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I need to measure the corticosterone level in rat blood by any calorimetric assay. If any one has experience with this parameter, please recommend a protocol, which is ideal to measure the blood corticosterone by using spectrophotometry (Just name of the paper is enough, i will grasp the methodology).
Thanking you in advance for your replies.
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Hi, arigo has a Mouse/Rat Corticosterone ELISA Kit which was validated by mouse and rat serum and plasma. Please refer to the detail at https://www.arigobio.com/Mouse-Rat-Corticosterone-ELISA-Kit-ARG80652.html
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There are reports of an association between autoimmune thyroid disease and vitamin D deficiency. Some patients, following a thyroidectomy for non-toxic goitres, are non responsive to supplementation with thyroxine [T4]. Has any colleague experience of this condition and its possible relationship to vitamin D deficiency
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Newer basal insulins have a very long half-life; eg: Degludec
[t1/2 of 40 hours]
Why does the insulin not 'stack' if it is given daily, but with a 40 hour half-life?
Are they safe to use and how do they compare to Glargine and Detemir?
How do we make this insulin ''safe'' to administer
What is your experience and opinion, please?
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it is safe with no risk of hypoglycaemia
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I am currently planning a study, where I want to administer hydrocortisone orally to impair hippocampal learning based on the idea that stress and cortisol impairs hippocampal function minutes to hours after the experience (Diamond, Campbell, Park, Halonen, & Zoladz, 2007).
There are a number of studies out there showing that hydrocortisone can de-activate the hippocampus: during a resting period of 35 minute episode immediately after injection (de Leon et al., 1997), during a resting period with a peak 35 min after injection (Lovallo, Robinson, Glahn, & Fox, 2010), during memory retrieval 60 min after oral hydrocortisone (de Quervain et al., 2003), during memory encoding with an effect 180 min after but not 30 min after oral hydrocortisone but no effect on memory (Henckens, Van Wingen, Joëls, & Fernández, 2012).
However there is also a study, which did not find an effect for the hippocampus 45 min after hydrocortisone alone (van Stegeren, Roozendaal, Kindt, Wolf, & Joëls, 2010).
Given that there is a delay introduced by given hydrocortisone orally when should I administer it before learning to impair hippocampal learning? Any recommendations? Some of these encoding studies even found a memory benefit rather than an impairment.
References
de Leon, M. J., McRae, T., Rusinek, H., Convit, A., De Santi, S., Tarshish, C., … McEwen, B. (1997). Cortisol Reduces Hippocampal Glucose Metabolism in Normal Elderly, but Not in Alzheimer’s Disease*. The Journal of Clinical Endocrinology & Metabolism, 82(10), 3251–3259. https://doi.org/10.1210/jcem.82.10.4305
de Quervain, D. J.-F., Henke, K., Aerni, A., Treyer, V., McGaugh, J., Berthold, T., … Hock, C. (2003). Glucocorticoid‐induced impairment of declarative memory retrieval is associated with reduced blood flow in the medial temporal lobe. European Journal of Neuroscience, 17(6), 1296–1302. https://doi.org/10.1046/j.1460-9568.2003.02542.x
Diamond, D. M., Campbell, A. M., Park, C. R., Halonen, J., & Zoladz, P. R. (2007). The Temporal Dynamics Model of Emotional Memory Processing: A Synthesis on the Neurobiological Basis of Stress-Induced Amnesia, Flashbulb and Traumatic Memories, and the Yerkes-Dodson Law. Neural Plasticity, 2007, 1–33. https://doi.org/10.1155/2007/60803
Henckens, M. J. A. G., Van Wingen, G. A., Joëls, M., & Fernández, G. (2012). Corticosteroid induced decoupling of the amygdala in men. Cerebral Cortex, 22(10), 2336–2345. https://doi.org/10.1093/cercor/bhr313
Lovallo, W. R., Robinson, J. L., Glahn, D. C., & Fox, P. T. (2010). Acute effects of hydrocortisone on the human brain: An fMRI study. Psychoneuroendocrinology, 35(1), 15–20. https://doi.org/10.1016/j.psyneuen.2009.09.010
van Stegeren, A. H., Roozendaal, B., Kindt, M., Wolf, O. T., & Joëls, M. (2010). Interacting noradrenergic and corticosteroid systems shift human brain activation patterns during encoding. Neurobiology of Learning and Memory, 93(1), 56–65. https://doi.org/10.1016/j.nlm.2009.08.004
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It depends on the type of memory and learning you are willing to investigate; whether you want study the working memory or declarative memory. It has been shown that hydrocortisone-induced declarative memory deficits is less severe than that of the working memory, probably because the mechanisms underlying the consolidation and retrieval of declarative memory is wide-ranging and involve a far more complex network of different brain regions as well. See below:
Papers often refer to a two weeks long safe window to induce detectable and reliable adverse responses.
But there are reports that used crossover trials with a couple of different treatments to see the effect of one treatment on subjects with already hydrocortisone-induced weorking or episodic memory impairment. In such cases a bit longer washout window (e.g. 21 days) for all trials seems more reliable. See this for instance:
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Can you recommend me a laboratory to assess cortisol and alfa-amilase in saliva? I am from Chile and I need to determine both biomarkers in infant's saliva. Any information or your experience in this research field can help me to develop my study. Thank you in advance.
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@Cara Skon Hegg - awesome, thank you. I will write you an email. Thanks :-) Teresa
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Isn't it the "Good Cholesterol"? What could be its consequences in the long run?
My father (49 years old) has elevated serum HDL levels, however LDL levels fall in normal limits. He has been prescribed Lipitor (Atorvastatin).
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i feel higher HDL helps in educing cardiovascular diseases.
Low HDL cholesterol is considered an independent risk factor for cardiovascular diseases, so increasing it helps reduce CVD risk
Regards
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clinically how can an ulcer be differentiated as Decubitus Ulcer or Diabetic Ulcer ??
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Patient who is age of 65 is suffering from Hyperglycemic Hyperosmolar Nonketotic Syndrome has elevated levels of Potassium levels on serum electrolytes, But has total body potassium depletion ?
what is the mechanism ?
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In HHS , there is insulin deficiency which causes hyperglycemia , but adequate production to prevent ketosis ( different from DKA in T1DM , in which there is no insulin production ) . Insulin deficiency causes efflux of potassium from the cells causing hyperkalemia . In addition , volume depletion due to osmotic diuresis causes AKI which can cause hyperkalemia . T2DM can cause hyperglycemia due to insulin resistance & later insulin deficiency , which can cause HHS .
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Hello,
I was looking at a couple of histological slides from a book. I was wondering if anyone knew how to determine whether a slide is from the pituitary gland just from looking at the features of the image and nothing else.
Thank you,
Timon S
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These are transmission electron micrographs - not the kind of histology appropriate for tissue identification.
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Fenofibrate treatment is found to decrease the level of VEGF in hyperlipidemic patients ...and this was the rationale for testing its effect on angiogenesis in cancer patients. Surprisingly VEGF level was increased among the mice that were treated with 200mg Fenofibrate/1kg/day ... Any explanation to the result!
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This is about six times the maximum safe dose in humans, is it not? Unpredictable things happen at high doses since fenofibrate has known and unknown off target effects.
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I want to induce diabetic kidney injury by using of SIRT inhibitors, Sirtinol and Ex-527 in csae of High fat diabetic rats. But I can not understand the dose(Rat) of these two compounds Sirtinol and Ex-527. Please suggest me the High fat diet rat dose so that I can carry on my further experiment?  
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why do not you use STZ? ,  or HFD and STZ depending on type od DM you want to induce !
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Can we create enough pressure on governments to provide the resources for adequate Diabetes Care?
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An'' International charter'' is a good concept. But regional implementation is a nightmare. In-spite of good research having been carried out and guidelines formulated, there is still a wide gap between service providers and the consumers.
From my view the disconnect lies in the knowledge gap, one can not implement what they don't know. Misplaced priorities and economic epitome for market produce in some regions is another handicap.
My question  is, will an international charter address the socio- economic and cultural diversities that exist?
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I'm planning to investigate the hyperthyroidism effects on some biochemical aspects in rats. I read various methods for hyperthyroidism induction in the publication. I've attached and would like some advice about the recommended techniques. I'm really looking to find out what you'd consider to be the most efficient method as cost and time are limiting factors.
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I understand that short term fasting in mice and men leads to a decrease in both glucose and lactate levels, with lactate being actively taken up by the liver for gluconeogenesis. I was wondering whether there were any good data on what happens to circulating pyruvate levels in plasma in response to short term and long term fasting? 
Any help and references would be most appreciated!
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google will help
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Has anyone come across clinical ECG data in hypo or hyperthyroid patients?
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According to available literature statins have equivocal effects on the risk of acute pancreatitis development. There are no RCTs available studying statins in acute pancreatitis. How would you perform database search to try to determine this effect by meta-analysis? Which search terms and type of studies would you include? Thank you.
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Hi Goran,
1. Specify your research question.
2. Identify keywords based on your research question. 
3. Develop a search string using "OR", "AND", and "NOT" boolean operators for the relevant database eg. Pubmed, EMBASE, etc.
I support 'Shamima Akter' suggestion, but she makes it simple. You have to be strict otherwise, you will miss important articles and your conclusion will be biased. 
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HYPOTHYROIDISM. OBESITY
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So do I
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According to Robbin's Pathology, hyperthyroidism leads to an overactivity of the sympathetic system.
It also goes on to mention that this sympathetic hyperstimulation in the gut leads to increased motility leading to diarrhea and malabsorption.
How would sympathetic stimulation cause hypermotility? Isn't the parasympathetic system responsible for it? I've read further that it rather is hyperdefecation. Does it make a difference?
Also, how does hyperthyroidism increase the sympathetic tone?
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Gastrointestinal motor dysfunction is widely accepted as the main cause of symptoms in hyperthyroidism.  Again, Intestinal hypermotility in thyrotoxicosis reduces small bowel transit time, especially when diarrhea is present.  Increased appetite and excessive fat-rich food intake may contribute to excessive fecal fat. Moreover, diarrhea may be related to a hypersecretory state within the intestinal mucosa. The adrenergic system may contribute to diarrhea as suggested by correction of transit in hyperthyroid patients treated with the β-adrenergic antagonist propranolol. A reduction in mixing of food with digestive secretions may also contribute to decreased fat absorption. 
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With the goals of reducing sample volume and sample stability, I am interested in any information or a review of the use (methods) of blood spots for later analysis of TSH, bound and free T3 and T4. How do results from blood spot analysis compare with traditional plasma EIA?
Thanks!
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The dentist referred the patient for a diabetic workup after he saw that the patient's mandibular trabecular bone appeared to be sparse (as in a diabetic patient) in a panoramic radiograph. Her 2-hr postprandial level is within range (135mg/dl) however it is close to the upper limit. The patient is worried and wants to do further workup. Is it necessary?
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How about her 3 independent fasting blood glucose levels? It is fairly inexpensive and straightforward.
If fasting levels are questionable, it would make sense to measure HA1c.
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It is generally agreed that insulin secretion increases as blood glucose increases, and the same is true for islets/beta-cells in a dish in response to glucose. I have been trying to locate definitive findings in the literature of what the glucose dose-response curve for insulin secretion looks like for rodent and/or human islets across a broad range of glucose concentrations (0-200 mM or more). At what glucose load does insulin secretion max out? My impression is that the range is far broader than I would have expected. Does secretion remain steady beyond this peak value or does it actually diminish if glucose loads become too high, thus creating the inverted U-shaped curve? I would greatly appreciate citations or links to well accepted publications on this matter.
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Dear Tausif,
Your response matches rather closely with what I teach in my lectures on basic beta-cell physiology. I don't exceed 28 mM glucose for my studies either because that's a plenty high concentration to maximize insulin release and reach the top of the glucose dose-response curve, right? Apparently, not. The few peer-reviewed studies I have been able to find suggest 50-200 mM glucose to reach maximum insulin secretion--much, much higher than I would have expected. 
I was eliciting help in finding a well-cited publication that includes a proper dose-response curve for insulin secretion in response to glucose stimulation. Sometimes Pubmed can be a bit unwieldy for this purpose.
Also, while I don't view 200 mM glucose as physiologically relevant either, it made me ask myself what is the highest blood glucose level a pancreas might see. I found this in the Guinness Book of World Records... "Michael Patrick Buonocore (USA) (b. 19 May 2001), survived a blood sugar level of 147.6 mmol/L (2,656 mg/dl) when admitted to the Pocono Emergency Room in East Stroudsburg, Pennsylvania, USA, on 23 March 2008."
I believe this was a  transient event in a child upon diagnosis with type 1 diabetes, but the previous record was in the same range, so it really makes one marvel at the limits of the human body!
Anyway, thanks for your response. Hopefully, I will track down a publication or two eventually.
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Does diabetes contribute significantly in pathogenesis of vascular dementia or are those two diseases with separate pathophysiological processes?
1/ If they're linked, what are these links?
2/ Should cognitive assessment be preformed on regular check-ups for patients with diabetes mellitus?
3/ Since Alzheimier disease (AD) is also recognized as diabates mellitus type 3, is diabetes mellitus type 2 generating a pathophysiological process towards AD, vascular dementia or both?
4/ How does chronic glucose regulation affect cognitive performance and would some other substances rather than glucoregulation per se improve diabetic patients cognitive status?
5/ Why isn't cognitive performance reported more in studies involving diabetic patients?
Hoping to get some answers to these questions. Related recent literature is in links, but doesn't provide answers to these questions.
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Dear Toljan,
First of all I appreciate you for asking such brain storming questions. The questions highlight your interest in the subject. I would like to answer a few of youur queries:
1/ Diabetes is basically a microangiopathy causing damage at the level of micro-vessels. These microvascular damage predisposes to micro-infarcts that may eventually lead to the development of vascular dementia. Hypertension is considered to be a more damaging risk factor for vascular dementia than diabetes. So, microangiopathy can a link between diabetes and vascular dementia.
2/ Though we do not have guidelines available today that recommend us to do this cognitive testing in diabetic patients. But it is advisable that if a diabetic patient presents with some neurological deficit of any kind, that patient must be checked for cognitive testing as well. We may have to wait for sometime and see the upcoming guidelines on this subject.
3/ Research is going on on this subject. And a substantial amount of research and evidence will be needed before declaring AD as DM type 3. As more and more pathophysiological processes become evident, we may be in a better position to describe an underlying relationship between these identities.
5/ Every research is done with a background and with a clearlt defined objective. So, it is quite possible that recent and future studies may be done with this point in mind to check cognitive status of the diabetic patients. 
Your post may turn out to a brain storming key for researchers on the subject and may lead to incorporation of your novel ideas in future studies.
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Most of the patients with chronic renal failure suffer from a decline in the level of the hormone Erythropoietin. Are there cases where the hormone levels rise in patients with renal failure? and whether research supports this opinion?? and why this increase there?
I hope the physiological explanation for this phenomenon
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there is no simple answer. As CKD progresses, epo levels increase almost as expected (about 2-3 fold) until a eGFR of ~35 to 40 is reached. At this point, Hb on average is ~ 12-13 g/dL and the anemia is mild. With further progression, epo levels fall but even in ESRD average levels are about 50% higher than in normal individuals without anemia and no kidney disease. These levels however are only 1/10 of those which would have been expected in anemic patients with Hb levels of 8 without kidney disease.
so what causes the mild "increase: in epo. probably output from the liver. However epo produced by the liver has a different glycosylation pattern and may be less active at the EpoR .
The issue whether cystic disease of the kidney increases epo levels is controversial. some studies have shown no increase . Similarly in acquired cystic disease of the kidney, epo levels do not differ from those of patients without cysts
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Salivary testosterone is reportedly representative of the free fraction of testosterone (T). Khan-Dawood et al. (1984) found that free testosterone constituted 78% of salivary testosterone but only 4% of plasma testosterone. However, I cannot find a paper reporting a correlation or regression between salivary T and serum T measured by equilibrium dialysis. Does anyone know of any?
Thanks.
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I don't think there is no other methods available in literature 
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HMG-CoA inhibitors dont really diminish cholesterol on N-S, and hypertrigliceridemia i havent found proper management of it on N-S, but searching for more information i found ideas of PPAR stimulation and potentiation of HMG-Coa Inhibitors, diminish lipid profile and better outcomes, and using ezetimibe and atorvastatine its better for cholesterol management and atorvastatine with a glitazone improves outcome, also that glitazone tend to protect the kidney, but i havent found studies using ezetimibe plus atorvastatine or simvastatine plus glitazone to try and improve outcome of dyslipidemia on N-S.
So can the triple therapy of glitazone plus ezetimibe plus atorvastatine or simvastine be used in N-S and would or can improve the outcome of dyslipidemia in N-S.
Can someone provide additional information, or ideas regarding the hypothetical treatment or some guidelines with information of dyslipidemias on N-S, preventing Cerebral Vascular Diseases.
Thanks
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No studies of lipid-lowering agents (statins or fibrates) in patients with NS have reported patient-centred outcomes including all-cause mortality, cardiovascular mortality, or non-fatal myocardial infarction; only single studies reported cholesterol (HDL, LDL and total cholesterol), There is no data on second-line agents (incl. ezetimibe) and outcomes in NS. 
There is also little evidence that secondary hyperlipidemia in NS has the same effect on cardiovascular outcomes. Bring the NS into remission and hyperlipidemia will resolve without the need of treating dylipidemia.
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I am interested in the side effects of overnight dexamethasone supression test. Could someone send me a reliable reference for that? I am referring to human subjects and I am interested in any kind of side effects (eg. effects on cognition, mood, subjective feelings, sleep, dreams). Thank you!
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The main effect would be a fall in the level of serum cortisol concentration (in normal subjects) through the effect of negative feedback on ACTH. The net "steroid load" is not significantly affected so as to cause any clinical consequence). The dose of dexamethasone is within the physiological tolerance fro a day, and the fall in ACTH and cortisol is due the effect on diurnal release of these hormones, but if there is any stress the hypothalamic-pituitary adrenal axis can still respond.
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is it up to 24 microU/L or it is up to 12 microU/L?
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Hi
Circulating insulin concentrations provide important information for the evaluation of insulin secretion and insulin resistance. Reference intervals are the most widely applied tool for the interpretation of clinical laboratory results, however, these will differ according to your study population. According to "Melmed S, et al 2011 Williams Textbook of Endocrinology. 12th ed.' a fasting insulin level < 25 mIU/L (< 174 pmol/L) is considered normal.
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In our institution, testosterone and androstenedione are measured simultaneously using LC-MS/MS and I have come across patients with clinical signs of androgen excess who have normal testosterone levels/FAI but have high androstenedione levels. I found that the correlation coefficient between the regular FAI and an androstenedione FAI in a healthy female subject group (n=75) to be r = 0.9004. I have come across one paper that touches on this subject, I'm just wondering is there any other information people might have regarding this topic
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Dear Shane,
I am just wondering how you calculated the FAI based on androstenedione (A), but I presume you calculated A/SHBG. However, A is not bound to SHBG, it is only loosely bound to albumin and other proteins in the circulation. As for testosterone (T), steroids bound to these proteins are usually considered as "free". It is not surprising that you find a good correlation between FAI based on T and FAI based on A, since levels of A and T in women are correlated with each other, If you divide both by the same SHBG concentration, you will get the same correlation you also find between the total T and A levels.
I hope this answers your question.
Frank de Jong 
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Does someone have any experience on the effects of chronic stress on tumor growth due to different mice strains outbred or inbred nude mice Foxn1 nu respect to Balb/c nude mice?
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I don't know Sara i used nude mice strain  Foxn1 nu purchased by Harlan Italy, but in international papers the authors use always Balb/c nude mouse strain.
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The use of Mineralocorticoid Receptor blocker triggers a positive feedback loop on aldosterone secretion (as well as of Renin-Angiotensin conversion), an effect more stable than changes in Na+/K+ reabsorption, according to Eudy et al. Journal of Translational Medicine 2011.
Since MR is blocked, one could speculate that even with higher levels of plasmatic adlosterone, there will have no effect through MR. However, this is uncertain as we do not know what is the mechanism of action of MR blockers (for instance, eplerenone may act as an inverse agonist, as aldosterone levels in human trials were actually low in treated patients).
Do we know whether aldosterone is able to bind to another receptor than the MR?
Also, does eplerenone treatment induce changes in blood pressure ? and what is the net effect of using MR blockers on the RAAS?
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You are right about cortisol in rodents. However, corticosterone is abundant in rodents and binds very effectively to MR. In epithelial tissues, the MR is protected by the activity of 11beta dehydrogenase type 2. In humans, the myocardial expression of this enzyme appears to be minimal (JCEM 99:915-22, 2014) but levels may be upregulated, depending on the biological setting (Endocrinology. 2009;150:4270-7, 2009). You may want to examine these issues in your studies.
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There is a tendency among doctors to assess thyroid function, i.e. hypo- and hyperthyroidism simply by measuring TSH. It is argued that clinical scores are complicated, difficult to obtain and imprecise. Notwithstanding the ongoing discussion of the "true" reference range for TSH, mere evaluation of a laboratory value will falsly classify 3% of euthyroid persons as either hypo- or hyperthyroid, as their TSH values will be outside the 97% normal range - assuming Gaussian distribution. On the other hand, patients report better quality of life when they are "on the edge of hyperthyroidism" although this - subclinical hyperthyroidism - is a known risk factor for cardiac arrhythmias and osteoporosis. Is there a simple way to assess thyroid function, maybe with questions about heat and cold intolerance, being tired or nervous and loss or gain of weight? Has some such score been evaluated in a study of long-term health effects of thyroid function?
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To my knowledge there is no study using a score for thyroid dysfunction and long-term outcome. The main problem is, as you mentioned, that most of those studies mainly measured TSH only once. There is an unfortunate misunderstanding concerning the normal range of TSH. Reference values are misinterpreted with the normal range. Whereas in a normal population the reference values for TSH is between 0.3 and 2.5 or even 0.2 and 2.1, this does not mean that individuals with a TSH of 3.6 mU/L are subclinical hypo as long as FT4 is within the normal range. In individuals with a TSH up to 4 mU/L nearly 100% have normal FT4 levels. The proportion of those with a low FT4 increases slightly,  when TSH is > 4 mU/L. Therefore the normal range for TSH is between 0.4 and 4 mU/L and this normal range is different from the reference values of a certain population.
For the clinical practice therefore the simply TSH measurement and classification only on this TSH level is not sufficient. But of course the history of the patient and specific complaints always have to be considered. It would be helpful to have a score system, but because the signs and symptoms of hypo- as well as hyperthyroidism are unspecific, this will not be easy to establish. Therefore the experience of the physician together with the lab test  results are still necessary for diagnosis and treatment of patients.
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We are going to evaluate the immunomodulatory effects of vitamin D in an intestinal mucosal injury model. What are the Pros and Cons of measuring 1,25(OH)2D in contrast to 25(OH)D for this investigation?
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The immuno modulatory effect is  1,25OH2 related, so it would make sense to measure 1,25 OH2. However, measuring 1,25OH2 gives you the blood / plasma level, when you want to know also the tissue level.
The mechanism of immunomodulatory effect of 1,25OH is clearly presented in a paper of van Etten and Mathieu in J Steroid Biochem Mol Biol 2005.
Another point to take into account:  the level of 1,25OH2 is maintained in a narrow range even over a wide range of 25OH concentrations, including severe deficiency.
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Chelators, i.e. trientine and penicillamine are regarded helpful in patients with Wilson's disease, given that they may stimulate the excretion of serum copper via the urine by elevating the serum free copper levels. In Wilson's disease patients, urinary copper content had already been dangerously increased as an indicator of raised serum free copper. Increasing this toxic level of copper paradoxically devastates the clinical situation of the treated patients and push them into hemolysis or death! However, there is a chance of improvement, in case of passing the so called "copper depletion" phase, and many patients do depending on their severity of clinical situations. There is a big question mark in front of the question whether shouldn't we rationally aim at normalization of the raised serum free copper values when there is no well-designed randomized clinical trial in the field and based on the available evidence, zinc therapy can safely and effectively suffice this?
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What about hemodilaysis using chelating agents?
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Cholesterol from animal sources are used to produce liposomes. Are there any potential threats? If so, what are these threats?
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Thanks Ali and Harita
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Plasma glucose was high but when insulin was given intraperitonially, blood glucose went down during the insulin tolerance test.
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Firstly, it should be noted that the effects of HFD depend upon the mouse strain selected (some are resistant). Secondly, HFD (60% fat) impairs glucose-stimulated insulin release even after one week of feeding (as determined following IPGTT/IVGTT) (http://diabetes.diabetesjournals.org/content/53/suppl_3/S215.full.pdf), although most people will investigate this at 6-8 wks. Both fasted insulin and glucose levels should be elevated, the likely explanation being the onset of compensatory beta cell expansion in the face of insulin resistance (the beta cells however don't respond normally to increased glucose; see above). Severity of the latter can depend on genetic background and can be crudely tested using ITT (or taking liver tissue and checking for insulin signaling). Beta cell failure occurs from around 18 wks of HFD onwards, again depending on genetic background. It is worth bearing in mind that effects of HFD depend on source of animals, gender, age, housing environment and diet manufacturer, so it is important to define the norms in your lab. 
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Some researchers focus on the relationship between sex hormones and concerned questions in humans. Many scientists may design animal and cell line experiments for further study. I am confused about the choice of different kinds of hormones, especially estrogen. Dose ethinylestradiol and 17β-estradiol have equal effects?
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EFFECT IS TRANSGENERATIONAL.
EH SIDIBE TROPICAL ENDOCRINOLOGIST POBOX 5062 DAKAR FANN 99000
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I would look up 'genorm' (or bestkeeper or normfinder).  You would run a PCR with samples from each of your tissues with a panel of housekeeping genes and then choose the most stable genes.  It is recommended that you use at least 3 reference or housekeeping genes for normalisation of qRT-PCR as no housekeeping gene is completely stable, especially when you are analysing expression across different tissues.  Primer Design are a small company who can supply Genorm kits (for SYBR green or taqman)  but you can also pick your own panel of genes and design your own primers of course.
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It is highly likely that the OGTT prediabetes (IGT) cutoff (7.8mmol/L; 140mg/dl) is too high and needs to be lowered to 6.7mmol/L; 120mg/dl - we have proposed this in the attached paper. Any thoughts? The full data-set is online and available from the authors for anyone interested in a re-analysis.
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Hi Ali,
Many thanks - that was really a very comprehensive chapter and documentation of current evidence. My question however was that of prediabetes - do we consider people with a 2h glucose <7.8 mmol/L as normal or should this be revised down to <6.7 mmol/L?
Regards
Suhail
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Dear all,
 I am looking for a protocol to induce insulin resistance in a hypothalamic cell line. Currently I am trying it by treating the cells with palmitic acid over night and challenge them with insulin to look at the phosphorylation of AKT. But the results are not satisfying. Hence I kindly request you to help me in this regard. If there are any other compounds or drugs available to induce insulin resistance kindly let me know. Any help in this regard will be greatly appreciable.
Many thanks in advance.
Cheers
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Dear Goutham, I hope that some articles will help you sort out this problem. All the best.
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What evidence based factors (other than significant visual field loss) would assist in the decision to use medical or surgical approaches to these lesions?
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I have treated maybe more than 200 patients with dopamine agonists, in the last years manly with cabergoline. Medical treatment is our clear first choice, even when visual field defects can be detected. We only consider surgery in the following cases:
- resistance to dopamin agonist therapy (meaning increasing prolactin levels or tumor size despite high doses of dopamine agonists
- increasing visual defects despite domain agonist therapy in large tumors
- severe sidefeffects of dopamine agonist therapy 
We feel that our approach is covered by most of the published guidelines. It should also be emphasized that macro adenomas often can't be removed completely even by experts so that dopamine agonist therapy has to be established anyway. 
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Has anyone experienced the effect of insulin by inhalation or injection?
We all know that the regular way is by insulin injection. I am trying to get an answer for the inhalation of insulin technique. One common thing we know that it is really easy and there is no pain with the injection, apart from what the real effect when it is in pulmonary.
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ok.
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I am studying a mouse model with reduced whole body development and I would need to evaluate if there is any alteration in the thyroid function. Some publications employed TSH levels, while others T3 or T4. Which one is more accurate?
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Hello, T4 is much better than T3 because thyroid gland release 90-95 % T4 and 5-10% T3. Hence, T4 is the best indicator of thyroid function. Too late, T4 is converted to T3 in the inner of the cells by deiodinase type II. Good Lucky.
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I want this information to my PhD project.
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there are two publications on betatrophin in humans. I do not believe either found a connection to diabetes or dyslipidemia
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see above
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Mattias:
I hope this question gets a lot of interdisciplinary responses because I believe it touches on a number of interesting, if not sometimes paradoxical, conditions.
For example, it has long been held that there is an apparent inequity within the order Primates in their need for UVB light and resultant synthesis of vitamin D3. New World primates are generally far more sunlight-dependent than their Old World counterparts, and the frequency of observable metabolic deficits in UV-deprived New World primates would seem to validate this. Therefore, is there a greater ability for Old World monkeys to satisfy their metabolic calcium requirements solely through diet? If so, what is the nutritional source? What evolutionary processes bought about such a discrepancy between Old World and New World primates?
Secondly, the degree to which nocturnal animals may be absorbing UV light while at rest (during the day) should not be overlooked. While touring in Costa Rica I was very surprised to see sloths sleeping high in the trees fully exposed to sunlight. While very nocturnal in behavior, this taxa certainly seemed to have ample opportunity to absorb UV light. I’d postulate that other species do likewise.
Lastly, on occasions of having to hand-rear infant armadillos, it has been found that those infants being reared in the absence of UV light tend to fair very poorly and show evidence of metabolic bone disease (as one would expect from a calcium deficiency). Others raised on the same diet and exposed to sunlight on a regular basis have faired much better. The paradox lies in the apparent requirement for UV light exposure by infants of a nocturnal, subterranean taxa. Is vitamin D normally passed from mother to her nursing infant through the milk and, if so, how is the mother armadillo synthesizing vitamin D?
My apologies for raising more questions while providing no answers. The question opens a number of intriguing side topics.
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MBG: Patients who had at least 6 previous Fasting BSL readings at the interval of at least 2 months prior to admission in the hospital were included in the study. MBG was calculated as an arithmetic mean of all the profile sets.
Kidney function: urea and creatinine values
Is there any clinical significance?
Is there any correlation significance?
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Occasional blood sugar may not have an automatic repercussion in the renal function. As a long standing issue, it is well known that high blood sugar correlates with nephropathy. We have known this for many years, but it was "evidence base" proven with the Diabetes Control and Complications Trial (DCCT) in type 1 diabetes and followed by other trials.
If you are interested in having mean BG and kidney function, it is more accurate to use Hemoglobin A1c that gives you a real average of the blood sugars in the past 3 months or fructosamine that covers for 15-30 days.
The blood sugar values will vary according to the time of the day. So, it is better to have the same time for your average BG.
You should also take in account what Dr. Smith and Dr Zhuo said in their interesting comments.
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Chronic opioid use can have negative effects on the endocrine system. Some of the published literature I have seen indicates that this is more likely with short acting than with long-acting opioids.
Is anyone aware of research specifically examining chronic (dependent) use of long-acting opioids (whether medical, illicit, or in agonist-replacement pharmacotherapy), and problems with hormone regulation?
I am particularly interested in anything that can demonstrate whether endocrine dysfunction generally, and/or hypo- or hyper-thyroidism are a more likely consequence of long-acting opioids or shorter acting ones, and also whether there is any evidence as to whether these problems are more likely with full-agonists (eg methadone) than with partial agonists (eg buprenorphine).
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Hi Paul:
You have it correct.
TSH responds to thyroid hormones, when they are low, TSH is high and viceversa. This happens in a normal environment. Primary hypothyroidism has low thyroid hormones and high TSH and primary hyperthyroidism occurs with high thyroid hormones and low TSH. In the case of secondary or tertiary hypothyroidism TSH is low and thyroid hormones are low. The difference between secondary and tertiary is in the TRH value, that cannot be measured peripherally that is low in tertiary and high in secondary. My comment about prolactin has to do with this issue of secondary or tertiary, because, as you know, prolactin has an inhibitor factor from the hypothalamus (Dopamine). In case of a tertiary problem TRH is low and TSH is low, but dopamine may be low and Prolactin will be high.
In reference to your question I see many Veteran patients who are on chronic opioid therapy and they develop secondary (or tertiary?) hypogonadism. I have no opportunity to see the effects of acute administration of opioids on the pituitary hormones, but what I see is that they have low gonadotropines and low testosterone values.
All the best,
Carlos
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This is quite true that endogenous estrogens protect female hearts and vessels prior to onset of menopause, they act as vasodilators, similarly to calcium channel blockers, have favorable effect on lipid metabolism and coagulation. But as for the application of HRT for primary or secondary prevention of CVD, it remains questioable due to the results of recent studies like HERS, WHI, PEPI, NHS, etc. which had demonstrated that selective beneficial effects of HRT on CVS doesnt overweight the possible risk of certain types of cancer, like invasive breast cancer, though decreasing the risk of colon cancer. Besides, HRT increses the overall risk of arterial and venous thrombosis in patients with trombophillia, EVTET trial.
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In our hospital various corticosteroid stress protocols are being used. At present I intend to create one uniform protocol (preferably evidence-based), which can be used in clinical practice in e.g. the perioperative setting for patients who are on long-term corticosteroid therapy (both replacement therapy and therapeutical dose). I would highly appreciate input from colleagues of other institutes.
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This paper reviews the evidence and provides some guidelines that are useful
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Why is the dexamethazone is not used widely as anti inflammatory agent compared to the prednizolone or methyleprednizolone inspite of being more potent than them and even not for short time use ( like the methylprednizolone use in the rapidly progressive glomerulonephritis for 5 days as pulse therapy)
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Sir the difference may be due to rapidity of action, of prednisolone rather than dexamethasone.
titering of the drug may be difficult in case of long acting potent steroid.
In case of any underlying infection steroid may be an inhibiting factor and dexamethasone may be a ditterent.
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Insulin has metabolic and mitogenic effect too. Thereby can be helpful in proliferation of neurons which are degenerated in certain brain diseases like Alzeihmer and Parkinson's.
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This is really an area worth pursuing. Brain insulin resistance can be shown not only in obesity and diabetes, but in some neurodegenerative conditions as well. Inflammatory cytokines may be the common denominator of brain insulin resistance in several neurodegenerative disorders ( Biochem Pharmacol. 2013 ;86:862-71). There is a real need for good basic research in well defined models of neurodegenerative diseases to identify1) how/whether such specific conditions are affected by insulin resistance and insulin re-sensitization; 2) new means to increase the brain's sensitivity to insulin;, 3) the role of peripheral vs. central insulin resistance in neurodegenerative diseases.
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Chronic opioid use can have negative effects on the endocrine system. Some of the published literature I have seen indicates that this is less likely with long-acting opioids.
Is anyone aware of research specifically examining chronic (dependent) use of long-acting opioids (whether medical, illicit, or in agonist-replacement pharmacotherapy), and problems with hormone regulation?
I am particularly interested in anything that can demonstrate whether endocrine dysfunction generally, and/or hypo- or hyper-thyroidism are a more likely consequence of long-acting opioids or shorter acting ones, and also whether there is any evidence as to whether these problems are more likely with full-agonists (eg methadone) than with partial agonists (eg buprenorphine).
Regards,
Paul
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Papillary Ca of Thyroid is known for metastasis in cervical lymph node. In a lady of 34 years, with Papillary ca in a sigle cervical lymph node, which was diagnosed after excision biopsy, with no focal lesion in Thyroid gland on Ultrasonography, what should be the plan of management?
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I think the need for aggressive treatment is not completely justified. The question about the origin of these metastasis of unknown primary is far from being solved.
I agree about the need for intensive scanning (PET, CT...) but if no primary is found there is enough evidence in the literature to support a strict follow-up, given the low aggressivity of these tumors and the favorable progostic factors (age <45, female).
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I am searching for a Cortisol assay (RIA or ELISA) that can detect low concentrations of cortisol in animal serum (< 10 nM; 0.3 ug/dL). I have a fairly large volume of serum, at least 500 uL for each sample. I know there are extraction methods available which I'll move to next but I've got a large number of samples (over 1000) and I'd like to avoid the time and error involved in adding these extraction steps. If there is a test or method that anyone has used or knows of that reliably detects these low cortisol concentrations directly in serum I'd appreciate it. Thanks!
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Hello, Corry!
I wonder if you can send a sample to a human clinical lab...If so, I would recommend you to try the ARUP lab that is assaying cortisol at very low concentration via LC-MS/MS. It is the most sensitive and specific method out there...
Try to contact them and submit a sample "for research"...
There is also a National Vet Lab in USA, where you can send samples. Contact them: http://natvetlab.com/index.php
If you need a good assay working well at very low concentrations, I would recommend you to go for a MS method rather than an immunoassay.
AGS
Alina G. Sofronescu PhD, MSC
Clinical Chemist
Technical Director Clinical Chemistry Laboratory
Assistant Professor
983135 University Nebraska Medical Center
Omaha, Nebraska 68198-5520
Ph: (402) 559-8335
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I'm trying to find out or estimate the total number of radioiodine treatments in the USA, EU or world wide. Have tried to look in different IRCP and UNSCEAR reports, but can't locate an answer. Does anybody know of other official sites or publications that can bring me closer to an estimate?
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Take a look at the following UNSCEAR Report - http://www.unscear.org/docs/reports/2008/09-86753_Report_2008_Annex_A.pdf Start with Table C19a.
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Do we need to get a baseline serum cortisol at 8 am?
How do we interprete and proceed?
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Thank you for the input
I exactly meant same , Do we need to rule out HPA suppression ?
Is single serum 8 am cortisol enough?
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I have the glucose values at -5, 0, 10, 15, 20 and 30 minutes.
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Glucose disappearance rate for ITT (KITT; %/min) is calculated as:
KITT=(0.693x100) / t1/2
where t1/2 is the "half life" calculated from the slope of the plasma glucose concentration.
The best calculation of t1/2 is to consider an exponential decrement of glucose concentration after insulin administration. A statistic software can calculate that using an exponential fit on the curve. I personally use GraphPad Prism.
Alternatively, a good approximation is to do a linear regression on the initial decrease of the curve and calculate the time where glucose concentration is 50% of the starting value.