Endocrinology RSS : Gourt

North Dartmouth :: Massachusetts :: New England Physician Recruitment Center

Endocrine-minutes to Boston and Providence. Salary and Compensation very, very competitive. Ideal Coastal Southern Massachusetts location. Outstanding opportunity for an additional BC/BE Endocrinologist

Williamstown :: Massachusetts :: New England Physician Recruitment Center

Subject: Endocrinology (predominately office based/no call) Great salary plus incentives plus productivity -College Town home of Williams College,Western Massachusetts- 4 day week, close to Albany,

Poughkeepsie :: New York :: New England Physician Recruitment Center

Endocrine Poughkeepsie, NY Southern NY, close to CT border and only 1 hour to NYC- join large multi specialty group with more than 55 providers. 15 primary care physicians. 3 office locations in the

Poughkeepsie :: New York :: New England Physician Recruitment Center

Endocrine Poughkeepsie, NY Southern NY, close to CT border and only 1 hour to NYC- join large multi specialty group with more than 55 providers. 15 primary care physicians. 3 office locations in the

Southbridge :: Massachusetts :: New England Physician Recruitment Center

Endocrinology- West of Boston - Seeking Endocrinologist for full time 100% Endocrine practice. Joining two other part time physicians. Hospital employed. Modern 113-bed hospital which provides quality

Manchester :: Connecticut :: New England Physician Recruitment Center

Endocrinologist needed to join multi-specialty group practice with more than 50 providers. One other Endocrinologist. Practice 100% Endocrine. Employed position. No call. EMR. Reputable group with several

Braintree :: Massachusetts :: New England Physician Recruitment Center

We are a Dyanamic, energetic group seeking Endocrine physicians for adult only practice in beautiful Oceanside community. Joining 5 other physicians and 2 Mid levels. Outpatient only. Office is located

Weymouth :: Massachusetts :: New England Physician Recruitment Center

Endocrinologist- Southshore Massachusetts --Great opportunity 20 minutes south of Boston to join 3 Endocrinologists in Multispecialty Group with 6 office locations south of Boston. 55 providers. All electronic

Hartford :: Connecticut :: New England Physician Recruitment Center

Endocrine-Hartford region-Connecticut Become a partner in one of the most well respected groups in the state of Connecticut. Large multispecialty group in central CT is seeking a third Endocrinologist

Southern :: New Hampshire :: New England Physician Recruitment Center

ENDO 105 -Endocrinologist needed in Southern New Hampshire community. Close to coast. 1 hour to Boston. Small well established group of physicians. Very well respected in the area. Currently have 8 Primary

Hyannis :: Massachusetts :: New England Physician Recruitment Center

Southeastern Massachusetts-Cape Cod- Endocrinologist Developing an endocrinology center of excellence - With more than 400 physicians and 4,600 employees, two acute care hospitals, the Cape's largest

Central :: Connecticut :: New England Physician Recruitment Center

Endocrine-Central Connecticut's leading Physician group. We would like you to join us. The group employs the latest technology to ensure Physician satsfaction and utilization of time. HER (electronic

Hanover :: Massachusetts :: New England Physician Recruitment Center

Great group covering Scituate, Pembroke, Hanover, Norwell , a number of the nicest towns South of Boston and the group admits to SouthShore Hospital with it's teaching affiliates to Brigham. Subject:

Eastern :: New York :: New England Physician Recruitment Center

Endo104-Southern NY, close to CT border-Seeking Endocrinologist to join large multi specialty group with several offices in Southern NY. then practice 100% specialty. well established multi-specialty

Nashua :: New Hampshire :: New England Physician Recruitment Center

Part of a 180-provider multispecialty group located in southern New Hampshire, has an outstanding opportunity for a BC/BE to join its dedicated practice. Call is 1:4. Nashua is located one hour north

Albany :: New York :: New England Physician Recruitment Center

. Academic Endocrinologist, Assistant/Associate Professor level New York, Albany region -650 bed tertiary care center - Working in a collegial environment. Patient care and research. Commitment to teaching

Exeter :: New Hampshire :: New England Physician Recruitment Center

Taxless NH near airport and Ocean and home of the finest prep school in the Country with full use of facilities We need another BC/BE endocrinologist needed immediately to practice in and office based

Boston :: Massachusetts :: New England Physician Recruitment Center

Endocrine-Boston area We are adding an Endocrinologist to join our established multi-specialty group 20 minutes north of Boston. Group has 25 providers. Endocrinologist would be supported by 1 NP,

Boston :: Massachusetts :: New England Physician Recruitment Center

Subject: ENDOCRINE BOSTON Endocrine-Western Boston suburbs with major Harvard teaching , internationally renowned institution at the center of medicine. Adding endocrine with strong emphasis on diabetes.

Boston :: Massachusetts :: New England Physician Recruitment Center

Boston-Lahey main campus-Advancing medicine is our practice. Lahey Clinic Medical Center, Burlington, Massachusetts, a 317-bed, state-of-the-art hospital and outpatient clinic, is a physician-led, multidisciplinary

Adenosine 5'-Monophosphate-Activated Protein Kinase-Mammalian Target of Rapamycin Cross Talk Regulates Brown Adipocyte Differentiation.

Adenosine 5'-Monophosphate-Activated Protein Kinase-Mammalian Target of Rapamycin Cross Talk Regulates Brown Adipocyte Differentiation. Endocrinology. 2010 Feb 4; Authors: Vila-Bedmar R, Lorenzo M, Fernández-Veledo S Brown adipose tissue (BAT) is considered of metabolic significance in mammalian physiology, because it plays an important role in regulating energy balance. Alterations in this tissue have been associated with obesity and type 2 diabetes. The molecular mechanisms modulating brown adipocyte differentiation are not fully understood. Using a murine brown preadipocyte cell line, primary cultures, and 3T3-L1 cells, we analyzed the contribution of various intracellular signaling pathways to adipogenic and thermogenic programs. Sequential activation of p38MAPK and LKB1-AMPK-tuberous sclerosis complex 2 (TSC2) as well as significant attenuation of ERK1/2 and mammalian target of rapamycin (mTOR)-p70 S6 kinase 1 (p70S6K1) activation was observed through the brown differentiation process. This study demonstrates a critical role for AMPK in controlling the mTOR-p70S6K1 signaling cascade in brown but not in 3T3-L1 adipocytes. We observed that mTOR activity is essential in the first stages of differentiation. Nevertheless, subsequent inhibition of this cascade by AMPK activation is also necessary at later stages. An in vivo study showed that prolonged 5-aminoimidazole-4-carboxamide ribonucleoside (AICAR)-induced AMPK activation increases uncoupling protein 1 expression and induces an accumulation of brown adipocytes in white adipose tissue (WAT), as revealed by immunohistology. Moreover, the induction of brown adipogenesis in areas of white fat partially correlates with the body weight reduction detected in response to treatment with AICAR. Taken together, our study reveals that differentiation of brown adipocytes employs different signaling pathways from white adipocytes, with AMPK-mTOR cross talk a central mediator of this process. Promotion of BAT development in WAT by pharmacological activation of AMPK may have potential in treating obesity by acting on energy dissipation. PMID: 20133456 [PubMed - as supplied by publisher]

Role of Estradiol in the Dynamic Control of Tanycyte Plasticity Mediated by Vascular Endothelial Cells in the Median Eminence.

Role of Estradiol in the Dynamic Control of Tanycyte Plasticity Mediated by Vascular Endothelial Cells in the Median Eminence. Endocrinology. 2010 Feb 4; Authors: de Seranno S, d'Anglemont de Tassigny X, Estrella C, Loyens A, Kasparov S, Leroy D, Ojeda SR, Beauvillain JC, Prevot V In the ever-changing physiological context of the neuroendocrine brain, the mechanisms by which cellular events involving neurons, astroglia, and vascular cells are coordinated to bring forth the appropriate neuronal signaling is not yet known but is amenable to examination. In the median eminence of the hypothalamus, endothelial cells are key players in the plasticity of tanycytes (specialized astroglia) and neuroendocrine synapse efficacy. Here we report that estradiol acts on both purified endothelial cells and isolated tanycytes to trigger endothelial-to-glial communication that leads to a sudden and massive retraction of tanycyte processes. The blockade of endothelial nitric oxide synthase by in vitro adenoviral-mediated gene transfer of a dominant-negative form of endothelial nitric oxide synthase abrogates the estradiol-induced tanycyte plasticity mediated by endothelial cells. In parallel, increases in prostaglandin-E2 (PGE2) due to changes in cyclooxygenase (COX)-1 and COX-2 expression induced by the exposure of tanycytes to estradiol promote acute tanycyte plasticity. We also demonstrate by electron microscopy that the administration of PGE2 to median eminence explants induces rapid neuroglial plasticity at the neurovascular junction of neurons that release GnRH (the neuropeptide controlling reproduction). Conversely, preventing local PGE2 synthesis in the median eminence of adult female rats with the COX inhibitor indomethacin impairs the ovarian cycle, a process that requires a pulsatile, coordinated delivery of GnRH into the hypothalamo-hypophyseal portal system. Taken together, our findings show that estradiol controls the dialog between endothelial cells and astroglia to regulate neuroglial plasticity in the neuroendocrine brain. PMID: 20133455 [PubMed - as supplied by publisher]

The Levels of the Endocannabinoid Receptor CB2 and Its Ligand 2-Arachidonoylglycerol Are Elevated in Endometrial Carcinoma.

The Levels of the Endocannabinoid Receptor CB2 and Its Ligand 2-Arachidonoylglycerol Are Elevated in Endometrial Carcinoma. Endocrinology. 2010 Feb 4; Authors: Guida M, Ligresti A, De Filippis D, D'Amico A, Petrosino S, Cipriano M, Bifulco G, Simonetti S, Orlando P, Insabato L, Nappi C, Di Spiezio Sardo A, Di Marzo V, Iuvone T The endocannabinoid system plays protective roles against the growth and the spreading of several types of carcinomas. Because estrogens regulate this system both in physiological states and cancer, in this paper we evaluated its involvement in endometrial carcinoma, a well-known estrogen-dependant tumor. To test whether the endocannabinoid system is expressed in endometrial cancer, tissue samples were collected both from 18 patients undergoing surgical treatment for endometrial adenocarcinoma and 16 healthy age-matched controls, and treated for Western blot and immunohistochemical analysis. Moreover, tissues were dounce homogenized and submitted to endocannabinoid measurement by liquid chromatography-mass spectrometry. To evaluate the physiological role of the endocannabinoid system, a human endometrial cancer cell-line (AN3CA) was used and transiently transfected with a plasmid containing the cDNA for the endocannabinoid receptor CB2. Cells were incubated for 48 h with an agonist (JWH133) (10 muM) or antagonist (SR144528) (1 muM) of CB2 24 h after transfection, and cell proliferation was measured by the 3-[4,5-dimethyltiazol-2yl]-2,5 diphenyltetrazolium bromide formazan assay. In human endometrial carcinoma biopsies the expression of CB2 receptor and the levels of its ligand, 2-arachidonoylglycerol increased, whereas monoacylglyerol lipase, an enzyme responsible for 2-arachidonoylglycerol degradation, was down-regulated. Immunohystochemical analysis revealed that CB2 was overexpressed only in malignant endometrial cells. CB2-overexpressing AN3CA cells showed a significant reduction in cell vitality compared with parental AN3CA cells: incubation with the selective CB2 antagonist SR144128 restored the viability of CB2-overexpressing cells to that of untransfected cells. In conclusion, the endocannabinoid system seems to play an important role in human endometrial carcinoma, and modulation of CB2 activity/expression may account for a tumor-suppressive effect. PMID: 20133454 [PubMed - as supplied by publisher]

Growth Activation Alone Is Not Sufficient to Cause Metastatic Thyroid Cancer in a Mouse Model of Follicular Thyroid Carcinoma.

Growth Activation Alone Is Not Sufficient to Cause Metastatic Thyroid Cancer in a Mouse Model of Follicular Thyroid Carcinoma. Endocrinology. 2010 Feb 4; Authors: Lu C, Zhao L, Ying H, Willingham MC, Cheng SY TSH is the major stimulator of thyrocyte proliferation, but its role in thyroid carcinogenesis remains unclear. To address this question, we used a mouse model of follicular thyroid carcinoma (FTC) (TRbeta(PV/PV) mice). These mice, harboring a dominantly negative mutation (PV) of the thyroid hormone-beta receptor (TRbeta), exhibit increased serum thyroid hormone and elevated TSH. To eliminate TSH growth-stimulating effect, TRbeta(PV/PV) mice were crossed with TSH receptor gene knockout (TSHR(-/-)) mice. Wild-type siblings of TRbeta(PV/PV) mice were treated with an antithyroid agent, propylthiouracil, to elevate serum TSH for evaluating long-term TSH effect (WT-PTU mice). Thyroids from TRbeta(PV/PV)TSHR(-/-) showed impaired growth with no occurrence of FTC. Both WT-PTU and TRbeta(PV/PV) mice displayed enlarged thyroids, but only TRbeta(PV/PV) mice developed metastatic FTC. Molecular analyses indicate that PV acted, via multiple mechanisms, to activate the integrins-Src-focal adhesion kinase-p38 MAPK pathway and affect cytoskeletal restructuring to increase tumor cell migration and invasion. Thus, growth stimulated by TSH is a prerequisite but not sufficient for metastatic cancer to occur. Additional genetic alterations (such as PV), destined to alter focal adhesion and migration capacities, are required to empower hyperplastic follicular cells to invade and metastasize. These in vivo findings provide new insights in understanding carcinogenesis of the human thyroid. PMID: 20133453 [PubMed - as supplied by publisher]

Prenatal Dexamethasone Programs Expression of Genes in Liver and Adipose Tissue and Increased Hepatic Lipid Accumulation But Not Obesity on a High-Fat Diet.

Prenatal Dexamethasone Programs Expression of Genes in Liver and Adipose Tissue and Increased Hepatic Lipid Accumulation But Not Obesity on a High-Fat Diet. Endocrinology. 2010 Feb 4; Authors: Drake AJ, Raubenheimer PJ, Kerrigan D, McInnes KJ, Seckl JR, Walker BR The association between low birth weight and cardiovascular disease is amplified by the development of obesity. We explored the effects of postnatal high-fat (HF) feeding in dexamethasone (Dex)-programmed rats, in which prenatal glucocorticoid overexposure is associated with reduced birth weight and adult glucose intolerance. Male Wistar rats exposed to Dex or vehicle (Veh) during the last week of gestation were weaned onto HF or control diets for 6 months. Dex-exposed animals were of lower birth weight and showed catch-up growth by 7 wk. There were no differences in obesity or hyperinsulinaemia between Dex-HF and Veh-HF animals. However, Dex-HF animals had increased hepatic triglyceride content compared with Veh-HF animals. mRNA transcript profiles in adipose tissue revealed depot-specific changes in the expression of genes involved in fatty acid esterification and triglyceride synthesis and storage with prenatal Dex exposure. Thus, antenatal glucocorticoid overexposure in rats does not confer increased sensitivity to HF diet-induced obesity, but increases susceptibility to fatty liver. This may be due to depot-specific-programmed alterations in fat metabolism in adipose tissue. PMID: 20133452 [PubMed - as supplied by publisher]

15-Deoxy-{Delta}12-14-Prostaglandin-J2 Induces Hypertrophy and Loss of Contractility in Human Testicular Peritubular Cells: Implications for Human Male Fertility.

15-Deoxy-{Delta}12-14-Prostaglandin-J2 Induces Hypertrophy and Loss of Contractility in Human Testicular Peritubular Cells: Implications for Human Male Fertility. Endocrinology. 2010 Feb 4; Authors: Schell C, Albrecht M, Spillner S, Mayer C, Kunz L, Köhn FM, Schwarzer U, Mayerhofer A The wall of the seminiferous tubules contains contractile smooth-muscle-like peritubular cells, thought to be important for sperm transport. Impaired spermatogenesis in men typically involves remodeling of this wall, and we now found that smooth muscle cell (SMC) markers, namely myosin heavy chain (MYH11) and smooth muscle actin (SMA) are often lost or diminished in peritubular cells of testes of men with impaired spermatogenesis. This suggests reduced contractility of the peritubular wall, which may contribute to sub- or infertility. In these cases, testicular expression of cyclooxygenase-2 (COX-2) implies formation of prostaglandins (PGs). When screening different PGs for their ability to target human testicular peritubular cells (HTPCs), only a PG metabolite, 15-deoxy-Delta(12-14)-prostaglandin-J2 (15dPGJ2), was effective. In primary cultures of HTPCs, 15dPGJ2 increased cell size in a reversible manner. Importantly, 15dPGJ2 treatment resulted in a loss of typical differentiation markers for SMCs, namely MYH11, calponin, and SMA, whereas fibroblast markers were unchanged. Collagen gel contraction assays revealed that this loss correlates with a reduced ability to contract. Experiments with an antagonist (bisphenol A diglycidyl ether) and agonist (troglitazone) for a cognate 15dPGJ2 receptor (i.e. peroxisome proliferator-activated receptor-gamma) indicated that peroxisome proliferator-activated receptor-gamma is not directly involved. Rather, the mode of action of 15dPGJ2 involves reactive oxygen species. The antioxidant N-acetylcysteine not only blocked ROS formation but also prevented the increase in cell size and the loss of contractility in HTPCs challenged with 15dPGJ2. We conclude that 15dPGJ2, via reactive oxygen species, influences SMC phenotype and contractility of human peritubular cells and possibly is involved in the development of human male sub-/infertility. PMID: 20133451 [PubMed - as supplied by publisher]

First report of combined ectopic ACTH-syndrome and PTHrP-induced hypercalcemia due to a hepatoblastoma.

First report of combined ectopic ACTH-syndrome and PTHrP-induced hypercalcemia due to a hepatoblastoma. Eur J Endocrinol. 2010 Feb 4; Authors: Grunewald T, von Luettichau I, Welsch U, Dörr H, Höpner FH, Kovacs K, Burdach S, Rabl W Context: Only occasionally endocrine active tumors develop directly from hepatic tissue and may lead to paraneoplastic syndromes (PNS). PNS mostly accompany malignancy of adulthood and are exceedingly rare in children. Patient: A 6 9/12 years old girl presented with a 2-month history of rapidly progressive weight gain, abdominal distension and polyuria/pollakisuria accompanied by short episodes of abdominal pain. She showed the typical clinical features of Cushing's syndrome and a huge hepatic mass. An abdominal CT scan revealed a large liver tumor. Blood glucose and serum calcium were greatly elevated. Design and objective: Case report describing the causative relationship of the clinical findings. Methods: Physical examination; ultrasound of the abdomen; CT scan of the abdomen and the chest; conventional X-rays; routine hematology; blood chemistry and multiple parameters of calcium and phosphorus metabolism; multi-steroid analysis in serum and urine; adrenocortical stimulation and suppression tests; histopathological assessment of the resected tumor; immunohistochemistry for ACTH, beta-endorphin, CRH and PTHrP; electron microscopy of tumor cells; ACTH and CRH extraction from the tumor tissue; clinical follow-up for more than 20 years. Results: Giant hepatoblastoma (approx. 1000 ml volume) of the right lobe of the liver with combined ectopic ACTH-syndrome and PTHrP-induced tumor-associated hypercalcemia. Wide local excision and polychemotherapy led to complete reversal of the paraneoplastic phenotype. Conclusions: This is the first report of an endocrine active hepatoblastoma causing both Cushing's syndrome and PTHrP-related "humoral hypercalcemia of malignancy". This information should be added to the well-known beta-hCG-related paraneoplastic effects of hepatoblastoma in children. PMID: 20133447 [PubMed - as supplied by publisher]

The impact of the CAG-repeat polymorphism of the androgen receptor gene on muscle and adipose tissues in 20-29 year-old Danish men: Odense Androgen Study.

The impact of the CAG-repeat polymorphism of the androgen receptor gene on muscle and adipose tissues in 20-29 year-old Danish men: Odense Androgen Study. Eur J Endocrinol. 2010 Feb 4; Authors: Nielsen T, Hagen C, Wraae K, Bathum L, Larsen R, Brixen K, Andersen M Background: The number of CAG-repeats (CAG(N)) within the CAG-repeat polymorphism of the androgen receptor gene correlates inversely with the transactivation of the receptor. Objective: To examine the impact of CAG(N) on muscle, fat distribution, and circulating androgen levels. Design, settings and participants: Population-based, cross-sectional study of 783 Danish men aged 20-29 years. Methods: Genotyping was performed in 767 men. Areas of thigh and lower trunk muscle (Muscle(Thigh) and Muscle(LowerTrunk)), subcutaneous adipose tissues (SAT(Thigh) and SAT(LowerTrunk)), and deep adipose tissues (intramuscular and visceral) were measured in 393 men by magnetic resonance imaging (MRI). Lean body mass (LBM) and fat mass (FM) were obtained in all men by whole body dual-energy X-ray absorptiometry (DXA). The absolute areas acquired by MRI were the main outcomes. The absolute DXA measurements and relative assessments of both modalities were considered secondary outcomes. Results: CAG(N) (range: 10-32) correlated inversely with absolute Muscle(Thigh) (r=0.108), absolute Muscle(LowerTrunk) (r=0.132), relative Muscle(Thigh) (r=0.128), relative Muscle(LowerTrunk) (r=0.126), relative LBM(LowerExtremity) (r=0.108), and relative LBM(Total) (r=0.082) and positively with relative SAT(Thigh) (r=0.137), relative SAT(LowerTrunk) (r=0.188), relative FM(LowerExtremity) (r=0.107), and relative FM(Total) (r=0.082). These relationships remained significant controlling for physical activity, smoking, chronic disease, and age. CAG(N) didn't correlate with any circulating androgen. Conclusions: The CAG-repeat polymorphism affects body composition in young men: Absolute Muscle(Thigh) and absolute Muscle(LowerTrunk) increase as CAG(N) decrease. Expressed relatively, muscle areas and LBM increase, while subcutaneous adipose tissues and FM decrease as CAG(N) decrease. The polymorphism does not affect deep adipose tissues or circulating androgens levels in young men. PMID: 20133446 [PubMed - as supplied by publisher]

Fractionated stereotactic radiotherapy in patients with acromegaly. Interim single centre audit.

Fractionated stereotactic radiotherapy in patients with acromegaly. Interim single centre audit. Eur J Endocrinol. 2010 Feb 4; Authors: Roug S, Rasmussen A, Juhler M, Kosteljanetz M, Poulsgaard L, Heeboell H, Roed H, Feldt-Rasmussen U Aim: To evaluate the effect of fractionated stereotactic radiotherapy (FSRT) in acromegaly in a retrospective analysis. Patients and methods: Thirty-four patients (17 females, median 43 years (range 30-74)) with acromegaly were treated with FSRT (conformal dynamic arcing, dose 54 Gy, 27-30 fractions) between January 1998 and April 2007. Thirty-two of the 34 patients had undergone transsphenoidal adenotomy, and 28 were on medical therapy before FSRT. Patients on medical therapy continued this during and after the irradiation. The treatment was gradually decreased/withdrawn after careful assessment. Results: MR scanning of the pituitary gland 34 months (median, range 11-95) after irradiation showed stable or reduced volume of the remaining tumour tissue in 31 of 34 patients (91%). Seventeen patients (50%) were biochemically controlled (normalised nadir growth hormone during OGTT and insulin-like growth factor-I (IGF-1) <+2SD) 30 months after FSRT (median, range 6-60), ten of them had true biochemical remission (off medical therapy) 30 months after FSRT (median, range 12-69). Eight of 28 patients (29%) with one or more functioning pituitary axes before irradiation developed further deficit of 1 or 2 pituitary axes 48 months (median, range 6-102) after FSRT. Twenty of 34 patients still required medical treatment for acromegaly at the end of this study, mainly those with a short follow-up period after irradiation. Conclusion: The FSRT treatment seems promising in terms of treatment of acromegaly. Longer follow-up is, however, needed to assess the overall efficacy and safety of FSRT for acromegaly. PMID: 20133445 [PubMed - as supplied by publisher]