Catliciousland

2011-09-22T16:07:00.001+09:30

I think Margaret has a few things absolutely nailed, Here...

2011-09-22T15:58:00.002+09:30

Snootchy Bootches!

well another week of flu has me burned out on Kevin Smith movies, enjoyed the rewatch for the most part, but really think that Jay and Silent Bob Strike Back is my fave of the ones I chose to watch (I don't count Jersey Girl coz it's rubbish!) .. because it doesn't really try to tell me anything, it's just a stupid fun romp.

Very little else happening, no riding walking or playing guitar... not enough concentration to read much, but lots of mindless tv and facebooking. I know, that's sad!!

heeeeeeeeeeeeeeeeeelllllllllppppppppppp meeeeeeeeeeeeeee!!!

:-)

Moving on from comp sys engineering and back to networking, really looking forward to this. Will be good also to be back in the old halls and hopefully, the coffee is still good there :-) Pity most of my old mates have moved on but there is one from the recent place there, and always room in my life for new cool people!! yay! :-)

I particularly love meeting people who inspire me and that I can respect, deep people who are unconcerned with the superficialities of life beyond that with which we are forced in some measure to comply in order to function within a city society. Outside of that, let the mind be free!

more to come? I hope so!!

wiigiiciaolicious!!!

2010-11-08T13:46:00.002+10:30

I promise to getting around to updatind my sidebar... very slack of me!!!

also, Cat's Computers... coming soon!! :)

2010-11-08T13:23:00.003+10:30

Sunday week ago... Elder park, 9am

after missing my ride buddies... (twice! oops) had some contemplative time on the River Torrens, and rode home via the River Torrens Linear park... nice :)

2010-10-05T13:42:00.003+10:30

Ok, so it's been a long time since I rock n rolled...
Doesn't mean I don't still rock out from time to time.
Not that I have been lately, rocking out that is, more drifting along, between occasional epiphanies and disillusionment... hoping for more of the former, less of the latter.

I need a hero...
Having experienced rather a lot of the less than stellar side of human nature during the non-delights of a workcover case... my natural idealism took a very large and almost fatal hit... my benevolence worn thin... I have struggled to find anyone to admire or be inspired by...

Then I met Joe ****** (haven't asked if I can blog him so asterisks will suffice for a surname).

Just the once, had a conversation in which the fire in my belly was lit again, albeit briefly. He told me what a priviledge it is to do the work he does, and support brave people working hard for everyone else, looking after the interests of those who look after the interests of all of us.
Well done :)

Tireless workers for the environment like my dear friend Margaret and her site: Re-earthing the Cities never cease to inspire me, but, I have become jaded after fighting and losing so much it would seem on the one hand. On the other, when I have the presence of mind to recollect, I have gained much more, and am abundant endlessly anyway.
The illusion of materialism drives our weakest darkest desires.

hmm that sounded a bit too philosophical for me today! Nevertheless, I'm back, I'm blogging, and I expect to become coherent sooner rather than later!!

Rock On!
Ride On!

Be happy!!!!!!!!!!!!!!!!!!!!

2010-07-03T18:04:00.003+09:30

hello :D

not a huge amount happening, the same amount of revelatory experience and time wasting :D

spending way too much time on the book of face these days but enjoyed reading back through some old posts here, lacking the inspiration to write a great deal, but I may type up some entries from my paper diary for posterity soon...

meanwhile, hooked on DANGER DANGER! High Voltage! from the Electric Six a the moment!!

Soooooooooooooo catchy :D

2010-06-01T19:38:00.000+09:30

greets peeps :D

have just added my bloggie pie to "blogthishere"
do check them out and let me know what you think.

Stay tuned for eventual resumption of regular posting thingies :D

2010-04-13T08:53:00.002+09:30

The doors of my life are beginning to creak open
and fresh breezes blow in
Adrift on a wide wide ocean
adrift no more
I am a sailor, and sail I shall
to new and undiscovered facets of what I thought I knew
I realise now, I know much less than I thought
and needing to "know", was my prison
I am reborn in an old body
that is new from not being known or appreciated fully
Will I ever know it fully?
Or can I embrace my mystery,
my strength and vulnerability
I can, I shall and I am.
I want to ponder and write of the magic within...

2009-01-01T13:51:00.002+10:30

Redundant Warning Labels:

I know I know, you've seen them all before, but this one gave me a good kak when I was cleaning out the stuff at the back of the pantry that will never get eaten....

good thing too!

Click to read the fine print - it's a packet of NUTS People!!!!

2008-11-18T19:31:00.001+10:30

Do flu shots really work? Ask the vaccine manufacturer:

2008-11-17T19:58:00.001+10:30

Damn this is catchy...

Empire of the sun, Walking on a Dream

2008-11-15T21:34:00.001+10:30

Someone who is definitely NOT ME is impersonating me on twitter.com.

Cease and desiste immediately! twitter have been contacted regarding this identity theft!!!

2008-10-10T16:08:00.000+10:30

2008-10-01T14:46:00.003+09:30

I never knew Adelaide was so full of youtubing plane spotters!

I was googling around, being an amateur plane spotter myself, to find the next arrival of the Qantas A380 training flight so we could try out the tripod for pics.. and found this (and way too many others):

I also found this lovely dedication of the first Spirit of Australia Qantas A380 to
Nancy Bird Walton

2008-09-30T16:55:00.004+09:30

The most Fantabulous

Stephen K. Amos starts his shows here in Adelaide at the Arts Theatre tomorrow.. I got my tix.. how about you? See you there....
Book Now

or if the stupid link doesn't work, go to Venuetix direct

2008-09-27T16:33:00.003+09:30

In case you don't believe me that it was packed to the rafters with Anoraks...

here's a small selection of geeks on a hill....

we were quite a distance away, thankyou zoom lens, and had trouble finding a spot to park, and a couple of minutes after we arrived, there was simply no more room for cars on any perimeter road there... plus, we didn't know the quarry road was open :-(

2008-09-27T15:41:00.003+09:30

Welcome to Blogging Ree of Flowers are Me! photography fame :-)

2008-09-27T13:35:00.005+09:30

Anorak Alert!!!

We went to Adelaide Airport today for the landing and take-off of the new Qantas Airbus A380

it was geeklicious!!!

PS: It was completely packed out - good to know I live in a city of complete nerds!!!!

you know the drill - if you click on the little piccies, big ones appear!! Yay!! :-)

2008-09-26T11:04:00.002+09:30

Have tix for Heath Franklin's Chopper: "Harden the Fuck up Australia" tour in Nov,

and Stephen K Amos in a couple of weeks!!!!

BooYAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAA!!! :-)

2008-09-26T11:02:00.002+09:30

Because I can...

flippin like a pancake, poppin like a cork,
Fleagle, Bingo, Drooper and Snork...

2008-09-20T19:27:00.003+09:30

Because I think the word needs to be spread, here is an unauthorised excerpt to whet your appetite that has been condensed from here:
SUGGESTIONS FOR AN APPROACH TO THE MANAGEMENT OF THYROID DEFICIENCY (full text with references)

SUGGESTIONS FOR AN

APPROACH TO THE

MANAGEMENT OF THYROID

DEFICIENCY

by Dr Barry J Durrant-Peatfield

M.B., B.S., LR.C.P., M.RCS.

Approved Civil Aviation Medical Examiner

The clinical syndrome of thyroid deficiency is very much more common than is generally realized; Barnes, in several publications, drew attention to this in the last two decades, as has the present writer more recently. One reason for this, is a tendency to think of hypothyroidism and myxoedema as one of the same thing, when this is quite wrong. Myxoedema, as doctors were taught in medical school, is the end result of a progressive disease process resulting in more or less total absence of thyroid hormone; whose symptoms and signs are no doubt perfectly familiar. But this state of deficiency has to start somewhere, winding down over a variable period to the terminal state of myxoedema. Symptoms and signs will naturally vary according to the extent of the level of deficiency reached. Clearly, a 10% loss may have little to show for it; whereas a 25% loss may have several very definite symptoms and signs; and a 40% loss even more so. Furthermore, patients show very individual response to any given level of dysfunction; while one may complain of excessive fatigue and weight gain, another may be more troubled by depression and menstrual problems.

That the diagnosis is all too frequently missed, is an inevitable result of this fundamental misunderstanding, and is commonly the result of an incomplete clinical appraisal in favor of the standard thyroid function tests. These tests are the real problem in diagnostic failure since there are inherent problems in interpreting blood levels of thyroxine and/or thyroid stimulating hormone (TSH) when blood levels may differ widely from tissue blood levels. Since the diagnosis may very properly, and easily, be made clinically, unreliable blood levels should NOT take precedence over clinical judgment.

Equally unsatisfactory is the acceptance by doctors and patients alike of poor response to thyroid replacement.

The present writer has been constantly alarmed and dismayed by hypothyroid patients who for years, all too often, have been obliged to accept a much less than satisfactory amelioration of their illness, being taught to expect no more than some improvement. It is perfectly possible that complete and long lasting remission should be obtained, and neither doctor nor patient should accept anything less. Further, the response should be monitored, not just by the doctor, but by the patients themselves. Since there often is a dynamic situation, the patients should be educated and taught to monitor themselves, making their own adjustments to dosage. In this connection, frequent monitoring by blood tests may be quite misleading and unhelpful. Surely it must be more satisfactory for the physician to ask the patients how they feel; and guide the informed patient in establishing the right dosage levels of replacement therapy.

One of the most taxing problems in diagnosis is the multiplicity of symptoms, which need not be rehearsed here. It is all too easy to pigeonhole the polysymptomatic patient as one of the heart sink variety, and much too often, for example, inappropriately prescribe anti-depressants. Thyroid deficiency may cause all sorts of major and minor symptoms and their very frequency should raise an index of suspicion for thyroid deficiency. The simple Basal Temperature Test, (see below), wrongly derided by many authorities, can provide valuable clinical backup. Finally, there is nothing wrong with a thoughtfully planned trial of treatment with an informed and cooperative patient.

2008-09-09T16:22:00.001+09:30

Definitely worth a read...

2008-08-24T18:11:00.001+09:30

A note from Cleo:
"As if you're ever going to catch me behaving like that shameless tabby... now keep the snacks coming!"

2008-08-10T14:16:00.001+09:30

I thought I was going to die from the cuteness... So I just had to share~!!! :-)

Funky Feline

2008-08-07T16:42:00.001+09:30

Stephanie from Real Thyroid Choices has created an Iodine pathway for us all.. Enjoy (and learn!) :-)

2008-08-05T14:57:00.001+09:30

2008-08-04T12:20:00.001+09:30

Gardasil - don't do it - need I say more? oh other than how did this idiot get the Nobel prize for this poison?

2008-07-31T14:12:00.001+09:30

Yeah Right... Monsanto told us it was safe to drink Roundup...

I don't think so

2008-07-31T13:45:00.004+09:30

I DETEST Monsanto!!!!!!!!!!!!!!!!!!!!!!!!

ever since my horticultural days when the Monsanto propaganda boasted that they had the only weed killer tested on live humans, the human test subjects apparently drank it no less, and the highest LD50 rating around (the dose needed to kill 50/100 laboratory rats), not once did they mention "Long term effects", simply touted their garbage as the safest POISON around, despite no information available to us at the time about topical absorption or inhalation of spray vapour, as these are the most common contacts in horticulture for Monsanto products, not oral ingestion.
Now they want to GM crops purely and simply so they can PATENT the modified gene pattern, and MAKE MONEY, this has nothing to do with feeding the world population, did you know that once a seed has been patented (this includes many cultivars actually in horticulture) that it is then illegal to propagate from any plant you have purchased previously whether by tissue culture or by seed collection? you MUST buy new seed from the owner of the patent rights, that's it people, this is all about making one small section of the world richer and the entire rest of the population poorer, and I am sick to death of it.

Read what Elaine Moore has to say about it

Monsanto seeds designed to die

Monsanto pushes farmers to go GM

Film - Monsanto's deadly sins

Monsanto acknowledges glyphosate resistance and pushes "management"

Millions AGAINST Monsanto (Yay!)

Monsanto, worlds most unethical and harmful investment

Monsanto loses law suit over GM canola contaminating GM free fields

Monsanto vs Farmers

and possibly the best for last:

monsantosucks.com

2008-07-20T17:01:00.007+09:30

Congratulations to Ree for getting her photography site up and running:
flowersareme.com check it out and drop her a line
info@flowersareme.com

2008-05-22T13:17:00.001+09:30

Fluoride Damages the Thyroid, report shows

Fluoride Damages the Thyroid, report shows
First-ever government review of fluoride/thyroid toxicology shows risk .

Print article
Refer to a friend
2008-05-19 15:54:10 - There is clear evidence that small amounts of fluoride, at or near levels added to U.S. water supplies,
present potential risks to the thyroid gland, according to the National Research Council's (NRC) first-ever published review of the fluoride/thyroid literature.(A)

Fluoride, in the form of silicofluorides, injected into 2/3 of U.S. public water supplies, ostensibly to reduce tooth decay, was never safety-tested.(B)

"Many Americans are exposed to fluoride in the ranges associated with thyroid effects, especially for people with iodine deficiency," says Kathleen Thiessen, PhD, co-author of the government-sponsored NRC report. "The recent decline in iodine intake in the U.S could
contribute to increased toxicity of fluoride for some individuals," says Thiessen.

"A low level of thyroid hormone can increase the risk of cardiac disease, high cholesterol, depression and, in pregnant woman, decreased intelligence of offspring," said Thiessen.(C)

Common thyroid symptoms include fatigue, weight gain, constipation, fuzzy thinking, low blood pressure, fluid retention, depression, body pain, slow reflexes, and more. It's estimated that 59 million
Americans have thyroid conditions.(D)

Robert Carton, PhD, an environmental scientist who worked for over 30 years for the U.S. government including managing risk assessments on high priority toxic chemicals, says "fluoride has detrimental effects on the thyroid gland of healthy males at 3.5 mg a day. With iodine deficiency, the effect level drops to 0.7 milligrams/day for an average male."(E) (1.0 mg/L fluoride is in most water supplies)

Among many others, the NRC Report cites human studies which show

- fluoride concentrations in thyroids exceeding that found in other soft tissues except kidney

- an association between endemic goiter and fluoride exposure or enamel fluorosis in human populations

- fluoride adversely affects thyroid and parathyroid hormones, which affect bone health

"If you have a thyroid problem, avoiding fluoride may be a good preventive health measure for you," writes Drs' Richard and Karilee Shames in "Thyroid Power."(F).

Over, 1,700 Physicians, Dentists, Scientists, Academics and Environmentalists urge Congress to stop water fluoridation until Congressional hearings are conducted. They cite new scientific evidence that fluoridation is ineffective and has serious health risks. (http://www.fluorideaction.org/statement.august.2007.html)

Please sign the petition and Congressional letter to support these
professionals http://www.FluorideAction.Net

References:

(A) "Fluoride in Drinking Water: A Scientific Review of EPA's
Standards," Committee on Fluoride in Drinking Water, Board on
Environmental Studies and Toxicology, Division on Earth and Life
Studies, National Research Council of the National Academies of
Science. March 2006 Chapter 8
http://www.nap.edu/catalog.php?record_id=11571

"Thyroid Function: Fluoride exposure in humans is associated with
elevated TSH concentrations, increased goiter prevalence, and altered
T4 and T3 concentrations." (Page 262)

"(The thyroid effects are associated with average fluoride intakes
that) will be reached by persons with average exposures at fluoride
concentrations of 1-4 mg/L in drinking water, especially the
children." (Page 260)

(B) Sodium Hexafluorosilicate and Fluorosilicic Acid
Review of Toxicological Literature, October 2001
http://ntp.niehs.nih.gov/ntp/htdocs/Chem_Background/ExSumPDF/Fluorosilicates.pdf

(C) Chemical & Engineering News, "Fluoride Risks Are Still A
Challenge," by Bette Hileman, September 4, 2006,
http://pubs.acs.org/cen/government/84/8436gov1.html

(D) Mary Shomon, About.com Thyroid editor, Patient Advocate --
Author of "The Thyroid Diet" and "Living Well With Hypothyroidism"
http://thyroid.about.com/

(E) Fluoride, "Review of the 2006 National Research Council Report:
Fluoride in Drinking Water," July-September 2006, by Robert J. Carton
http://www.fluorideresearch.org/393/files/FJ2006_v39_n3_p163-172.pdf

(F) Thyroid Power and Feeling Fat Fuzzy or Frazzeled"by Richard
Shames MD & Karilee Shames RN, PhD http://www.thyroidpower.com
http://www.feelingfff.com/

Fluoride/Thyroid Health Effects
http://www.fluoridealert.org/health/thyroid/

Sources of Fluoride
http://www.fluoridealert.org/f-sources.htm

Sulfuryl Fluoride Pesticide Residues Allowed on Foods
http://www.fluoridealert.org/pesticides/sulfuryl.f.all.food.html
United States Department of Agriculture (USDA) National Fluoride
Database of Selected Beverages and Foods
http://www.nal.usda.gov/fnic/foodcomp/Data/Fluoride/Fluoride.html

2008-05-07T13:39:00.002+09:30

Read My blog While at work...

While I'm no fan of cheating or lying, or nicking stuff, I had include this because I think it is very clever, heard of it many times but was surprised to find my bloggie here: Catlicious via Workfriendly

enjoy and don't get caught!!

2008-05-05T15:36:00.005+09:30

You've read it right here, T3 and T4 auto antibodies cause spuriously high free T3 serum levels and continuing hypothyoid symptoms when patients are treated to lab reference ranges instead of to cessation of symptoms, Now read on regarding the genetic resistance to thyroid hormone that does exactly the same thing.
Yes, this is why some people need to take much more than the reccommended dosage of thyroid hormone.

http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=296951
Furthermore, the dominant negative inhibition elicited by the P448H receptor mutant at higher T3 concentrations was reversed in the presence of high doses of T3

Dr Lowe in France

(1) is euthyroid before beginning the use of T3, according to thyroid function test results, including a TRH stimulation test;
(2) markedly improves or completely recovers from hypothyroid-like FMS symptoms and signs with supraphysiologic dosages of T3;
(3) after beginning T3 therapy has an extremely high free T3 blood level;
(4) has no evidence of tissue thyrotoxicosis due to the high free T3 level, according to the results of serial ECGs, serum and urine biochemical tests, and bone densitometry.

Most of our euthyroid patients who improve or recover with metabolic rehabilitation involving T3 therapy meet these four criteria. Clearly, this set of findings in many treated euthyroid FMS patients shows that they meet Refetoff's definition of thyroid hormone resistance: "reduced responsiveness of target tissues to concentrations of thyroid hormone that under normal conditions would be excessive" (23).

http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6T3G-3YDGFYR-D&_user=10&_coverDate=01%2F25%2F2000&_rdoc=1&_fmt=high&_orig=browse&_cdi=4946&_sort=d&_docanchor=&view=c&_ct=1&_refLink=Y&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=0d9bd777c0288fd48c19d5e77c212a5f

Abstract
Thyroid hormone receptors (T3Rs) both repress and activate gene transcription by interacting with auxiliary factors denoted corepressors and coactivators. Resistance to thyroid hormone (RTH) syndrome in humans is manifested as a failure to respond properly to elevated circulating thyroid hormone. RTH syndrome has been mapped to T3Râ mutations that alter the transcriptional properties of the receptor, resulting in a dominant negative phenotype. We report here a characterization of a series of RTH mutant T3Rs that exhibit unusual interactions with corepressor. Two mutations in receptor helix 11 (Ä430, Ä432) greatly enhance the ability of the mutant receptors to bind to corepressor. A distinct mutation, V264D, in an 'omega loop' region of the receptor, impairs corepressor release but does not fully eliminate the ability to recruit coactivator. These mutations reveal novel determinants that regulate the interaction of the T3R with important ancillary cofactors, and that are disrupted in a human endocrine disease.

http://books.google.com.au/books?id=B9z1W9JNA64C&pg=PA119&lpg=PA119&dq=thyroid+cellular+resistance&source=web&ots=bqImsvUHpn&sig=cWw4WXZBds8OSIgHBRYgEU92kTs&hl=en#PPA121,M1

Dr Gina Honeyman.com
"What lab tests do you want to see to know if I'm on the right thyroid'hormone dosage? My doctor says that lab tests, particularly my TSH, are'the only way to know if I need to change my thyroid medication." –Bob.

While the standard thyroid lab tests including TSH, free T4, free T3, and thyroid antibody group are necessary for your initial evaluation, I do not recheck them to see if you're on the correct dosage. However, if either the thyroid peroxidase antibodies or thyroglobulin antibodies have been elevated I certainly will recheck them to be sure they are being suppressed by your thyroid hormone therapy. The usual system of diagnosis and adjusting thyroid medication dosages
keeps so many people undiagnosed and under-treated that I consider it a threat to public health. I've participated in research projects that have proven that the TSH, free T3 and free T4 do not correlate with patients' metabolic rates. These articles that I coauthored about these studies can be found online at no cost so please feel free to copy them and share them with your prescribing physicians. You can find the studies at these links:
Medical Science Monitor
Thyroid Science online journal
Your prescribing doctor may insist on checking the lab tests since that is the standard of care to which they are held. I'm always glad to discuss this research and my metabolic rehab protocol with your other physicians. The best way to know if you're on the optimal dosage of thyroid hormone is to monitor your responses according to the metabolic rehab protocol and recheck your resting metabolic rate at intervals. Be sure to use my "Are you overstimulated?" form to watch for signs or symptoms of excessive dosing with your thyroid hormone. Please share these forms with your prescribing doctor to let him or her know that
you are carefully watching for this possibility. Some doctors have asked for permission to use my copyrighted form with all of their patients on thyroid medications and I'm always pleased to share this with others.

"I started metabolic rehab because of the same symptoms as a friend of mine, but she's on a much higher dose of Cytomel than I am, and she's not getting well as fast as I am. Do you think she's doing something wrong?" –Maureen R.

There is no way to predict how one person will respond to metabolic rehab compared to another. We all have individual responses and there's no magic in a particular dosage of Cytomel or other thyroid hormone medications. Your friend most likely has a greater degree of cellular resistance to thyroid hormone, meaning that she may have a greater number of thyroid hormone receptors that are not working properly. I can speculate about the reasons this can happen, but the greater value is in your friend continuing to persist with her treatment. She needs to be sure she is using all parts of the protocol. Sometimes people
decline to take nutritional supplements, for example, and this compromises their treatment outcome. She may have other health issues to address at the same time she is dealing with her hypometabolism.

http://www.medscimonit.com/fulltxt.php?ICID=452199

http://www.thyroidscience.com/Criticism/lowe.dec.2006/lowe.critique.T4.T4&T3.Studies.pdf

I looked up the endocrinologist that Dr Lowe referred to and thought this line was important re; treating t3 resistance (TH = thyroid
hormone)

The optimal dose of TH is variable among individuals, and doses of L-T4 as high as 1,000 µg per day may be necessary to achieve the desired effects.
http://jcem.endojournals.org/cgi/content/full/84/2/401

http://www.ncbi.nlm.nih.gov/pubmed/17574009?ordinalpos=4&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

Syndromes of reduced sensitivity to thyroid hormone: genetic defects in hormone receptors, cell transporters and deiodination.Refetoff S, Dumitrescu AM.
Department of Medicine, University of Chicago, Chicago, IL 60637, USA. refetoff@uchicago.edu

At least six major steps are required for secreted thyroid hormone (TH) to exert its action on target tissues. Mutations interfering with three of these steps have been so far identified. The first recognized defect, which causes resistance to TH, involves the TH receptor beta gene and has been given the acronym RTH. Occurring in approximately 1 per 40,000 newborns, more than 1000 affected subjects, from 339 families, have been identified. The gene defect remains unknown in 15% of subjects with RTH. Two novel syndromes causing reduced sensitivity to TH were recently identified. One, producing severe psychomotor defects in > 100 males from 26 families, is caused by mutations in the cell-membrane transporter of TH, MCT8; the second, affecting the intracellular metabolism of TH in four individuals from two families, is caused by mutations in the SECISBP2 gene, which is required for the synthesis of selenoproteins, including TH deiodinases.

http://www.ncbi.nlm.nih.gov/pubmed/1580595?ordinalpos=5&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

Thyroid hormone resistance.Weiss RE, Refetoff S.
Department of Medicine, University of Chicago, Illinois 60637.

Generalized resistance to thyroid hormone (GRTH) encompasses a heterogeneous group of conditions characterized by reduced responses of target tissues to thyroid hormone due to defects at the site of hormone action. In the majority of patients, GRTH is inherited as a dominant trait associated with mutations in the hormone-binding domain of the thyroid hormone receptor. GRTH serves as a prototype of other resistance syndromes for hormones that act via nuclear receptors.

http://www.ncbi.nlm.nih.gov/pubmed/10487671?ordinalpos=6&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

The thyroid hormone receptor-beta gene mutation R383H is associated with isolated central resistance to thyroid hormone.Safer JD, O'Connor MG, Colan SD, Srinivasan S, Tollin SR, Wondisford FE.
Thyroid Unit, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts 02215, USA. Jsafer@bu.edu

Resistance to thyroid hormone (RTH) action is due to mutations in the beta-isoform of the thyroid hormone receptor (TR-beta). RTH patients display inappropriate central secretion of TRH from the hypothalamus and of TSH from the anterior pituitary despite elevated levels of thyroid hormone (T4 and T3). RTH mutations cluster in three hot spots in the C-terminal portion of the TR-beta. Most individuals with TR-beta mutations have generalized resistance to thyroid hormone, where most tissues in the body are hyporesponsive to thyroid hormone. The affected individuals are clinically euthyroid or even hypothyroid depending on the severity of the mutation. Whether TR-beta mutations cause a selective form of RTH that only leads to central thyroid hormone resistance is debated. Here, we describe an individual with striking peripheral sensitivity to graded T3 administration. The subject was enrolled in a protocol in which she received three escalating T3 doses over a 13-day period. Indexes of central and peripheral thyroid hormone action were measured at baseline and at each T3 dose. Although the patient's resting pulse rose only 11% in response to T3, her serum ferritin, alanine aminotransferase, aspartate transaminase, and lactate dehydrogenase rose 320%, 117%, 121%, and 30%, respectively. In addition, her serum cholesterol, creatinine phosphokinase, and deep tendon reflex relaxation time fell (25%, 36%, and 36%, respectively). Centrally, the patient was sufficiently resistant to T3 that her serum TSH was not suppressed with 200 microg T3, orally, daily for 4 days. The patient's C-terminal TR exons were sequenced revealing the mutation R383H in a region not otherwise known to harbor TR-beta mutations. Our clinical evaluation presented here represents the most thorough documentation to date of the central thyroid hormone resistance phenotype in an individual with an identified TR-beta mutation.

http://www.ncbi.nlm.nih.gov/pubmed/15815068?ordinalpos=7&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

Resistance to thyroid hormone in a Chinese family with R429Q mutation in the thyroid hormone receptor beta gene.Kong AP, Lam CW, Chan AO, Yiu SF, Tiu SC.
Department of Medicine, Queen Elizabeth Hospital, 30 Gascoigne Road, Hong Kong.

The combination of elevated serum levels of free thyroid hormones with non-suppressed thyroid-stimulating hormone suggests the differential diagnoses of resistance to thyroid hormone or thyroid-stimulating hormone-secreting pituitary tumour. Clinical differentiation of these two conditions can be difficult, because patients with thyroid hormone resistance may exhibit various combinations of hypermetabolic and hypometabolic features, and laboratory results have limited sensitivity and specificity. We report a case of resistance to thyroid hormone in a Chinese family that illustrates this difficulty. The diagnosis could only be confirmed by the identification of a known disease-causing mutation in the thyroid hormone receptor beta gene in peripheral leukocytes. Availability of genetic tests will identify more cases in the future and improve our understanding of this condition.

http://www.ncbi.nlm.nih.gov/pubmed/12946875?ordinalpos=8&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

Molecular basis of resistance to thyroid hormone.Yen PM.
Molecular Regulation and Neuroendocrinology Section, Clinical Endocrinology Branch, NIDDK/NIH, Bethesda, MD 20892, USA. pauly@intra.niddk.nih.gov

Resistance to thyroid hormone (RTH) is a syndrome in which patients have raised serum thyroid hormone (TH) levels and raised or inappropriately normal thyrotropin (TSH) levels. In general, patients exhibit TH resistance in the pituitary and peripheral tissues. Novel techniques and genetically engineered mouse model systems have increased our understanding of thyroid hormone receptor (TR) action, and shed new light on the underlying molecular mechanisms for RTH. In particular, we are learning how mutant TRs from RTH patients can block wild-type TR function, with consequent effects in various tissues and cells. This dominant-negative activity has important implications for other hormone-resistant conditions and in hormone-sensitive tumors. This article examines the molecular basis of RTH.

http://www.ncbi.nlm.nih.gov/pubmed/9350446?ordinalpos=9&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

Resistance to thyroid hormone.Chatterjee VK.
Department of Medicine, University of Cambridge, Addenbrooke's Hospital, UK. kkc1@mole.bio.cam.ac.uk

Resistance to thyroid hormone (RTH) is usually dominantly inherited and is characterized by elevated free thyroid hormones in the serum and failure to suppress pituitary thyroid stimulating hormone (TSH) secretion with variable refractoriness to hormone action in peripheral tissues. Two major forms of the disorder are recognized: asymptomatic individuals with generalized resistance (GRTH) and patients with thyrotoxic features, suggesting predominant pituitary resistance (PRTH). Molecular genetic analyses indicate that both GRTH and PRTH are associated with diverse mutations in the thyroid hormone receptor beta gene, which localize to three regions in the hormone binding domain of the receptor. In addition to being functionally impaired, the mutant receptors are also able to inhibit their wild-type counterparts in a dominant negative manner. Recognized features of RTH include failure to thrive, growth retardation and attention-deficit hyperactivity disorder in childhood, and goitre and thyrotoxic cardiac symptoms in adults. The pathogenesis of variable tissue resistance is not fully understood but may be related to the differing tissue distributions of a and b thyroid hormone receptors and variable dominant negative activity of mutant receptors on different target genes.

http://www.ncbi.nlm.nih.gov/pubmed/15611821?ordinalpos=12&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

[Thyroid hormone resistance syndrome][Article in Portuguese]

Carvalho GA, Ramos HE.
Serviço de Endocrinologia e Metabologia, Universidade Federal do Paraná, Curitiba, PR. carvalho@mais.sul.com.br

Resistance to thyroid hormone (RTH) is a syndrome characterized by elevated serum thyroid hormone (TH) levels and elevated or inappropriately normal thyrotropin levels. In general, patients exhibit TH resistance in the pituitary and peripheral tissues. The phenotype of RTH is variable; the affected individuals are clinically euthyroid or even hypothyroid depending on the severity of the mutation, the variable hyposensitivity to TH among individuals as well as in different tissues. In almost all cases the genetic basis of RTH lies in mutation of the carboxyl-terminus of the ss-thyroid hormone receptor. RTH is a dominant disorder, except in one family; most individuals are heterozygous for the mutant allele. New standard techniques and genetically engineered mouse model systems have increased our understanding on TH receptor action, in particular, how mutant thyroid receptors from RTH patients can block wild-type thyroid receptor function (dominant negative activity), and how the mutant receptors can differently affect various tissues and individuals.

http://www.ncbi.nlm.nih.gov/pubmed/8594618?ordinalpos=14&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

Syndrome of resistance to thyroid hormone: insights into thyroid hormone action.Kopp P, Kitajima K, Jameson JL.
Division of Endocrinology, Metabolism, and Molecular Medicine, Northwestern University Medical School, Chicago, Illinois 60611, USA.

Thyroid hormones (T3, T4) exert multiple cellular effects through nuclear thyroid hormone receptors (TR alpha, TR beta). Thyroid hormone receptors are transcription factors that act by altering patterns of gene expression. Resistance to thyroid hormone (RTH) is a rare disorder caused by mutations in the TR beta gene. Biochemically, the syndrome is defined by elevated circulating levels of free thyroid hormones due to reduced target tissue responsiveness and normal, or elevated, levels of thyroid-stimulating hormone (TSH). This "inappropriate" TSH elevation contrasts with the situation in hyperthyroidism, where the pituitary secretion of TSH is suppressed. Patients with RTH usually present with goiter and an euthyroid or mildly hypothyroid metabolic state. Thus, pituitary resistance results in hypersecretion of TSH, which compensates, at least in part, for hormone resistance in peripheral tissues. Despite this compensation, clinical effects of RTH can include short stature, delayed bone maturation, hyperactivity, learning disabilities, and hearing defects, as well as variable features of hyper- and hypothyroidism. With the exception of a single sibship, which harbored a deletion of the entire coding sequence of the TR beta gene and a recessive pattern of inheritance, all other cases of RTH have been inherited in an autosomal dominant manner or have been de novo heterozygous mutations of the TR beta gene. The dominant pattern of inheritance is explained by the functional properties of the mutant receptors which act in a dominant negative manner to block the activity of normal TR alpha and TR beta receptors. Now that a large number of different RTH mutations have been identified, it is striking that the mutations are clustered within restricted domains in the carboxyterminal region of the receptor. Mutations in these regions have been shown to preserve critical receptor functions such as dimerization and DNA binding, while inactivating other activites such as T3 binding and transcriptional activation. The examination of patients with RTH and their mutated receptors has provided important insights into the mechanisms of thyroid hormone action, the structure-function relationship of the receptors, and the molecular mechanisms of dominant negative activity.

http://www.ncbi.nlm.nih.gov/pubmed/7998483?ordinalpos=15&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

Resistance to thyroid hormone--an uncommon cause of thyroxine excess and inappropriate TSH secretion.Chatterjee VK.
Department of Medicine, University of Cambridge, Addenbrooke's Hospital, United Kingdom.

Resistance to thyroid hormone (RTH) is an uncommon inherited cause of hyperthyroxinemia with inappropriate TSH secretion. The syndromes are characterized by reduced target tissue responsiveness to circulating free thyroid hormones. The differential diagnosis to other diseases with similar laboratory results (high T4 with normal TSH) like familial dysalbuminemia or antibodies against iodothyronines or TSH is now possible with the appropriate use of new assays for free thyroid hormones. In the presence of thyrotoxic symptoms it may be difficult to differentiate the syndrome from a TSH-secreting pituitary tumour. Familial occurrence and a normal TSH-response to TRH that can not be suppressed by T3 are characteristic features of RTH, that may be helpful in that respect. The majority of RTH cases are dominantly inherited and have highly variable clinical signs and symptoms. There are, however, mainly two forms of the syndrome that have been shown to overlap clinically and biochemically, namely a generalised resistance (GRTH) and a more "selective" pituitary resistance to thyroid hormones (PRTH). The absence of thyrotoxic symptoms rather suggests GRTH, whereas thyrotoxic signs seem to be characteristic for PRTH. Following the cloning of thyroid hormone receptors, familial GRTH was shown to be tightly linked to the TR-(Thyroid hormone receptor)-beta gene locus. Molecular genetic studies have shown that even within a single kindred the same receptor mutation was associated with both, GRTH or PRTH, and therefore suggest that these two forms represent part of a variable clinical spectrum of a single genetic disorder.

http://www.ncbi.nlm.nih.gov/pubmed/8954015?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus

Dominant inheritance of resistance to thyroid hormone not linked to defects in the thyroid hormone receptor alpha or beta genes may be due to a defective cofactor.Weiss RE, Hayashi Y, Nagaya T, Petty KJ, Murata Y, Tunca H, Seo H, Refetoff S.
Department of Medicine, University of Chicago, Illinois 60637, USA. rweiss@medicine.bsd.uchicago.edu

Resistance to thyroid hormone (RTH) is an inherited syndrome of reduced tissue responsiveness to thyroid hormone. To date, all individuals expressing the RTH phenotype have been found to harbor mutations in the thyroid hormone receptor beta (TR beta) gene that impair T3-mediated function. We describe a unique family in which the dominantly inherited RTH is not associated with abnormalities in the TR beta or TR alpha genes, as determined by gene sequencing and linkage analysis. However, affected family members manifest a severe form of RTH, with reduced responses of thyrotrophs and peripheral tissues requiring 8- to 10-fold the normal replacement doses of L-T4 and L-T3. No other endocrine abnormalities were detected. The defect developed de novo in the proposita and was transmitted to her two children of unrelated fathers. As cultured fibroblasts from the proposita responded poorly to T3 despite a normal concentration of TR, other abnormalities in the mediation of T3 action were sought. Nucleotide sequences of the TSH beta promoter, containing thyroid hormone response elements, and TR-interacting protein 1 were normal. Nuclear extracts (NE) of cultured skin fibroblasts from affected individuals of this family were tested for their interaction with normal TR beta and thyroid hormone response elements by the electrophoretic mobility shift assay. NE from the proposita showed a strong additional band compared to NEs from normal individuals and patients with RTH caused by TR beta mutations or deletion. Far Western analysis of NE from the affected daughter hybridized with labeled TR beta demonstrated an additional band that was not seen in NEs from a normal control or patients with TR beta gene defects. It is concluded that the etiology of RTH is not confined to abnormalities in the TR beta gene. An abnormal cofactor with a specific function in the regulation of thyroid hormone action is probably involved in the expression of the RTH phenotype in this family.

http://www.ncbi.nlm.nih.gov/pubmed/15860414?ordinalpos=18&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

Thyroid hormone receptor mutations and disease: beyond thyroid hormone resistance.Cheng SY.
Laboratory of Molecular Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892-4264, USA. sycheng@helix.nih.gov

Thyroid hormone receptors (TRs) are ligand-dependent transcription factors that mediate the biological activities of thyroid hormone (T3). Two THR genes (A and B), located on different chromosomes, yield four T3-binding isoforms with highly conserved sequences in the DNA- and ligand-binding domains. Mutations of THRB cause a human genetic disease, thyroid hormone resistance syndrome (RTH). Comprehensive genomic profiling unveiled the contribution of novel change-of-function mutations of TRbeta to the pathogenesis of RTH. In addition, abnormalities associated with mutations of the THRA gene have been uncovered recently. The phenotypic manifestations of mutated THRB and THRA genes are distinct, indicating isoform-dependent actions of TR mutants in vivo. Therefore, mutant TRs provide a new paradigm to understand the molecular basis of receptor disease.

http://www.ncbi.nlm.nih.gov/pubmed/15543767?ordinalpos=19&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

[Familial generalized thyroid hormone resistance. Report of one case][Article in Spanish]

López JM, Jiménez M, Campino C.
Departamento de Endocrinología, Facultad de Medicina, Pontificia Universidad Católica de Chile. jmlopez@med.puc.cl

Thyroid hormone resistance is a rare autosomal dominant disease associated, in more than 90% of cases, to mutations in the beta thyroid hormone receptor. We report a 23 years old male that consulted for a psychiatric condition. Clinically, the patient was euthyroid in spite of high total and free T4 and T3 concentrations, while TSH remained normal. Also, TSH showed a five fold increase under TRH stimulation. The mother and one of his brothers had the same pattern of abnormal serum thyroid hormones. We discuss the diagnostic considerations and the protocol to study this rare pathology.

http://www.ncbi.nlm.nih.gov/pubmed/8954015?ordinalpos=20&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

Dominant inheritance of resistance to thyroid hormone not linked to defects in the thyroid hormone receptor alpha or beta genes may be due to a defective cofactor.Weiss RE, Hayashi Y, Nagaya T, Petty KJ, Murata Y, Tunca H, Seo H, Refetoff S.
Department of Medicine, University of Chicago, Illinois 60637, USA. rweiss@medicine.bsd.uchicago.edu

Resistance to thyroid hormone (RTH) is an inherited syndrome of reduced tissue responsiveness to thyroid hormone. To date, all individuals expressing the RTH phenotype have been found to harbor mutations in the thyroid hormone receptor beta (TR beta) gene that impair T3-mediated function. We describe a unique family in which the dominantly inherited RTH is not associated with abnormalities in the TR beta or TR alpha genes, as determined by gene sequencing and linkage analysis. However, affected family members manifest a severe form of RTH, with reduced responses of thyrotrophs and peripheral tissues requiring 8- to 10-fold the normal replacement doses of L-T4 and L-T3. No other endocrine abnormalities were detected. The defect developed de novo in the proposita and was transmitted to her two children of unrelated fathers. As cultured fibroblasts from the proposita responded poorly to T3 despite a normal concentration of TR, other abnormalities in the mediation of T3 action were sought. Nucleotide sequences of the TSH beta promoter, containing thyroid hormone response elements, and TR-interacting protein 1 were normal. Nuclear extracts (NE) of cultured skin fibroblasts from affected individuals of this family were tested for their interaction with normal TR beta and thyroid hormone response elements by the electrophoretic mobility shift assay. NE from the proposita showed a strong additional band compared to NEs from normal individuals and patients with RTH caused by TR beta mutations or deletion. Far Western analysis of NE from the affected daughter hybridized with labeled TR beta demonstrated an additional band that was not seen in NEs from a normal control or patients with TR beta gene defects. It is concluded that the etiology of RTH is not confined to abnormalities in the TR beta gene. An abnormal cofactor with a specific function in the regulation of thyroid hormone action is probably involved in the expression of the RTH phenotype in this family.

http://jcem.endojournals.org/cgi/reprint/86/11/5142?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&searchid=1&FIRSTINDEX=0&minscore=5000&resourcetype=HWCIT

http://jcem.endojournals.org/cgi/reprint/84/9/3099?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&searchid=1&FIRSTINDEX=0&minscore=5000&resourcetype=HWCIT

http://jcem.endojournals.org/cgi/content/full/84/2/401?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&searchid=1&FIRSTINDEX=0&minscore=5000&resourcetype=HWCIT

http://jcem.endojournals.org/cgi/reprint/84/11/3919?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&searchid=1&FIRSTINDEX=0&minscore=5000&resourcetype=HWCIT

http://jcem.endojournals.org/cgi/reprint/84/2/401

2008-04-21T10:33:00.002+09:30

It's finally here!

The most patient focussed useful tried and true (not lies created by drug companies) book on Thyroid information ever!

the Stop the Thyroid Madness book... I'll be buying a copy.. how about you?

2008-04-20T10:57:00.003+09:30

I've had my Care2 wildmail account for 8 years now, and though the site is going strong, it probably still needs more people to help change the world...

here are some things you can do:

Stop all animal testing in the UK and replace with viable alternatives

There are many petitions here that may be close to your heart, go on, sign them! The Petition Site

One click a day can make so much difference Click to Donate

This is where it all started, The Hunger Site, one of the first "home pages" i ever had on the net... and my favourite: The Animal Rescue Site

2008-04-20T08:57:00.003+09:30

Hysone 20mg back on the shelves..

According to the Alphapharm Website 20mg Hysone tablets should be back on the pharmacy shelves soon.

Apparently, this is a new "re-formulated" Hysone, so what has changed Alphapharm?

information from their site in italics below:

UPDATE APRIL 2008

HYSONETM (HYDROCORTISONE) 20mg TABLETS

RETURN TO USUAL SUPPLY

Alphapharm is pleased to inform consumers and health care professionals that a re-formulated HYSONE 20mg tablet is now available through usual supply channels.

This means that supply of this medicine can be obtained via the usual prescription and pharmacy dispensing process, without the need to seek supply through the Special Access Scheme (SAS).

Our wholesale partners have advised us that Hysone 20mg tablets will begin to be available through pharmacy by the end of this week (18th April 2008).

We ask you please to remain patient if your pharmacy takes a little longer to obtain supplies. Experience shows that a return to supply after an extended out of stock period can take a few weeks.

Alphapharm would like to thank our customers for their understanding and patience during the period when the company could not manufacture the tablets.

If you have difficulties in obtaining supplies, please contact the Alphapharm Sales Support team on 1800 274 276.

2008-04-20T08:52:00.002+09:30

My latest book purchase...

but I haven't had the time to start reading it yet :-(

End of America by Naomi Wolf

2008-04-01T12:14:00.002+10:30

Fiona O'Loughlin - Thyroid problems?

Get thee to Stop the Thyroid Madness immediately...

god help her if the medical establishment get hold of her thyroid with their crappy TSH testing and T4 only medications....
Oh and get your adrenals tested too girlfriend before you start anything...

PS Julia Morris - are you out there? You have a Goitre girlfriend, get thee into some Lugol's drops from a compounding pharmacy immediately, and follow up on Stop the Thyroid Madness too...

you'll be happy you did :-)

2008-02-27T13:45:00.003+10:30

I have been searching high and low for a dvd version of Marilyn Waring's "Sex Lies and Economics" or "who's counting?"

This documentary changed my life some 10 years ago, please spend one hour of your life, download the audio version of this in two parts and listen carefully.

Maybe this will change your life like it changed mine

2008-02-25T11:34:00.001+10:30

Wish I'd thought of it...

Valentine's message in our local rag...

2008-02-22T14:51:00.000+10:30

You are in my power...

2008-02-22T14:43:00.003+10:30

Cat's Life Tips 101

Assemble lasagne in the nude.

I find it useful to assemble lasagne in the nicky noo nah.

Yesterday I made my famous vego lasagne and while I don't actually cook the red sauce in the buff, who wants to be scalded by burning sauce rosa? I do find it helps with the cleaning up if assembling is done in the nakey, or at least topless.
Those red spots are so hard to get out otherwise!! The white sauce isn't an issue.
Here's one I prepared earlier:

2008-02-22T08:56:00.000+10:30

Never done this before, but, this post was so popular I'm repeating it...

Monday, February 11, 2008

Never treat hypoT on free T3 without taking symptoms into account

aka - never discount the T3 auto antibodies....

Ok we all know that using the TSH to dose thyroid meds is like trying to navigate a shopping mall using a soccer ball as a map - or maybe even less useful.

TSH only has a useful relationship to serum thyroid hormones when all systems are working properly, failing that, all bets are off.

As thyroid stimulating hormone is actually produced in the pituitary, and is released in response to the body perceiving a need for more thyroid hormone, a number of things can go wrong. The body may be in thyroid hormone conservation mode, this can happen after a number of years of being hypothyroid without treatment, or in the case of some, extreme dieting can bring it on, shock etc. The pituitary may not be unable to produce enough TSH to stimulate the thyroid gland, the body may not sense the lack and stimulate the pituitary to produce TSH, and you may have antibodies to the TSH itself, so the body attacks it's own hormone, and your thyroid doesn't get stimulated.

To get around this, most forward thinking people use the free t3 test to indicate how one should be replaced, correlating this to symptoms for "most" people has shown that with a freeT3 in the top 1/4 of the lab range, or just over, most hypothyroid people begin to feel well and regain some of the life they have lost to the illness.

But what if your free T3 is at the top of the range with no cessation of symptoms?

What if, like me, you can go for a week with no thyroid hormone supplement, and your symptoms worsen to the point of being bedridden, but your free T3 still shows on the top of range on a serum test while free T4 and TSH are both below range?

T3 has a half life of up to 10 hours, so after a week, it should be gone right?

Not neccesarily, what has been proven in case after case after case where an elevated T3 in the presence of hypothyroid symptoms has been evaluated, is the presence of antibodies to the T3 itself, which causes it to become bound in the serum, unavailable to the cells where it is needed for metabolism, causing high so called "free" T3 testing, and persistent hypothyroid symptoms.

Don't take my word for it, read the research, and DEMAND better treatment to the cessation of symptoms, rather than just to make some numbers on some paper look pretty.

http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&uid=3224724&cmd=showdetailview&indexed=google

[Triiodothyronine(T3) autoantibodies in a woman with nonthyroidal disorder: a study on preparation of serum IgG fraction employing protein A column chromatography]
[Article in Japanese]
Mizuno E, Sugenoya A, Haniuda M, Sakai R, Kameko M, Kato M, Iida F.
Department of Surgery, Shinshu University School of Medicine.
A 48-year-old non-goitrous woman, who had undergone cardiac surgery for mitral stenosis under the extracorporeal circulation, showed high levels of serum T3 and free T3 in a recent follow-up study, employing antibody coated-bead RIA for T3 and -Amerlex M particle RIA for free T3. However, other thyroid function tests (T4, free T4, TSH and TBG) were normal. We suspected that thyroid hormone autoantibodies (THAA) in her serum interfered with T3 and free T3 analyses. The presence of THAA was demonstrated by the use of various procedures as follows. Firstly, the patient's serum was directly incubated with 125I-T3 or -T4 analog which did not bind to TBG, followed by B/F separation with polyethyleneglycol, counting the precipitates. Secondly, after the serum was treated with an acid-charcoal solution to remove circulating thyroid hormone, the measurement of THAA was made as stated above. Normal sera were used as controls. Both the non- and acid-charcoal-treated sera showed much higher percentages of 125I-T3 analog precipitation as compared with controls. In the case of 125I-T4 analog, there was no difference between them. In the third study, the presence of IgG antibodies that bound T3 but not T4 was investigated. The IgG fraction of the patient's serum was separated employing a Protein A-Sepharose CL-4B column chromatography. Then, the prepared IgG fraction was purified by a technique of gel filtration chromatography (Sephacryl S 200). Non-purified and purified-IgG fractions both revealed higher binding percentages of 125I-T3 analog than the control IgG fraction and non-IgG fraction of the patient. Furthermore, a good dose response was observed between the binding percentage of 125I-T3 analog and each dose of the patient's serum or IgG fraction. From these observations, it was clarified that this woman had anti-T3 IgG autoantibodies using a Protein A column chromatography with confirmation of gel filtration chromatography.
PMID: 3224724 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/pubmed/8006324?ordinalpos=14&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

Thyroid hormone autoantibodies and their implications for free thyroid hormone measurement.
Vyas SK, Wilkin TJ.
Endocrine Section, University Medicine, Southampton General Hospital, UK.
Thyroid hormone autoantibodies (THAA) disrupt the equilibrium between thyroid hormones and their binding proteins. This may lead to spurious estimations of free thyroxine (FT4) and triiodothyronine (FT3) by radioimmunoassay (RIA). In the present study we highlight the importance of THAA by examining the frequency of THAA in consecutive sera sent to a routine district hospital laboratory. Over a period of six months, sera were collected from 200 consecutive hypothyroid, 200 hyperthyroid and seven patients whose clinical and biochemical thyroid status were contradictory. A further 200 patients with non-thyroid autoimmune conditions, 20 patients with insulin autoantibodies and 100 healthy blood transfusion donors were studied. In all sera, both effects of antigen removal on THAA detection and where THAA were found, the effect of their removal on FT4, were examined. The frequencies of THAA amongst hypothyroid, hyperthyroid and non-thyroid autoimmune conditions were 7%, 1.5% and 7.5% respectively, whilst no THAA were found in insulin autoantibody positive patients and 100 blood transfusion donors. However, THAA frequency was highest in those patients whose biochemical thyroid status was widely inappropriate to clinical state (5/7 = 64%). Sera stripped of thyroid hormones prior to THAA detection had significantly higher antibody activity than unstripped sera (p = 0.0027 and p = 0.0123 for T3 and T4 binding respectively). Free thyroxine levels measured by the Amerlex-M RIA kit after antibody removal fell in all 21 THAA positive sera tested. The correlation coefficient between antibody activity in serum with percentage fall in FT4 was 0.79 (Spearman's Rank Correlation Test).(ABSTRACT TRUNCATED AT 250 WORDS)
PMID: 8006324 [PubMed - indexed for MEDLINE]

http://www.clinchem.org/cgi/reprint/41/1/117

Spuriously High Concentration of Serum Free Thyroxine due to Anti-Trilodothyronine Antibodies ,
R#{233}S maypin, 1.3 Fran#{231}oiGseasser,' Andreas Boehn,2 and Muriel Rondeau2 ['Inst. de Phys. Biol. (Dir. Pr. J.
Chambron), Facultd de Med., F-67085 Strasbourg Cedex, France;2 Med. Interne A (Pr. D. Christmann), Clin. Med.
A, Hopital Central, CHRU, F-67091 Strasbourg Cedex, France; 3Author for correspondence: Fax Tnt + 33 88 3714 97, E-mail sapin@alsace.u-strasbg.frI
Free thyroxine (Fr4) is now frequently measured in serum by one-step labeled antibody assays based on a Solid-Phase Antigen-Linked Technique (SPALT) (1). In this assay the serum sample is incubated with a large excess of triiodothyronine (T3)-coupled solid phase and with a limited amount of labeled anti-T4 antibody. Because the solid phase acts as a ligand of low affinity for the anti-T4 antibody, interference from circulating anti-thyroid hormone (anti-T4 or anti-T3) autoantibodies (THAA) is theoretically possible.
However, until now, to our knowledge, this assay was considered to be only slightly affected by THAA (2-4).
The highest measured FT4 values (up to 35 pmol/L) could be related to therapy with T4 (4). Nevertheless, recently we observed a very high FT4 value (131 pmol/L) measured by a SPALT assay (Amerlex- MAB; Kodak Clinical Diagnostics, Amersham, UK) in the serum of a hospitalized patient with Crohn disease. This 33-year-old man was euthyroid by clinical evaluation and by his normal thyrotropin serum concentration (0.59 mIUIL, normal range 0.15-4.5 mIUfL) determined with BeriLux kit (Behring, Marburg, Germany). The biological evaluation showed a moderate hypergammaglobulinemia (17 g/L, normal range <14 g/L) with increased IgG concentration (21.8 g/L, normal range <17 g/L). The followed procedures were in accordance with the Helsinid Declaration of 1975 as revised in 1983.
This patient's serum contained anti-T3 but no anti-T4 antibodies, as identified with the technique of Allan et a!. (5) by using the analog T3 or T4 radioactive tracer of the Amerlex-M FT3 or FT4 kits, respectively (Kodak Clinical Diagnostics). The percentage of radioactive T3 analog tracer precipitated by polyethylene glycol, 12%, was above normal (5% in absence of THAA) but still quite low. The measurement of Amerlex-M FT3 remained normal ( 4.1 pmol/L, reference range 3.7-9.2 pmol/L). Fixation of a radioactive '251-labeled native T3 tracer on the fraction pre cipitated by polyethylene glycol was also not very high: 7.1% (vs normal of <5% in absence of THAA). That the free thyroidhormone concentrations were normal was confirmed by two-step RIAs known to be unaffected by the presence of THAA: FT4 24.8 pmol/L (normal range 9-25.7 pmol/L by Gammacoat"; Incstar, Stifiwater, MN); FT3 3.7 pmol/L (normal range 3.1-6.1 pmol/L by Ria-gnost; Behring). This very marked interference in the FT4 Amerlex-MAB assay shows an interaction of anti-T3 autoantibodies with the T3 immobilized on the solid phase. This interaction can occur in the presence of THAA of high affinity for the T3 fixed on the solid phase; perhaps the serum of this patient contains an antibody with a high affinity towards the T3- bridge that is used to link the solid phase to T3. This interaction can also occur with THAA of low affinity but of high capacity (i.e., the ligand is present in high concentration) (4).
The prevalence of THAA seems to be low (1/2360) (2) but the frequency of THAA is much higher in hypothyroid (7%), hyperthyroid (1.5%), and nonthyroid autoimmune ( 7.5%) patients (6). Compared with other one-step FT4 kits, the Amerlex-MAB assay is considered to be little affected by THAA (4), with only one of eight Amerlex-MAB FT4 results being higher than two-step values in the study by John et al. (2). However, users of this FT4 kit, and more generally of SPALT Fr4 kits with a T3-coupled solid phase, should be aware that such methods can give grossly misleading overestimates of FT., in presence of anti-T3 autoantibodies and produce a misclassification of thyroid sta tus. Therefore, not only anti-T4 but also anti-T3 antibodies should be suspected when a FT4 result does not correspond to the clinical state of the patient.

References
1. Christofides ND, Sheehan CP, Midgley JEM. One-step, labeledantibody assay for measuring free thyroxin. I. Assay development and validation. Cliii Chem 1992;38:11-8.
2. John R, Henley R, Shankland D. Concentrations of free thyroxunand free triiodothyronine in serum of patients with thyroxinand triiodothyronine-bindung autoantibodies. Clin Chem 1990;36: 470-3.
3. Sapin R, Gasser F, Schlienger JL, Chambron J. Analytical and clinical evaluation of a new one-step non-analogue radioimmuno assay for serum free thyroxin. Ear J Nucl Med 1990;17:111-5.
4. Sheehan CP, Christofides ND. One-step, labeled-antibody assay for measuring free thyroxine. II. Performance in a multicenter trial. Clin Chem 1992;38:19-25.
5. Allan DJ, Murphy F, Needham CA, Barron N, Wilkins TA, Midgley JEM. Sensitive test for thyroid hormone autoantibodies in serum [Letter!. Lancet 1982;ii:824.
6. Vyas SK, Wilkin TJ. Thyroid hormone autoantibodies and their implications for free thyroid hormone measurement. J Endocrino! Invest 1994;17:15-21.

http://www.clinchem.org/cgi/content/full/51/6/1071

Letters to the Editor

Falsely High Serum Free Triiodothyronine and Free Thyroxine Concentrations Attributable to Anti-Diiodothyronine and Anti-Triiodothyronine Antibodies
Kunihiro Iwahara1, Chizuko Tanabe1, Kozo Nishiyama2, Hiroyuki Ohashi 3 and Masato Maekawa1,a
1 Department of Laboratory Medicine
2 2nd Department of Internal Medicine and3 3rd Department of Internal Medicine, Hamamatsu University, School of Medicine, Hamamatsu, Japan
aAddress correspondence to this author at: Department of Laboratory Medicine, Hamamatsu University School of Medicine, 1-20-1 Handayama, Hamamatsu, 431-3192 Japan. Fax 81-53-435-2794; e-mail mmaekawa@hama-med.ac.jp

To the Editor:
We observed a patient with markedly increased free triiodothyronine (FT3) and free thyroxine (FT4) concentrations measured on a Vitros ECi analyzer (Ortho Clinical Diagnostics). The patient was a hospitalized 42-year-old woman with lupus erythematosus who appeared euthyroid and had normal thyroid-stimulating hormone (TSH) concentrations (Table 1 in the Data Supplement that accompanies the online version of this letter at http://www.clinchem.org/content/vol51/issue6/). Thyroid peroxidase antibody and thyroglobulin antibody were <0.3 kilounits/L, and rheumatoid factor was < 6.0 kilounits/L. We suspected interference from heterophilic antibodies (1 )(2), but our experiments suggested interference from antibodies to diiodothyronine (T2), T3, or their conjugates, as have been described (3 )(4)( 5). The procedures in this study were in accordance with the Helsinki Declaration of 1975 and the subsequent 1996 amendments.
In contrast to results of the Vitros ECi FT3 and FT4 assays, which use solid phases with T2 - and T3-gelatin, respectively, and labeled sheep antibodies, FT3 and FT4 were normal by the Elecsys assays (Roche Diagnostics), which use biotinylated antibodies in a one-step method.
To the Vitros FT3II and FT4 assay wells we added 0.05 mL of serum from the patient or from controls (n = 5) and 0.1 mL of diluent [phosphate-buffered saline (PBS) containing, per liter, 2 mL of Tween 20 (Sigma) and 10 g of bovine globulin (Sigma)], and incubated them at 37 °C for 18 min. After washing each well, we added 0.125 mL of horseradish peroxidase-labeled goat anti-human IgG antibody conjugate (Chemicon International. Inc.), diluted 50 000-fold in the same diluent, and incubated the mixtures at 37 °C for 18 min. After each well was washed, the Vitros Signal Reagent was added to the well, and the luminescence was measured (ALOKA luminometer). The IgG fraction of serum samples from the patient and from five control individuals was purified with a MAbTrapTM Kit (Amersham Biosciences), and the IgG concentration was adjusted to 4.0 g/L. The purified IgG (0.08 mL) was incubated at 4 °C for 24 h with 0.08 mL of PBS alone or with T2, T3, or T4 (Sigma; at 4570, 42, and 768 nmol/L, respectively) dissolved in PBS. Each sample was mixed vigorously with 1.2 mL of polyethylene glycol (PEG; 125 g/L), centrifuged at 2800g for 30 min, aspirated, and washed with 1.2 mL of PEG (125 g/L). After the precipitates were dissolved in 0.001 mol/L hydrochloric acid ( 0.04 mL) and neutralized by equal amounts of 0.001 mol/L sodium hydroxide, T2 and T3 were measured by the FT3 assay and T4 by the FT4 assay. The concentrations of T2 were expressed as T3 concentrations. Each sample was analyzed in duplicate. The ability of the purified IgG to bind T2, T3, or T 4 was defined as the difference between the FT3 or FT4 assay result and the respective blank value and is reported as the T2 , T3, or T4 value.
The ratios of FT3 and FT4 concentrations in PEG-treated samples ( 6) to those in untreated samples were significantly lower for the patient than for 37 other patients (Table 1 in the online Data Supplement); therefore, immunoglobulins in the patient's serum interfered with both the FT3 and FT4 assays. FT3 and FT4 values in the mixtures of serum with sheep IgG, bovine globulin, and gelatin did not differ significantly from those in the mixtures of serum and PBS only, suggesting that heterophilic antibodies and anti-gelatin antibodies did not cause the high FT3 and FT4 values.
When we examined the patient's IgG binding with Vitros FT3II and FT4 assay wells, the luminescence generated by the patient's serum was higher than that of the 5 control individuals (Table 1 in the online Data Supplement). This suggested that the patient's IgG bound to T2- and T3-gelatin.
The FT3 and FT4 concentrations in purified IgG and in treated samples of purified IgG ( 6) were below the lower detection limits of the Elecsys assays, suggesting an absence of T3 and T4 contamination in the IgG fractions. The patient's T2 and T3 values were higher than those of the 5 control individuals, but the T4 value was within 2 SD of the values for the 5 controls (Table 1 in the online Data Supplement). This finding implies that the patient's IgG interacted with T 2 and T3 but not with T4. The cross-reactivity of the anti-T3 antibody with T2 in the Vitros FT3II assay was very low, whereas the patient's T2 value was evidently higher than that of 5 control individuals. We conclude that T2 was bound to the patient's IgG.
Because anti-gelatin antibodies in the patient's serum were not recognized, we suggest that the interfering substance were antibodies to T2 and T3. As the interfering antibodies did not interfere with the Elecsys FT3 assay, the interfering antibody in the patient's serum may recognize T 2 and T3 conjugates used in the Vitros ECi FT3 and FT4 assays, as reported for a labeled-antibody assay ( 7). We suggest that this interference in the Vitros ECi FT3 and FT4 assays arose from antibodies to T2 , T3, or their conjugates.

References
1. Fiad TM, Duffy J, McKenna TJ. Multiple spuriously abnormal thyroid function indices due to heterophilic antibodies. Clin Endocrinol (Oxf) 1994;41:391-395. [Medline] [Order article via Infotrieve]
2. Kricka LJ. Human anti-animal antibody interferences in immunological assays. [Review]Clin Chem 1999;45:942-956. [Abstract/Free Full Text]
3. Lai LC, Day JA, Clark F, Peaston RT. Spuriously high free thyroxine with the Amerlite MAB FT4 assay. J Clin Pathol 1994;47:181-182. [Abstract/Free Full Text]
4. Sapin R, Gasser F, Boehn A, Rondeau M. Spuriously high concentration of serum free thyroxine due to anti-triiodothyronine antibodies. Clin Chem 1995;41:117-118. [Free Full Text]
5. John R, Henley R, Shankland D. Concentrations of free thyroxin and free triiodothyronine in serum of patients with thyroxin- and triiodothyronine-binding autoantibodies. Clin Chem 1990;36:470-473. [Abstract/Free Full Text]
6. Kuzuya H, Blix PM, Horwitz DL, Steiner DF, Rubenstein AH. Determination of free and total insulin and C-peptide in insulin-treated diabetics. Diabetes 1977;26:22-29. [Abstract]
7. Westerhuis LW, Venekamp WJ. Falsely high serum free thyroxine concentration measured with Amerlite-MAB FT4. Clin Chem 1995;41:633-634. [Free Full Text]

http://www.ncbi.nlm.nih.gov/pubmed/7535535?ordinalpos=15&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

Autoimmunity against thyroid hormones.
Sakata S.
Third Department of Internal Medicine, Gifu University School of Medicine, Japan.
The presence of thyroid hormone autoantibodies (THAA) is a common phenomenon. More than 270 cases have been reported by the end of 1993 involving not only thyroidal but also nonthyroidal disorders. Clinically, THAA in a patient's serum produces variation in thyroid hormone metabolism and, in particular, may interfere with the radioimmunoassay (RIA) results of total or free thyroid hormone measurements, which can cause unusually high or low values of the hormones depending on the B/F separation method used. This in vitro interference can give clinicians confusing information about the patient's thyroid state. As a result, the patient may receive inappropriate treatment from physicians who are unaware of this disorder. The presence of THAA has been reported not only in humans but also in dogs, chickens, and rats. In this review article, clinical features of THAA and the mechanism of autoantibody production are discussed.
PMID: 7535535 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/pubmed/7958106?ordinalpos=12&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

[Studies on patients with a discrepancy between free thyroid hormones and thyrotropin values]
[Article in Japanese]
Hisaoka T, Iino S, Saitoh H, Yoshimura H, Ishikawa N, Momotani N, Ito K.
Department of Internal Medicine, Showa University Fujigaoka Hospital, Yokohama, Japan.
Thyroid function has been almost exactly evaluated by the measurement of serum free thyroxine (FT4), free triiodothyronine (FT3) and thyrotropin (TSH) concentrations. However, we occasionally experience patients who show a discrepancy between free thyroid hormones and TSH values, and the assessment of thyroid function in such cases is extremely difficult. Thyroid hormone autoantibodies (THAA) interfere with radioimmunoassay (RIA) of FT4 and FT3 by giving inappropriate values. To investigate the incidence of THAA, immune precipitation of patients' sera after incubation with labelled T4 (125I-T4) or T3 (125I-T3) analog tracer was done in 394 patients with thyroid diseases. 9 patients ( 2.3%) showed an increased binding of 125I-T4 or 125I-T3 analog. Heterophilic antimouse antibodies in a patient's serum (human antimouse immunoglobulin antibodies: HAMA) can interfere in two-site immunometric assays (IMA) using mouse monoclonal antibodies and result in spuriously increased serum TSH concentrations. Manufacturers now customarily add nonspecific mouse immunoglobulins into their assay kits to absorb HAMA and prevent such interference. This approach may not always be enough to prevent HAMA interference in all samples. In 14 thyrotoxic patients with inappropriately high TSH measured by an IMA kit, we measured the levels of TSH by the further addition of mouse serum into this kit. Their serum TSH levels were fully suppressed except for 2 patients with a syndrome of inappropriate secretion of TSH (SITSH). The presence of abnormal albumin in the serum also interferes with RIA of FT4 and FT3. We experienced a female case of Graves' disease treated with methimazole who showed an inappropriately high serum FT3 measured by an analog tracer RIA kit, whose serum FT4, FT3 and TSH were 1.31 ng/dl, 19.3 pg/ml and 1.9 mu U/ml respectively. Although the anti-T3 autoantibody was considered to be present initially, immune precipitation of her serum with 125I-T3 analog tracer gave a negative result. In order to elucidate this finding, Sephadex-G200 chromatography of her serum after incubation with 125I-T3 analog tracer was done. Radioactivity of her serum in albumin fraction was significantly higher than that of normal control serum to indicate the presence of abnormal albumin in the serum. In conclusion, to assess the thyroid function of a patient with a discrepancy between free thyroid hormones and TSH values, it is important to consider the presence of THAA, HAMA, or rarely, an abnormal albumin.
PMID: 7958106 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/pubmed/7556780?ordinalpos=11&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

[Three thyroid patients showing fluctuation of thyroid hormone autoantibody titers during long-term treatment]
[Article in Japanese]
Ikekubo K, Hino M, Saiki Y, Kajikawa M, Hattori N, Ishihara T, Moridera K, Kurahachi H.
Department of Nuclear Medicine, Kobe City General Hospital.
Development and fluctuation of thyroid hormone autoantibody (THAA) titers were observed during long-term treatment of thyroid diseases in three patients. The presence of THAA was noticed by spuriously high serum free thyroid hormone levels measured with an analog tracer RIA (Amerlex-M FT3, FT4) in all three patients. Amerlex-M FT3 or FT4 levels gradually decreased to appropriate values for the clinical status according to the decreasing titers of THAA. Free thyroid hormone levels with radiolabeled antibody radioassay (Amerlex-MAB FT3, FT4) were not affected by the THAA and always reflected actual thyroid function. Case 1 was a 46-year-old man with untreated primary hypothyroidism. Auti-T4 autoantibody was detected in his serum. The 125I-T4 analog binding to the autoantibody (125I-T4 analog binding ratio) gradually declined after L-T4 therapy and finally almost disappeared two years and four months later. Amerlex-MAB FT4 level rose to the normal range two months after T4 therapy, but TSH level remained slightly elevated ( 5.4-13 microU/ml) for five months during T4 therapy. The 125I-T4 analog binding ratio and anti-Tg autoantibody (TgAb) titer were inversely correlated. Case 2 was a 72-year-old woman had received desiccated thyroid for a long time. Sequential changes of 125I-T4 analog binding ratio were very similar to those of TgAb titer. Case 3 was a 74-year-old woman with Graves' disease. She had been treated with methimazole (MMI) and desiccated thyroid for three years and five months. Ten months after stopping both drugs, anti-T3 autoantibody was detected. The 125I-T3 analog binding ratio was transiently elevated and gradually declined to reference range for four years during L-T4 therapy. 125I-T3 analog binding ratio and TgAb titer changed in a similar way. These results suggest that desiccated thyroid hormone therapy and TgAb formation are related to the development of THAA and that L-T4 therapy reduces the THAA titer.
PMID: 7556780 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/pubmed/8697622?ordinalpos=10&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

Autoantibodies to thyroid hormones: the role of thyroglobulin.
Erregragui K, Cheillan F, Defoort JP, Prato S, Fert V.
Immunotech, Marseille, France.
Autoantibodies against thyroid hormones (THAA) are frequently detected in the sera of patients with thyroid disorders together with autoantibodies against thyroglobulin (TGAA). THAA are considered to be a subset of TGAA, but alternative possibilities have not been excluded. We hypothesize that if THAA arise through an immune response to iodothyronines carried by circulating thyroglobulin (hTg), THAA should be found together with autoantibodies against the peptide backbone of hTg (TPAA) close to the hormone-forming sites. We measured TPAA in 178 serum samples, obtained from healthy subjects and patients with thyroid disorders, using two hormone-forming peptides isolated from hTg. The occurrence of TPAA was much lower than that of TGAA. Autoantibodies to the hormone-rich peptide, P3, were significantly more common than autoantibodies to the hormone-poor peptide, P1 (111/178 = 62.3% for TGAA versus 21/178 = 11.8% for anti-P3 TPAA and 7/178 = 3.9% for anti-P1 TPAA). The presence of autoantibodies to thyroid hormones was investigated in 25 TPAA+ and 26 TPAA- sera. THAA were found more frequently in TPAA+ sera (10/25 = 40% for TPAA+ and 4/26 = 15.3% for TPAA-). Correlation analysis shows that the anti-P3, but not the anti-P1 binding activity, correlates positively with the THAA-binding activity (P < 0.001 for anti-T4 THAA; P < 0.01 for anti-T3 THAA). Specificity of anti-P3 TPAA indicates that a subset of the anti-P3 antibodies is directed against the thyroid hormone moiety and another subset is directed against the peptide backbone near the hormone-forming peptide, according to our hypothesis. These results indicate that the THAA response is an anti-hTg response directed, in a significant number of cases, against the hormone-forming site included in the P3 peptide. This response seems to be elicited by either native hormone-rich hTg or by hTg fragments.
PMID: 8697622 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/pubmed/9175389?ordinalpos=9&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

Antitriiodothyronine antibody in patient with Hashimoto's thyroiditis.
Plengvidhya N, Sunthornthepvarakul T, Vannasaeng S.
Department of Medicine, Faculty of Medicine, Siriraj Hospital, Mahidol University, Bangkok, Thailand.
We described a 44-year-old female patient with a history of goiter for 2 months. Physical examination revealed a diffusely enlarged thyroid gland weighing 40 g firm to hard in consistency. She was clinically euthyroid and had neither ophthalmopathy nor dermopathy. Serum thyroid hormone levels revealed total T4 (RIA) of 4.8 micrograms/dL (normal, 4-11 micrograms/dL), total T3 (RIA) of above 600 ng/dL (70-175 ng/dL), and TSH (IRMA) of 54 mU/L (0.3-6 mU/L). Antithyroglobulin and antiperoxidase antibody titers were 1:5,120 and 1:409,260, respectively. Because of the discrepancy between the patient's clinical status and laboratory values, assay for thyroid hormone autoantibodies (THAA) was done and subsequently demonstrated antitriiodothyronine antibody with percentage of precipitation by polyethylene of 98.4 per cent (normal range, 3.06 +/- 8.58%). In conclusion, THAA should be suspected in patients whose clinical status is incoherent with the thyroid function test.
PMID: 9175389 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/pubmed/6896035?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVAbstractPlus

[A study on anti-T3 and anti-T4 autoantibodies found in two sisters with juvenile hypothyroidism due to Hashimoto's thyroiditis (author's transl)]
[Article in Japanese]
Nakamura S, Fushimi K, Okuyama M, Miura K.
Anti-thyroid hormone autoantibodies were found in two sisters of short stature (case 1: 13 years old, case 2: 10 years old). Physical examination revealed clinical findings of hypothyroidism with diffuse goiter. A diagnosis of Hashimoto's thyroiditis was made by open biopsy of the thyroid gland in both patients. Serum levels of T3 and T4 were assayed by double antibody radioimmunoassay. In case 1, serum T3 level was 16 ng/dl and serum T4 level was 2.0 microgram/dl. In case 2, serum T3 levels were high (range, 375 approximately 1660 ng/dl), while serum T4 remained at a very low level (0.9 microgram/dl). On the other hand, the level of T3 in case 2 as well as the level of T4 in case 1 was not detectable by a single antibody radioimmunoassay using dextran-coated charcoal or polyethylene glycol separation. In each case, the serum TSH level measured by double antibody radioimmunoassay was extremely high (255 microunits/ml in case 1, 240 microunits/ml in case 2), which was compatible with the clinical features of primary hypothyroidism. Sera from both patients were incubated with 125I-T3 and 125I-T4, followed by precipitation with polyethylene glycol. The binding of 125I-T3 with serum from case 2 and the binding of 125I-T4 with serum from case 1 were markedly high, suggesting the presence of T3- and T4-binding substance(s) in the sera. IgG prepared from the sera of both cases showed marked and specific binding with T3 in case 2 and T4 in case 1. The association constant for T4-antibody in case 1 was 5.2 x 10(8) M-1 and for T3-antibody in case 2 was 5.0 x 10(9) M-1. The binding capacity for T4 was 1.2 ng/ml.IgG and for T3 was 0.3 ng/mg.IgG.
PMID: 6896035 [PubMed - indexed for MEDLINE]

2008-02-18T10:46:00.001+10:30

Absolute Must read...

http://www.geocities.com/organdonate/trustingyourhospital.html

The Nasty Side Of
Organ Transplanting
The Cannibalistic Nature of Transplant Medicine

Norm Barber

Third Edition 2007

“Transplant technology may be compared to an evil genie let out of a bottle and now won’t return.”
Nancy Scheper-Hughes, Organs Watch

Copyright 2007 Norm Barber, Adelaide, South Australia, Australia, standardoil@hotmail.com; gumflat88@hotmail.com . All Rights Reserved. This publication may not be reproduced, stored in a retrieval system or transmitted, in any form or by any means, without the author’s written prior permission. However, a single copy may be printed from an electronic database for the exclusive use of the person authorising or doing the printing. More generous copying and printing rights may be given upon application to the author, who encourages the wide reading of this text.

Acknowledgments

Dr David Wainwright Evans, Cardiologist, Queens' College, Cambridge, U.K.; Dr David Hill, Emeritus Consultant Anaesthetist, Cambridgeshire, U.K.; Dr R.G. Nilges, Emeritus Neurosurgeon, Swedish Covenant Hospital, Chicago, U.S.A.; Associate Professor Cicero Galli Coimbra, Head of the Neurology and Neurosurgery Department at the Federal University of Sao Paulo, Brazil; the late Dr Phillip Keep, former Consultant Anaesthetist, Norfolk and Norwich Hospital, U.K; Professor Nancy Scheper-Hughes, Director, Organs Watch, University of California; Associate Professor Mario C. Deng of Columbia University College of Physicians and Surgeons, New York; Dr Yoshio Watanabe, Consultant Cardiologist, Chiba Tokushu-kai Hospital, Funbashi, Japan; Duane Horton of OrganKeeper, Rhode Island, U.S.A.; Dr Peter Doyle of the British Department of Health; Berendina Schermers van Straalen, Kluwer Academic Publishers, PO Box 17, 3300AA Dordrecht, The Netherlands; David Brockschmidt and Vita Vitols of Skye, Australia, Anton Keijzer, Susan Mitchell, The Staff at the Port Adelaide Library; Karen Herbertt of the South Australia Organ Donation Agency; Bob Spieldenner of the United Network for Organ Sharing, U.S.A.; The Staff at the Disability Information and Resource Centre, Adelaide.

Contents

Foreword to the Third Edition
1. An Invented Death
2. Donors May Need Anaesthetic
3. The Apnoea "Brain Death" Test May Kill Patient
4. Organ Rejection
5. Battle for the Body
6. Aggressive Hospital Harvest Teams
7. Harvest Time
8. The Nurse’s Tale
9. Types of Donors
10. Donation after Cardiac Death
11. Futile transplants and flexible survival statistics
12. Body Parts and Business
13. Coercion, Live Donation and Slippery Ethics
14. Deception by Organ Donor Agencies
15. Australian Transplant Legislation
16. Avoiding Harvest Time
17. Societal Consensus and the Slippery Slope
18. Terminology and Gender Donor Rates
19. Getting A Transplant
20. Religion, Culture and Harvesting
21. The Politics of Suppressed Death Statistics
22. A Short History of Human and Xeno Transplanting
23. Trusting Your Hospital
24. Organ Selling, Organ Theft
25. Sociological Implications
Appendix One: Some Comments on Testing for Brain Death
Appendix Two: Some Comments on Treating Brain Injury
End Notes

2008-02-14T11:13:00.003+10:30

Two Miracles

The legend of the Happy Plant says that when it flowers, a miracle happens.. My happy plant that I have been caring for for 23 years, since 1985, through 11 houses, is currently flowering for the first time...

I knew this was a time for miracles...
Please watch this video, please, it will continue to heal you as it heals all Australians

http://www.video.news.com.au/newsinteractive/videopage/videoplayer/?Channel=National+News&ClipId=1094_238199&bitrate=300&Format=wmp

The draceana fragrans massangiana, or I didn't know this but it is called a corn plant in the states, is known locally as a happy plant, or a chinese money tree, even though it is from Africa... the legend goes that you must never buy one for yourself, but only give them as gifts, or receive them as gifts, and when they flower, a miracle will occur... looks like we got ours :-)

The blooms have a deep frangipani like scent, which is interesting because it is dwarfed by my back neighbour's border of native frangipani (hymenosporum flavum) which also give off that scent, but they are not in flower currently.

It looks like this one:

I see these days the lucky bamboo and jade tree have taken over from the dracaena fragrans as the "Chinese Money Tree"

2008-02-11T11:34:00.000+10:30

Never treat hypoT on free T3 without taking symptoms into account

aka - never discount the T3 auto antibodies....

Ok we all know that using the TSH to dose thyroid meds is like trying to navigate a shopping mall using a soccer ball as a map - or maybe even less useful.

TSH only has a useful relationship to serum thyroid hormones when all systems are working properly, failing that, all bets are off.

As thyroid stimulating hormone is actually produced in the pituitary, and is released in response to the body perceiving a need for more thyroid hormone, a number of things can go wrong. The body may be in thyroid hormone conservation mode, this can happen after a number of years of being hypothyroid without treatment, or in the case of some, extreme dieting can bring it on, shock etc. The pituitary may not be unable to produce enough TSH to stimulate the thyroid gland, the body may not sense the lack and stimulate the pituitary to produce TSH, and you may have antibodies to the TSH itself, so the body attacks it's own hormone, and your thyroid doesn't get stimulated.

To get around this, most forward thinking people use the free t3 test to indicate how one should be replaced, correlating this to symptoms for "most" people has shown that with a freeT3 in the top 1/4 of the lab range, or just over, most hypothyroid people begin to feel well and regain some of the life they have lost to the illness.

But what if your free T3 is at the top of the range with no cessation of symptoms?

What if, like me, you can go for a week with no thyroid hormone supplement, and your symptoms worsen to the point of being bedridden, but your free T3 still shows on the top of range on a serum test while free T4 and TSH are both below range?

T3 has a half life of up to 10 hours, so after a week, it should be gone right?

Not neccesarily, what has been proven in case after case after case where an elevated T3 in the presence of hypothyroid symptoms has been evaluated, is the presence of antibodies to the T3 itself, which causes it to become bound in the serum, unavailable to the cells where it is needed for metabolism, causing high so called "free" T3 testing, and persistent hypothyroid symptoms.

Don't take my word for it, read the research, and DEMAND better treatment to the cessation of symptoms, rather than just to make some numbers on some paper look pretty.

http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&uid=3224724&cmd=showdetailview&indexed=google

[Triiodothyronine(T3) autoantibodies in a woman with nonthyroidal disorder: a study on preparation of serum IgG fraction employing protein A column chromatography]
[Article in Japanese]
Mizuno E, Sugenoya A, Haniuda M, Sakai R, Kameko M, Kato M, Iida F.
Department of Surgery, Shinshu University School of Medicine.
A 48-year-old non-goitrous woman, who had undergone cardiac surgery for mitral stenosis under the extracorporeal circulation, showed high levels of serum T3 and free T3 in a recent follow-up study, employing antibody coated-bead RIA for T3 and -Amerlex M particle RIA for free T3. However, other thyroid function tests (T4, free T4, TSH and TBG) were normal. We suspected that thyroid hormone autoantibodies (THAA) in her serum interfered with T3 and free T3 analyses. The presence of THAA was demonstrated by the use of various procedures as follows. Firstly, the patient's serum was directly incubated with 125I-T3 or -T4 analog which did not bind to TBG, followed by B/F separation with polyethyleneglycol, counting the precipitates. Secondly, after the serum was treated with an acid-charcoal solution to remove circulating thyroid hormone, the measurement of THAA was made as stated above. Normal sera were used as controls. Both the non- and acid-charcoal-treated sera showed much higher percentages of 125I-T3 analog precipitation as compared with controls. In the case of 125I-T4 analog, there was no difference between them. In the third study, the presence of IgG antibodies that bound T3 but not T4 was investigated. The IgG fraction of the patient's serum was separated employing a Protein A-Sepharose CL-4B column chromatography. Then, the prepared IgG fraction was purified by a technique of gel filtration chromatography (Sephacryl S 200). Non-purified and purified-IgG fractions both revealed higher binding percentages of 125I-T3 analog than the control IgG fraction and non-IgG fraction of the patient. Furthermore, a good dose response was observed between the binding percentage of 125I-T3 analog and each dose of the patient's serum or IgG fraction. From these observations, it was clarified that this woman had anti-T3 IgG autoantibodies using a Protein A column chromatography with confirmation of gel filtration chromatography.
PMID: 3224724 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/pubmed/8006324?ordinalpos=14&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

Thyroid hormone autoantibodies and their implications for free thyroid hormone measurement.
Vyas SK, Wilkin TJ.
Endocrine Section, University Medicine, Southampton General Hospital, UK.
Thyroid hormone autoantibodies (THAA) disrupt the equilibrium between thyroid hormones and their binding proteins. This may lead to spurious estimations of free thyroxine (FT4) and triiodothyronine (FT3) by radioimmunoassay (RIA). In the present study we highlight the importance of THAA by examining the frequency of THAA in consecutive sera sent to a routine district hospital laboratory. Over a period of six months, sera were collected from 200 consecutive hypothyroid, 200 hyperthyroid and seven patients whose clinical and biochemical thyroid status were contradictory. A further 200 patients with non-thyroid autoimmune conditions, 20 patients with insulin autoantibodies and 100 healthy blood transfusion donors were studied. In all sera, both effects of antigen removal on THAA detection and where THAA were found, the effect of their removal on FT4, were examined. The frequencies of THAA amongst hypothyroid, hyperthyroid and non-thyroid autoimmune conditions were 7%, 1.5% and 7.5% respectively, whilst no THAA were found in insulin autoantibody positive patients and 100 blood transfusion donors. However, THAA frequency was highest in those patients whose biochemical thyroid status was widely inappropriate to clinical state (5/7 = 64%). Sera stripped of thyroid hormones prior to THAA detection had significantly higher antibody activity than unstripped sera (p = 0.0027 and p = 0.0123 for T3 and T4 binding respectively). Free thyroxine levels measured by the Amerlex-M RIA kit after antibody removal fell in all 21 THAA positive sera tested. The correlation coefficient between antibody activity in serum with percentage fall in FT4 was 0.79 (Spearman's Rank Correlation Test).(ABSTRACT TRUNCATED AT 250 WORDS)
PMID: 8006324 [PubMed - indexed for MEDLINE]

http://www.clinchem.org/cgi/reprint/41/1/117

Spuriously High Concentration of Serum Free Thyroxine due to Anti-Trilodothyronine Antibodies ,
R#{233}S maypin, 1.3 Fran#{231}oiGseasser,' Andreas Boehn,2 and Muriel Rondeau2 ['Inst. de Phys. Biol. (Dir. Pr. J.
Chambron), Facultd de Med., F-67085 Strasbourg Cedex, France;2 Med. Interne A (Pr. D. Christmann), Clin. Med.
A, Hopital Central, CHRU, F-67091 Strasbourg Cedex, France; 3Author for correspondence: Fax Tnt + 33 88 3714 97, E-mail sapin@alsace.u-strasbg.frI
Free thyroxine (Fr4) is now frequently measured in serum by one-step labeled antibody assays based on a Solid-Phase Antigen-Linked Technique (SPALT) (1). In this assay the serum sample is incubated with a large excess of triiodothyronine (T3)-coupled solid phase and with a limited amount of labeled anti-T4 antibody. Because the solid phase acts as a ligand of low affinity for the anti-T4 antibody, interference from circulating anti-thyroid hormone (anti-T4 or anti-T3) autoantibodies (THAA) is theoretically possible.
However, until now, to our knowledge, this assay was considered to be only slightly affected by THAA (2-4).
The highest measured FT4 values (up to 35 pmol/L) could be related to therapy with T4 (4). Nevertheless, recently we observed a very high FT4 value (131 pmol/L) measured by a SPALT assay (Amerlex- MAB; Kodak Clinical Diagnostics, Amersham, UK) in the serum of a hospitalized patient with Crohn disease. This 33-year-old man was euthyroid by clinical evaluation and by his normal thyrotropin serum concentration (0.59 mIUIL, normal range 0.15-4.5 mIUfL) determined with BeriLux kit (Behring, Marburg, Germany). The biological evaluation showed a moderate hypergammaglobulinemia (17 g/L, normal range <14 g/L) with increased IgG concentration (21.8 g/L, normal range <17 g/L). The followed procedures were in accordance with the Helsinid Declaration of 1975 as revised in 1983.
This patient's serum contained anti-T3 but no anti-T4 antibodies, as identified with the technique of Allan et a!. (5) by using the analog T3 or T4 radioactive tracer of the Amerlex-M FT3 or FT4 kits, respectively (Kodak Clinical Diagnostics). The percentage of radioactive T3 analog tracer precipitated by polyethylene glycol, 12%, was above normal (5% in absence of THAA) but still quite low. The measurement of Amerlex-M FT3 remained normal ( 4.1 pmol/L, reference range 3.7-9.2 pmol/L). Fixation of a radioactive '251-labeled native T3 tracer on the fraction pre cipitated by polyethylene glycol was also not very high: 7.1% (vs normal of <5% in absence of THAA). That the free thyroidhormone concentrations were normal was confirmed by two-step RIAs known to be unaffected by the presence of THAA: FT4 24.8 pmol/L (normal range 9-25.7 pmol/L by Gammacoat"; Incstar, Stifiwater, MN); FT3 3.7 pmol/L (normal range 3.1-6.1 pmol/L by Ria-gnost; Behring). This very marked interference in the FT4 Amerlex-MAB assay shows an interaction of anti-T3 autoantibodies with the T3 immobilized on the solid phase. This interaction can occur in the presence of THAA of high affinity for the T3 fixed on the solid phase; perhaps the serum of this patient contains an antibody with a high affinity towards the T3- bridge that is used to link the solid phase to T3. This interaction can also occur with THAA of low affinity but of high capacity (i.e., the ligand is present in high concentration) (4).
The prevalence of THAA seems to be low (1/2360) (2) but the frequency of THAA is much higher in hypothyroid (7%), hyperthyroid (1.5%), and nonthyroid autoimmune ( 7.5%) patients (6). Compared with other one-step FT4 kits, the Amerlex-MAB assay is considered to be little affected by THAA (4), with only one of eight Amerlex-MAB FT4 results being higher than two-step values in the study by John et al. (2). However, users of this FT4 kit, and more generally of SPALT Fr4 kits with a T3-coupled solid phase, should be aware that such methods can give grossly misleading overestimates of FT., in presence of anti-T3 autoantibodies and produce a misclassification of thyroid sta tus. Therefore, not only anti-T4 but also anti-T3 antibodies should be suspected when a FT4 result does not correspond to the clinical state of the patient.

References
1. Christofides ND, Sheehan CP, Midgley JEM. One-step, labeledantibody assay for measuring free thyroxin. I. Assay development and validation. Cliii Chem 1992;38:11-8.
2. John R, Henley R, Shankland D. Concentrations of free thyroxunand free triiodothyronine in serum of patients with thyroxinand triiodothyronine-bindung autoantibodies. Clin Chem 1990;36: 470-3.
3. Sapin R, Gasser F, Schlienger JL, Chambron J. Analytical and clinical evaluation of a new one-step non-analogue radioimmuno assay for serum free thyroxin. Ear J Nucl Med 1990;17:111-5.
4. Sheehan CP, Christofides ND. One-step, labeled-antibody assay for measuring free thyroxine. II. Performance in a multicenter trial. Clin Chem 1992;38:19-25.
5. Allan DJ, Murphy F, Needham CA, Barron N, Wilkins TA, Midgley JEM. Sensitive test for thyroid hormone autoantibodies in serum [Letter!. Lancet 1982;ii:824.
6. Vyas SK, Wilkin TJ. Thyroid hormone autoantibodies and their implications for free thyroid hormone measurement. J Endocrino! Invest 1994;17:15-21.

http://www.clinchem.org/cgi/content/full/51/6/1071

Letters to the Editor

Falsely High Serum Free Triiodothyronine and Free Thyroxine Concentrations Attributable to Anti-Diiodothyronine and Anti-Triiodothyronine Antibodies
Kunihiro Iwahara1, Chizuko Tanabe1, Kozo Nishiyama2, Hiroyuki Ohashi 3 and Masato Maekawa1,a
1 Department of Laboratory Medicine
2 2nd Department of Internal Medicine and3 3rd Department of Internal Medicine, Hamamatsu University, School of Medicine, Hamamatsu, Japan
aAddress correspondence to this author at: Department of Laboratory Medicine, Hamamatsu University School of Medicine, 1-20-1 Handayama, Hamamatsu, 431-3192 Japan. Fax 81-53-435-2794; e-mail mmaekawa@hama-med.ac.jp

To the Editor:
We observed a patient with markedly increased free triiodothyronine (FT3) and free thyroxine (FT4) concentrations measured on a Vitros ECi analyzer (Ortho Clinical Diagnostics). The patient was a hospitalized 42-year-old woman with lupus erythematosus who appeared euthyroid and had normal thyroid-stimulating hormone (TSH) concentrations (Table 1 in the Data Supplement that accompanies the online version of this letter at http://www.clinchem.org/content/vol51/issue6/). Thyroid peroxidase antibody and thyroglobulin antibody were <0.3 kilounits/L, and rheumatoid factor was < 6.0 kilounits/L. We suspected interference from heterophilic antibodies (1 )(2), but our experiments suggested interference from antibodies to diiodothyronine (T2), T3, or their conjugates, as have been described (3 )(4)( 5). The procedures in this study were in accordance with the Helsinki Declaration of 1975 and the subsequent 1996 amendments.
In contrast to results of the Vitros ECi FT3 and FT4 assays, which use solid phases with T2 - and T3-gelatin, respectively, and labeled sheep antibodies, FT3 and FT4 were normal by the Elecsys assays (Roche Diagnostics), which use biotinylated antibodies in a one-step method.
To the Vitros FT3II and FT4 assay wells we added 0.05 mL of serum from the patient or from controls (n = 5) and 0.1 mL of diluent [phosphate-buffered saline (PBS) containing, per liter, 2 mL of Tween 20 (Sigma) and 10 g of bovine globulin (Sigma)], and incubated them at 37 °C for 18 min. After washing each well, we added 0.125 mL of horseradish peroxidase-labeled goat anti-human IgG antibody conjugate (Chemicon International. Inc.), diluted 50 000-fold in the same diluent, and incubated the mixtures at 37 °C for 18 min. After each well was washed, the Vitros Signal Reagent was added to the well, and the luminescence was measured (ALOKA luminometer). The IgG fraction of serum samples from the patient and from five control individuals was purified with a MAbTrapTM Kit (Amersham Biosciences), and the IgG concentration was adjusted to 4.0 g/L. The purified IgG (0.08 mL) was incubated at 4 °C for 24 h with 0.08 mL of PBS alone or with T2, T3, or T4 (Sigma; at 4570, 42, and 768 nmol/L, respectively) dissolved in PBS. Each sample was mixed vigorously with 1.2 mL of polyethylene glycol (PEG; 125 g/L), centrifuged at 2800g for 30 min, aspirated, and washed with 1.2 mL of PEG (125 g/L). After the precipitates were dissolved in 0.001 mol/L hydrochloric acid ( 0.04 mL) and neutralized by equal amounts of 0.001 mol/L sodium hydroxide, T2 and T3 were measured by the FT3 assay and T4 by the FT4 assay. The concentrations of T2 were expressed as T3 concentrations. Each sample was analyzed in duplicate. The ability of the purified IgG to bind T2, T3, or T 4 was defined as the difference between the FT3 or FT4 assay result and the respective blank value and is reported as the T2 , T3, or T4 value.
The ratios of FT3 and FT4 concentrations in PEG-treated samples ( 6) to those in untreated samples were significantly lower for the patient than for 37 other patients (Table 1 in the online Data Supplement); therefore, immunoglobulins in the patient's serum interfered with both the FT3 and FT4 assays. FT3 and FT4 values in the mixtures of serum with sheep IgG, bovine globulin, and gelatin did not differ significantly from those in the mixtures of serum and PBS only, suggesting that heterophilic antibodies and anti-gelatin antibodies did not cause the high FT3 and FT4 values.
When we examined the patient's IgG binding with Vitros FT3II and FT4 assay wells, the luminescence generated by the patient's serum was higher than that of the 5 control individuals (Table 1 in the online Data Supplement). This suggested that the patient's IgG bound to T2- and T3-gelatin.
The FT3 and FT4 concentrations in purified IgG and in treated samples of purified IgG ( 6) were below the lower detection limits of the Elecsys assays, suggesting an absence of T3 and T4 contamination in the IgG fractions. The patient's T2 and T3 values were higher than those of the 5 control individuals, but the T4 value was within 2 SD of the values for the 5 controls (Table 1 in the online Data Supplement). This finding implies that the patient's IgG interacted with T 2 and T3 but not with T4. The cross-reactivity of the anti-T3 antibody with T2 in the Vitros FT3II assay was very low, whereas the patient's T2 value was evidently higher than that of 5 control individuals. We conclude that T2 was bound to the patient's IgG.
Because anti-gelatin antibodies in the patient's serum were not recognized, we suggest that the interfering substance were antibodies to T2 and T3. As the interfering antibodies did not interfere with the Elecsys FT3 assay, the interfering antibody in the patient's serum may recognize T 2 and T3 conjugates used in the Vitros ECi FT3 and FT4 assays, as reported for a labeled-antibody assay ( 7). We suggest that this interference in the Vitros ECi FT3 and FT4 assays arose from antibodies to T2 , T3, or their conjugates.

References
1. Fiad TM, Duffy J, McKenna TJ. Multiple spuriously abnormal thyroid function indices due to heterophilic antibodies. Clin Endocrinol (Oxf) 1994;41:391-395. [Medline] [Order article via Infotrieve]
2. Kricka LJ. Human anti-animal antibody interferences in immunological assays. [Review]Clin Chem 1999;45:942-956. [Abstract/Free Full Text]
3. Lai LC, Day JA, Clark F, Peaston RT. Spuriously high free thyroxine with the Amerlite MAB FT4 assay. J Clin Pathol 1994;47:181-182. [Abstract/Free Full Text]
4. Sapin R, Gasser F, Boehn A, Rondeau M. Spuriously high concentration of serum free thyroxine due to anti-triiodothyronine antibodies. Clin Chem 1995;41:117-118. [Free Full Text]
5. John R, Henley R, Shankland D. Concentrations of free thyroxin and free triiodothyronine in serum of patients with thyroxin- and triiodothyronine-binding autoantibodies. Clin Chem 1990;36:470-473. [Abstract/Free Full Text]
6. Kuzuya H, Blix PM, Horwitz DL, Steiner DF, Rubenstein AH. Determination of free and total insulin and C-peptide in insulin-treated diabetics. Diabetes 1977;26:22-29. [Abstract]
7. Westerhuis LW, Venekamp WJ. Falsely high serum free thyroxine concentration measured with Amerlite-MAB FT4. Clin Chem 1995;41:633-634. [Free Full Text]

http://www.ncbi.nlm.nih.gov/pubmed/7535535?ordinalpos=15&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

Autoimmunity against thyroid hormones.
Sakata S.
Third Department of Internal Medicine, Gifu University School of Medicine, Japan.
The presence of thyroid hormone autoantibodies (THAA) is a common phenomenon. More than 270 cases have been reported by the end of 1993 involving not only thyroidal but also nonthyroidal disorders. Clinically, THAA in a patient's serum produces variation in thyroid hormone metabolism and, in particular, may interfere with the radioimmunoassay (RIA) results of total or free thyroid hormone measurements, which can cause unusually high or low values of the hormones depending on the B/F separation method used. This in vitro interference can give clinicians confusing information about the patient's thyroid state. As a result, the patient may receive inappropriate treatment from physicians who are unaware of this disorder. The presence of THAA has been reported not only in humans but also in dogs, chickens, and rats. In this review article, clinical features of THAA and the mechanism of autoantibody production are discussed.
PMID: 7535535 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/pubmed/7958106?ordinalpos=12&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

[Studies on patients with a discrepancy between free thyroid hormones and thyrotropin values]
[Article in Japanese]
Hisaoka T, Iino S, Saitoh H, Yoshimura H, Ishikawa N, Momotani N, Ito K.
Department of Internal Medicine, Showa University Fujigaoka Hospital, Yokohama, Japan.
Thyroid function has been almost exactly evaluated by the measurement of serum free thyroxine (FT4), free triiodothyronine (FT3) and thyrotropin (TSH) concentrations. However, we occasionally experience patients who show a discrepancy between free thyroid hormones and TSH values, and the assessment of thyroid function in such cases is extremely difficult. Thyroid hormone autoantibodies (THAA) interfere with radioimmunoassay (RIA) of FT4 and FT3 by giving inappropriate values. To investigate the incidence of THAA, immune precipitation of patients' sera after incubation with labelled T4 (125I-T4) or T3 (125I-T3) analog tracer was done in 394 patients with thyroid diseases. 9 patients ( 2.3%) showed an increased binding of 125I-T4 or 125I-T3 analog. Heterophilic antimouse antibodies in a patient's serum (human antimouse immunoglobulin antibodies: HAMA) can interfere in two-site immunometric assays (IMA) using mouse monoclonal antibodies and result in spuriously increased serum TSH concentrations. Manufacturers now customarily add nonspecific mouse immunoglobulins into their assay kits to absorb HAMA and prevent such interference. This approach may not always be enough to prevent HAMA interference in all samples. In 14 thyrotoxic patients with inappropriately high TSH measured by an IMA kit, we measured the levels of TSH by the further addition of mouse serum into this kit. Their serum TSH levels were fully suppressed except for 2 patients with a syndrome of inappropriate secretion of TSH (SITSH). The presence of abnormal albumin in the serum also interferes with RIA of FT4 and FT3. We experienced a female case of Graves' disease treated with methimazole who showed an inappropriately high serum FT3 measured by an analog tracer RIA kit, whose serum FT4, FT3 and TSH were 1.31 ng/dl, 19.3 pg/ml and 1.9 mu U/ml respectively. Although the anti-T3 autoantibody was considered to be present initially, immune precipitation of her serum with 125I-T3 analog tracer gave a negative result. In order to elucidate this finding, Sephadex-G200 chromatography of her serum after incubation with 125I-T3 analog tracer was done. Radioactivity of her serum in albumin fraction was significantly higher than that of normal control serum to indicate the presence of abnormal albumin in the serum. In conclusion, to assess the thyroid function of a patient with a discrepancy between free thyroid hormones and TSH values, it is important to consider the presence of THAA, HAMA, or rarely, an abnormal albumin.
PMID: 7958106 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/pubmed/7556780?ordinalpos=11&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

[Three thyroid patients showing fluctuation of thyroid hormone autoantibody titers during long-term treatment]
[Article in Japanese]
Ikekubo K, Hino M, Saiki Y, Kajikawa M, Hattori N, Ishihara T, Moridera K, Kurahachi H.
Department of Nuclear Medicine, Kobe City General Hospital.
Development and fluctuation of thyroid hormone autoantibody (THAA) titers were observed during long-term treatment of thyroid diseases in three patients. The presence of THAA was noticed by spuriously high serum free thyroid hormone levels measured with an analog tracer RIA (Amerlex-M FT3, FT4) in all three patients. Amerlex-M FT3 or FT4 levels gradually decreased to appropriate values for the clinical status according to the decreasing titers of THAA. Free thyroid hormone levels with radiolabeled antibody radioassay (Amerlex-MAB FT3, FT4) were not affected by the THAA and always reflected actual thyroid function. Case 1 was a 46-year-old man with untreated primary hypothyroidism. Auti-T4 autoantibody was detected in his serum. The 125I-T4 analog binding to the autoantibody (125I-T4 analog binding ratio) gradually declined after L-T4 therapy and finally almost disappeared two years and four months later. Amerlex-MAB FT4 level rose to the normal range two months after T4 therapy, but TSH level remained slightly elevated ( 5.4-13 microU/ml) for five months during T4 therapy. The 125I-T4 analog binding ratio and anti-Tg autoantibody (TgAb) titer were inversely correlated. Case 2 was a 72-year-old woman had received desiccated thyroid for a long time. Sequential changes of 125I-T4 analog binding ratio were very similar to those of TgAb titer. Case 3 was a 74-year-old woman with Graves' disease. She had been treated with methimazole (MMI) and desiccated thyroid for three years and five months. Ten months after stopping both drugs, anti-T3 autoantibody was detected. The 125I-T3 analog binding ratio was transiently elevated and gradually declined to reference range for four years during L-T4 therapy. 125I-T3 analog binding ratio and TgAb titer changed in a similar way. These results suggest that desiccated thyroid hormone therapy and TgAb formation are related to the development of THAA and that L-T4 therapy reduces the THAA titer.
PMID: 7556780 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/pubmed/8697622?ordinalpos=10&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

Autoantibodies to thyroid hormones: the role of thyroglobulin.
Erregragui K, Cheillan F, Defoort JP, Prato S, Fert V.
Immunotech, Marseille, France.
Autoantibodies against thyroid hormones (THAA) are frequently detected in the sera of patients with thyroid disorders together with autoantibodies against thyroglobulin (TGAA). THAA are considered to be a subset of TGAA, but alternative possibilities have not been excluded. We hypothesize that if THAA arise through an immune response to iodothyronines carried by circulating thyroglobulin (hTg), THAA should be found together with autoantibodies against the peptide backbone of hTg (TPAA) close to the hormone-forming sites. We measured TPAA in 178 serum samples, obtained from healthy subjects and patients with thyroid disorders, using two hormone-forming peptides isolated from hTg. The occurrence of TPAA was much lower than that of TGAA. Autoantibodies to the hormone-rich peptide, P3, were significantly more common than autoantibodies to the hormone-poor peptide, P1 (111/178 = 62.3% for TGAA versus 21/178 = 11.8% for anti-P3 TPAA and 7/178 = 3.9% for anti-P1 TPAA). The presence of autoantibodies to thyroid hormones was investigated in 25 TPAA+ and 26 TPAA- sera. THAA were found more frequently in TPAA+ sera (10/25 = 40% for TPAA+ and 4/26 = 15.3% for TPAA-). Correlation analysis shows that the anti-P3, but not the anti-P1 binding activity, correlates positively with the THAA-binding activity (P < 0.001 for anti-T4 THAA; P < 0.01 for anti-T3 THAA). Specificity of anti-P3 TPAA indicates that a subset of the anti-P3 antibodies is directed against the thyroid hormone moiety and another subset is directed against the peptide backbone near the hormone-forming peptide, according to our hypothesis. These results indicate that the THAA response is an anti-hTg response directed, in a significant number of cases, against the hormone-forming site included in the P3 peptide. This response seems to be elicited by either native hormone-rich hTg or by hTg fragments.
PMID: 8697622 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/pubmed/9175389?ordinalpos=9&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

Antitriiodothyronine antibody in patient with Hashimoto's thyroiditis.
Plengvidhya N, Sunthornthepvarakul T, Vannasaeng S.
Department of Medicine, Faculty of Medicine, Siriraj Hospital, Mahidol University, Bangkok, Thailand.
We described a 44-year-old female patient with a history of goiter for 2 months. Physical examination revealed a diffusely enlarged thyroid gland weighing 40 g firm to hard in consistency. She was clinically euthyroid and had neither ophthalmopathy nor dermopathy. Serum thyroid hormone levels revealed total T4 (RIA) of 4.8 micrograms/dL (normal, 4-11 micrograms/dL), total T3 (RIA) of above 600 ng/dL (70-175 ng/dL), and TSH (IRMA) of 54 mU/L (0.3-6 mU/L). Antithyroglobulin and antiperoxidase antibody titers were 1:5,120 and 1:409,260, respectively. Because of the discrepancy between the patient's clinical status and laboratory values, assay for thyroid hormone autoantibodies (THAA) was done and subsequently demonstrated antitriiodothyronine antibody with percentage of precipitation by polyethylene of 98.4 per cent (normal range, 3.06 +/- 8.58%). In conclusion, THAA should be suspected in patients whose clinical status is incoherent with the thyroid function test.
PMID: 9175389 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/pubmed/6896035?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVAbstractPlus

[A study on anti-T3 and anti-T4 autoantibodies found in two sisters with juvenile hypothyroidism due to Hashimoto's thyroiditis (author's transl)]
[Article in Japanese]
Nakamura S, Fushimi K, Okuyama M, Miura K.
Anti-thyroid hormone autoantibodies were found in two sisters of short stature (case 1: 13 years old, case 2: 10 years old). Physical examination revealed clinical findings of hypothyroidism with diffuse goiter. A diagnosis of Hashimoto's thyroiditis was made by open biopsy of the thyroid gland in both patients. Serum levels of T3 and T4 were assayed by double antibody radioimmunoassay. In case 1, serum T3 level was 16 ng/dl and serum T4 level was 2.0 microgram/dl. In case 2, serum T3 levels were high (range, 375 approximately 1660 ng/dl), while serum T4 remained at a very low level (0.9 microgram/dl). On the other hand, the level of T3 in case 2 as well as the level of T4 in case 1 was not detectable by a single antibody radioimmunoassay using dextran-coated charcoal or polyethylene glycol separation. In each case, the serum TSH level measured by double antibody radioimmunoassay was extremely high (255 microunits/ml in case 1, 240 microunits/ml in case 2), which was compatible with the clinical features of primary hypothyroidism. Sera from both patients were incubated with 125I-T3 and 125I-T4, followed by precipitation with polyethylene glycol. The binding of 125I-T3 with serum from case 2 and the binding of 125I-T4 with serum from case 1 were markedly high, suggesting the presence of T3- and T4-binding substance(s) in the sera. IgG prepared from the sera of both cases showed marked and specific binding with T3 in case 2 and T4 in case 1. The association constant for T4-antibody in case 1 was 5.2 x 10(8) M-1 and for T3-antibody in case 2 was 5.0 x 10(9) M-1. The binding capacity for T4 was 1.2 ng/ml.IgG and for T3 was 0.3 ng/mg.IgG.
PMID: 6896035 [PubMed - indexed for MEDLINE]

2008-02-07T09:01:00.000+10:30

Kung Hi Fat Chow!!!

2008-01-15T15:13:00.000+10:30

Disgusting

That's what I Think of the Australian Government's decision to ban raw milk from sale for consumption.

For many years I have consumed bio-dynamic unpasteurised unhomogenised cows milk, and for many years before that, raw goats milk (quite different to the crap in the supermarket i assure you) and was deeply saddened by this patronising nanny state country that we live in banning something so good and nourishing.

Then I found this site, we can do something about it, please consider lending your voice:

Real Milk Australia

2008-01-10T09:46:00.000+10:30

Girls Just Want to have Fun!

Gang, if you've a hankering for an evening chock full of laughs at a very good price, then don't miss this Fringe event: Girls Just Want to Have Fun
Hosted by Jess McKenzie, all the proceeds go to children's charities, and it really is the best value for money anyway at the Fringe, so please, make a donation too if you can convince a comedian to take some cash from you while you are there :-)

Last year's was magnificent, with some of the best local and interstate talent available - Hannah Gadsby (excellent), Kehau Jackson (supendous) and Fiona O'Loughlin (say no more), and a token male (Mark Trenwith), who was perhaps left a little deranged by the crazy frog thing being in the top 40 for so long - you be the judge!

I shall say no more, except, Support local talent! Support children's charities!

go and have a giggle or 20 thousand, you deserve it!!

2008-01-02T17:30:00.000+10:30

My latest most admired person, Vandana Shiva

2007-12-24T18:47:00.000+10:30

Merry Christmas Everyone!!

2007-12-12T11:07:00.000+10:30

Just wanted to know what you're reading right now..

I'm reading The Shock Doctrine by Naomi Klein

watch the short film here:

2007-12-06T09:42:00.000+10:30

He may be male...

He may be a cat.....

but we still call him....

THE BAG LADY!!!

2007-12-02T08:47:00.001+10:30

Why not to use Aldara

2007-12-02T08:35:00.000+10:30

When people speak the truth, not for spite but for the public good, it is not considered libellous.

Doctors are Dangerous - so are Dentists!

2007-11-28T08:15:00.000+10:30

|\|3r|) /\|_3rT

You can download Microsoft Visual Studio 2008 Express here

2007-11-27T08:18:00.000+10:30

Waiting to exhale, for more than 11 years...

finally, a new Prime Minister who is willing to say Sorry, something many of us did on behalf of ourselves, seeing the previous idiot would not.

I am less ashamed of my country today than I have been in a very long time.

2007-11-21T08:34:00.000+10:30

The Joys of Ageing

Just before the funeral services, the undertaker came up to the very
elderly widow and asked, 'How old was your husband?' '98,' she replied.
'Two years older than me.' 'So you're 96,' the undertaker commented. She
responded, 'Hardly worth going home, is it?'
_________________________________

Reporters interviewing a 104-year-old woman: 'And what do you think is
the best thing about being 104?' the reporter asked. She simply replied,
'No peer pressure.'
_______________________________

The nice thing about being senile is you can hide your own Easter eggs .
__________________________________________________________

I've sure gotten old! I've had two bypass surgeries, a hip replacement,
new knees, fought prostate cancer and diabetes; I'm half blind, can't
hear anything quieter than a jet engine, take 40 different medications
that make me dizzy, winded, and subject to blackouts. Have bouts with
dementia. Have poor circulation; hardly feel my hands and feet anymore.
Can't remember if I'm 85 or 92. Have lost all my friends but, thank God,
I still have my driver's license
_______________________________
I feel like my body has gotten totally out of shape, so I got my doctor's
permission to join a fitness club and start exercising I decided to take
an aerobics class for seniors. I bent, twisted, gyrated, jumped up and
down, and perspired for an hour. By the time I got my leotards on, the
class was over.
_______________________________

An elderly woman decided to prepare her will and told her preacher she
had two final requests. First, she wanted to be cremated, and second, she
wanted her ashes scattered over Coles. 'Coles?' the preacher exclaimed.
'Why Coles?'
'Then I'll be sure my daughters visit me twice a week '
____________________________________________________________

My memory's not as sharp as it used to be. Also, my memory's not as sharp
as it used to be.
_______________________________

Know how to prevent sagging? Just eat till the wrinkles fill out.
_______________________________

It's scary when you start making the same noises as your coffee-maker.
______________________________

These days about half the stuff in my shopping trolley says, 'For fast
relief.'
______________________________

Remember: You don't stop laughing because you grow old, You grow old
because you stop laughing.
________________________________

THE SENILITY PRAYER : Grant me the senility to forget the people I never
liked anyway, the good fortune to run into the ones I do, and the
eyesight to tell the difference.

I've just found an Easter Egg!!!

2007-11-19T12:13:00.000+10:30

ikebana workshop

2007-11-15T07:10:00.000+10:30

Thyroid Article by Dr Barry Durrant Peatfield

2007-11-14T14:33:00.001+10:30

thyroid movie for you - forget the supplements - I'm not selling anything for this guy!

2007-11-14T13:47:00.000+10:30

I nearly forgot the five things!

from Sunshine, I think I've done more than five pics about me so here's five facts:

1 - I got my semi-trailer license when I was 19 years old.
2 - I suffered a closed head injury with mild traumatic brain injury in 2006 - hence my endocrine system is now dysfunctional.
3 - I love humour above most things, the blacker the better :-D
4 - I name all of my cars and all of my guitars, currently own Ruby, Rosie, Wilbur, Eppie and Piggie - now you get to guess which are guitars and which are cars :-)
5 - After trying really really hard for a couple of years to eat "good quality protein and fats" - I have given up a couple of days ago and gone back to being vegetarian, a land far more comfortable to me, that's vego + dairy no whole eggs but eggs in cooking ok. I suspect a choline issue.

Oh and .. NO SOY.. SOY IS BAD

2007-11-14T13:44:00.000+10:30

Scarey Mary...

Nearly 25 years on and I still remember this one all too well...

2007-11-13T16:36:00.000+10:30

International bad products awards

and you thought taking Bindeez was bad, hmmm one wonders about those "toy of the year" awards it won....

2007-11-13T16:03:00.000+10:30

Mobile Phone pics:

I'm too sexy for this pic:

Clee Clee does her "Nessy" impression:

How I cooked myself in the window alt= curses! foiled again!

Disaster in the backyard - didn't anyone tell the pipes we're in a drought?

2007-11-13T15:05:00.000+10:30

feeling a bit exposed!

2007-11-13T14:53:00.000+10:30

Why My house is dusty...

just snapped this with my mobile while stopped at the lights cnr sth and anzac hwy, metres from my home...

This is why:
underpass

and yes, I do have lilac wiper blades :-D

because I can...

:-D

Scientific Misconduct Blog: The GMC vs Dr Rita Pal. A story about those who pretend to regulate integrity in medicine

2007-11-12T10:51:00.000+10:30

Scientific Misconduct Blog: The GMC vs Dr Rita Pal. A story about those who pretend to regulate integrity in medicine

Bullying of Academics in Higher Education: The victimization of Lisa Blakemore Brown

2007-11-12T10:49:00.000+10:30

Bullying of Academics in Higher Education: The victimization of Lisa Blakemore Brown

Scientific Misconduct Blog: The General Medical Council - in whose interests?

2007-11-12T10:42:00.000+10:30

Scientific Misconduct Blog: The General Medical Council - in whose interests?

Scientific Misconduct Blog: Memory Hole (7 November): Boots payout for scientific misconduct

2007-11-11T14:10:00.000+10:30

A must read....

Scientific Misconduct Blog: Memory Hole (7 November): Boots payout for scientific misconduct

2007-11-11T13:55:00.000+10:30

One of the best road work signs I've ever seen;
Marion Rd 11 Nov 2007

It looks like a lambada dance instruction mat or something, yes, we passed by unscathed... just :-\

click for biggies

2007-11-08T18:17:00.000+10:30

2007-11-08T12:43:00.001+10:30

I submit to you...

That the Hyundai Sonata is the Toyota Crown of the naughties.

I seem to find myself gazing at that ubiquitous creamy white broad rump far too often while dawdling in traffic...

with it's rear parcel shelf full of good things for lawn bowls, an afternoon jaunt or a day trip, including tissues, a broad brimmed hat with a ribbon band and a plaid knee ruggie...

not that there's anything wrong with that :-)

2007-10-27T09:07:00.000+09:30

Leafy Sea Dragon movie in recognition of my visit to the Sea Horse Farm

2007-10-25T19:06:00.000+09:30

Blackle - worth thinking about

How is Blackle saving energy?
Blackle was created by Heap Media to remind us all of the need to take small steps in our everyday lives to save energy. Blackle searches are powered by Google Custom Search.
Blackle saves energy because the screen is predominantly black. "Image displayed is primarily a function of the user's color settings and desktop graphics, as well as the color and size of open application windows; a given monitor requires more power to display a white (or light) screen than a black (or dark) screen." Roberson et al, 2002
In January 2007 a blog post titled Black Google Would Save 750 Megawatt-hours a Year proposed the theory that a black version of the Google search engine would save a fair bit of energy due to the popularity of the search engine. Since then there has been skepticism about the significance of the energy savings that can be achieved and the cost in terms of readability of black web pages.
We believe that there is value in the concept because even if the energy savings are small, they all add up. Secondly we feel that seeing Blackle every time we load our web browser reminds us that we need to keep taking small steps to save energy.
How can you help?
We encourage you to set Blackle as your home page ( set ). This way every time you load your Internet browser you will save a little bit of energy. Remember every bit counts! You will also be reminded about the need to save energy each time you see the Blackle page load.
Help us spread the word about Blackle by telling your friends and family to set it as their home page. If you have a blog then give us a mention. Or put the following text in your email signature: "Blackle.com - Saving energy one search at a time".
Have a look at our energy saving tips page for ideas on steps you can take to save energy.
There are a lot of great web sites about saving energy and being more environmentally friendly. They are full of great tips covering the little things that we can all do to make a difference today. Try Blackling "energy saving tips" or visit treehugger.com a great blog dedicated to environmental awareness.

Contact Blackle - Blackle FAQ
© 2007 Heap Media

2007-10-23T14:29:00.000+09:30

Re; Sunshine's comment..

No, that's not me in the video, I'm blonde and Australian, but I still don't like Landmark!

refer: http://catlicious.blogspot.com/search/label/Cult

I lost a friend to Landmark Education, it certainly never felt right to me but I gave it the benefit of the doubt and went with her to the information session.
We were asked to give our names addresses and phone numbers at the desk - I asked why my phone number was required when I was only attending for the sake of my friend and this was a "no - obligation information session"... I was allowed to enter but the red flags had gone up around me and looks were exchanged and my friend was in the bad books after that.
They had some inspiring speakers from higher up the echelons... but when members who were new-ish got up and spoke I felt decidedly ill at ease, these people were basically putting themselves down in order to win the acceptance of the group... " I was a bad person.. but Landmark changed me!!" that kind of thing.
They split us up into groups and the group leader that I had seemed to think he could find a vulnerability in the group that we would identify with and "break down" emotionally to be guided and built back up by landmark (standard brainwashing 101), I however didn't suffer the low self esteem that he expected and the opportunity to create a possibility for myself (the supposed purpose of the small group) I decided would be best spent creating the possibility of leaving the group - right now.
There were protests, I was stopped several times on the way out, but I was set on leaving with my finances and self esteem intact, so I did.
Prior to this I had received numerous phone calls to attend, join up whatever, and to tell me how to be in integrity with herself she had to tell me all these things that I wasn't aware of, resentments she had for me etc. afterwards I was to be quizzed about why I left, and to receive constant updates about the "education" but to tell you the truth my friend did spare me most of it.
The worst of it was the changes that happened to her, she became so insecure that it was impossible to be around her, she became obsessive over trivial things, OCD like, having to touch and check everything, over and over and over, critical of everything and really competitive and critical and bitchy, the way people with extreme low self esteem can become. All the while telling me how great Landmark is and how it had saved her life and how she was about to plunge another 10 grand into more and more endless seminars... the few throwaway quotes she did get out of it she could have easily got for 20 bucks from a self help book... :-(
After being told by others (didn't want to admit it to myself) that it would take me 3 or 4 days to get over spending time with her, it was that exhausting, she was always crying and really emotional... still spouting the virtues of Landmark between sniffles, I finally realised that there was nothing more that I could do so I left the friendship, and decided to post information about Landmark as it comes to hand so that fewer people have to go through that if at all possible.

:-(

2007-10-22T14:33:00.000+09:30

Ya know I despise Landmark right?

This cracked me up!!

2007-10-16T15:59:00.000+09:30

from here

ADRENAL FATIGUE AND THE SAFE USES OF CORTISOL

BASED MOSTLY ON THE BOOK SAFE USES OF CORTISOL (3rd Edition)
BY U.S. ENDOCRINOLOGIST WILLIAM McCORMACK JEFFERIES
AND ALSO YOUR THYROID AND HOW TO KEEP IT HEALTHY
BY DR BARRY DURRANT-PEATFIELD
AND ALSO ADRENAL FATIGUE THE 21ST CENTURY STRESS SYNDROME
BY JAMES L. WILSON, ND, DC, PHD
By Kyle Grimshaw-Jones ND, RT www.conscioushealing.com.au
Sep 30th, 2007

This five page educational article is written for health professionals and their clients, in the hope of stimulating interest and discussion in this vital area for the alleviation of human suffering. The author is a naturopath, not a doctor, and does not claim definitive knowledge in this area. This article is a summary of the above literature, and other research and personal experience and observation of the author.
This article is not intended as a substitute for proper medical advice or training. It is written largely from memory so it may be best to check details by purchasing the original books.
The author does not accept any liability for negative effects from any action or inaction, taken or not taken, by any person or group of persons in connection in any way with the information presented in this article. If in doubt consult your physician…Just pray he’s read these books!
CONTEMPT PRIOR TO THOROUGH INVESTIGATION WILL CONDEMN A PERSON TO IGNORANCE!
BOTTOM LINE: SAFE LOW PHYSIOLOGIC DOSES OF CORTISOL GIVEN APPROX. EVERY SIX HOURS HAVE BEEN SAFELY AND SUCCESSFULLY USED FOR OVER 40 YEARS AND 40,000 PATIENT HOURS. THIS HAS OFTEN INVOLVED LONG-TERM SUPPLEMENTATION FOR YEARS OR DECADES, GIVING DRAMATIC PATIENT BENEFIT, AND HAS PRODUCED NO OBSERVABLE LONG-TERM NEGATIVE EFFECTS AS IS COMMONLY SUPPOSED.
‘CORTISOL IS A NORMAL HORMONE, ESSENTIAL FOR LIFE.’ - McCormack Jefferies
(In fact it is the only hormone you die without!)
‘MOST PHYSICIANS TODAY ARE UNDER THE IMPRESSION THAT ANY DOSAGE OF CORTISOL CAN PRODUCE SIDE EFFECTS THAT OCCUR WITH ANY EXCESSIVE DOSES.’ - McCormack Jefferies
1. Most physicians and pharmacists do not appear to understand the safe uses of cortisol, and are biased against its use by outdated generalised information based on beliefs about other substances/glucocorticoids that are chemically similar to cortisol but not the same, such as prednisone, or cortisone, and/or based on ‘pharmacologic’ dosages that are far above what can be termed safe low ‘physiologic’ doses. After safe low physiologic doses are administered, patient peak blood cortisol levels still fall within normal physiological ranges.
2. The cortisol that can be ordered in standard blood, urine, and saliva pathology tests is the same chemical as what is termed hydrocortisone which is sold under the brand name of Hysone in Australia, and can also be manufactured by compounding pharmacists. Hydrocortisone can therefore be defined as ‘biodentical’. Hydrocortisone is somewhat inappropriately named, as it does not have a ketone side chain as its last three letters ‘one’ would suggest. Many years ago Cortisol was originally classified as Compound F in the early research work by Kendall, as distinct from Cortisone which was originally classified as Compound E. Cortisone must be turned into Cortisol in the body for it to have its full effect.
3. Jefferies has used safe physiological dosage cortisol for over four decades, and has documented his findings as a summary of over 40,000 patient hours. As far as I can tell, despite multiple published papers in the medical literature, nobody has been able to refute his observations and recommendations.
4. The original patent rights on cortisol and related natural compounds have expired. In order for new usage claims to be made about a drug new trials would have to be run. This would require funding. This would normally only come from drug companies. These companies are unlikely to fund research into usages of a drug which they cannot patent, as any other company could profit from their research and market their own equivalent product.
5. Many different disease patterns have responded favourably to Jefferies low-dose physiological protocol of cortisol administration, sometimes in conjunction with other hormone supplementation. These include allergies, amenorrhoea, low stomach acid, low secretory IgA production, poor resistance to infection/frequent infection (poor immunity), infertility, tendency to miscarriage, inflammation, autoimmune thyroiditis, lupus, and rheumatoid arthritis.
6. The negative effects from the gross heavy-handed pharmacologic dosages of the cortisone compounds that occurred in the early days of experimentation do not occur with safe low dose physiological cortisol, even when prolonged for decades. In addition, women who had previously miscarried repeatedly only managed to carry their pregnancy to full term when supplemented with cortisol, and no negative effects on mother or child have been observed in over 40 years and 40,000 patient hours. These negative side effects of high-pharmacologic doses of compounds that are in the same family as cortisol, include ‘moon face’, ‘buffalo hump’, shut-down of the hypothalamus-pituitary-adrenal axis, osteoporosis, gastrointestinal ulcerations, and immune suppression.
7. Many clinicians, even if they may begrudgingly be persuaded to prescribe low dose cortisol to a patient, are very reticent to do so, very nervous and cautious, and usually have the viewpoint that the client should not be allowed to remain on this dosage medium or long term. Many pharmacists share this belief. I believe this attitude should change. If a patient has a degree of under responsiveness of the hypothalamus-pituitary-adrenal axis which is contributing to their health condition, then this can and perhaps often should be supplemented for as long as necessary, while every attempt is made to support the patient’s body in eventually being able to produce adequate cortisol in response to various types of stressors. This may include nutritional, herbal, dietary, or other methods. Specific examples include vitamin C, B complex, Rehmannia, Licorice, Eleutherococcus, Withania, raw bovine or porcine adrenal, adrenal cortex, (and other) glandular extracts, and Iodine (which appears to influence steroid hormone receptor sensitivity).
8. Jefferies points out that even if blood cortisol, ACTH, ACTH stimulation tests, and CRF stimulation tests all show as normal, then low-dose cortisol supplementation may still be indicated and is worth trialling. It appears that certain types of feedback to the hypothalamus can sometimes not result in an adequate response down the endocrine chain. Interleukin I feedback from monocytes has been shown to influence this process through its effect on the hypothalamus, as has the influenza virus. This connection between the hypothalamus-pituitary-adrenal axis and the immune system has been reported in medical literature since the 1980s.
9. In the 1918 flu epidemic, many victims who were fatally affected were shown on autopsy to have exhausted their adrenal glands, which had ruptured, not from direct infection per se, but from trying to respond to the infection.
10. It can happen that 8am blood cortisol and DHEA levels, and even supposed 24 hr urinary ‘free’ cortisol tests can all appear in normal limits, yet saliva tests that show the amount of actual free hormone that is available to the body cells can be grossly deficient indicating that biodentical supplementation is likely to be required. Standard 8am blood cortisol or DHEA indicate the combined amount of both free and globulin-bound hormones. (Globulin-bound hormone is unavailable to the body cells.) Saliva cortisol or DHEA indicate the amount of free hormone available to the body cells. Salivary cortisol is usually tested at 6am, 12pm, 6pm, and 10pm in order to assess the diurnal pattern of cortisol production/cell availability. DHEA cortisol is usually tested at 6 am.
11. Jefferies would use dosages of up to 40 mg/day, excepting in severe conditions requiring very strong short-term intervention. 40mg/day is the amount that in unstressed circumstances will temporarily shut down the endogenous production of cortisol by negative feedback to the pituitary gland. Dosages below this, in unstressed circumstances, result in only partial shut down of endogenous production, and when gradually reduced do not impair long-term or medium-term endogenous production.
12. For the purposes of dosage comparisons, Prednisone is considered as four times stronger than cortisol. So a 20 mg/day dose of cortisol could be comparable to a 5 mg/day dose of prednisone.
13. Typically, Jefferies patients would end up on maintenance dosages of 5 mg four times per day. This would often be increased during times of infectious stress/exposure (e.g. pre and post-operatively), or other periods of heightened stress, or if slightly higher dosages were needed to maintain symptom remission. Other common dosages were therefore 7.5 mg four times per day, 10 mg four times per day, and sometimes 2.5 mg four times per day. These dosages were administered with breakfast, lunch, dinner, and before bed. The dose before bed was taken with some light food or milk if it created any tummy upset (cortisol is a gastric acid stimulant).
14. Some physicians have tried to follow the diurnal pattern by giving dosages of 12, 8, 4, and 1 mgs throughout the day. Some suggest omitting the evening dose. Taking such a small dose at bed time does not support the body in it’s early morning rise towards the normally and ideally highest cortisol level of the day. This is when it is needed the most. Therefore the evening dose is essential, and should probably not be omitted, but may need to be tapered slightly if any sleeplessness results.
15. Some authors have cautioned that stomach acid supplementation (with betaine hydrochloride for example) may need to be lowered or discontinued if cortisol supplementation is commenced. It can be observed that people with mild adrenal insufficiency often appear to have low stomach acid production also. These individuals may still need stomach acid supplementation however. In Australia direct measurement of stomach acid production seems to be a grossly underused diagnostic procedure. For more information read Lawrence Wight’s work, including Why Stomach Acid is Good for You.
16. Typically, Jefferies would attempt to lower the dose in stages over time. If symptoms returned then he would slightly increase the dose again. People would often remain supplemented for years or decades, with no ill effects, and certainly NONE of the ill effects reported during the early work using high pharmacologic dosages (as distinct from low physiologic dosages). Jefferies has noted that a typical scenario is that a physician attempts to remove cortisol supplementation far too quickly because of biased and incorrect education in this area, and the false belief that prolonged supplementation is always harmful no matter what the dosage (or which glucocorticoid is used!), instead of experimenting to find the safe physiologic dose that allows the patient to live free of their symptoms with no ill effects, even if supplementation is required for many decades and even through pregnancies.
17. Jefferies noted, as have others, that it appears to take 2 weeks for full effect of the dosage that is being used to become apparent. It is important to consider this when finding the necessary dose. A cautious and patient attitude should be employed, beginning with small dosages, and making small changes followed by 2 week observation periods at each stage. Some physicians begin with 2.5 mg four times daily.
18. Jefferies also noted and demonstrated the importance of dividing the dosages of the cortisol throughout the day. It is extremely important to understand that 20 mg of cortisol given once by mouth in the morning is very different in its effect than 5 mg given four times (once every 6 hours, or as close to this as is practical), even though the overall daily intake is the same in both cases. Three or four divided doses have been found to be most effective. Two divided doses has not. One is out of the question.
19. Contrary to popular belief, cortisol given in safe low physiologic dosages is an immune stimulant. Jefferies has convincingly demonstrated this with graphs of immunoglobulin levels over time relative to supplemental cortisol, and also with case history reports and observations that repeatedly demonstrate the dramatically improved immunity to infection of those supplementing with safe low physiological doses of cortisol. To put it simply, people who used to get sick at the drop of a hat turned into the only people in the office who didn’t catch the bug that laid everyone else up in bed for a week! To be cautious, he still would increase the dosage of cortisol during times of likely infection. This is in stark contrast to conventional conditioned thinking which is basically that ‘cortisone suppresses the immune system’.
20. Apart from dramatically improved resistance to infection, the following effects are notable in people on safe low medium to long-term physiological dose cortisol supplementation: increased alertness, better digestion (return of desire for food!), more sustained energy levels/better endurance, better ability to concentrate, dramatic relief or remission of rheumatoid arthritis and other autoimmune disease, disappearance of chronic allergies, return of colour to the face - normalisation of low blood pressure, disappearance of postural hypotension (getting dizzy when you stand up quick!), and more stable blood sugar levels.
21. Cortisol increases the conversion of T4 (thyroxine) to T3 (triiodothyronine) at the cell level, and so interrelationships between the adrenals and the thyroid glands must be considered. For further information on this area the book Your Thyroid and how to keep it healthy by Dr Barry Durrant-Peatfield is highly recommended. Here’s a hint - supplement the adrenals first, and don’t rely on blood tests for assessing thyroid function - test basal temperature and interview and assess the case based on signs and symptoms!
22. Durrant-Peatfield lists the following signs and symptoms as indicating low thyroid function disorder:
SYMPTOMS SIGNS
Weight Gain Reduced pulse pressure (difference between systolic and diastolic)
Lowered Body Temperature Slowed pulse
Lack of Energy Slowed reflexes (e.g. Achilles)(common to adrenal dysfunction also)
Fluid Retention Lab tests taken alone can be grossly and dangerously unreliable.
Chronic Constipation Lowered basal temperature
Nervous Disorders (taken upon waking under armpit - some recommend testing both armpits)
Loss of memory and thinking ability (to understand this in more detail refer to the work of Dr Broda Barnes)
Headaches
Skin troubles
Hair Loss
Changes in the Voice
Poor resistance to infection
Atherosclerosis
Anaemia
Loss of libido
Infertility
Effects on Menstruation, Childbirth and Postnatal Depression
Raynaud’s phenomenon
23. For more understanding of adrenal insufficiency that is not classic Addison’s disease, the book Adrenal Fatigue by James L Wilson is recommended. Any condition that improves with low dose physiological supplementation of cortisol is very likely to have a component of adrenal fatigue involved with it! Mainstream medical syndrome classification does not usually include a category for adrenal insufficiency unless it is formally diagnosed as classic Addison’s disease. This is a problem.
24. Wilson lists the following symptoms and signs as indications of adrenal fatigue. Clinicians may find these useful in identifying adrenal fatigue in their patients.
SYMPTOMS
Difficulty getting up in the morning.
Continuing fatigue not relieved by sleep
Craving for salt or salty foods
Lethargy (lack of energy)
Increased effort to do every day tasks
Decreased sex drive
Decreased ability to handle stress
Increased time to recover from illness, injury or trauma
Light-headed when standing up quickly
Mild Depression
Less enjoyment or happiness with life
Increased PMS
Symptoms increase if meals are skipped or inadequate
Thoughts less focused, more fuzzy
Memory less accurate
Decreased tolerance
Don’t really wake up until 10am, afternoon low between 3 and 4 pm, feels better after evening meal
Decreased productivity
SIGNS
On exposure to a light source the iris of the eye contracts, but then it oscillates wider and narrower instead of holding a stable increased tone. In severe cases it hardly responds at all.
Low blood pressure and postural low blood pressure - pressure drops on standing up from lying down - this is known as Raglan’s sign, and getting dizzy when you stand up quick is called postural hypotension.
Sergent’s White Line (present in about 40% of people with adrenal fatigue)
- with the dull end of ballpoint pen lightly stroke the skin of abdomen - within few seconds a reddened line should appear
- if it stays white for about 2 minutes and widens you probably have adrenal fatigue!
Lab tests taken alone can be grossly and dangerously unreliable and misinterpreted.
25. Supplementation with DHEA, 7-keto DHEA, or other hormones may be indicated concurrently in cases of adrenal insufficiency.
26. Jefferies used cortisone acetate for some time, but reached the conclusion over the decades that it was far better to use the biodentical cortisol (hydrocortisone).
27. Much human suffering has been caused by ignorance of the information contained in this document. Please feel free to photocopy it and distribute it, on the condition that you do not edit or modify it in any way, and ensure that each copy is complete. Please give this to all people you know with autoimmune diseases, and all doctors, rheumatologists, etc. that you come across.
THIS DOCUMENT IS RESPECTFULLY DEDICATED TO ALL THOSE WHO:
HAVE WORKED TO EASE HUMAN SUFFERING,
ARE WILLING TO THOROUGHLY INVESTIGATE AN AREA OF CONCERN BEFORE ARRIVING AT AN OPINION,
ARE WILLING TO REVISE THEIR OPINIONS AND PRACTICES IN THE LIGHT OF NEW INFORMATION,
WHO PLACE THE LONG-TERM WELFARE OF THE PERSON ABOVE PROFIT MOTIVES, AND THEIR PERSONAL NEED TO BE RIGHT OR TO STAND UNCORRECTED, AND
WHO HAVE SOUGHT AND FOUND HOW TO SERVE.
- Kyle Grimshaw-Jones ND

2007-10-03T15:41:00.000+09:30

the catlicious SG custom...

here's one I prepared earlier:

I think it's the filtertrons that make it :-)

2007-10-02T10:23:00.000+09:30

Why I don't use flu shots...

2007-10-01T09:14:00.000+09:30

Just in case you thought I was stuck getting my 70's freak on...

Here's proof that being sick means
a) I have too much time on my hands
and
b)I watch too much tv...

I keep thinking that Liam, left in this pick from Puzzle play

looks just like Ian McCulloch from Echo and the Bunnymen:

2007-09-27T13:19:00.000+09:30

Just in case...

you thought that Blake's 7 was the only place that I've been getting my 70's freak on...

I have been ebaying myself cd's to replace my old stretched cassettes of...

2007-09-24T18:12:00.000+09:30

Finally found it

So, who wore it first?

Kerr Avon?

Or Ace Frehley?

2007-09-24T16:07:00.001+09:30

Great text

I do concur with this summary of Kerr Avon, pity the pics are a little distorted... or_are_they?? 8-|

http://homepages.tesco.net/~N.Faulkner/blakes7/avontrib.htm

2007-09-22T10:17:00.000+09:30

Guilty Pleasures...

Dare I say it? Lately, my guilty pleasure has been the sight of Paul Darrow, playing Kerr Avon in Blake's 7, in really tight red leather pants... Ohhhhhhhhhh!!!!

There's something there that appeals to the geek lover in me, and I am a geekophile for sure, and the bad boy thing, and the sometimes noble cause thing, sometimes selfish bastard thing, and then theres the black skivvy, tight red leather pants, beatles hair and cuban heeled boots...

never thought I'd long for the 70's, Paul Darrow is just as enigmatic interesting and windswept as ever these days, Kerr Avon has served him, and me well ...

If you watch enough eps it works people, I tells ya!

never mind the shoulder pads!

2007-08-23T09:16:00.000+09:30

End of an Era.... Beginning of an Era...

Some of you may know about the closure of the patient advice forums at Stop the Thyroid Madness, but what you may not know, is that there are new patient advice forums available in just 24 hours from now, at Real Thyroid Help.

Many of the same people you know and love from Stop the Thyroid Madness will be there, and come along and visit me at the Australian forum :)

Cat

2007-08-22T18:11:00.000+09:30

Five More Things...

Sunshine offered us the list of five things she can't leave home without... now it's my turn :)

1, mobile phone - it has all of my appointments as well as my contacts and a video and still camera in one unit, very versatile :)

2, sunglasses - I still can't get around without sunglasses, glare and my eyes don't go together well.

3, water - just need my H2O

4, warm clothing - I don't thermoregulate well so I usually lug a jacket around with me even in the warmest weather, never know when I'm going to shiver.

5, keys - my memory is bad, so to make sure I can always get into whatever I want to get into, keys are permanently on hand.

Hmm I feel a bit boring after that, it would have been wonderful to say I carry a notebook or a sketch pad and record scenes of life as they strike me, or a petition for world peace and invite everyone I meet to sign it, the complete works of Shakespeare trying to access classical literature, mind you, I never could get into Shakespeare, my parents had the complete works of George Bernard Shaw, Shakespeare and a King James Bible, the only one I ever read and enjoyed was the Shaw, not for lack of trying, but I guess the language of the other two, being much older English, was much harder to access as I did begin reading them before I attained double digits of age. Wonder what I'd make of them now? :)

2007-08-21T18:46:00.000+09:30

Just to mock me

because they honestly never really share, here they are sharing a "blankie". They have separate blankies so that they can have their own territory and yet be close together, this time, they went for sharesies.

The bright green flashes on the collar are the free petregister.com.au registration tags, the white blob is my thumb in front of the camera and the general crumminess is the indoor potential of my mobile phone camera (2mp) with flash.

2007-08-18T11:37:00.000+09:30

Shaun Micallef, an underrated comedy genius of whom we now only get tantalising glimpses on Thank God You're Here, hopefully he'll still be there if they get to season 3.

For now, go back in time a decade or more, and see Shaun Micallef as David McGahan playing Roger Explosion...

2007-08-18T11:32:00.000+09:30

Not sure how I stumbled across this very young looking Shaun Micallef clip, this must be at least 10 years old? now to find me some roger explosion clips!

2007-08-15T18:01:00.000+09:30

Because I don't have any pics for you today

here's a fave lolcat from I can has cheezburger

2007-08-12T10:35:00.000+09:30

Someone to watch over me...

At least until she gets bored...

While he is busy herding Pandas....

2007-08-09T12:55:00.000+09:30

More Market...

I first started shopping at the Market regularly in about 1986 or so, Fiona and I used to shop there, we were very enamoured of Ally Fricker's Food Conspiracy, the only 100% organic fruit and vegetable stall there at the time.
You can imagine my disappointment that I was unable to google any reference to Ally Fricker's Food Conspiracy all these years later, such a landmark stall it was.
The same stall is still organic, it just isn't Fricker's Food Conspiracy any longer, and is no longer the only organic stall around either.

Market days involved lunch at the Malacca Corner which was always vegetarian poh pia, vego laksa and a coconut bun, or Clearlight Cafe back when it was in Rundle Street and several owners and incarnations ago - well it was the 80's :)

It was quite a treat to fire up Frieda, my HD Holden, lug my backpack around and fill it with fresh goodies, then savour an afternoon of delightful cafe fare. :-)

2007-08-08T09:50:00.000+09:30

Central Market

I just tried to post these links on Sunshine's blog, and they were truncated.

I love the Adelaide Central Market!!!

I only recently found out it's the largest fresh food market in the Southern Hemisphere, that's a double happiness for me :)

Market

More

Even More

Yes, there's more

Still more..

Just a bit more

Had enough yet?

One more.....

2007-08-06T10:50:00.000+09:30

I've been tagged for the "Five Things" meme!

Angela, from Domestic Divapalooza has tagged me to list 5 things about the following:

5 things in my refrigerator:

1. Paris Creek BioDynamic unhomogenised whole milk

2. Paris Creek natural yoghurt

3. Crumpets :)

4. St Dalfour Black Cherry no sugar Fruit Spread

5. P's half finished Farmer's Union Iced Mocha

5 things in my wardrobe:

1. Long Leather Jacket

2. Shoes that are too high for me :) - thankyou arthritic knees

3. All my packing and moving bags - I live in perpetual awareness that home is not permanent from having moved so much

4. Handbags that I currently don't use, not that there's a lot of them :), 2 I think

5. P's Navy mementos

5 things in my bag or backpack:

1. My wallet

2. Sunglasses

3. Fascia plate for my car stereo

4. Lip Balm

5. Japanese language cd's (thanks P) so I can learn a language while I drive - idea thanks to the stig from Top Gear who is learning Spanish while test driving for the show

I'm a sucker for Top Gear - just a childish rev head I suppose :)

5 things in my vehicle:

1. Spring water bottle

2. Sun visor for me

3. Reflective sun visor for Ruby (my car)

4. Cd's

5. Lots of mini tissue packets - I get stirred for this!

5 things in the world I want to see before I die:

1. Holyrood Palace

2. Japan

3. Yorkshire

4. New Zealand

5. Ireland

4 people I’m going to tag to participate in the 5 things meme:

1. Jenny

2. Julez

3. Sunshine

4. Ashlar

2007-08-02T08:00:00.000+09:30

petregister.com.au

have been doing some upgrades, hence the missing button from my sidebar.
There is a temporary one up now, but if it changes again, the linkie is still clickable so please do visit them if you're in Oz and would like your pet registered and tags for free!

2007-07-30T13:55:00.000+09:30

I found...

A packet of Tim Tams that said "Hide Me" instead of Tim Tams on the packet.
I thought I would be the first to blog about it, but apparently,
I'm not

2007-07-28T10:40:00.000+09:30

As you wish...

2007-07-27T14:08:00.000+09:30

Wow what a treat!

A real tonic to being down with the flu was being nominated as a Rockin Girl Blogger by Angela , which was started by Roberta

I'm really chuffed by this nomination, and in turn, would like to make some Rockin Girl Bloggie nominations of my own.

Angela of course
Jenny
Sunshine
Laurie
Julez

Honorable mentions to some blogs I love that are no longer updated regularly:

Sharn
Pookie

Keep on rockin girls!!

Cat