Alternative meaning: Organisation (band).

An organization or organisation (read more about -ize vs -ise) is a formal group of people with one or more shared goals. The word itself is derived from the Greek word ὄργανον (organon) meaning tool. The term is used in both daily and scientific English in multiple ways.

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Permanent Endocrinology Job in Greater Kansas City metropolitan area Missouri with BioPointe
Endocrinologist needed for a practice located in the Greater Kansas City metropolitan area. The practice is an independent, well-established, freestanding mid-sized endocrine practice, which is 100%
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Seeking ambitious Endocrinologist to join progressive group that consists of 100% endocrinology.3 Endocrinologists and 6 Physician Assistants. Will consider flexible employment options. Call every
Permanent Endocrinology Job in Southern MI Michigan with BioPointe
A private practice consisting of three Internists, a Geriatrician, and three Rheumatologists wants to add an Endocrinologist to meet the need resulting from the relocation of an Endocrinologist who practiced

pubmed: 0013-7227

Effects of maternal global nutrient restriction on fetal baboon hepatic IGF system genes and gene products.
Li C, Schlabritz-Loutsevitch NE, Hubbard GB, Han V, Nygard K, Cox LA, McDonald TJ, Nathanielsz PW Effects of maternal global nutrient restriction on fetal baboon hepatic IGF system genes and gene products. Endocrinology. 2009 Jul 2; Authors: Li C, Schlabritz-Loutsevitch NE, Hubbard GB, Han V, Nygard K, Cox LA, McDonald TJ, Nathanielsz PW Knowledge of altered maternal nutrition effects on growth regulating systems is critical to understanding normal and abnormal fetal development. There are many reports of hepatic fetal insulin-like growth factor (IGF) system responses to maternal nutrient restriction (MNR) during pregnancy in rodents and sheep, but none in nonhuman primates. We determined effects of MNR on the fetal baboon hepatic IGF system. Social groups of female baboons were fed ad libitum, controls (CTR) or 70% CTR (MNR) from 0.16 - 0.5 gestation and fetuses delivered by cesarean section. Fetal liver tissue was analyzed for IGF-I, IGF-II and IGFBP-3 mRNA by in situ hybridization (ISH) and QRT-PCR and protein by immunohistochemistry (IHC); IGF-1R, IGF-2R by QRT-PCR and IHC and IGFBP-1 by ISH and IHC. MNR did not alter fetal body or liver weight. Fetal hepatic glycogen staining increased with MNR. MNR reduced fetal hepatic IGF-I and IGF-II and increased IGFBP-1 mRNA and decreased IGF-I, IGF-II, IGF-1R and IGF-2R protein while increasing protein for IGFBP-1 and IGFBP-3. MNR increased Caspase-3 indicating apoptosis and decreased Akt staining indicating decreased nutrient sensing. In conclusion, while fetal body and liver weights did not change in response to moderate MNR during the first half of baboon pregnancy, the major indices of function of the hepatic IGF system measured were all reduced. PMID: 19574404 [PubMed - as supplied by publisher]
Developmental Changes in Pituitary PACAP Expression during the Perinatal Period: Possible Role in Fetal Gonadotroph Regulation.
Moore JP, Villafuerte BC, Unick CA, Winters SJ Developmental Changes in Pituitary PACAP Expression during the Perinatal Period: Possible Role in Fetal Gonadotroph Regulation. Endocrinology. 2009 Jul 2; Authors: Moore JP, Villafuerte BC, Unick CA, Winters SJ Normal reproductive functioning may require secretion of LH independently of FSH. Variation in GnRH pulse frequency and inhibin negative feedback are mechanisms for differential gonadotropin regulation; however, the first instance of differential regulation in rats is during fetal development, prior to the establishment of GnRH connections, when LH accumulates appreciably 2-4 days prior to FSH. PACAP can differentially regulate the gonadotropins in vitro by stimulating alpha-subunit transcription, lengthening LHbeta transcripts and decreasing FSHbeta mRNA levels probably through stimulation of follistatin transcription. These experiments are the first to examine whether PACAP influences gonadotroph function in perinatal pituitaries. In vivo, pituitary PACAP mRNA and peptide levels were high at E19 and declined by 94% and 85%, respectively, after parturition. This was accompanied by a decrease of 65% and 96% in total follistatin and follistatin-288 mRNAs. These changes were temporally associated with a 20-and 6.5-fold rise in FSHbeta and GnRH-R mRNAs respectively, with no significant increase in LHbeta mRNA. In pituitary cell cultures from fetal and postnatal male rats, PACAP mRNA levels were likewise highest in fetal cultures in which the PACAP 6-38 antagonist decreased alpha-subunit and increased FSHbeta mRNA. PACAP 6-38 also reduced basal and GnRH-stimulated LH secretion with little effect on FSH. These data support the hypothesis that PACAP expressed at high levels in the fetal pituitary stimulates alpha-subunit expression and LH secretion, and restrains FSH synthesis relative to LH, and that a decline in PACAP allows for the neonatal rise in FSH and GnRH-R because follistatin is decreased. PMID: 19574403 [PubMed - as supplied by publisher]
The Human Lipodystrophy Gene Product BSCL2/Seipin Plays a Key Role in Adipocyte Differentiation.
Chen W, Yechoor VK, Chang BH, Li MV, March KL, Chan L The Human Lipodystrophy Gene Product BSCL2/Seipin Plays a Key Role in Adipocyte Differentiation. Endocrinology. 2009 Jul 2; Authors: Chen W, Yechoor VK, Chang BH, Li MV, March KL, Chan L Mutations in the Berardinelli-Seip congenital lipodystrophy 2 gene (BSCL2) are the underlying defect in patients with congenital generalized lipodystrophy type 2. BSCL2 encodes a protein called seipin, whose function is largely unknown. In this study, we investigated the role of Bscl2 in the regulation of adipocyte differentiation. Bscl2 mRNA is highly upregulated during standard hormone-induced adipogenesis in 3T3-L1 cells in vitro. However, this upregulation does not occur during mesenchymal stem cell (C3H10T1/2 cells) commitment to the preadipocyte lineage. Knockdown of Bscl2 by short hairpin RNA (shRNA) in C3H10T1/2 cells has no effect on BMP4-induced preadipocyte commitment. However, knockdown in 3T3-L1 cells prevents adipogenesis induced by a standard hormone cocktail but adipogenesis can be rescued by the addition of PPARgamma agonist pioglitazone at an early stage of differentiation. Interestingly, pioglitazone-induced differentiation in the absence of standard hormone is not associated with upregulated Bscl2 expression. On the other hand, shRNA-knockdown of Bscl2 largely blocks pioglitazone-induced adipose differentiation. These experiments suggest that Bscl2 may be essential for normal adipogenesis; it works upstream or at the level of PPARgamma, enabling the latter to exert its full activity during adipogenesis. Loss of Bscl2 function thus interferes with the normal transcriptional cascade of adipogenesis during fat cell differentiation, resulting in near total loss of fat or lipodystrophy. PMID: 19574402 [PubMed - as supplied by publisher]
INSULIN RECEPTOR SUBSTRATE 2 IN {beta}-CELLS DECREASES DIABETES IN NON-OBESE DIABETIC (NOD) MICE.
Norquay LD, D'Aquino KE, Opare-Addo LM, Kuznetsova A, Haas M, Bluestone JA, White MF INSULIN RECEPTOR SUBSTRATE 2 IN {beta}-CELLS DECREASES DIABETES IN NON-OBESE DIABETIC (NOD) MICE. Endocrinology. 2009 Jul 2; Authors: Norquay LD, D'Aquino KE, Opare-Addo LM, Kuznetsova A, Haas M, Bluestone JA, White MF Insulin receptor substrate-2 (Irs2) integrates insulin-like signals with glucose and cAMP agonists to regulate beta-cell growth, function and survival. This study investigated whether increased Irs2 concentration in beta-cells could reduce beta-cell destruction and the incidence of type 1 diabetes in non-obese diabetic (NOD) mice. NOD-mice were intercrossed with C57Bl/6 mice overexpressing Irs2 specifically in beta-cells to create NOD(Irs2)-mice. After backcrossing NOD(Irs2)-mice for 12 generations, glucose homeostasis and diabetes incidence were compared against NOD littermates. Compared to 12-week old NOD-mice, the progression of severe insulitis was reduced and islet mass was increased in NOD(Irs2)-mice. Moreover, the risk of diabetes decreased 50% in NOD(Irs2)-mice until the experiment was terminated at 40 weeks of age. Nondiabetic NOD(Irs2)-mice displayed better glucose tolerance than nondiabetic NOD-mice throughout the duration of the study and up to the age of 18 months. The effect of Irs2 to increase islet mass and improve glucose tolerance raised the possibility that NOD(Irs2)-mice might have an increased capacity to respond to anti-CD3 antibody, which can induce remission of overt diabetes in some NOD mice. Anti-CD3 antibody injections restored glucose tolerance in newly diabetic NOD- and NOD(Irs2)-mice; however, anti-CD3-treated NOD(Irs2)-mice were less likely than NOD-mice to relapse during the experimental period, as they displayed 10-fold greater beta-cell mass and mitogenesis. In conclusion, increased Irs2 attenuated the progression of beta-cell destruction, promoted beta-cell mitogenesis, and reduced diabetes incidence in NOD(Irs2)-mice. PMID: 19574401 [PubMed - as supplied by publisher]
Epigenetic Changes in Ovarian Cancer.
Balch C, Fang F, Matei DE, Huang TH, Nephew KP Epigenetic Changes in Ovarian Cancer. Endocrinology. 2009 Jul 2; Authors: Balch C, Fang F, Matei DE, Huang TH, Nephew KP Epigenetic aberrations, including DNA methylation, histone modifications, and microRNA dysregulation, are now well established in the development and progression of ovarian cancer, and their gradual accumulation is associated with advancing disease stage and grade. Epigenetic aberrations are relatively stable, associated with distinct disease subtypes, and present in circulating serum, representing promising diagnostic, prognostic, and pharmacodynamic biomarkers. In contrast to DNA mutations and deletions, aberrant gene-repressive epigenetic modifications are potentially reversible by epigenetic therapies, including inhibitors of DNA methylation or histone-modifying enzymes. Although epigenetic monotherapies have not shown activity against solid tumors, including ovarian cancer, preclinical studies suggest they will be effective when used in combination with one another or with conventional chemotherapeutics, and combinatorial epigenetic therapy regiments are being examined in cancer clinical trials. A greater understanding of the role of epigenetics in ovarian neoplasia will provide for improved interventions against this devastating malignancy. PMID: 19574400 [PubMed - as supplied by publisher]
Gonadotropin releasing hormone-mediated phosphorylation of estrogen receptor {alpha} contributes to fosB expression in mouse gonadotrophs.
Chen J, An BS, Cheng L, Hammond GL, Leung PC Gonadotropin releasing hormone-mediated phosphorylation of estrogen receptor {alpha} contributes to fosB expression in mouse gonadotrophs. Endocrinology. 2009 Jul 2; Authors: Chen J, An BS, Cheng L, Hammond GL, Leung PC Estrogen receptors (ERs) are activated by their ligands as well as by signaling pathways that alter ER phophorylation in response to peptide hormones and growth factors. In pituitary gonadotrophs, gonadotropin releasing hormones (GnRHs) act via the type I GnRH receptor (GnRHR). Both GnRH subtypes (GnRH-I and GnRH-II) activate an estrogen response element (ERE)-driven luciferase reporter gene in LbetaT2 mouse pituitary cells, and GnRH-I is most potent in this regard. Moreover, antide (a GnRH antagonist) and a GnRHR siRNA abrogate this effect, while an ERalpha antagonist (ICI 182,780) does not. The ERalpha in LbetaT2 cells is phosphorylated at Ser(118) in the nucleus and at Ser(167) in both nucleus and cytoplasm after GnRH treatments, coincided with increased ERalpha binding to its co-activator, the p300/CBP-associated factor (PCAF). Moreover, siRNA-mediated knockdown of PCAF levels attanuated GnRH-induced ERE-luciferase trans-activation in these cells. Most importantly, both GnRH subtypes robustly up-regulated expression of the immediate early response gene, fosB, while co-treatment with ERalpha siRNA or PCAF siRNA attenuated this effect. This appears to occur at the transcriptional level because co-recruitment of ERalpha and PCAF to an ERE within the endogenous fosB promoter was increased by GnRH treatments, as shown by chromatin immunoprecipitation assays. These data demonstrate that GnRH-mediated phosphorylation of ERalpha in mouse LbetaT2 pituitary cells results in its rapid association with PCAF and the transcriptional activation of fosB, and we demonstrate that this in turn likely activates other genes in pituitary cells including the follicle-stimulating hormone beta subunit gene. PMID: 19574399 [PubMed - as supplied by publisher]
Metformin inhibits aromatase via an ERK (extracellular signal-regulated kinase) - mediated pathway.
Rice S, Pellatt L, Ramanathan K, Whitehead SA, Mason HD Metformin inhibits aromatase via an ERK (extracellular signal-regulated kinase) - mediated pathway. Endocrinology. 2009 Jul 2; Authors: Rice S, Pellatt L, Ramanathan K, Whitehead SA, Mason HD Metformin treatment, now widely prescribed in PCOS, is aimed at correcting the associated insulin resistance, but it has also been shown to directly inhibit ovarian steroidogenesis. The mechanisms however, by which metformin inhibits oestradiol production in human granulosa cells remain unknown. Granulosa luteal cells were incubated with metformin, insulin or combined metformin and insulin treatment and aromatase mRNA expression was quantified using real-time PCR. Enzyme activity was assessed by the conversion of (3)H-androstenedione to oestrone and oestradiol. Metformin's effect on the expression of specific untranslated first exon aromatase promoters was analyzed using semi-quantitative PCR. The involvement of MEK/ERK pathway was investigated by immunoblotting for aromatase, phosphorylated and total ERK-1,2 from cells cultured as above with/without the MEK inhibitor PD98059. Metformin significantly inhibited basal and insulin-stimulated aromatase mRNA expression, with parallel results from the aromatase activity assay and protein assessment. This suppression was via down-regulation of aromatase promoter II, I.3 and I.4 expression and was reversed by the addition of PD98059. Involvement of the ERK signalling pathway was demonstrated by the significant increase in phosphorylated ERK- 1,2 with the combined metformin and insulin treatement. We have shown for the first time in human granulosa cells that metformin significantly attenuated basal and insulinstimulated P450 aromatase mRNA expression and activity, via silencing of key promoters. This occurred by activation of MEK/ERK pathway which negatively regulates aromatase production. This is an important consideration given metformin's widespread use in PCOS and may further support a possible therapeutic indication in oestrogendependent breast tumours. PMID: 19574398 [PubMed - as supplied by publisher]
AN IN VIVO STUDY ON ADJUDIN AND BLOOD-TESTIS BARRIER DYNAMICS.
Kopera IA, Su L, Bilinska B, Cheng CY, Mruk DD AN IN VIVO STUDY ON ADJUDIN AND BLOOD-TESTIS BARRIER DYNAMICS. Endocrinology. 2009 Jul 2; Authors: Kopera IA, Su L, Bilinska B, Cheng CY, Mruk DD Adjudin is known to specifically affect Sertoli-germ cell adhesion, resulting in germ cell loss from the seminiferous epithelium and transient infertility. The apical ectoplasmic specialization (apical ES) was shown to be the primary target of adjudin since adhesion was unaffected in organs which lack this structure. Herein, we expand previous findings by treating rat pups with adjudin, and we aim to address two questions. First, can adjudin perturb germ cell adhesion in the seminiferous epithelium of testes in which the apical ES is not yet present? Second, can adjudin affect assembly of the blood-testis barrier (BTB) at approximately 15-18 days of age? Interesting changes were noted when aged-matched testes from control and adjudin-treated rats were examined, including a delay in the appearance of developing germ cells, as well as a delay in the formation of the tubule lumen. Immunoblotting using antibodies against BTB-constituent proteins indicated that formation of the BTB was affected in rat pups gavaged with adjudin. These results were corroborated by immunofluorescence microscopy which showed profound changes in the cellular distribution of tight junction (TJ) and basal ES proteins. Moreover, the BTB was shown to be compromised in 30-day old rats when its integrity was assessed by a functional in vivo assay. By 45 days of age, however, the seminiferous epithelium of treated rats was indistinguishable from that of control rats. Collectively, these results demonstrate that adjudin targets the apical ES, as well as the basal ES and TJ, which in turn delays assembly of the BTB. PMID: 19574397 [PubMed - as supplied by publisher]
Hypothalamic Leptin Signaling Regulates Hepatic Insulin Sensitivity via a Neurocircuit Involving the Vagus Nerve.
German J, Kim F, Schwartz GJ, Havel PJ, Rhodes CJ, Schwartz MW, Morton GJ Hypothalamic Leptin Signaling Regulates Hepatic Insulin Sensitivity via a Neurocircuit Involving the Vagus Nerve. Endocrinology. 2009 Jul 2; Authors: German J, Kim F, Schwartz GJ, Havel PJ, Rhodes CJ, Schwartz MW, Morton GJ Recent evidence suggests that hormones such as insulin and leptin act in the hypothalamus to regulate energy balance and glucose metabolism. Here, we show that in leptin receptor-deficient Koletsky (fa(k)/fa(k)) rats, adenovirally-induced expression of leptin receptors in the area of the hypothalamic arcuate nucleus improved peripheral insulin sensitivity via enhanced suppression of hepatic glucose production, with no change of insulin-stimulated glucose utilization. This effect was associated with increased insulin signal transduction via phosphatidylinositol-3-OH kinase (as measured by pY-IRS-1 and pS-PKB/Akt) in liver, but not skeletal muscle, and with reduced hepatic expression of the gluconeogenic genes, glucose-6-phosphatase and phosphoenolpyruvate kinase. Moreover, the beneficial effects of hypothalamic leptin signaling on hepatic insulin sensitivity were blocked by selective hepatic vagotomy. We conclude that hypothalamic leptin action increases peripheral insulin sensitivity primarily via effects on the liver, and that the mechanism underlying this effect is dependent on the hepatic branch of the vagus nerve. PMID: 19574396 [PubMed - as supplied by publisher]

pubmed: 0804-4643

BRAF V600E mutation analysis increases diagnostic accuracy for papillary thyroid carcinoma in fine needle aspiration biopsies.
Zatelli MC, Trasforini G, Leoni S, Frigato G, Buratto M, Tagliati F, Rossi R, Cavazzini L, Roti E, Degli Uberti E BRAF V600E mutation analysis increases diagnostic accuracy for papillary thyroid carcinoma in fine needle aspiration biopsies. Eur J Endocrinol. 2009 Jul 2; Authors: Zatelli MC, Trasforini G, Leoni S, Frigato G, Buratto M, Tagliati F, Rossi R, Cavazzini L, Roti E, Degli Uberti E Objective: Papillary thyroid carcinoma (PTC) represents the majority of differentiated thyroid cancers, presenting the V600E activating BRAF mutation in 29-83% o f cases. The aim of our study is to analyze the influence of BRAF mutation analysis on the diagnostic accuracy of fine needle aspiration biopsy (FNAB) in patients with suspected PTC. Design and methods: Thyroid cytoaspirates from 469 nodules (size: 1.1 +/- 0.8 cm) with ultrasonographic features suspicious of malignant lesion, performed in 374 patients, were submitted to cytological evaluation and to biomolecular analysis, carried out after somatic DNA isolation, specific PCR amplification and subsequent automated direct sequencing. All PCR fragments were also processed by specific enzyme restriction analysis. Results: V600E BRAF mutation was found in 48 samples, 41 of which were also cytologically diagnosed as PTC, with histologic confirmation after thyroidectomy. Total thyroidectomy was perfomed also in 7 patients with negative cytology but positive BRAF mutation, with histological confirmation of PTC in all. Among the 429 BRAF negative samples, 407 had negative cytology for PTC, while 22 were diagnosed as suspected PTC and underwent total thyroidectomy with histological diagnosis of PTC in 17 and of benign lesion in 5. The prevalence of V600E BRAF mutation among histologically diagnosed PTC patients was 64%. Biomolecular analysis significantly increased cytology sensitivity for PTC from 77.3% to 86.7% (P<0.01). Conclusions: These data indicate that V600E BRAF mutation analysis can significantly improve FNAB diagnostic accuracy. However, biomolecular analysis is complementary to cytology, which should always be performed. PMID: 19574281 [PubMed - as supplied by publisher]
Association study of AMP-activated protein kinase (AMPK) subunit genes in polycystic ovary syndrome.
Sproul K, Jones M, Azziz R, Goodarzi M Association study of AMP-activated protein kinase (AMPK) subunit genes in polycystic ovary syndrome. Eur J Endocrinol. 2009 Jul 2; Authors: Sproul K, Jones M, Azziz R, Goodarzi M Objective: To examine the genes for AMP-activated protein kinase (AMPK) subunits alpha2 (PRKAA2) and gamma3 (PRKAG3) as candidates for polycystic ovary syndrome (PCOS) and its component traits. Design and methods: 287 White PCOS women were recruited from the reproductive endocrinology clinic at the University of Alabama at Birmingham and 187 White control subjects were recruited from the surrounding community. Seven PRKAA2 single nucleotide polymorphisms (SNPs) and four PRKAG3 SNPs were genotyped in PCOS cases and controls. Genotyping and association analysis were performed at Cedars-Sinai Medical Center. Results: Nominal associations of PRKAA2 variants with insulin-related traits and the PRKAG3 Pro71Ala variant with PCOS were not statistically significant after multiple testing correction. Among PCOS patients, there were no associations between variants in AMPK subunit genes and androgenic or reproductive traits. Conclusions: Variants in genes for AMPKalpha2 and AMPKgamma3 were not associated with PCOS or its component traits. Our evidence does not demonstrate AMPK is a major genetic risk factor for PCOS. PMID: 19574280 [PubMed - as supplied by publisher]
Germline VHL gene mutations in Hungarian families with von Hippel-Lindau disease and patients with apparently sporadic unilateral phaeochromocytomas.
Gergics P, Patócs A, Toth M, Igaz P, Szucs N, Liko I, Fazakas F, Szabo I, Kovács B, Glaz E, Racz K Germline VHL gene mutations in Hungarian families with von Hippel-Lindau disease and patients with apparently sporadic unilateral phaeochromocytomas. Eur J Endocrinol. 2009 Jul 2; Authors: Gergics P, Patócs A, Toth M, Igaz P, Szucs N, Liko I, Fazakas F, Szabo I, Kovács B, Glaz E, Racz K Objective: Von Hippel-Lindau (VHL) disease is a hereditary tumor syndrome caused by mutations or deletions of the VHL tumor-suppressor gene. Germline VHL gene alterations may be also present in patients with apparently sporadic phaeochromocytoma (ASP), although a wide variation in mutation frequencies has been reported in different patient cohorts. Design: Herein we report the analysis of the VHL gene in Hungarian families with VHL disease and in those with ASP. Methods: Seven families (35 members) with VHL disease and 37 unrelated patients with unilateral ASP were analysed. Patients were clinically evaluated and the VHL gene was analysed using direct sequencing, multiplex ligation probe amplification and real-time polymerase chain reaction with SYBRGreen chemistry. Results: Disease-causing genetic abnormalities were identified in each of the 7 VHL families and in 3 of the 37 patients with ASP (one nonsense and 6 missense mutations, 2 large gene deletions and one novel 2 bp deletion). Large gene deletions and other genetic alterations resulting in truncated VHL protein were found only in families with VHL type 1, whereas missense mutations were associated mainly, although not exclusively with VHL type 2B and type 2C. Conclusions: The spectrum of VHL gene abnormalities in Hungarian population is similar to that observed in Western, Japanese or Chinese VHL kindreds. The presence of VHL gene mutations in 3 of the 37 patients with ASP suggests that genetic testing is useful not only in patients with VHL disease but also in those with ASP. PMID: 19574279 [PubMed - as supplied by publisher]

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