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drmeriftr

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About drmeriftr

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  1. Hi Meri! Thanks for your comment a long time ago, thought I would say hi back!:)

  2. Scientists Unravel Clue in Cortisol Production Atlanta (April 24, 2007) ? When a person?s under stress or injured, the adrenal gland releases cortisol to help restore the body?s functions to normal. But the hormone?s effects are many and varied, lowering the activity of the immune system, helping create memories with short-term exposure, while impairing learning if there?s too much for too long. Given the variety of its effects,understanding how cortisol is made is essential to producing medications that can alter its production. Scientists at the Georgia Institute of Technology have discovered an important step in cortisol production, finding that although the output of the hormone is continuous, the molecular production is cyclic in nature ? involving a rhythmic binding and unbinding of a protein essential to its production. The research, which increases understanding of how the brain and the endocrine system work together to regulate health, appears in the February issue of the journal Molecular Endocrinology. Turning cholesterol into the stress hormone cortisol involves many reactions and begins when the hypothalamus sends a signal to the adrenal glands. Proteins then flood into the nucleus to bind to the DNA, creating the gene CYP 17. What happens next is well understood; CYP 17, along with a battery of other enzymes, transforms cholesterol into cortisol. But what isn?t understood is how this protein binding creates CYP 17, or which proteins are important. So, graduate students Eric Dammer and Adam Leon, along with Marion Sewer, assistant professor in Georgia Tech?s School of Biology, decided to model the events that occur after the adrenal gland receives the signal. One of the things the signal does is cause adrenal cells to increase their production of cyclic AMP (cAMP), a chemical that encourages proteins to interact. So they began by causing the cells to make more cAMP. Then as the proteins assembled on the DNA, they tested the cells at different intervals in order to get a snapshot of which proteins were interacting, both with each other and the DNA and in which order this occurred. Then they mutated the proteins to stop them from fulfilling their roles. "One of the best ways to try and figure out the function of a protein or a gene is to get rid of it or mutate it so that it?s not acting normally. Then you compare it with one that is acting normally,? said Sewer. In this study, they focused on a protein known as steriodogenic factor 1 (SF-1), which is essential for making all steroid hormones. Researchers were interested in discovering what events have to occur in order for SF-1 to bind to DNA. The first thing they found was that because DNA is so tightly packed in the nucleus, SF-1 can?t bind to it until it?s unpacked by a group of proteins. Once that happens, SF-1 binds to the genes, beginning the process that makes CYP 17 and ultimately cortisol. But it?s not a continuous process, they found. "Once SF-1 binds, it leaves. A few minutes later other proteins come in and condense the DNA,? said Sewer. ?After that SF-1 binds again, then leaves, and the proteins cause the DNA to contract again.? This cycle goes on as long as the adrenal gland is receiving the signal. "Even though you get a sustained production of cortisol, the actual molecular events that happen in the nucleus are dynamic,? said Sewer. ?It?s an extremely complex series of events that starts within minutes of the adrenal gland receiving the signal. Without all these transient binding events, the adrenal gland fails to produce optimal levels of cortisol.? Next the team will investigate how small molecules ? ligands ? regulate cortisol production by binding to SF-1 and controlling the receptor?s ability to bind to DNA. This research was supported by the National Institutes of Health, the National Science Foundation and the Georgia Cancer Coalition. http://www.gatech.edu/news-room/release.php?id=1355
  3. Congratulations to everyone who worked on Officially Designating April 8th as Cushing's Awareness Day!! This is awesome!! I found the bill here: http://thomas.loc.gov/cgi-bin/query/z?c110:S.RES.127: Designating April 8, 2007, as `National Cushing's Syndrome Awareness Day'. (Agreed to by Senate) SRES 127 ATS 110th CONGRESS 1st Session S. RES. 127 Designating April 8, 2007, as `National Cushing's Syndrome Awareness Day'. IN THE SENATE OF THE UNITED STATES March 27, 2007 Mr. INHOFE (for himself and Mr. DODD) submitted the following resolution; which was considered and agreed to -------------------------------------------------------------------------------- RESOLUTION Designating April 8, 2007, as `National Cushing's Syndrome Awareness Day'. Whereas Cushing's Syndrome annually affects an estimated 10 to 15 people per million, most of whom are currently between the ages of 20 and 50; Whereas Cushing's Syndrome is an endocrine or hormonal disorder caused by prolonged exposure of the body's tissue to high levels of the hormone cortisol; Whereas exposure to cortisol can occur by overproduction in the body or by taking glucocorticoid hormones, which are routinely prescribed for asthma, rheumatoid arthritis, lupus, or as an immunosuppressant following transplantation; Whereas the syndrome may also result from pituitary adenomas, ectopic ACTH syndrome, adrenal tumors, and Familial Cushing's Syndrome; Whereas Cushing's Syndrome can cause abnormal weight gain, skin changes, and fatigue and ultimately lead to diabetes, high blood pressure, depression, osteoporosis, and death; Whereas Cushing's Syndrome is diagnosed through a series of tests, often requiring x-ray examinations of adrenal or pituitary glands to locate tumors; Whereas many people who suffer from Cushing's Syndrome are misdiagnosed or go undiagnosed for years because many of the symptoms are mirrored in milder diseases, thereby delaying important treatment options; Whereas treatments for Cushing's Syndrome include surgery, radiation, chemotherapy, cortisol-inhibiting drugs, and reducing the dosage of glucocorticoid hormones; Whereas Cushing's Syndrome was discovered by Dr. Harvey Williams Cushing, who was born on April 8th, 1869; Whereas the Dr. Harvey Cushing stamp was part of the United States Postal Service's `Great American' series, initiated in 1980 to recognize individuals for making significant contributions to the heritage and culture of the United States; Whereas President Ronald Reagan spoke on April 8, 1987, in the Rose Garden at a White House ceremony to unveil the commemorative stamp honoring Dr. Harvey Cushing; Whereas following the ceremony, President Reagan hosted a reception in the State Dining Room for Mrs. John Hay Whitney, Dr. Cushing's daughter, and representatives of the American Association of Neurological Surgeons; and Whereas the Senate is an institution that can raise awareness in the general public and the medical community of Cushing's Syndrome: Now, therefore, be it Resolved, That the Senate-- (1) designates April 8, 2007, as `National Cushing's Syndrome Awareness Day'; (2) recognizes that all Americans should become more informed and aware of Cushing's Syndrome; (3) calls upon the people of the United States to observe the date with appropriate ceremonies and activities; and (4) directs the Secretary of the Senate to transmit a copy of this resolution to the Cushing's Understanding, Support & Help Organization.
  4. Hey! Thought I'd say "hi!" Hava great day!!:~P

  5. A study by University College London (Oct. 2006) revealed that people who drank tea after stressful events were able to de-stress more quickly than those who did not drink tea. The researchers discovered that black tea lowers the levels of cortisol, a harmful stress hormone, by a significant average of 47 percent. No distinction was referenced between decafinated or regular tea. http://www.businessportal24.com/en/Black_T...ing_143589.html
  6. Mortality in Patients Treated for Cushing?s Disease Is Increased, Compared with Patients Treated for Nonfunctioning Pituitary Macroadenoma O. M. Dekkers, N. R. Biermasz, A. M. Pereira, F. Roelfsema, M. O. van Aken, J. H. C. Voormolen and J. A. Romijn Departments of Endocrinology and Metabolic Diseases (O.M.D., N.R.B., A.M.P., F.R., M.O.v.A., J.A.R.), Neurosurgery (J.H.C.V.), and Clinical Epidemiology (O.M.D.), Leiden University Medical Center, 2300 RC Leiden, The Netherlands Address all correspondence and requests for reprints to: O. M. Dekkers, M.D., M.A., Department of Endocrinology and Metabolic Diseases C4-R, Leiden University Medical Center, P.O. Box 9600, 2300 RC Leiden, The Netherlands. E-mail: o.m.dekkers@lumc.nl. Context: Increased mortality in patients with pituitary tumors after surgical treatment has been reported. However, it is unknown to what extent excess mortality is caused by pituitary tumors and their treatment in general and to what extent by previous exposure to hormonal overproduction. Objective: The aim of the study was to compare mortality between patients treated for Cushing?s disease and nonfunctioning pituitary macroadenomas (NFMAs). Design: This was a follow-up study. Patients: We included 248 consecutive patients with pituitary adenomas treated by transsphenoidal surgery in our hospital for NFMAs (n = 174) and ACTH-producing adenomas (n = 74). The mean duration of follow-up after surgery was 10.1 ? 7.2 yr for the whole cohort. Outcome Measures: The standardized mortality ratio (SMR) was calculated for the whole cohort and also for the two diseases separately. Cox regression analysis was used to compare mortality in patients with Cushing?s disease with NFMA patients. Results: Patients with Cushing?s disease (39.1 ? 16.1 yr) were significantly younger at time of operation than NFMA patients (55.3 ? 13.4 yr). The SMR for the whole cohort was 1.41 [95% confidence interval (CI), 1.05?1.86]. The SMR in NFMA patients was 1.24 (95% CI, 0.85?1.74) vs. 2.39 (95% CI, 1.22?3.9) in patients with Cushing?s disease. In patients with Cushing?s disease, compared with NFMAs, the age-adjusted mortality was significantly increased: hazard ratio 2.35 (95% CI, 1.13?4.09, P = 0.008). Conclusions: Mortality in patients previously treated for Cushing?s disease is increased, compared with patients treated for NFMAs. This implies that previous, transient overexposure to cortisol is associated with increased mortality. http://jcem.endojournals.org/cgi/content/abstract/92/3/976
  7. http://www.primenewswire.com/newsroom/news.html?d=113205 Samaritan Pharma Aims At SP-6300 as New Innovative Treatment for Cushing's Syndrome Files New Patent Application for SP-6300 Making Use of SP-01A's Phase II Study Data Drug SP-01A (HIV), SP-6300 (Cushing's) Demonstrates a Statistically Significant Ability to Normalize High Cortisol in Humans High Cortisol Cushing's is Caused by a Long-Term Use of Corticosteroid Medications (Normally Administered to Lupus, Asthma, and Rheumatoid Arthritis Patients) LAS VEGAS, Feb. 6, 2007 (PRIME NEWSWIRE) (PRIMEZONE) -- Samaritan Pharmaceuticals Inc. (AMEX:LIV) a developer of innovative drugs, announced today its drug candidate SP-6300 has shown the ability to modulate excessive cortisol levels by lowering the hormone-stimulated corticosteroid formation in adrenal cells, and as a result could be a potentially new treatment for Cushing's Syndrome. Cushing's Syndrome is a disorder of the adrenal glands leading to excess cortisol secretion. This means that there is too much cortisol hormone in the blood. Cushing's Syndrome is a hormonal disorder caused by prolonged exposure of the body's tissues to high levels of the hormone cortisol. It is sometimes called "hypercortisolism," and an estimated 10 to 15 of every million people are affected each year. Long-term (chronic) use of corticosteroid medications, for the treatment of conditions such as lupus, asthma, and rheumatoid arthritis, is the most common cause of Cushing's Syndrome. Patients who develop Cushing's exhibit a variety of symptoms including weight gain, fatigue, muscle weakness, diabetes, high blood pressure, depression, and osteoporosis. If left untreated, Cushing's Syndrome can lead to death. Dr. Greeson, CEO of Samaritan Pharmaceuticals stated, "There is an urgent need to develop new therapeutic agents, with a new and different mechanism of action, for Cushing's. It is commonly held that the cause of Cushing's is related to patients taking too much corticosteroid medications. We believe the addition of SP-6300 to normally prescribed medications might allow doctors to prescribe smaller doses of corticosteroid medications; to possibly decrease corticosteroid side effects, and increase their efficacy, at the same time." Samaritan Pharmaceuticals: "We LIV... to Save Lives." Samaritan is a small-cap Biotech, driven to discover, develop and commercialize innovative therapeutics' for AIDS, Alzheimer's, Cancer and Heart disease patients. Look at www.samaritanpharma.com. Please register on Website so we can notify you of upcoming conference calls, news and events. Click here: Samaritan Pharmaceuticals -- Samaritan Technology Videos (http://www.samaritanpharma.com/html/videos.html) The Samaritan Pharmaceuticals Inc. logo is available at http://www.primezone.com/newsroom/prs/?pkgid=2670 Disclaimer The company disclaims any information that is created by an outside party and endorses only information that is communicated by its press releases, filings and Website. This news release contains forward-looking statements that reflect management's current beliefs about the potential for its drug candidates, science and technology. However, as with any biopharmaceutical under development, there are significant risks and uncertainties in the process of development and regulatory review. There are no guarantees that products will prove to be commercially successful. For additional information about the factors that affect the company's business, please read the company's latest Form 10-K/A filed November 2, 2006. The company undertakes no duty to update forward-looking statements. CONTACT: Samaritan Pharmaceuticals, Inc. Richard Brown (702) 735-7001 rbrown@SamaritanPharma.com
  8. Hi MaryO, I would also be interested in car ribbon magnets for Cushing's Awareness. Are they available? Thank you!! Meri
  9. Novartis Highlights Strong R&D Pipeline, Plans for Multiple New Product Launches and Novel Projects Moving Into Late-stage Trials (bits & pieces of the press release) ...Late-stage compounds moving into pivotal trials - FTY720 (multiple sclerosis), QAB149 (COPD/asthma), AGO178 (depression), ABF656 (hepatitis C), RAD001 (cancer) and SOM230 (Cushing's disease) ... ...The following compounds are moving into pivotal late-stage trials: FTY720 (fingolimod) for multiple sclerosis, QAB149 (indacaterol) for COPD and asthma, AG0178 (agomelatine) for depression and ABF656 (Albuferon) for hepatitis C as well as RAD001 (everolimus) for cancer and SOM230 (pasireotide) for Cushing's disease. ... ...SOM230 (pasireotide), a next-generation somatostatin analogue therapy, has completed Phase II studies in Cushing's disease, a rare disorder characterized by excessive excretion of the hormone cortisol from a pituitary adenoma (tumor), a condition for which there is no approved medical therapy. Registration studies are set to begin by year end. A registration trial in refractory carcinoid tumors is set to begin in the first quarter of 2007. ... http://www.medadnews.com/News/index.cfm?articleid=394765
  10. The Effects of SOM230 on Cell Proliferation and Adrenocorticotropin Secretion in Human Corticotroph Pituitary Adenomas Dalia L. Batista, Xun Zhang, Roger Gejman, Peter J. Ansell, Yunli Zhou, Sarah A. Johnson, Brooke Swearingen, E. Tessa Hedley-Whyte, Constantine A. Stratakis and Anne Klibanski Neuroendocrine Unit (D.L.B., X.Z., P.J.A., Y.Z., S.A.J., A.K.), Neuropathology Unit (R.G., E.T.H.-W.), and Division of Neurosurgery (B.S.), Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02114; and Section on Endocrinology and Genetics (D.L.B., C.A.S.), Developmental Endocrinology Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 02892 Address all correspondence and requests for reprints to: Anne Klibanski, M.D. Neuroendocrine Unit, Massachusetts General Hospital, 55 Fruit Street, BUL457, Boston, Massachusetts 02114. E-mail: aklibanski@partners.org. Context: There is no tumor-directed medical therapy available for Cushing?s disease. Objective: The objective was to determine the in vitro effect of the somatostatin analog pasireotide (SOM230) on cell proliferation in human corticotroph tumors. Design/Methods: Expression of somatostatin receptors (SSTR 1?5) was determined by quantitative RT-PCR in 13 human corticotroph tumors and by immunohistochemistry (IHC) in 12 of the 13 tumors. SOM230 effects on cell proliferation and ACTH release were evaluated in vitro using primary cultures of six of the 13 human corticotroph adenomas. Results: In our series, we found expression of SSTR subtypes 1, 2, 4, and 5 in human corticotroph tumors by quantitative RT-PCR. All receptor subtypes were detected by IHC, with SSTR subtype 5 having the highest IHC score in 83% (10 of 12) of the cases. Significant suppression of cell proliferation was observed in all tumors cultured (percent suppression range: 10?70%; P = 0.045?0.001). SOM230 inhibited ACTH secretion in five of the six tumors cultured (percent suppression range: 23?56%; P = 0.042?0.001). Conclusion: Corticotroph tumors express multiple SSTR subtypes. SOM230 significantly suppressed cell proliferation and ACTH secretion in primary cultures of human corticotroph tumors. These in vitro results support the hypothesis that SOM230 may have a role in the medical therapy of corticotroph tumors. http://jcem.endojournals.org/cgi/content/abstract/91/11/4482
  11. Sorry, I did not realize that the article had already been posted here-I was just so surprised that my sister told me about it! I have not been able to keep up with the boards recently, otherwise, it appears I would have known about it ten days ago! Thanx for sharing the article and information! Take care. Meri
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