Endocrinology RSS : Gourt

Spectacular Washington State Has it All - Now They Just Need an Endocrinologist! Is That You? :: Washington :: CompHealth Inc

Job 6512322 Board Certified / Board Eligible Endocrinologist to join an established practice with 1 other Endo and 1 NP Special attention paid to an Endocrinologist who has diabetes and thyroid experience

NEW MEDICAL BUILDING UNDER CONSTRUCTION - Outstanding Endocrinology New Mexico Practice :: New Mexico :: CompHealth Inc

Job 6511958 Excellent compensation & benefits that include 5 weeks PTO Plus CME Time 100% Endocrine Practice 100% Outpatient - No Hospital work 4-1/2 day work week J1 Opportunity Malpractice Paid 5

Endocrinologist Sought For Beautiful Maryland Location Just 2 Hours From Baltimore or DC :: Maryland :: CompHealth Inc

Job 6512006 Large multi-specialty practice seeks a 2nd Endocrine Practice 100% Endocrinology 5 day work week; mostly outpatient Outstanding salary and benefits Lovely community with colleges and private

Endocrinologist Needed with a Busy Cardiology Group in Metro Oklahoma !!! :: Oklahoma :: CompHealth Inc

Job 6512430 Join an established group and a waiting patient base in this growing cosmopolitan city Strong interest in diabetes and general Endocrinology is needed Trained or willing to be trained in

Premier MSG Outside of Boston Seeking Experienced Endocrinologist :: Massachusetts :: CompHealth Inc

Job 6512744 Relaxing lifestyle with mainly outpatient practice Established Hospitalist group takes first call -- primarily phone call to offer support regarding the management of gestational diabetes

Endocrinologist Needed on the Space Coast of Sunny Florida! :: Florida :: CompHealth Inc

Job 41280 MD trained Endocrinologist to join one other in a 100% Endocrinology practice with NO CALL! Just an hour away from Orlando Receive production bonuses in year one Must be MD, no DO's, Sorry!

Endocrinology ... Beautiful Maryland Eastern Shore Location :: Maryland :: CompHealth Inc

Job 6512391 Easy drive to Baltimore & Washington, DC 100% Endocrine Well known health system has opened an OUTPATIENT CLINIC on its hospital campus Leadership option available Excellent compensation

100% ENDOCRINOLOGY PRACTICE IN FAIRFIELD COUNTY CONNECTICUT :: Connecticut :: CompHealth Inc

Job 6511770 Well established, 120 doctor multispecialty group with 5 Endos High earning potential 100% outpatient Excellent compensation and great benefits Academic affiliation with top medical school

Pediatric Endocrinologist Position in a outpatient setting :: Missouri :: CompHealth Inc

Job 3114611 Existing patient base awaits Hospitalist in place who cover inpatient duties No procedures - mostly diagnostic Call is done by pager - nurse helps with call Compensation 200K will be discussed

General Pediatrician with Background in Diabetes & Obesity :: Tennessee :: CompHealth Inc

Job 3114452 Join Multi Specialty Group Practice 100% outpatient No C-Section or Delivery Partnership after 2 years MGMA Standards Must be fluent in Spanish 3 Weeks Vacation 1 Week CME with Stipend Medical,

Outstanding Endocrinology Opportunity in Metro Milwaukee ! :: Wisconsin :: CompHealth Inc

Job 6511782 Join a well established, very successful, multi-specialty group Attractive two year guaranteed salary with a bonus formula from day one Wisconsin's most advanced outpatient facility with

Pennsylvania Waterfront Area Needs Endocrinologist !!!!! :: Pennsylvania :: CompHealth Inc

Job 6511783 100% Endocrinology Work New Office Space - Moved in 2 years ago. Majority of work will be office based. Great Call Schedule - Open 4 days per week ADA Certified Diabetes Center - Bone

ENDOCRINOLOGISTS - - COME TO THE CAPITAL OF WISCONSIN! :: Wisconsin :: CompHealth Inc

Job 6511738 Well-established health system 4 to 4 ? day workweek 100% Endo Physician-owned multispecialty group Shareholder opportunity Fabulous benefits Bonus/incentives Malpractice paid PTO, vacation

School of Medicine seeks Pediatric Endocrinologist :: West Virginia :: CompHealth Inc

Job 3114556 Clinical focus rather than research Growing practice 6-8 half days per week Two person team Malpractice with tail Vacation CME with stipend Culturally diverse area Strong public & private

Endocrinologist Sought In Metro Madison, Wisconsin :: Wisconsin :: CompHealth Inc

Job 6511964 100% Endocrinology Join one other Endo in multi-specialty practice Employed position No Call Safe community of 60,000 Full Benefits Excellent compensation Malpractice Paid 20 Days Vacation,

Practice Endocrinology In Beautiful Wisconsin.... :: Wisconsin :: CompHealth Inc

Job 6512297 100% Endocrinology Well established practice with one other Endo in State-of-the-Art Diabetes Center Metropolitan location Affordable Living One of the best states to practice medicine Very

Endocrinology Practice - Cape Cod, Massachusetts :: Massachusetts :: CompHealth Inc

Job 6511786 Outstanding Endocrine opportunity in one of the most scenic areas of New England Full time practice - Can set your schedule (either 4, ten hour days or 5 days 8:30-5 p.m.) No Hospital work

100% Endocrinology On The West Coast of Florida :: Florida :: CompHealth Inc

Job 6512458 100% Endocrinology Partnership after Year 1 Top Multi-Specialty group in the State Walk into ready made practice Generous compensation Great life-style practice Relocation Malpractice Vacation,

DIRECTOR OF ENDOCRINOLOGY IN BOSTON METRO .... :: Massachusetts :: CompHealth Inc

Job 6512607 Outstanding suburban Boston hospital seeks well-trained specialist for administrative/directorship position Practice will encompass inpatient, outpatient, administrative and academic responsibilities

Reproductive Endocrinology Need :: Arizona :: CompHealth Inc

Job 1724562-0001 Assisted Reproductive Therapy OB/GYN Fellowship required Monday through Friday Schedule with some weekends. Sunny Arizona Location Immediate Need Will License for this position We

Expression of Ankyrin Repeat and Suppressor of Cytokine Signaling Box Protein 4 (Asb-4) in Proopiomelanocortin Neurons of the Arcuate Nucleus of Mice Produces a Hyperphagic, Lean Phenotype.

Expression of Ankyrin Repeat and Suppressor of Cytokine Signaling Box Protein 4 (Asb-4) in Proopiomelanocortin Neurons of the Arcuate Nucleus of Mice Produces a Hyperphagic, Lean Phenotype. Endocrinology. 2009 Nov 24; Authors: Li JY, Chai BX, Zhang W, Wang H, Mulholland MW Ankyrin repeat and suppressor of cytokine signaling box-containing protein 4 (Asb-4) is specifically expressed in the energy homeostasis-related brain areas and colocalizes with proopiomelanocortin (POMC) neurons of the arcuate nucleus (ARC). Injection of insulin into the third ventricle of the rat brain increased Asb-4 mRNA expression in the paraventricular nucleus but not in the ARC of the hypothalamus, whereas injection of leptin (ip) increased Asb-4 expression in both mouse paraventricular nucleus and ARC. A transgenic mouse in which Myc-tagged Asb-4 is specifically expressed in POMC neurons of the ARC was made and used to study the effects of Asb-4 on ingestive behavior and metabolic rate. Animals with overexpression of Asb-4 in POMC neurons demonstrated an increase in food intake. However, POMC-Asb-4 transgenic animals gained significantly less weight from 6-30 wk of age. The POMC-Asb-4 mice had reduced fat mass and increased lean mass and lower levels of blood leptin. The transgenic animals were resistant to high-fat diet-induced obesity. Transgenic mice had significantly higher rates of oxygen consumption and carbon dioxide production than wild-type mice during both light and dark periods. The locomotive activity of transgenic mice was increased. The overexpression of Asb-4 in POMC neurons increased POMC mRNA expression in the ARC. The transgenic animals had no observed effect on peripheral glucose metabolism and the activity of the autonomic nervous system. These results indicate that Asb-4 is a key regulatory protein in the central nervous system, involved in the control of feeding behavior and metabolic rate. PMID: 19934378 [PubMed - as supplied by publisher]

Nephroblastoma Overexpressed (Nov) Inactivation Sensitizes Osteoblasts to Bone Morphogenetic Protein-2, But Nov Is Dispensable for Skeletal Homeostasis.

Nephroblastoma Overexpressed (Nov) Inactivation Sensitizes Osteoblasts to Bone Morphogenetic Protein-2, But Nov Is Dispensable for Skeletal Homeostasis. Endocrinology. 2009 Nov 24; Authors: Canalis E, Smerdel-Ramoya A, Durant D, Economides AN, Beamer WG, Zanotti S Overexpression of nephroblastoma overexpressed (Nov), a member of the Cyr 61, connective tissue growth factor, Nov family of proteins, inhibits osteoblastogenesis and causes osteopenia. The consequences of Nov inactivation on osteoblastogenesis and the postnatal skeleton are not known. To study the function of Nov, we inactivated Nov by homologous recombination. Nov null mice were maintained in a C57BL/6 genetic background after the removal of the neomycin selection cassette and compared with wild-type controls of identical genetic composition. Nov null mice were identified by genotyping and absent Nov mRNA in calvarial extracts and osteoblast cultures. Nov null mice did not exhibit developmental skeletal abnormalities or postnatal changes in weight, femoral length, body fat, or bone mineral density and appeared normal. Bone volume and trabecular number were decreased only in 1-month-old female mice. In older mice, after 7 months of age, osteoblast surface and bone formation were increased in females, and osteoclast and eroded surfaces were increased in male Nov null mice. Calvarial osteoblasts from Nov null mice displayed enhanced alkaline phosphatase activity, alkaline phosphatase mRNA, and transactivation of a bone morphogenetic protein (BMP)/phosphorylated mothers against decapentaplegic reporter construct in response to BMP-2. Similar results were obtained after the down-regulation of Nov by RNA interference in ST-2 stromal and MC3T3 cells. Osteoclast number was increased in marrow stromal cell cultures from Nov null mice. Surface plasmon resonance demonstrated direct interactions between Nov and BMP-2. In conclusion, Nov sensitizes osteoblasts to BMP-2, but Nov is dispensable for the maintenance of bone mass. PMID: 19934377 [PubMed - as supplied by publisher]

Functional Effects of Polymorphisms in the Human Gene Encoding 11{beta}-Hydroxysteroid Dehydrogenase Type 1 (11{beta}-HSD1): A Sequence Variant at the Translation Start of 11{beta}-HSD1 Alters Enzyme Levels.

Functional Effects of Polymorphisms in the Human Gene Encoding 11{beta}-Hydroxysteroid Dehydrogenase Type 1 (11{beta}-HSD1): A Sequence Variant at the Translation Start of 11{beta}-HSD1 Alters Enzyme Levels. Endocrinology. 2009 Nov 24; Authors: Malavasi EL, Kelly V, Nath N, Gambineri A, Dakin RS, Pagotto U, Pasquali R, Walker BR, Chapman KE Regeneration of active glucocorticoids within liver and adipose tissue by the enzyme 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1) may be of pathophysiological importance in obesity and metabolic syndrome and is a therapeutic target in type 2 diabetes. Polymorphisms in HSD11B1, the gene encoding 11beta-HSD1, have been associated with metabolic phenotype in humans, including type 2 diabetes and hypertension. Here, we have tested the functional consequences of two single nucleotide polymorphisms located in contexts that potentially affect tissue levels of 11beta-HSD1. We report no effect of allelic variation at rs846910, a polymorphism within the 5'-flanking region of the gene on HSD11B1 promoter activity in vitro. However, compared with the common G allele, the A allele of rs13306421, a polymorphism located two nucleotides 5' to the translation initiation site, gave higher 11beta-HSD1 expression and activity in vitro and was translated at higher levels in in vitro translation reactions, possibly associated with a lower frequency of "leaky scanning." These data suggest that this polymorphism may have direct functional consequences on levels of 11beta-HSD1 enzyme activity in vivo. However, the rs13306421 A sequence variant originally reported in other ethnic groups may be of low prevalence because it was not detected in a population of 600 European Caucasian women. PMID: 19934376 [PubMed - as supplied by publisher]

Molecular Mechanism of the Inhibition of Estradiol-Induced Endometrial Epithelial Cell Proliferation by Clomiphene Citrate.

Molecular Mechanism of the Inhibition of Estradiol-Induced Endometrial Epithelial Cell Proliferation by Clomiphene Citrate. Endocrinology. 2009 Nov 24; Authors: Amita M, Takahashi T, Tsutsumi S, Ohta T, Takata K, Henmi N, Hara S, Igarashi H, Takahashi K, Kurachi H We examined the molecular mechanisms of the antiestrogenic effects of clomiphene citrate (CC) in the endometrium using two types of cell lines, Ishikawa and EM-E6/E7/hTERT cells. CC or ICI182780 inhibited 17beta-estradiol (E2)-induced endometrial cell proliferation and transcriptional activation of the estrogen response element (ERE) gene. We directly visualized the ligand-estrogen receptor (ER)alpha interaction using green fluorescent protein (GFP)-tagged ERalpha in a single living cell. Whereas E2 changed the nuclear localization of GFP-ERalpha to a punctate distribution within 5 min, CC or ICI182780 changed the slower and less mobilization of GFP-ERalpha compared with E2. Pretreatment with CC or ICI182780 partly prevented the E2-induced nuclear redistribution of GFP-ERalpha. Fluorescence recovery after photobleaching revealed that GFP-ERalpha mobility treated with E2 was more rapid than that treated by CC or ICI182780. As coactivator recruitment to the ER is essential for ER-dependent transcription, we examined the interaction between ERalpha and steroid receptor coactivator-1 (SRC-1). The complex formation between ERalpha and SRC-1 was significantly increased by E2 but was prevented in the presence of CC or ICI182780 by coimmunoprecipitation. Moreover, the E2-induced colocalization of GFP-ERalpha and SRC-1 was prevented in the presence of CC or ICI182780 according to an immunofluorescence assay. We also observed that the reduction of SRC-1 using small interfering RNA for SRC-1 resulted in the inhibition of E2-induced cell proliferation and transcriptional activation of the ERE gene. Collectively, these results suggest that CC may inhibit E2-induced endometrial epithelial cell proliferation and ERE transactivation by inhibiting the recruitment of SRC-1 to ERalpha. PMID: 19934375 [PubMed - as supplied by publisher]

Senescence Marker Protein-30/Gluconolactonase Deletion Worsens Glucose Tolerance through Impairment of Acute Insulin Secretion.

Senescence Marker Protein-30/Gluconolactonase Deletion Worsens Glucose Tolerance through Impairment of Acute Insulin Secretion. Endocrinology. 2009 Nov 24; Authors: Hasegawa G, Yamasaki M, Kadono M, Tanaka M, Asano M, Senmaru T, Kondo Y, Fukui M, Obayashi H, Maruyama N, Nakamura N, Ishigami A Senescence marker protein-30 (SMP30) is an androgen-independent factor that decreases with age. We recently identified SMP30 as the lactone-hydrolyzing enzyme gluconolactonase (GNL), which is involved in vitamin C biosynthesis in animal species. To examine whether the age-related decrease in SMP30/GNL has effects on glucose homeostasis, we used SMP30/GNL knockout (KO) mice treated with L-ascorbic acid. In an ip glucose tolerance test at 15 wk of age, blood glucose levels in SMP30/GNL KO mice were significantly increased by 25% at 30 min after glucose administration compared with wild-type (WT) mice. Insulin levels in SMP30/GNL KO mice were significantly decreased by 37% at 30 min after glucose compared with WT mice. Interestingly, an insulin tolerance test showed a greater glucose-lowering effect in SMP30/GNL KO mice. High-fat diet feeding severely worsened glucose tolerance in both WT and SMP30/GNL KO mice. Morphometric analysis revealed no differences in the degree of high-fat diet-induced compensatory increase in beta-cell mass and proliferation. In the static incubation study of islets, insulin secretion in response to 20 mM glucose or KCl was significantly decreased in SMP30/GNL KO mice. On the other hand, islet ATP content at 20 mM in SMP30/GNL KO mice was similar to that in WT mice. Collectively, these data indicate that impairment of the early phase of insulin secretion due to dysfunction of the distal portion of the secretion pathway underlies glucose intolerance in SMP30/GNL KO mice. Decreased SMP30/GNL may contribute to the worsening of glucose tolerance that occurs in normal aging. PMID: 19934374 [PubMed - as supplied by publisher]

Urocortin: a few inflammatory remarks.

Urocortin: a few inflammatory remarks. Endocrinology. 2009 Dec;150(12):5205-7 Authors: Davidson SM, Yellon DM PMID: 19933398 [PubMed - in process]

Insulin-regulated glucagon-like peptide-1 release from L cells: actin' out.

Insulin-regulated glucagon-like peptide-1 release from L cells: actin' out. Endocrinology. 2009 Dec;150(12):5202-4 Authors: Thurmond DC PMID: 19933397 [PubMed - in process]

Lighting up neuronal pathways: the development of a novel transgenic rat that identifies Fos-activated neurons using a red fluorescent protein.

Lighting up neuronal pathways: the development of a novel transgenic rat that identifies Fos-activated neurons using a red fluorescent protein. Endocrinology. 2009 Dec;150(12):5199-201 Authors: Appleyard SM PMID: 19933396 [PubMed - in process]

If I only had a whole brain: the importance of extrahypothalamic areas in the energy balance equation.

If I only had a whole brain: the importance of extrahypothalamic areas in the energy balance equation. Endocrinology. 2009 Dec;150(12):5195-8 Authors: Schneider JE PMID: 19933395 [PubMed - in process]

Pregnancy and pituitary disorders.

Pregnancy and pituitary disorders. Eur J Endocrinol. 2009 Nov 24; Authors: Karaca Z, Tanriverdi F, Unluhizarci K, Kelestimur F Major hormonal changes emerge during pregnancy. The pituitary gland is one of the most affected organs with altered anatomy and physiology. The pituitary gland is enlarged as a result of lactotroph hyperplasia. Due to physiological changes in the pituitary and target hormone levels, binding globulins and placental hormones, hormonal evaluation becomes more complex in pregnant women. As a consequence of physiological hormonal changes, the evaluation of pituitary functions in pregnant women is quite different from the prepregnant state. Pituitary adenomas may cause problems by their hormone secretion that affect the mother and the fetus besides causing an increased risk of tumour growth. Furthermore, diagnosis, course and treatment of pituitary diseases point out differences. The changes in anatomy and physiology of the pituitary gland during pregnancy are reviewed. Pituitary disorders namely Cushing's disease, acromegaly, prolactinoma, TSH secreting, gonadotropin producing and clinically non-functioning adenomas, craniopharingioma, Sheehan's syndrome which is one of the most common causes of hypopituitarism, lymphocytic hypophysitis and hypopituitarism in relation to pregnancy are discussed. Being aware of all this information will prevent any serious problems which mother and child will be exposed to. PMID: 19934270 [PubMed - as supplied by publisher]

Circulating white blood cell count and measures of adipose tissue inflammation predict higher 24 hour energy expenditure.

Circulating white blood cell count and measures of adipose tissue inflammation predict higher 24 hour energy expenditure. Eur J Endocrinol. 2009 Nov 24; Authors: He J, Le DS, Xu X, Scalise M, Ferrante A, Krakoff J Abstract: Objective: Energy expenditure (EE) and measures of inflammation increase with adiposity, and this obesity induced chronic and sub-clinical inflammation was extensively reported to be a cause of insulin resistance. However, whether sub-clinical inflammation has a role in increasing EE to prevent further weight gain which may be at the cost of developing insulin resistance is not clear. Methods: We investigated the association between circulating white blood cell count (WBC) in a population of Native Americans (n=243) with measurement of EE in a respiratory chamber, and in a subset of the same population (n=34), with gene expression measures of inflammation in subcutaneous abdominal adipose tissue (SAAT). All subjects are healthy with oral glucose tolerance test. Statistically, non-normally distributed variables were logarithmically transformed before analyses to approximate normal distributions. Results: WBC was associated with 24EE adjusted for age, sex, fat free mass (FFM) and fat mass (FM) (r=0.13, p=0.04). In SAAT, TNF-alpha shown as log10 transformed TNF-alpha (lTNF-alpha ) (r=0.36, p=0.05) and PAI-1, shown as log10 transformed PAI-1 (lPAI-1) (r=0.41, p=0.02) expression were also positively correlated with adjusted 24hEE. lPAI-1 was also correlated with adjusted sleep EE (r=0.34, p=0.07). Conclusions: In conclusion, circulating markers of inflammation (WBC) and markers of inflammation within adipose tissue (TNF-alpha and PAI-1) are positively associated with energy expenditure indicating expenditure indicating a role of chronic sub-clinical inflammation in the regulation of metabolic rate. PMID: 19934269 [PubMed - as supplied by publisher]

Hemostatic abnormalities in endocrine and metabolic disorders.

Hemostatic abnormalities in endocrine and metabolic disorders. Eur J Endocrinol. 2009 Nov 24; Authors: Franchini M, Lippi G, Manzato F, Vescovi PP, Targher G The hemostatic balance is a complex system where the delicate equilibrium is regulated by several factors, including hormones. This review summarizes current knowledge of the effects of most frequent endocrine and metabolic diseases (such as hypothyroidism, hyperthyroidism, Cushing's syndrome, growth hormone-related pituitary dysfunctions, pituitary prolactin producing adenomas, polycystic ovary syndrome, primary hyperparathyroidism and metabolic syndrome) on coagulation and fibrinolysis. Overt hypothyroidism appears to be associated with a bleeding tendency, whereas all other endocrine diseases appear to be associated with a thrombotic tendency. Globally, the disorders of coagulation and fibrinolysis usually range from mild to moderate, and, rarely, to severe laboratory abnormalities (for example, bleeding diathesis in overt hypothyroidism mainly due to an acquired von Willebrand's disease type 1). Further larger and high-quality studies are needed to provide more definitive information on the effects of endocrine disorders on coagulation and fibrinolysis. PMID: 19934268 [PubMed - as supplied by publisher]

ADMA concentration changes across the menstrual cycle and during oral contraceptive use. The Cardiovascular Risk in Young Finns Study.

ADMA concentration changes across the menstrual cycle and during oral contraceptive use. The Cardiovascular Risk in Young Finns Study. Eur J Endocrinol. 2009 Nov 24; Authors: Valtonen P, Punnonen K, Saarelainen H, Heiskanen N, Raitakari O, Juonala M, Viikari J, Alfthan G, Kähönen M, Laaksonen R, Lyyra-Laitinen T, Laitinen T, Heinonen S Objective: The aim of this study was to evaluate changes in the nitric oxide synthase inhibitor, asymmetric dimethylarginine (ADMA) levels during different menstrual cycle phases in young adult women with or without oral contraceptive (OC) use. Design and Methods: The subjects (n = 1079) originated from a large population-based, prospective cohort study conducted in Finland. Plasma ADMA, symmetric dimethylarginine (SDMA), L-arginine, C-reactive protein, creatinine and brachial artery flow-mediated dilatation (FMD) were measured. The use of OC and menstrual cycle phase were determined from a questionnaire. Results: In non-OC users, ADMA (P = 0.017), L-arginine (P = 0.002) and ADMA/SDMA ratio (P < 0.001) were significantly lower in the luteal phase compared to the follicular phase of the menstrual cycle. Non-OC users also had significantly higher ADMA and SDMA concentrations (P < 0.001) and lower L-arginine concentrations (P < 0.001) compared to OC users with estrogen containing pills. Progestin-only contraceptive pills (POP) did not lower the ADMA level but maintained it at the same level as in non-users. In OC-users, there were no significant differences found in ADMA, FMD or FMD% across menstrual cycle, whereas brachial artery diameter was significantly decreased in the luteal phase (P = 0.013) compared to the follicular phase. Conclusions: We observed that the circulating ADMA concentration varies across the menstrual cycle in young women not using OC and women on OCs displayed significantly lower circulating ADMA concentrations than non-users though this was not the case with POP contraception. PMID: 19934267 [PubMed - as supplied by publisher]

Allelic variations of RANKL/OPG signaling system is related to bone mineral density and in vivo gene expression.

Allelic variations of RANKL/OPG signaling system is related to bone mineral density and in vivo gene expression. Eur J Endocrinol. 2009 Nov 24; Authors: Takacs I, Lazary A, Kosa J, Kiss J, Balla B, Nagy Z, Bacsi K, Speer G, Lakatos P Objective: RANKL/OPG signaling system plays a crucial role in the regulation of bone resorption. Polymorphic variations in the genes may have an influence on gene expression and bone metabolism. In present study, we aimed to investigate the influence of RANKL/OPG allelic variations on the in vivo human gene 5 expression, on bone mineral density (BMD) and on fracture incidence in Hungarian postmenopausal women. Methods: 360 postmenopausal women (61.6 +/- 7.9 years) were genotyped. All together, 5 single nucleotide polymorphisms (SNP) in the 2 genes have been investigated. In addition, bone samples from 17 examined subjects were acquired for gene expression studies. Bone 10 densities and fracture data have also been collected. Results: All 2 SNPs in OPG and 3 SNPs in RANKL genes showed correlation with BMD. Haplotype analysis of these genes gave similar results. The 'CCT' haplotype of RANKL promoter region, that was associated with decreased BMD, exhibited a significantly upregulated expression of RANKL mRNA, while the other haplotypes of RANKL or OPG 15 genes did not. No correlation between genetic variations and fracture data was found. Conclusion: We have demonstrated associations between RANKL and OPG haplotypes and BMD as well as RANKL haplotypes and in vivo RANKL expression in Hungarian postmenopausal population. Moreover we have found a new RANKL haplotype associating with reduced BMD and increased in vivo RANKL expression in human bone tissue. PMID: 19934266 [PubMed - as supplied by publisher]

Cardiac dysfunction is reversed upon successful treatment of Cushing's syndrome.

Cardiac dysfunction is reversed upon successful treatment of Cushing's syndrome. Eur J Endocrinol. 2009 Nov 23; Authors: Pereira A, Delgado V, Romijn J, Smit J, Bax J, Feelders R Objective: In patients with active Cushing's Syndrome (CS), cardiac structural and functional changes have been described in a limited number of patients. It is unknown whether these changes reverse after successful treatment. We therefore evaluated the changes in cardiac structure and dysfunction after successful treatment of CS, using more sensitive echocardiographic parameters (based on 2-dimensional strain imaging) to detect subtle changes in cardiac structure and function. Methods: In a prospective study design, we studied 15 consecutive CS patients and 30 controls (matched for age, sex, body surface area, hypertension, and left ventricular [LV] systolic function). Multidirectional LV strain was evaluated by 2-dimensional speckle tracking strain imaging. Systolic (radial thickening and circumferential and longitudinal shortening) and diastolic (longitudinal strain rate at the isovolumic relaxation time [SRIVRT]) parameters were measured. Results: At baseline, CS patients had similar LV diameters but significantly more LV hypertrophy and impaired LV diastolic function, compared to controls. In addition, CS patients showed impaired LV shortening in the circumferential (-16.5+/-3.5% vs. -19.7+/-3.4%, p=0.013) and longitudinal (-15.9+/-1.9% vs. -20.1+/-2.3%, p<0.001) directions and decreased SRIVRT (0.3+/-0.15 s-1 vs. 0.4+/-0.2 s-1, p=0.012) compared to controls. After normalization of corticosteroid excess, LV structural abnormalities reversed and LV circumferential and longitudinal shortening and SRIVRT normalized. Conclusion: CS not only induces LV hypertrophy and diastolic dysfunction but also subclinical LV systolic dysfunction, that reverses upon normalization of corticosteroid excess. PMID: 19933822 [PubMed - as supplied by publisher]