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O Dobozy G Csaba M A Shahin G Lazáry 《Acta morphologica Academiae Scientiarum Hungaricae》1980,28(1-2):11-20
Histological examination of cockerel testes revealed the overlapping effects of FSH and TSH. Within the dose-range studied (20-160 microgram FSH and 27.5-220 microgram TSH), both hormones increased the cell number in the seminiferous cords including the number of spermatogonia, primary spermatocytes and pre-Sertoli cells. They also enhanced the mitotic activity of spermatogonia and accelerated spermatogenesis. Peak effects were observed after treatment with 160 microgram FSH and 55 microgram TSH dose. Liquefaction of cords due to hormone treatment was indicative of an acceleration of testicular ontogeny. Cross-effects of the two hormones were explained by receptor immaturity i.e. in the early stage of ontogenesis the receptors can bind both hormones due to the similarities in their structure. The maximum effects of the hormones were different, that of FSH being more marked. 相似文献
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Tom Walsh Hashem Shahin Tal Elkan-Miller Anne M. Thornton Amal Abu Rayyan Karen B. Avraham Moien Kanaan 《American journal of human genetics》2010,87(1):90-94
Massively parallel sequencing of targeted regions, exomes, and complete genomes has begun to dramatically increase the pace of discovery of genes responsible for human disorders. Here we describe how exome sequencing in conjunction with homozygosity mapping led to rapid identification of the causative allele for nonsyndromic hearing loss DFNB82 in a consanguineous Palestinian family. After filtering out worldwide and population-specific polymorphisms from the whole exome sequence, only a single deleterious mutation remained in the homozygous region linked to DFNB82. The nonsense mutation leads to an early truncation of the G protein signaling modulator GPSM2, a protein that is essential for maintenance of cell polarity and spindle orientation. In the mouse inner ear, GPSM2 is localized to apical surfaces of hair cells and supporting cells and is most highly expressed during embryonic development. Identification of GPSM2 as essential to the development of normal hearing suggests dysregulation of cell polarity as a mechanism underlying hearing loss. 相似文献
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Caitrin W. McDonough Nancy K. Gillis Abdullah Alsultan Shin-Wen Chang Marina Kawaguchi-Suzuki Jason E. Lang Mohamed Hossam A. Shahin Thomas W. Buford Nihal M. El Rouby Ana C.C. Sá Taimour Y. Langaee John G. Gums Arlene B. Chapman Rhonda M. Cooper-DeHoff Stephen T. Turner Yan Gong Julie A. Johnson 《PloS one》2013,8(10)
We sought to identify novel pharmacogenomic markers for HDL-C response to atenolol in participants with mild to moderate hypertension. We genotyped 768 hypertensive participants from the Pharmacogenomic Evaluation of Antihypertensive Responses (PEAR) study on the Illumina HumanCVD Beadchip. During PEAR, participants were randomized to receive atenolol or hydrochlorothiazide. Blood pressure and cholesterol levels were evaluated at baseline and after treatment. This study focused on participants treated with atenolol monotherapy. Association with atenolol induced HDL-C change was evaluated in 232 whites and 152 African Americans using linear regression. No SNPs achieved a Bonferroni corrected P-value. However, we identified 13 regions with consistent association across whites and African Americans. The most interesting of these regions were seven with prior associations with HDL-C, other metabolic traits, or functional implications in the lipid pathway: GALNT2, FTO, ABCB1, LRP5, STARD3NL, ESR1, and LIPC. Examples are rs2144300 in GALNT2 in whites (P=2.29x10-4, β=-1.85 mg/dL) and rs12595985 in FTO in African Americans (P=2.90x10-4, β=4.52 mg/dL), both with consistent regional association (P<0.05) in the other race group. Additionally, baseline GALNT2 expression differed by rs2144300 genotype in whites (P=0.0279). In conclusion, we identified multiple gene regions associated with atenolol induced HDL-C change that were consistent across race groups, several with functional implications or prior associations with HDL-C. 相似文献
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Karim Aghcheli Haji-Amin Marjani Dariush Nasrollahzadeh Farhad Islami Ramin Shakeri Masoud Sotoudeh Behnoush Abedi-Ardekani Mohammad-Reza Ghavamnasiri Ezzatollah Razaei Elias Khalilipour Samira Mohtashami Yasha Makhdoomi Rabea Rajabzadeh Shahin Merat Rasoul Sotoudehmanesh Shahryar Semnani Reza Malekzadeh 《PloS one》2011,6(7)
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Fan Zhang Shirling Tsai Kaori Kato Dai Yamanouchi Chunjie Wang Shahin Rafii Bo Liu K. Craig Kent 《The Journal of biological chemistry》2009,284(26):17564-17574
Bone marrow-derived progenitor cells have recently been shown to be involved in the development of intimal hyperplasia after vascular injury. Transforming growth factor-β (TGF-β) has profound stimulatory effects on intimal hyperplasia, but it is unknown whether these effects involve progenitor cell recruitment. In this study we found that although TGF-β had no direct effect on progenitor cell recruitment, conditioned media derived from vascular smooth muscle cells (VSMC) stimulated with TGF-β induced migration of both total bone marrow (BM) cells and BM-mesenchymal stem cells (MSC) and also induced MSC differentiation into smooth muscle like cells. Furthermore, overexpression of the signaling molecule Smad3 in VSMC via adenovirus-mediated gene transfer (AdSmad3) enhanced the TGF-β''s chemotactic effect. Microarray analysis of VSMC stimulated by TGF-β/AdSmad3 revealed monocyte chemoattractant protein-1 (MCP-1) as a likely factor responsible for progenitor cell recruitment. We then demonstrated that TGF-β through Smad3 phosphorylation induced a robust expression of MCP-1 in VSMC. Recombinant MCP-1 mimicked the stimulatory effect of conditioned media on BM and MSC migration. In the rat carotid injury model, Smad3 overexpression significantly increased MCP-1 expression after vascular injury, consistent with our in vitro results. Interestingly, TGF-β/Smad3-induced MCP-1 was completely blocked by both Ro-32-0432 and rotterlin, suggesting protein kinase C-δ (PKCδ) may play a role in TGF-β/Smad3-induced MCP-1 expression. In summary, our data demonstrate that TGF-β, through Smad3 and PKCδ, stimulates VSMC production of MCP-1, which is a chemoattractant for bone marrow-derived cells, specifically MSC. Manipulation of this signaling system may provide a novel approach to inhibition of intimal hyperplasia. 相似文献