Database : MEDLINE
Search on : pituitary and gland [Words]
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[PMID]: 29095280
[Au] Autor:Zeng MF; Chen L; Ye HY; Gong W; Zhou LN; Li YM; Zhao XL
[Ad] Address:aDepartment of Endocrinology, Huashan Hospital North bDepartment of Endocrinology, Huashan Hospital, Fudan University, Shanghai, China.
[Ti] Title:Primary hypothyroidism and isolated ACTH deficiency induced by nivolumab therapy: Case report and review.
[So] Source:Medicine (Baltimore);96(44):e8426, 2017 Nov.
[Is] ISSN:1536-5964
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:RATIONALE: Nivolumab is a monoclonal IgG antibody blocking programmed death receptor-1 (PD1), leading to restoration of the natural T-cell-mediated immune response against the cancer cells. However, it also causes plenty of autoimmune-related adverse events, which often involves endocrine system. PATIENT CONCERNS: A 54-year-old male with renal clear cell carcinoma was treated with nivolumab intravenously. Routine monitoring showed elevated thyroid-stimulating hormone and low free thyroxine after the 6th administration of nivolumab. After the 12th administration, he developed general fatigue, recurrent hypoglycemia, and relative hypotension. Laboratory tests showed low sodium, low morning cortisol without correspondence increase of corticotrophin (ACTH). Other pituitary hormones were normal. MRI showed no space-occupying lesions, but heterogeneous enhancement of the pituitary gland. DIAGNOSES: Primary hypothyroidism and isolated ACTH deficiency. The etiologies were assumed to be nivolumab induced autoimmune lymphocytic thyroiditis and hypophysitis, respectively. INTERVENTIONS: Hormone replacements with levothyroxine and acetate cortisone were given orally. Nivolumab was adjusted to lower dose and longer interval. OUTCOMES: The patient felt good after adequate replacement. Nivolumab was returned to routine dose and interval six months later. And the metastasis was not obviously progressed during this time. LESSONS: The present report provides the first detailed presentation of combined hypothyroidism and isolated ACTH deficiency induced by nivolumab. Adrenal deficiency often develops insidiously. We suggest routine monitoring of fasting blood-glucose, blood pressure and serum sodium as well as thyroid function during nivolumab and other cancer immunotherapies. When unexpected fatigue, hypoglycemia, hypotension or hyponatremia appeared, adrenal deficiency should be taken into consideration.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1711
[Cu] Class update date: 171102
[Lr] Last revision date:171102
[St] Status:In-Process
[do] DOI:10.1097/MD.0000000000008426

  2 / 71203 MEDLINE  
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[PMID]: 29093382
[Au] Autor:Koide H; Shiga A; Komai E; Yamato A; Fujimoto M; Tamura A; Kono T; Nakayama A; Takiguchi T; Higuchi S; Sakuma I; Nagano H; Hashimoto N; Suzuki S; Takeda Y; Shibuya M; Nishioka H; Yamada S; Inoshita N; Ishiwatari N; Horiguchi K; Yokote K; Tanaka T
[Ad] Address:Department of Medicine, Division of Diabetes, Metabolism and Endocrinology, Chiba University Hospital, Japan.
[Ti] Title:Prednisolone-responsive Postpartum IgG4-related Hypophysitis.
[So] Source:Intern Med;, 2017 Nov 01.
[Is] ISSN:1349-7235
[Cp] Country of publication:Japan
[La] Language:eng
[Ab] Abstract:We herein report the case of a 25-year-old woman who presented with severe headache and visual field defects after childbirth. Magnetic resonance imaging revealed marked swelling of the pituitary gland, and an endocrinological examination revealed panhypopituitarism and diabetes insipidus. An immunohistological analysis of a transsphenoidal biopsy sample of the pituitary gland showed the significant accumulation of an immunogloblin G4 (IgG4)-positive population, leading to the diagnosis of IgG4-related hypophysitis. The patient was treated with prednisolone, which markedly reduced the swelling of the pituitary gland, in association with recovery of the pituitary function. This is a rare case of biopsy-proven IgG4-related hypophysitis with a postpartum onset.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1711
[Cu] Class update date: 171102
[Lr] Last revision date:171102
[St] Status:Publisher
[do] DOI:10.2169/internalmedicine.8446-16

  3 / 71203 MEDLINE  
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[PMID]: 29092962
[Au] Autor:Kumawat BL; Sharma C; Shah MJ; Panchal M
[Ad] Address:Department of Neurology, Sawai Mansingh Medical College and Hospital, Jaipur, India.
[Ti] Title:Multiple endocrine neoplasia type 1 presenting with refractory seizures.
[So] Source:BMJ Case Rep;2017, 2017 Nov 01.
[Is] ISSN:1757-790X
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:We report a case of 29-year-old woman referred to us for management of refractory epilepsy. Under observation, she was detected to have recurrent hypoglycaemia during the episodes of seizures. On investigation, she was found to have hyperinsulinemic hypoglycaemia. Her triple-phase CT scan of abdomen showed neuroendocrine tumour of pancreatic head, with bilateral renal calculi. Screening of other endocrine glands revealed pituitary microadenoma and parathyroid adenoma on imaging, which was also supported by biochemical and hormonal profile. On the basis of tumours involving parathyroid, pancreatic islets and pituitary gland, she was diagnosed as a case of multiple endocrine neoplasia type 1. Pancreatic tumour removal was done and bromocriptine was started. She was followed up for 6 months postoperatively and never had seizures even without antiepileptic drugs. This case report highlights an exceptional treatable cause of uncontrolled seizures.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1711
[Cu] Class update date: 171102
[Lr] Last revision date:171102
[St] Status:In-Process

  4 / 71203 MEDLINE  
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[PMID]: 29065362
[Au] Autor:Surkin PN; Gallino SL; Luce V; Correa F; Fernandez Solari J; De Laurentiis A
[Ad] Address:Cátedra de Fisiología, Facultad de Odontología, Universidad de Buenos Aires, Argentina; Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Argentina.
[Ti] Title:Pharmacological augmentation of endocannabinoid signaling reduces the neuroendocrine response to stress.
[So] Source:Psychoneuroendocrinology;87:131-140, 2017 Oct 18.
[Is] ISSN:1873-3360
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Activation of the hypothalamic-pituitary-adrenal axis (HPA) is critical for survival when the organism is exposed to a stressful stimulus. The endocannabinoid system (ECS) is currently considered an important neuromodulator involved in numerous pathophysiological processes and whose primary function is to maintain homeostasis. In the tissues constituting the HPA axis, all the components of the ECS are present and the activation of this system acts in parallel with changes in the activity of numerous neurotransmitters, including nitric oxide (NO). NO is widely distributed in the brain and adrenal glands and recent studies have shown that free radicals, and in particular NO, may play a crucial role in the regulation of stress response. Our objective was to determine the participation of the endocannabinoid and NOergic systems as probable mediators of the neuroendocrine HPA axis response to a psychophysical acute stress model in the adult male rat. Animals were pre-treated with cannabinoid receptors agonists and antagonists at central and systemic level prior to acute restraint exposure. We also performed in vitro studies incubating adrenal glands in the presence of ACTH and pharmacological compounds that modifies ECS components. Our results showed that the increase in corticosterone observed after acute restraint stress is blocked by anandamide administered at both central and peripheral level. At hypothalamic level both cannabinoid receptors (CB1 and CB2) are involved, while in the adrenal gland, anandamide has a very potent effect in suppressing ACTH-induced corticosterone release that is mainly mediated by vanilloid TRPV1 receptors. We also observed that stress significantly increased hypothalamic mRNA levels of CB1 as well as adrenal mRNA levels of TRPV1 receptor. In addition, anandamide reduced the activity of the nitric oxide synthase enzyme during stress, indicating that the anti-stress action of endocannabinoids may involve a reduction in NO production at hypothalamic and adrenal levels. In conclusion, an endogenous cannabinoid tone maintains the HPA axis in a stable basal state, which is lost with a noxious stimulus. In this case, the ECS dampens the response to stress allowing the recovery of homeostasis. Moreover, our work further contributes to in vitro evidence for a participation of the endocannabinoid system by inhibiting corticosterone release directly at the adrenal gland level.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1710
[Cu] Class update date: 171103
[Lr] Last revision date:171103
[St] Status:Publisher

  5 / 71203 MEDLINE  
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[PMID]: 28951438
[Au] Autor:Bargi-Souza P; Goulart-Silva F; Nunes MT
[Ti] Title:Novel aspects of T actions on GH and TSH synthesis and secretion: physiological implications.
[So] Source:J Mol Endocrinol;59(4):R167-R178, 2017 11.
[Is] ISSN:1479-6813
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Thyroid hormones (THs) classically regulate the gene expression by transcriptional mechanisms. In pituitary, the encoding genes for growth hormone (GH) and thyroid-stimulating hormone (TSH) are examples of genes regulated by triiodothyronine (T ) in a positive and negative way, respectively. Recent studies have shown a rapid adjustment of GH and TSH synthesis/secretion induced by T posttranscriptional actions. In somatotrophs, T promotes an increase in mRNA content, poly(A) tail length and binding to the ribosome, associated with a rearrangement of actin cytoskeleton. In thyrotrophs, T reduces mRNA content, poly(A) tail length and its association with the ribosome. In parallel, it promotes a redistribution of TSH secretory granules to more distal regions of the cell periphery, indicating a rapid effect of T inhibition of TSH secretion. T was shown to affect the content of tubulin and the polymerization of actin and tubulin cytoskeletons in the whole anterior pituitary gland, and to increase intracellular alpha (CGA) content. This review summarizes genomic and non-genomic/posttranscriptional actions of TH on the regulation of several steps of GH and TSH synthesis and secretion. These distinct mechanisms induced by T can occur simultaneously, even though non-genomic effects are promptly elicited and precede the genomic actions, coexisting in a functional network within the cells.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1709
[Cu] Class update date: 171103
[Lr] Last revision date:171103
[St] Status:In-Process
[do] DOI:10.1530/JME-17-0068

  6 / 71203 MEDLINE  
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[PMID]: 28920935
[Au] Autor:Prüss H; Tedeschi A; Thiriot A; Lynch L; Loughhead SM; Stutte S; Mazo IB; Kopp MA; Brommer B; Blex C; Geurtz LC; Liebscher T; Niedeggen A; Dirnagl U; Bradke F; Volz MS; DeVivo MJ; Chen Y; von Andrian UH; Schwab JM
[Ad] Address:Department of Microbiology and Immunobiology, Division of Immunology, Harvard Medical School, Boston, Massachusetts, USA.
[Ti] Title:Spinal cord injury-induced immunodeficiency is mediated by a sympathetic-neuroendocrine adrenal reflex.
[So] Source:Nat Neurosci;20(11):1549-1559, 2017 Nov.
[Is] ISSN:1546-1726
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Acute spinal cord injury (SCI) causes systemic immunosuppression and life-threatening infections, thought to result from noradrenergic overactivation and excess glucocorticoid release via hypothalamus-pituitary-adrenal axis stimulation. Instead of consecutive hypothalamus-pituitary-adrenal axis activation, we report that acute SCI in mice induced suppression of serum norepinephrine and concomitant increase in cortisol, despite suppressed adrenocorticotropic hormone, indicating primary (adrenal) hypercortisolism. This neurogenic effect was more pronounced after high-thoracic level (Th1) SCI disconnecting adrenal gland innervation, compared with low-thoracic level (Th9) SCI. Prophylactic adrenalectomy completely prevented SCI-induced glucocorticoid excess and lymphocyte depletion but did not prevent pneumonia. When adrenalectomized mice were transplanted with denervated adrenal glands to restore physiologic glucocorticoid levels, the animals were completely protected from pneumonia. These findings identify a maladaptive sympathetic-neuroendocrine adrenal reflex mediating immunosuppression after SCI, implying that therapeutic normalization of the glucocorticoid and catecholamine imbalance in SCI patients could be a strategy to prevent detrimental infections.
[Mh] MeSH terms primary: Adrenal Glands/immunology
Hypothalamo-Hypophyseal System/immunology
Immune Tolerance/immunology
Pituitary-Adrenal System/immunology
Reflex/immunology
Spinal Cord Injuries/immunology
[Mh] MeSH terms secundary: Adrenal Glands/transplantation
Adrenalectomy/adverse effects
Adrenalectomy/methods
Adult
Aged
Animals
Female
Humans
Male
Mice
Mice, Inbred C57BL
Mice, Knockout
Mice, Transgenic
Middle Aged
Single-Blind Method
Spinal Cord Injuries/complications
Spinal Cord Injuries/surgery
Thoracic Vertebrae/injuries
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1711
[Cu] Class update date: 171102
[Lr] Last revision date:171102
[Js] Journal subset:IM
[Da] Date of entry for processing:170918
[St] Status:MEDLINE
[do] DOI:10.1038/nn.4643

  7 / 71203 MEDLINE  
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[PMID]: 28885086
[Au] Autor:Kamei T; Nonaka M; Uemura Y; Yamanouchi Y; Komori Y; Iwata R; Takeda J; Hashiba T; Yoshimura K; Asai A
[Ad] Address:Departments of 1 Neurosurgery and.
[Ti] Title:Enlarging pediatric ectopic Rathke's cleft cyst in the prepontine cistern: case report.
[So] Source:J Neurosurg Pediatr;20(5):480-484, 2017 Nov.
[Is] ISSN:1933-0715
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Rathke's cleft cyst is a cystic disease that occurs in the sella turcica or, occasionally, in the suprasellar area. An ectopic Rathke's cleft cyst is extremely rare, and its nature is less well understood. The authors report the case of a 14-year-old girl who presented with a growing cystic lesion in the prepontine cistern, immediately behind the dorsum sellae. Preoperative imaging and intraoperative investigation showed part of the cyst wall continuing into the dorsum sellae, to the pituitary gland. The cisternal portion of the cyst wall was totally resected via a right subtemporal approach. Histopathological examination of the cyst wall showed a monolayer of ciliated cells, identical to those of Rathke's cleft cyst. To the best of the authors' knowledge, this represents the first pediatric case of Rathke's cleft cyst occurring in the prepontine cistern.
[Mh] MeSH terms primary: Central Nervous System Cysts/diagnostic imaging
Central Nervous System Cysts/surgery
Pituitary Gland/diagnostic imaging
Pituitary Gland/surgery
Subarachnoid Space
[Mh] MeSH terms secundary: Adolescent
Central Nervous System Cysts/pathology
Female
Humans
Magnetic Resonance Imaging
Pituitary Gland/pathology
Pons
[Pt] Publication type:CASE REPORTS; JOURNAL ARTICLE
[Em] Entry month:1711
[Cu] Class update date: 171102
[Lr] Last revision date:171102
[Js] Journal subset:IM
[Da] Date of entry for processing:170908
[St] Status:MEDLINE
[do] DOI:10.3171/2017.6.PEDS1727

  8 / 71203 MEDLINE  
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[PMID]: 28629513
[Au] Autor:Dey S; Noguchi CT
[Ad] Address:National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, United States.
[Ti] Title:Erythropoietin and Hypothalamic-Pituitary Axis.
[So] Source:Vitam Horm;105:101-120, 2017.
[Is] ISSN:0083-6729
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Erythropoietin (EPO), known primarily for its erythropoietic activity, is commonly used clinically to treat anemia of chronic kidney disease. However, the expression of EPO receptor (EpoR) beyond erythroid tissue provides for potential extrahematopoietic effects of EPO, including EPO regulation of metabolic homeostasis (Zhang et al., 2014). Small clinical studies have shown that EPO treatment in patients with end-stage renal disease improved glycemic control and insulin sensitivity. Studies in animal models have shown that EPO regulation of metabolism is mainly attributed to its response in fat, and the hypothalamus-pituitary axis (Dey et al., 2016; Dey, Scullen, & Noguchi, 2015; Teng, Gavrilova, et al., 2011; Wang et al., 2013) and is not dependent on its hematopoietic activity. EpoR expression in the hypothalamus is localized to the neurons expressing proopiomelanocortin (POMC) in the arcuate nucleus region, the most important site in the brain for the regulation of physiological energy expenditure. EPO treatment increases POMC production in anorexigenic POMC neurons in the hypothalamus. In the pituitary, EPO modulates the secretion of the POMC-derived peptide, adrenocorticotropic hormone (ACTH) that regulates physiological and metabolic stress response. With EPO produced by cells in the brain, such as astrocytes, and with EPO-stimulated POMC expression in the hypothalamus and EPO-inhibited ACTH secretion in the pituitary, EPO signaling contributes to the hypothalamic-pituitary axis as a major regulator of glucose metabolism and energy homeostasis.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1706
[Cu] Class update date: 171102
[Lr] Last revision date:171102
[St] Status:In-Process

  9 / 71203 MEDLINE  
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[PMID]: 28255689
[Au] Autor:El Sanharawi I; Tzarouchi L; Cardoen L; Martinerie L; Leger J; Carel JC; Elmaleh-Berges M; Alison M
[Ad] Address:Service de Radiologie Pédiatrique, Hôpital Robert Debré, APHP, 48 boulevard Sérurier, 75019, Paris, France.
[Ti] Title:High-resolution heavily T2-weighted magnetic resonance imaging for evaluation of the pituitary stalk in children with ectopic neurohypophysis.
[So] Source:Pediatr Radiol;47(5):599-605, 2017 May.
[Is] ISSN:1432-1998
[Cp] Country of publication:Germany
[La] Language:eng
[Ab] Abstract:BACKGROUND: In anterior pituitary deficiency, patients with non visible pituitary stalk have more often multiple deficiencies and persistent deficiency than patients with visible pituitary stalk. OBJECTIVE: To compare the diagnostic value of a high-resolution heavily T2-weighted sequence to 1.5-mm-thick unenhanced and contrast-enhanced sagittal T1-weighted sequences to assess the presence of the pituitary stalk in children with ectopic posterior pituitary gland. MATERIALS AND METHODS: We retrospectively evaluated the MRI data of 14 children diagnosed with ectopic posterior pituitary gland between 2010 and 2014. We evaluated the presence of a pituitary stalk using a sagittal high-resolution heavily T2-weighted sequence and a 1.5-mm sagittal T1-weighted turbo spin-echo sequence before and after contrast medium administration. RESULTS: A pituitary stalk was present on at least one of the sequences in 10 of the 14 children (71%). T2-weighted sequence depicted the pituitary stalk in all 10 children, whereas the 1.5-mm-thick T1-weighted sequence depicted 2/10 (20%) before contrast injection and 8/10 (80%) after contrast injection (P=0.007). CONCLUSION: Compared with 1.5-mm-thick contrast-enhanced T1-weighted sequences, high-resolution heavily T2-weighted sequence demonstrates better sensitivity in detecting the pituitary stalk in children with ectopic posterior pituitary gland, suggesting that contrast injection is unnecessary to assess the presence of a pituitary stalk in this setting.
[Mh] MeSH terms primary: Magnetic Resonance Imaging/methods
Pituitary Diseases/diagnostic imaging
Pituitary Gland, Posterior/abnormalities
Pituitary Gland, Posterior/diagnostic imaging
[Mh] MeSH terms secundary: Adolescent
Child
Child, Preschool
Contrast Media
Female
Humans
Image Enhancement/methods
Infant
Male
Meglumine
Organometallic Compounds
Reproducibility of Results
Retrospective Studies
Sensitivity and Specificity
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Contrast Media); 0 (Organometallic Compounds); 6HG8UB2MUY (Meglumine); L0ND3981AG (gadoterate meglumine)
[Em] Entry month:1711
[Cu] Class update date: 171102
[Lr] Last revision date:171102
[Js] Journal subset:IM
[Da] Date of entry for processing:170303
[St] Status:MEDLINE
[do] DOI:10.1007/s00247-017-3784-2

  10 / 71203 MEDLINE  
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[PMID]: 28104302
[Au] Autor:Fragiadaki M; Lannoy M; Themanns M; Maurer B; Leonhard WN; Peters DJ; Moriggl R; Ong AC
[Ad] Address:Academic Nephrology Unit, Department of Infection, Immunity and Cardiovascular Disease, The Medical School, University of Sheffield, Sheffield, UK. Electronic address: m.fragiadaki@sheffield.ac.uk.
[Ti] Title:STAT5 drives abnormal proliferation in autosomal dominant polycystic kidney disease.
[So] Source:Kidney Int;91(3):575-586, 2017 Mar.
[Is] ISSN:1523-1755
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Autosomal dominant polycystic kidney disease (ADPKD) leads to renal failure. The hallmark of ADPKD is increased epithelial proliferation, which has been proposed to be due to atypical signaling including abnormal JAK-STAT activity. However, the relative contribution of JAK-STAT family members in promoting proliferation in ADPKD is unknown. Here, we present siRNA JAK-STAT-focused screens discovering a previously unknown proliferative role for multiple JAK-STAT components (including STAT1, STAT2, STAT4, STAT5a, and STAT5b). Amongst these, we selected to study the growth hormone/growth hormone receptor/STAT5-axis because of its known role as a regulator of growth in nonrenal tissues. Loss of STAT5 function, facilitated by pharmacological inhibition or siRNAs, significantly reduced proliferation with an associated reduction in cyst growth in vitro. To study whether STAT5 is abnormally activated in vivo, we analyzed its expression using two independent mouse models of ADPKD. STAT5 was nuclear, thus activated, in renal epithelial cyst lining cells in both models. To test whether forced activation of STAT5 can modulate proliferation of renal cells in vivo, irrespective of the Pkd1 status, we overexpressed growth hormone. These mice showed increased STAT5 activity in renal epithelial cells, which correlated with de novo expression of cyclin D1, a STAT5 target gene. Chromatin immunoprecipitation experiments revealed that STAT5 transcriptionally activated cyclin D1 in a growth hormone-dependent fashion, thus providing a mechanism into how STAT5 enhances proliferation. Finally, we provide evidence of elevated serum growth hormone in Pkd1 mutant mice. Thus, the growth hormone/STAT5 signaling axis is a novel therapeutic target in ADPKD.
[Mh] MeSH terms primary: Cell Proliferation
Epithelial Cells/metabolism
Kidney/metabolism
Polycystic Kidney, Autosomal Dominant/metabolism
STAT5 Transcription Factor/metabolism
Tumor Suppressor Proteins/metabolism
[Mh] MeSH terms secundary: Animals
Carrier Proteins/metabolism
Cell Line
Cell Nucleus/metabolism
Cell Proliferation/drug effects
Cyclin D1/genetics
Cyclin D1/metabolism
Disease Models, Animal
Epithelial Cells/drug effects
Epithelial Cells/pathology
Genotype
Growth Hormone/genetics
Growth Hormone/metabolism
Humans
Janus Kinases/antagonists & inhibitors
Janus Kinases/genetics
Janus Kinases/metabolism
Kidney/drug effects
Kidney/pathology
Mice, Transgenic
Phenotype
Polycystic Kidney, Autosomal Dominant/drug therapy
Polycystic Kidney, Autosomal Dominant/genetics
Polycystic Kidney, Autosomal Dominant/pathology
Protein Kinase Inhibitors/pharmacology
RNA Interference
STAT5 Transcription Factor/antagonists & inhibitors
STAT5 Transcription Factor/genetics
Signal Transduction
TRPP Cation Channels/genetics
TRPP Cation Channels/metabolism
Time Factors
Transfection
Tumor Suppressor Proteins/antagonists & inhibitors
Tumor Suppressor Proteins/genetics
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (CCND1 protein, human); 0 (Carrier Proteins); 0 (Protein Kinase Inhibitors); 0 (STAT5 Transcription Factor); 0 (STAT5A protein, human); 0 (STAT5B protein, human); 0 (Stat5a protein, mouse); 0 (Stat5b protein, mouse); 0 (TRPP Cation Channels); 0 (Tumor Suppressor Proteins); 0 (polycystic kidney disease 1 protein); 0 (somatotropin-binding protein); 136601-57-5 (Cyclin D1); 9002-72-6 (Growth Hormone); EC 2.7.10.2 (Janus Kinases)
[Em] Entry month:1711
[Cu] Class update date: 171102
[Lr] Last revision date:171102
[Js] Journal subset:IM
[Da] Date of entry for processing:170120
[St] Status:MEDLINE


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