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[PMID]: 29524673
[Au] Autor:Raghunathan V; Benoit J; Kasetti R; Zode G; Salemi M; Phinney BS; Keller KE; Staverosky JA; Murphy CJ; Acott T; Vranka J
[Ad] Address:Department of Basic Sciences, University of Houston, Houston, TX, 77204, USA; The Ocular Surface Institute, University of Houston, Houston, TX, 77204, USA. Electronic address: vraghunathan@uh.edu.
[Ti] Title:Glaucomatous cell derived matrices differentially modulate non-glaucomatous trabecular meshwork cellular behavior.
[So] Source:Acta Biomater;, 2018 Mar 07.
[Is] ISSN:1878-7568
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Ocular hypertension is a causal risk-factor to developing glaucoma. This is associated with stiffening of the trabecular meshwork (TM), the primary site of resistance to aqueous-humor-outflow. The mechanisms underlying this stiffening or how pathologic extracellular matrix (ECM) affects cell function are poorly understood. It is recognized that mechanotransduction systems allow cells to sense and translate the intrinsic biophysical properties of ECM into intracellular signals to control gene transcription, protein expression, and cell behavior. Using an anterior segment perfusion model, we document that there are significantly more low flow regions that are much stiffer, and fewer high flow regions that are less stiff in glaucomatous TM (GTM) when compared to non-glaucomatous TMs (NTM). GTM tissue also has fewer cells overall when compared with NTM tissue. In order to study the role of pathologic ECM in glaucoma disease progression, we conducted studies using cell derived matrices (CDM). First, we characterized the mechanics, composition and organization of fibronectin in ECM deposited by GTM and NTM cells treated with glucocorticosteroids. Then, we determined that these GTM-derived ECM are able to induce stiffening of normal NTM cells, and alter their gene/protein expression to resemble that of a glaucomatous phenotype. Further, we demonstrate that GTM-derived ECM causes endoplasmic reticular stress in NTM. They also became resistant to being reorganized by these NTM cells. These phenomena were exacerbated by ECMs obtained from steroid treated glaucoma model groups. Collectively, our data demonstrates that CDMs represent a novel tool for the study of bidirectional interactions between TM cells and their immediate microenvironment. STATEMENT OF SIGNIFICANCE: Extracellular matrix (ECM) changes are prevalent in a number of diseases. The precise mechanisms by which changes in the ECM contribute to disease progression is unclear, primarily due to absence of appropriate models. Here, using glaucoma as a disease model, we document changes in cell derived matrix (CDM) and tissue mechanics that contribute to the pathology. Subsequently, we determine the effect that ECMs from diseased and healthy individuals have on healthy cell behaviors. Data emanating from this study demonstrate that CDMs are a potent tool for the study of cell-ECM interactions.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  2 / 461457 MEDLINE  
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[PMID]: 29524630
[Au] Autor:Zhou Y; Horowitz JC; Naba A; Ambalavanan N; Atabai K; Balestrini J; Bitterman PB; Corley RA; Ding BS; Engler AJ; Hansen KC; Hagood JS; Kheradmand F; Lin QS; Neptune E; Niklason L; Ortiz LA; Parks WC; Tschumperlin DJ; White ES; Chapman HA; Thannickal VJ
[Ad] Address:Division of Pulmonary, Allergy and Critical Care Medicine, University of Alabama at Birmingham, United States. Electronic address: yongzhou@uabmc.edu.
[Ti] Title:Extracellular matrix in lung development, homeostasis and disease.
[So] Source:Matrix Biol;, 2018 Mar 07.
[Is] ISSN:1569-1802
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:The lung's unique extracellular matrix (ECM), while providing structural support for cells, is critical in the regulation of developmental organogenesis, homeostasis and injury-repair responses. The ECM, via biochemical or biomechanical cues, regulates diverse cell functions, fate and phenotype. The composition and function of lung ECM become markedly deranged in pathological tissue remodeling. ECM-based therapeutics and bioengineering approaches represent promising novel strategies for regeneration/repair of the lung and treatment of chronic lung diseases. In this review, we assess the current state of lung ECM biology, including fundamental advances in ECM composition, dynamics, topography, and biomechanics; the role of the ECM in normal and aberrant lung development, adult lung diseases and autoimmunity; and ECM in the regulation of the stem cell niche. We identify opportunities to advance the field of lung ECM biology and provide a set recommendations for research priorities to advance knowledge that would inform novel approaches to the pathogenesis, diagnosis, and treatment of chronic lung diseases.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  3 / 461457 MEDLINE  
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[PMID]: 29524606
[Au] Autor:Zhuang H; Li Q; Zhang X; Ma X; Wang Z; Liu Y; Yi X; Chen R; Han F; Zhang N; Li Y
[Ad] Address:Key Laboratory of Breast Cancer Prevention and Therapy, Laboratory of Cancer Cell Biology, Tianjin Medical University Cancer Institute and Hospital; Research Center of Basic Medical Sciences; Department of Pathogen Biology & Department of Genetics, School of Basic Medical Sciences; Tianjin Medic
[Ti] Title:Downregulation of Glycine Decarboxylase Enhanced Cofilin-mediated Migration in Hepatocellular Carcinoma Cells.
[So] Source:Free Radic Biol Med;, 2018 Mar 07.
[Is] ISSN:1873-4596
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Metabolic reprogramming is a hallmark of cancer. Glycine decarboxylase (GLDC), an oxidoreductase, plays an important role in amino acid metabolism. While GLDC promotes tumor initiation and proliferation in non-small cell lung cancer and glioma and it was reported as a putative tumor suppressor gene in gastric cancer, the role of GLDC in hepatocellular carcinoma (HCC) is unknown. In the current study, microarray-based analysis suggested that GLDC expression was low in highly malignant HCC cell lines, and clinicopathological analysis revealed a decrease in GLDC in HCC tumor samples. While the knockdown of GLDC enhanced cancer cell migration and invasion, GLDC overexpression inhibited them. Mechanistic studies revealed that GLDC knockdown increased the levels of reactive oxygen species (ROS) and decreased the ratio of glutathione/oxidized glutathione (GSH/GSSG), which in turn dampened the ubiquitination of cofilin, a key regulator of actin polymerization. Consequently, the protein level of cofilin was elevated, which accounted for the increase in cell migration. The overexpression of GLDC reversed the phenotype. Treatment with N-acetyl-L-cysteine decreased the protein level of cofilin while treatment with H O increased it, further confirming the role of ROS in regulating cofilin degradation. In a tumor xenographic transplant nude mouse model, the knockdown of GLDC promoted intrahepatic metastasis of HCC while GLDC overexpression inhibited it. Our data indicate that GLDC downregulation decreases ROS-mediated ubiquitination of cofilin to enhance HCC progression and intrahepatic metastasis.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  4 / 461457 MEDLINE  
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[PMID]: 29524590
[Au] Autor:Barnhart K; Giudice L; Young S; Thomas T; Diamond MP; Segars J; Youssef WA; Krawetz S; Santoro N; Eisenberg E; Zhang H; NICHD Cooperative Reproductive Medicine Network
[Ad] Address:Department of Obstetrics and Gynecology, University of Pennsylvania School of Medicine, Philadelphia, PA, United States. Electronic address: kbarnhart@obgyn.upenn.edu.
[Ti] Title:Evaluation, validation and refinement of noninvasive diagnostic biomarkers for endometriosis (ENDOmarker): A protocol to phenotype bio-specimens for discovery and validation.
[So] Source:Contemp Clin Trials;, 2018 Mar 07.
[Is] ISSN:1559-2030
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:OBJECTIVE: Endometriosis is a chronic, estrogen dependent condition that affects 5-10% of reproductive aged women and is associated with pelvic pain and infertility. As the approach to therapy shifts from surgical ablation to pharmacological control, a non-surgical mode of diagnosis would be desirable. The ENDOmarker study was designed by the NICHD Reproductive Medicine Network (RMN) to obtain well characterized and phenotyped bio specimens in a standardized fashion from women with and without endometriosis. DESIGN: Development of a diagnostic test. SETTING: Academic medical centers. PATIENTS: This study will enroll up to 500 participants, and follow them for up to 5 months. Included subjects are aged 18-44, scheduled to undergo gynecologic surgery (laparoscopy/laparotomy) for clinical reasons. INTERVENTIONS: Presence and stage of endometriosis (or its absence) is characterized by visual examination at the time of surgery. Subjects will undergo extensive clinical evaluation pre-operatively and at visits one and four months postoperatively. Endometrial biopsy, blood, urine and disease specific questionnaires will be collected at each visit. MAIN OUTCOME: Samples will be placed in a bio-repository to be used to validate and optimize the clinical use of genomic classifiers of the endometrium alone or in combination with serum cytokines as a non-surgical composite marker of endometriosis. CONCLUSION: This protocol can serve as a reference for objective collection of high quality bio specimens for discovery or validation of potential nonsurgical diagnosis of presence or severity of disease.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  5 / 461457 MEDLINE  
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[PMID]: 29524578
[Au] Autor:Katkam SK; Indumathi B; Tasneem FSD; Rajasekhar L; Kutala VK
[Ad] Address:Departments of Clinical Pharmacology and Therapeutics, Nizam's Institute of Medical Sciences (NIMS), Telangana, Hyderabad, India.
[Ti] Title:Impact of eNOS 27-bp VNTR (4b/a) gene polymorphism with the risk of Systemic Lupus Erythematosus in south Indian subjects.
[So] Source:Gene;, 2018 Mar 07.
[Is] ISSN:1879-0038
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:OBJECTIVE: Endothelial nitric oxide synthase (eNOS) is constitutively expressed by vascular endothelium including glomerular endothelium. Functional polymorphisms, -786T>C (rs2070744) promoter variant, 27 bp VNTR (4b/a) in intron 4 and 894G>T (rs1799983) exon variant of eNOS are known to alter the eNOS expression and activity leading to altered NO levels and contribute to the development of vascular and renal disease risk. Thus it might have a role in SLE risk and development of glomerulonephritis. Hence, the present study is aimed to investigate the role of eNOS polymorphisms in South Indian SLE patients. METHODS: Five hundred and four subjects (219 SLE cases and 285 controls) were included in the present case-control study. Genotyping was done using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) for -786T>C and 894G>T SNPs. Another, 4a4b variable number of tandem repeat polymorphism was genotyped using direct PCR method using primer pairs flanking the 27 bp direct repeat region in intron 4 of eNOS gene. RESULTS: Our analysis revealed that intron 4 27 bp VNTR genotype frequency differ significantly between the SLE patients and controls (OR: 1.73, 95% CI %:1.18-2.54, P = 0.004). Further, "a allele" frequency was significantly higher in SLE patients as compared to the controls (20 vs. 13.8%) (OR: 1.56, 95%CI: 1.11-2.18, P = 0.01). However, promoter polymorphism -786T>C and missense variant 894G>T werenot significantly different between the SLE cases and controls (OR: 0.92, 95%CI: 0.64-1.33, P = 0.7 and OR: 1.4, 95%CI: 0.95-2.06, P = 0.095 respectively). Furthermore, no association was found between any of the three polymorphisms with lupus nephritis phenotype. Increased plasma nitrate levels were observed in SLE patients (36.79  2.83 M/L) as compared to healthy controls (28.53  1.94 M/L) (P = 0.01). In addition, the genotype-based simulations have indicated that combined effect of eNOS polymorphisms contribute to 30.5% variability in NO production. CONCLUSION: Results of the present study indicate that 27-bp VNTR polymorphism in intron 4 of eNOS gene polymorphism may be the significant risk factor for SLE in south Indian subjects.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  6 / 461457 MEDLINE  
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[PMID]: 29524576
[Au] Autor:Kumari P; Singh SK; Raman R
[Ad] Address:Cytogenetics Laboratory, Department of Zoology, Banaras Hindu University, Varanasi 221005, Uttar Pradesh, India.
[Ti] Title:A novel non-coding RNA within an intron of CDH2 and association of its SNP with non-syndromic cleft lip and palate.
[So] Source:Gene;, 2018 Mar 07.
[Is] ISSN:1879-0038
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:BACKGROUND: Genome-wide linkage analysis and whole genome sequencing in a Van der Woude syndrome (VWS) family revealed that the SNP, rs539075, within intron 2 of the cadherin 2 gene (CDH2) co-segregated with the disease phenotype. RESULTS: A study with nonsyndromic cleft lip with or without cleft palate (NSCL  P) cases (N = 292) and controls (N = 287) established association of this SNP with NSCL  P as a risk factor. RT-PCR based expression analysis of the SNP-harbouring region of intron 2 of CDH2 in the clefted lip and/or palate tissues of 16 patients revealed that the mutant allele expressed in all those individuals having it (hetero-/homozygous), whereas the wild type allele expressed in <50% of the samples in which it was present. The intronic transcript was also present in the prospective lip and palate region of 13.5 dpc mouse embryo, detected by RNA in situ hybridization and RT-PCR. CONCLUSIONS: These results including the in silico, characterization of the ~200 nt-intronic transcript showed that conformationally it fits best with noncoding small RNA, possibly a precursor of miRNA. Its function in the orofacial organogenesis remains to be elucidated which will enable us to define the role of this mutant ncRNA in the clefting of lip and palate.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  7 / 461457 MEDLINE  
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[PMID]: 29524567
[Au] Autor:Hollinger MK; Giudice V; Cummings NA; Rivell G; Zhang H; Kajigaya S; Keyvanfar K; Chen J; Feng X; Young NS
[Ad] Address:Hematology Branch, National Heart, Lung, and Blood Institute (NHLBI), NIH, Bethesda, MD 20892-1202, USA.
[Ti] Title:PD-1 deficiency augments bone marrow failure in a minor-histocompatibility antigen mismatch lymphocyte infusion model.
[So] Source:Exp Hematol;, 2018 Mar 07.
[Is] ISSN:1873-2399
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:While PD-1 blockade has revolutionized cancer immunotherapy, immune-related adverse events (irAEs) present life-threatening complications. Recent reports of aplastic anemia (AA) as irAEs implicate PD-1/PD-L1 as important in preventing immune-mediated destruction of the hematopoietic niche. Infusion of PD-1-deficient (PD-1 KO) lymph node (LN) cells into minor-antigen mismatched mice resulted in early mortality, as well as more severe BM hypoplasia, anemia, and BM microarchitecture disruption in PD-1 KO LN-infused mice relative to mice that received B6 LN cell infusion. Mice that received PD-1 KO LN cells had more CD8 T cell infiltration of the BM and greater expansion of H60-specific CD8 T cells than did their B6 LN-infused counterparts. In the spleen, CD8 T cells were skewed to an effector memory phenotype, suggesting accelerated differentiation of PD-1 KO T cells. Our data suggest that PD-1 dysregulation has a role in murine BM failure, and vigilance in irAE monitoring may be desirable to treat early AA and related cytopenias.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  8 / 461457 MEDLINE  
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[PMID]: 29524426
[Au] Autor:Chiba-Falek O; Gottschalk WK; Lutz MW
[Ad] Address:Department of Neurology, Duke University Medical Center, Durham, NC, USA; Center for Genomic and Computational Biology, Duke University Medical Center, Durham, NC, USA. Electronic address: o.chibafalek@duke.edu.
[Ti] Title:The effects of the TOMM40 poly-T alleles on Alzheimer's disease phenotypes.
[So] Source:Alzheimers Dement;, 2018 Mar 07.
[Is] ISSN:1552-5279
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The TOMM40 poly-T is a polymorphism in intron 6 of the TOMM40 gene, which is adjacent to and in linkage disequilibrium with APOE. Roses etal identified the association between the length of TOMM40 poly-T with the risk and age of onset of late-onset Alzheimer's disease (LOAD). Following the original discovery, additional studies found associations between the TOMM40 poly-T and LOAD-related phenotypes independent of APOE genotypes, while others did not replicate these associations. Furthermore, the identity of the TOMM40 poly-T risk allele has been controversial between different LOAD-related phenotypes. Here, we propose a framework to address the conflicting findings with respect to the TOMM40 poly-T allele associations with LOAD phenotypes and their functional effects. The framework is used to interpret previous studies as means to gain insights regarding the nature of the risk allele, very long versus short. We suggest that the identity of the TOMM40 poly-T risk allele depends on the phenotype being evaluated, the ages of the study subjects at the time of assessment, and the context of the APOE genotypes. In concluding remarks, we outline future studies that will inform the mechanistic interpretation of the genetic data.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  9 / 461457 MEDLINE  
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[PMID]: 29520342
[Au] Autor:Schwiesow L; Mettert E; Wei Y; Miller HK; Herrera NG; Balderas D; Kiley PJ; Auerbuch V
[Ad] Address:Department of Molecular, Cell, and Developmental Biology, University of California, Santa Cruz, Santa Cruz, CA, United States.
[Ti] Title:Control of Heme Uptake Genes in in Response to Iron Sources.
[So] Source:Front Cell Infect Microbiol;8:47, 2018.
[Is] ISSN:2235-2988
[Cp] Country of publication:Switzerland
[La] Language:eng
[Ab] Abstract:Despite the mammalian host actively sequestering iron to limit pathogenicity, heme (or hemin when oxidized) and hemoproteins serve as important sources of iron for many bloodborne pathogens. The HmuRSTUV hemin uptake system allows species to uptake and utilize hemin and hemoproteins as iron sources. HmuR is a TonB-dependent outer membrane receptor for hemin and hemoproteins. HmuTUV comprise a inner membrane ABC transporter that transports hemin and hemoproteins from the periplasmic space into the bacterial cytoplasm, where it is degraded by HmuS. Here we show that but not are expressed under iron replete conditions, whereas as well as are expressed under iron limiting conditions, suggesting complex transcriptional control. Indeed, expression of in the presence of inorganic iron, but not in the presence of hemin, requires the global regulator IscR acting from a promoter in the intergenic region between and . This effect of IscR appears to be direct by binding a site mapped by DNaseI footprinting. In contrast, expression of under iron limiting conditions requires derepression of the ferric uptake regulator Fur acting from the promoter, as Fur binding upstream of was demonstrated biochemically. Differential expression by both Fur and IscR would facilitate maximal hemin uptake and utilization when iron and heme availability is low while maintaining the capacity for periplasmic removal and cytosolic detoxification of heme under a wider variety of conditions. We also demonstrate that a Δ mutant has a survival defect when incubated in whole blood, in which iron is sequestered by heme-containing proteins. Surprisingly, this phenotype was independent of the Hmu system, the type III secretion system, complement, and the ability of to replicate intracellularly. These results suggest that IscR regulates multiple virulence factors important for survival and growth in mammalian tissues and reveal a surprising complexity of heme uptake expression and function under differing conditions of iron.
[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:10.3389/fcimb.2018.00047

  10 / 461457 MEDLINE  
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[PMID]: 29515676
[Au] Autor:Borssn M; Nordlund J; Haider Z; Landfors M; Larsson P; Kanerva J; Schmiegelow K; Flaegstad T; Jnsson G; Frost BM; Palle J; Forestier E; Heyman M; Hultdin M; Lnnerholm G; Degerman S
[Ad] Address:1Department of Medical Biosciences, Ume University, Blg 6M, 2nd floor, SE-90185 Ume, Sweden.
[Ti] Title:DNA methylation holds prognostic information in relapsed precursor B-cell acute lymphoblastic leukemia.
[So] Source:Clin Epigenetics;10:31, 2018.
[Is] ISSN:1868-7083
[Cp] Country of publication:Germany
[La] Language:eng
[Ab] Abstract:Background: Few biological markers are associated with survival after relapse of B-cell precursor acute lymphoblastic leukemia (BCP-ALL). In pediatric T-cell ALL, we have identified promoter-associated methylation alterations that correlate with prognosis. Here, the prognostic relevance of CpG island methylation phenotype (CIMP) classification was investigated in pediatric BCP-ALL patients. Methods: Six hundred and one BCP-ALL samples from Nordic pediatric patients (age 1-18) were CIMP classified at initial diagnosis and analyzed in relation to clinical data. Results: Among the 137 patients that later relapsed, patients with a CIMP- profile ( = 42) at initial diagnosis had an inferior overall survival (pOS 33%) compared to CIMP+ patients ( = 95, pOS 65%) ( = 0.001), which remained significant in a Cox proportional hazards model including previously defined risk factors. Conclusion: CIMP classification is a strong candidate for improved risk stratification of relapsed BCP-ALL.
[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:10.1186/s13148-018-0466-3


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