Database : MEDLINE
Search on : adrenal and glands [Words]
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[PMID]: 29524503
[Au] Autor:Huang H; Liu L; Li J; Zhu C; Xie X; Ao Y; Wang H
[Ad] Address:Department of Pharmacology, School of Basic Medical Sciences, Wuhan University, Wuhan 430071, China; Department of Pharmacy, Wuhan No. 1 Hospital, Wuhan 430022, China.
[Ti] Title:Autophagy as a compensation mechanism participates in ethanol-induced fetal adrenal dysfunction in female rats.
[So] Source:Toxicol Appl Pharmacol;, 2018 Mar 07.
[Is] ISSN:1096-0333
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Autophagy plays a vital role in embryonic development and cell differentiation. Our previous study demonstrated that prenatal ethanol exposure (PEE) resulted in intrauterine growth retardation (IUGR) and adrenal developmental toxicities in rat offspring. The present study focused on PEE-induced autophagy as an underlying mechanism and its biological significance in female fetal rats. Female fetuses in the PEE group exhibited lower body weights and suffered adrenal structural abnormalities compared to the controls. Cell proliferation was inhibited, the insulin-like growth factor 1 (IGF1) pathway was reduced, and autophagy was activated in the glands of female fetal rats. Ethanol increased the ratio of microtubule-associated protein light chain 3 beta-II (LC3ß-II) to LC3ß-I in vitro, and it reduced cortisol levels in time- and concentration-dependent manners in human adrenocortical carcinoma cells (NCI-H295A). Bafilomycin A1 inhibited autophagy, steroidogenic factor 1 (SF1) protein and steroidogenesis in the present study. Rapamycin with ethanol up-regulated autophagy and SF1 expression and activated steroidogenesis when compared with ethanol alone. In addition, ethanol inhibited IGF1 receptor (IGF1R) and phospho-mTOR (Ser2448) expression in a concentration-dependent manner. These results demonstrate that PEE activated autophagy in fetal adrenal glands, and the underlying mechanism may be associated with inhibition of the IGF1R/phospho-mTOR (Ser2448) pathway. Autophagy may be a compensatory mechanism for the PEE-induced inhibition of fetal adrenal steroidogenesis to maintain fetal adrenal development.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  2 / 45819 MEDLINE  
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[PMID]: 29520185
[Au] Autor:Ahn H; Chun EJ; Lee HJ; Hwang SI; Choi DJ; Chae IH; Lee KW
[Ad] Address:Department of Radiology, Seoul National University Bundang Hospital, Seongnam 13620, Korea.
[Ti] Title:Multimodality Imaging in Patients with Secondary Hypertension: With a Focus on Appropriate Imaging Approaches Depending on the Etiologies.
[So] Source:Korean J Radiol;19(2):272-283, 2018 Mar-Apr.
[Is] ISSN:2005-8330
[Cp] Country of publication:Korea (South)
[La] Language:eng
[Ab] Abstract:Although the causes of hypertension are usually unknown, about 10% of the cases occur secondary to specific etiologies, which are often treatable. Common categories of secondary hypertension include renal parenchymal disease, renovascular stenosis, vascular and endocrinologic disorders. For diseases involving the renal parenchyma and adrenal glands, ultrasonography (US), computed tomography (CT) or magnetic resonance (MR) imaging is recommended. For renovascular stenosis and vascular disorders, Doppler US, conventional or noninvasive (CT or MR) angiography is an appropriate modality. Nuclear imaging can be useful in the differential diagnosis of endocrine causes. Radiologists should understand the role of each imaging modality and its typical findings in various causes of secondary hypertension. This article focuses on appropriate imaging approaches in accordance with the categorized etiologies leading to hypertension.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review
[do] DOI:10.3348/kjr.2018.19.2.272

  3 / 45819 MEDLINE  
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[PMID]: 29462703
[Au] Autor:Pietrelli A; Di Nardo M; Masucci A; Brusco A; Basso N; Matkovic L
[Ad] Address:Department of Basic Sciences Research, School of Health Sciences, University of Business and Social Sciences (UCES), Buenos Aires, Argentina; CONICET-Universidad de Buenos Aires, Instituto de Biología Celular y Neurociencia (IBCN), Buenos Aires, Argentina. Electronic address: apietrelli@uces.edu.ar.
[Ti] Title:Lifelong Aerobic Exercise Reduces the Stress Response in Rats.
[So] Source:Neuroscience;376:94-107, 2018 Feb 17.
[Is] ISSN:1873-7544
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The aim of this study was to analyze the effects of lifelong aerobic exercise (AE) on the adaptive response of the stress system in rats. It is well known that hypothalamic-pituitary-adrenal axis (HPA) activity differs when triggered by voluntary or forced exercise models. Male Wistar rats belonging to exercise (E) or control (C) groups were subjected to chronic AE, and two cutoff points were established at 8 (middle age) and 18 months (old age). Behavioral, biochemical and histopathological studies were performed on the main components/targets of the stress system. AE increased adrenal sensitivity (AS), brain corticosterone (CORT) and corticotropin-releasing factor (CRF), but had no effect on the thymus, adrenal glands (AGs) weight or plasma CORT. In addition, AE exerted no effect on the sympathetic tone, but significantly reduced anxiety-related behavior and emotionality. Aging decreased AS and deregulated neuroendocrine feedback, leading to an anxiogenic state which was mitigated by AE. Histopathological and morphometric analysis of AGs showed no alterations in middle-aged rats but adrenal vacuolization in approximately 20% old rats. In conclusion, lifelong AE did not produce adverse effects related to a chronic stress state. On the contrary, while AE upregulated some components of the HPA axis, it generated an adaptive response to cumulative changes, possibly through different compensatory and/or super compensatory mechanisms, modulated by age. The long-term practice of AE had a strong positive impact on stress resilience so that it could be recommended as a complementary therapy in stress and depression disease.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  4 / 45819 MEDLINE  
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[PMID]: 29524270
[Au] Autor:Kaaja RJ; Nicholls MG
[Ad] Address:Institute of Clinical Medicine, Internal Medicine, University of Turku and Turku University Hospital, Finland.
[Ti] Title:Does the hormone "endogenous ouabain" exist in the human circulation?
[So] Source:Biofactors;, 2018 Mar 10.
[Is] ISSN:1872-8081
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Studies in the early 1990s suggested that a hormone identical to ouabain or an isomer of ouabain is secreted by the adrenal glands into the circulation and plays a role in the regulation of arterial pressure and cardiac and renal function. This hormone, known as endogenous ouabain (EO), was claimed to contribute to the pathophysiology of a number of disorders including heart failure, renal failure, pregnancy-induced, and essential hypertension. However, some research groups have been unable to confirm the presence of EO in the human circulation and the issue remains in dispute. In that the implications are of considerable importance to clinicians who, like the authors, lack biochemical expertise, it would be useful if the dispute could be addressed by disinterested scientists with long-standing and acknowledged expertise in analytical chemistry who could opine as to whether the evidence is, or is not, sufficient to state categorically that EO does (or does not) exist in the circulation in man. This brief review does not present new data but, rather, recommends that adjudication is needed regarding this important issue. © 2018 BioFactors, 2018.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher
[do] DOI:10.1002/biof.1421

  5 / 45819 MEDLINE  
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[PMID]: 29516208
[Au] Autor:Noguchi G; Nakaigawa N; Taguri M; Tsutsumi S; Saito Y; Fukui S; Yasui M; Tokita T; Mitome T; Tatenuma T; Kuroda S; Abe K; Ueno D; Namura K; Umemoto S; Takizawa A; Ohta J; Ueki T; Watanabe T; Kobayashi K; Kondo K; Kishida T; Kanno H; Kitami K; Yamanaka T; Yao M
[Ad] Address:Department of Urology, Yokohama City University Graduate School of Medicine, Yokohama, Japan.
[Ti] Title:Time-dependent change in relapse sites of renal cell carcinoma after curative surgery.
[So] Source:Clin Exp Metastasis;, 2018 Mar 07.
[Is] ISSN:1573-7276
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:We investigated time-dependent changes in the relapse features of renal cell carcinoma (RCC) after curative surgery. Between 1985 and 2015, 1398 patients with RCC (1226 clear cell RCC, 89 papillary RCC, and 53 chromophobe RCC) underwent curative surgery at Yokohama City University Hospital and its affiliated hospitals. We retrospectively reviewed the clinicopathologic factors of patients with relapse after surgery. Median follow-up was 56.3 months. Recurrence occurred in 245 patients (217 clear cell RCC, 12 papillary RCC, and 3 chromophobe RCC). Papillary RCC and chromophobe RCC had no recurrence beyond 5 years after surgery, but 20 cases of clear cell carcinoma had recurrence beyond 10 years after surgery. The typical recurrence sites of clear cell RCC were lung (46.6%), bone (17.9%), liver (7.6%), and lymph nodes (6.5%). The proportion of recurrences at these typical sites was 83.9% for recurrences within 5 years, 76.3% between 5 and 10 years, and 40.0% beyond 10 years. In contrast, the proportion of retroperitoneal organ recurrence, including contralateral kidney, pancreas, and adrenal glands, increased with increasing time after surgery. Interestingly, the hazard ratio of typical site relapse decreased whereas that of retroperitoneal organ relapse increased in a time-dependent manner. In summary, clear cell RCC showed potential to relapse beyond 10 years after surgery. Recurrence at typical sites decreased whereas retroperitoneal organ recurrence increased in a time-dependent manner. Clinicians should check for recurrence at various sites beyond 10 years, especially in clear cell RCC.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[St] Status:Publisher
[do] DOI:10.1007/s10585-018-9883-0

  6 / 45819 MEDLINE  
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[PMID]: 29399828
[Au] Autor:Lin Z; Zhang L; Zhang D; Huo G; Zhou X; Yang YW; Huo Y; Li B; Geng XC
[Ad] Address:National Institute for Food and Drug Control, National Center for Safety Evaluation of Drugs, Beijing Key Lab for Pre-clinical Safety Evaluation of Drugs, Beijing, China.
[Ti] Title:A case report of spontaneous staphylococcal meningitis in a cynomolgus monkey.
[So] Source:J Med Primatol;47(2):132-135, 2018 Apr.
[Is] ISSN:1600-0684
[Cp] Country of publication:Denmark
[La] Language:eng
[Ab] Abstract:This report describes a suppurative meningitis in a young cynomolgus. The animal had neutrophil aggregation in the subarachnoid space and hemorrhage in bilateral adrenal glands. Staphylococcus was identified by FISH in brain. To our knowledge, this is the first case of staphylococcal meningitis with Waterhouse-Friderichsen syndrome in a cynomolgus monkey.
[Pt] Publication type:CASE REPORTS
[Em] Entry month:1802
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[St] Status:In-Data-Review
[do] DOI:10.1111/jmp.12330

  7 / 45819 MEDLINE  
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[PMID]: 29486221
[Au] Autor:Wang C; Du J; Du S; Liu Y; Li D; Zhu X; Ni X
[Ad] Address:Department of Physiology, Second Military Medical University, Shanghai, China.
[Ti] Title:Endogenous H S resists mitochondria-mediated apoptosis in the adrenal glands via ATP5A1 S-sulfhydration in male mice.
[So] Source:Mol Cell Endocrinol;, 2018 Feb 24.
[Is] ISSN:1872-8057
[Cp] Country of publication:Ireland
[La] Language:eng
[Ab] Abstract:In a previous study, we showed that endogenous hydrogen sulfide (H S) plays a key role in the maintenance of intact adrenal cortex function via the protection of mitochondrial function during endoxemia. We further investigated whether mitochondria-mediated apoptosis is involved in H S protection of adrenal function. LPS treatment resulted in mitochondria-mediated apoptosis in the adrenal glands of male mice, and these effects were prevented by the H S donor GYY4137. In the model of Y1 cells, the LPS-induced mitochondria-mediated apoptosis and blunt response to ACTH were rescued by GYY4137. The H S-generating enzyme cystathionine-ß-synthase (CBS) knockout heterozygous (CBS ) mice showed mitochondria-mediated apoptosis in the adrenal gland and adrenal insufficiency. GYY4137 treatment restored adrenal function and eliminated mitochondria-mediated apoptosis. Maleimide assay combined with mass spectrometry analysis showed that a number of proteins in mitochondria were S-sulfhydrated in the adrenal gland. ATP5A1 was further confirmed as S-sulfhydrated using a modified biotin switch assay. The level of S-sulfhydrated ATP5A1 was decreased in the adrenal gland of endotoxemic and CBS mice, which was restored by GYY4137. ATP5A1 was identified as sulfhydrated at cysteine 244 by H S. Overexpression of the cysteine 244 mutant ATP5A1 in Y1 cells resulted in a loss of LPS-induced mitochondria-mediated apoptosis and GYY4137 restoration of LPS-induced hyporesponsiveness to ACTH. Collectively, the present study revealed that decreased H S generation leads to mitochondrial-mediated apoptosis in the adrenal cortex and a blunt response to ACTH. S-sulfhydration of ATP5A1 at cysteine 244 is an important molecular mechanism by which H S maintains mitochondrial function and steroidogenesis in the adrenal glands.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180306
[Lr] Last revision date:180306
[St] Status:Publisher

  8 / 45819 MEDLINE  
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[PMID]: 29313945
[Au] Autor:Barroso-Sousa R; Ott PA; Hodi FS; Kaiser UB; Tolaney SM; Min L
[Ad] Address:Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts.
[Ti] Title:Endocrine dysfunction induced by immune checkpoint inhibitors: Practical recommendations for diagnosis and clinical management.
[So] Source:Cancer;124(6):1111-1121, 2018 Mar 15.
[Is] ISSN:1097-0142
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Immune checkpoint inhibitors (ICIs) have revolutionized cancer therapy. However, because ICIs block coinhibitory molecules on T cells and other immune cells, unleashing them to mediate tumor cell killing, they also can disrupt the maintenance of immunological tolerance to self-antigens. Compared with chemotherapy, ICIs have a different toxicity profile, especially the occurrence of autoimmune-like manifestations against multiple organ systems, including endocrine glands, commonly referred to as immune-related adverse events. The aim of this review was to provide practical recommendations regarding the proper assessment and clinical management related to the new onset of endocrinopathies after the use of ICIs in patients with cancer. Cancer 2018;124:1111-21. © 2018 American Cancer Society.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1801
[Cu] Class update date: 180306
[Lr] Last revision date:180306
[St] Status:In-Data-Review
[do] DOI:10.1002/cncr.31200

  9 / 45819 MEDLINE  
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[PMID]: 29307715
[Au] Autor:Medwid S; Guan H; Yang K
[Ad] Address:Children's Health Research Institute & Lawson Health Research Institute, Departments of Obstetrics & Gynaecology and Physiology & Pharmacology, Western University, 800 Commissioners Rd. E., N6C 2V5, London, Ontario, Canada.
[Ti] Title:Bisphenol A stimulates adrenal cortical cell proliferation via ERß-mediated activation of the sonic hedgehog signalling pathway.
[So] Source:J Steroid Biochem Mol Biol;178:254-262, 2018 Apr.
[Is] ISSN:1879-1220
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:We previously demonstrated that prenatal exposure to bisphenol A (BPA) resulted in increased adrenal gland weight independent of changes in plasma ACTH levels in adult mouse offspring. This finding suggested that BPA exposure likely had a direct effect on adrenal development. Given that (1) sonic hedgehog (Shh) signaling is essential for adrenal development; (2) deletion of the Shh gene in mice results in adrenal hypoplasia; (3) BPA is known to signal through estrogen receptor ß (ERß); and (4) ERß is highly expressed in adrenal glands; we hypothesized that BPA stimulates adrenal cell proliferation via ERß-mediated activation of the Shh pathway. To test this hypothesis, the human adrenal cell line, H295A cells, was used as an in vitro model system. Our main findings were: (1) BPA increased cell number and protein levels of proliferating cell nuclear antigen (PCNA; a universal marker of cell proliferation), cyclin D1 and D2 (key proliferation factors), as well as Shh and its key transcriptional regulator Gli1; (2) cyclopamine, a Shh pathway inhibitor, blocked these stimulatory effects of BPA on cell proliferation; (3) BPA increased the nuclear translocation of ERß; and (4) the ERß-specific agonist DPN mimicked while the ERß-specific antagonist PHTPP abrogated the stimulatory effects of BPA on cell proliferation and Shh signaling. Taken together, these findings demonstrate that BPA stimulates adrenal cell proliferation likely through ERß-mediated activation of the Shh signaling pathway. Thus, the present study provides novel insights into the molecular mechanisms underlying our previously reported BPA-induced aberrant adrenal phenotype.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180304
[Lr] Last revision date:180304
[St] Status:In-Data-Review

  10 / 45819 MEDLINE  
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[PMID]: 29223003
[Au] Autor:Sanders K; Mol JA; Slob A; Kooistra HS; Galac S
[Ad] Address:Department of Clinical Sciences of Companion Animals, Faculty of Veterinary Medicine, Utrecht University, Yalelaan 108, 3584 CM Utrecht, The Netherlands.
[Ti] Title:Steroidogenic factor-1 inverse agonists as a treatment option for canine hypercortisolism: in vitro study.
[So] Source:Domest Anim Endocrinol;63:23-30, 2018 Apr.
[Is] ISSN:1879-0054
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Hypercortisolism is one of the most commonly diagnosed endocrinopathies in dogs, and new targeted medical treatment options are desirable. Steroidogenic factor-1 (SF-1), an orphan nuclear hormone receptor, is a key regulator of adrenal steroidogenesis, development, and growth. In pituitary-dependent hypercortisolism (PDH), high plasma ACTH concentrations increase the transcriptional activity of SF-1. In adrenal-dependent hypercortisolism, SF-1 expression is significantly greater in dogs with recurrence after adrenalectomy than in those without recurrence. Inhibition of SF-1 could therefore be an interesting treatment option in canine spontaneous hypercortisolism. We determined the effects of 3 SF-1 inverse agonists, compounds IsoQ A, #31, and #32, on cortisol production, on the messenger RNA (mRNA) expression of steroidogenic enzymes and SFs, and on cell viability, in primary adrenocortical cell cultures of 8 normal adrenal glands and of 3 cortisol-secreting adrenocortical tumors (ATs). To mimic PDH, the normal adrenocortical cell cultures were stimulated with ACTH. The results show that only compound #31 inhibited cortisol production and SF-1 target gene expression in non-ACTH-stimulated and ACTH-stimulated normal adrenocortical cells but did not affect cell viability. In the AT cell cultures, the effects of #31 on cortisol production and target gene expression were variable, possibly caused by a difference in the SF-1 mRNA expressions of the primary tumors. In conclusion, inhibition of SF-1 activity shows much promise as a future treatment for canine hypercortisolism.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 180305
[Lr] Last revision date:180305
[St] Status:In-Data-Review


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