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  1 / 15542 MEDLINE  
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PMID:28647348
Autor:Yuan H; Zhou S; Liu Z; Cong W; Fei X; Zeng W; Zhu H; Xu R; Wang Y; Zheng J; Pan M
Dirección:Department of Dermatology, Rui Jin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Título:Pivotal Role of Lesional and Perilesional T/B Lymphocytes in Pemphigus Pathogenesis.
Fuente:J Invest Dermatol; 137(11):2362-2370, 2017 Nov.
ISSN:1523-1747
País de publicación:United States
Idioma:eng
Resumen:Pemphigus is a skin and mucosal membrane-targeting autoimmune bullous disease. Previous studies have shown that circulating anti-desmoglein1/3 antibodies are pathogenic and mediate blister formation. However, the role of infiltrating immune cells in lesional skin has not been fully investigated. In this study we showed that there existed a large number of B and T lymphocytes and plasma cells in the skin lesions by immunohistochemistry and immunofluorescence staining. In addition, a significantly increased number of Dsg1- and Dsg3-specific B cells could be identified by flow cytometric analysis or enzyme-linked immunospot technique (i.e., ELISPOT) assay. Furthermore, anti-Dsg1 and Dsg3 antibodies could be detected from the supernatant of in vitro cultures with isolated lymphocytes from lesional skin. We found that most T lymphocytes infiltrating pemphigus vulgaris lesions were CD4 T helper cells expressing IL-21 and IL-17a but not typical T follicular helper cells expressing CXCR5. Additionally, our microarray assay showed that the level of chemokine CCL19 was significantly elevated, suggesting active T-/B-lymphocyte trafficking and aggregation in the pemphigus vulgaris lesions. Collectively, our results suggest a critical role of locally infiltrating lymphocytes in pemphigus pathogenesis.
Tipo de publicación:JOURNAL ARTICLE
Nombre de substancia:0 (Desmoglein 1); 0 (Interleukin-17); 0 (Interleukins); 0 (interleukin-21)


  2 / 15542 MEDLINE  
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PMID:28634035
Autor:Niehues H; Tsoi LC; van der Krieken DA; Jansen PAM; Oortveld MAW; Rodijk-Olthuis D; van Vlijmen IMJJ; Hendriks WJAJ; Helder RW; Bouwstra JA; van den Bogaard EH; Stuart PE; Nair RP; Elder JT; Zeeuwen PLJM; Schalkwijk J
Dirección:Department of Dermatology, Radboud University Medical Center, Radboud Institute for Molecular Life Sciences, Nijmegen, The Netherlands.
Título:Psoriasis-Associated Late Cornified Envelope (LCE) Proteins Have Antibacterial Activity.
Fuente:J Invest Dermatol; 137(11):2380-2388, 2017 Nov.
ISSN:1523-1747
País de publicación:United States
Idioma:eng
Resumen:Terminally differentiating epidermal keratinocytes express a large number of structural and antimicrobial proteins that are involved in the physical barrier function of the stratum corneum and provide innate cutaneous host defense. Late cornified envelope (LCE) genes, located in the epidermal differentiation complex on chromosome 1, encode a family of 18 proteins of unknown function, whose expression is largely restricted to epidermis. Deletion of two members, LCE3B and LCE3C (LCE3B/C-del), is a widely-replicated psoriasis risk factor that interacts with the major psoriasis-psoriasis risk gene HLA-C*06. Here we performed quantitative trait locus analysis, utilizing RNA-seq data from human skin and found that LCE3B/C-del was associated with a markedly increased expression of LCE3A, a gene directly adjacent to LCE3B/C-del. We confirmed these findings in a 3-dimensional skin model using primary keratinocytes from LCE3B/C-del genotyped donors. Functional analysis revealed that LCE3 proteins, and LCE3A in particular, have defensin-like antimicrobial activity against a variety of bacterial taxa at low micromolar concentrations. No genotype-dependent effect was observed for the inside-out or outside-in physical skin barrier function. Our findings identify an unknown biological function for LCE3 proteins and suggest a role in epidermal host defense and LCE3B/C-del-mediated psoriasis risk.
Tipo de publicación:JOURNAL ARTICLE
Nombre de substancia:0 (Anti-Bacterial Agents); 0 (Cornified Envelope Proline-Rich Proteins); 0 (LCE3B protein, human); 0 (LCE3C protein, human)


  3 / 15542 MEDLINE  
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PMID:28664920
Autor:Gasser E; Moutos CP; Downes M; Evans RM
Dirección:Gene Expression Laboratory, Salk Institute for Biological Studies.
Título:FGF1 - a new weapon to control type 2 diabetes mellitus.
Fuente:Nat Rev Endocrinol; 13(10):599-609, 2017 Oct.
ISSN:1759-5037
País de publicación:England
Idioma:eng
Resumen:A hypercaloric diet combined with a sedentary lifestyle is a major risk factor for the development of insulin resistance, type 2 diabetes mellitus (T2DM) and associated comorbidities. Standard treatment for T2DM begins with lifestyle modification, and includes oral medications and insulin therapy to compensate for progressive ß-cell failure. However, current pharmaceutical options for T2DM are limited in that they do not maintain stable, durable glucose control without the need for treatment intensification. Furthermore, each medication is associated with adverse effects, which range from hypoglycaemia to weight gain or bone loss. Unexpectedly, fibroblast growth factor 1 (FGF1) and its low mitogenic variants have emerged as potentially safe candidates for restoring euglycaemia, without causing overt adverse effects. In particular, a single peripheral injection of FGF1 can lower glucose to normal levels within hours, without the risk of hypoglycaemia. Similarly, a single intracerebroventricular injection of FGF1 can induce long-lasting remission of the diabetic phenotype. This Review discusses potential mechanisms by which centrally administered FGF1 improves central glucose-sensing and peripheral glucose uptake in a sustained manner. Specifically, we explore the potential crosstalk between FGF1 and glucose-sensing neuronal circuits, hypothalamic neural stem cells and synaptic plasticity. Finally, we highlight therapeutic considerations of FGF1 and compare its metabolic actions with FGF15 (rodents), FGF19 (humans) and FGF21.
Tipo de publicación:JOURNAL ARTICLE; REVIEW
Nombre de substancia:0 (Blood Glucose); 0 (Insulin); 104781-85-3 (Fibroblast Growth Factor 1)


  4 / 15542 MEDLINE  
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PMID:28971825
Autor:Abdel-Wahab M; Lahoupe B; Polo A; Zubizarreta E; Adnan RR; Johnston P; Juric A; Haffar FE; Andre M; Meghzifene A
Dirección:Division of Human Health, International Atomic Energy Agency, Vienna, Austria. Electronic address: wahabmay@hotmail.com.
Título:Assessment of cancer control capacity and readiness: the role of the International Atomic Energy Agency.
Fuente:Lancet Oncol; 18(10):e587-e594, 2017 Oct.
ISSN:1474-5488
País de publicación:England
Idioma:eng
Resumen:During the past six decades, the International Atomic Energy Agency (IAEA) has helped to address the growing cancer burden, by delivering substantial cancer-related assistance to low-income and middle-income member states. IAEA assistance has primarily been facilitated through sustainable radiotherapy and nuclear medicine programmes to establish safe and effective diagnostic imaging, nuclear medicine, and radiotherapy capacity to safely treat patients with cancer. Planning of a National Cancer Control Programme starts with a needs assessment of all aspects of cancer control in the country to ensure evidence-based strategies are adapted to the country's specific needs. The IAEA offers its member states a tool, known as an integrated mission of Programme of Action for Cancer Therapy Review, to assess the status of national capacities for implementation and delivery of cancer control plans and activities and the readiness to develop and implement a long-term radiation medicine infrastructure and plan to improve capacity.
Tipo de publicación:EVALUATION STUDIES; JOURNAL ARTICLE; REVIEW


  5 / 15542 MEDLINE  
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PMID:28911146
Autor:van Gucht ALM; Meima ME; Moran C; Agostini M; Tylki-Szymanska A; Krajewska MW; Chrzanowska K; Efthymiadou A; Chrysis D; Demir K; Visser WE; Visser TJ; Chatterjee K; van Dijk TB; Peeters RP
Dirección:Department of Internal Medicine, Erasmus University Medical Center, 3000 Rotterdam, The Netherlands.
Título:Anemia in Patients With Resistance to Thyroid Hormone α: A Role for Thyroid Hormone Receptor α in Human Erythropoiesis.
Fuente:J Clin Endocrinol Metab; 102(9):3517-3525, 2017 Sep 01.
ISSN:1945-7197
País de publicación:United States
Idioma:eng
Resumen:Context: Patients with resistance to thyroid hormone (TH) α (RTHα) are characterized by growth retardation, macrocephaly, constipation, and abnormal thyroid function tests. In addition, almost all RTHα patients have mild anemia, the pathogenesis of which is unknown. Animal studies suggest an important role for TH and TH receptor (TR)α in erythropoiesis. Objective: To investigate whether a defect in TRα affects the maturation of red blood cells in RTHα patients. Design, Setting, and Patients: Cultures of primary human erythroid progenitor cells (HEPs), from peripheral blood of RTHα patients (n = 11) harboring different inactivating mutations in TRα (P398R, F397fs406X, C392X, R384H, A382fs388X, A263V, A263S), were compared with healthy controls (n = 11). During differentiation, erythroid cells become smaller, accumulate hemoglobin, and express different cell surface markers. We assessed cell number and cell size, and used cell staining and fluorescence-activated cell sorter analysis to monitor maturation at different time points. Results: After ∼14 days of ex vivo expansion, both control and patient-derived progenitors differentiated spontaneously. However, RTHα-derived cells differentiated more slowly. During spontaneous differentiation, RTHα-derived HEPs were larger, more positive for c-Kit (a proliferation marker), and less positive for glycophorin A (a differentiation marker). The degree of abnormal spontaneous maturation of RTHα-derived progenitors did not correlate with severity of underlying TRα defect. Both control and RTHα-derived progenitors responded similarly when differentiation was induced. T3 exposure accelerated differentiation of both control- and RTHα patient-derived HEPs. Conclusions: Inactivating mutations in human TRα affect the balance between proliferation and differentiation of progenitor cells during erythropoiesis, which may contribute to the mild anemia seen in most RTHα patients.
Tipo de publicación:COMPARATIVE STUDY; JOURNAL ARTICLE
Nombre de substancia:0 (Thyroid Hormone Receptors alpha)


  6 / 15542 MEDLINE  
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PMID:28637297
Autor:Delaney MA; Wan YW; Kim GE; Creighton CJ; Taylor MG; Masand R; Park A; Valdes C; Gibbons W; Liu Z; Anderson ML
Dirección:Department of Obstetrics & Gynecology, Baylor College of Medicine, Houston, Texas 77030.
Título:A Role for Progesterone-Regulated sFRP4 Expression in Uterine Leiomyomas.
Fuente:J Clin Endocrinol Metab; 102(9):3316-3326, 2017 Sep 01.
ISSN:1945-7197
País de publicación:United States
Idioma:eng
Resumen:Context: Despite progesterone's key role in uterine smooth muscle tumorigenesis, the mechanisms by which it promotes the growth of uterine leiomyomas remain poorly understood. Objective: The aim of this study was to identify gene products mediating the effects of progesterone in uterine leiomyomas. Design: Gene expression profiling was used to identify putative progesterone-regulated genes differentially expressed in uterine leiomyomas, which were then studied in vitro. Methods: Gene expression was comprehensively profiled with the Illumina WG BeadChip (version 2.6) and analyzed with a bioinformatic algorithm that integrates known protein-protein interactions. Genomic binding sites for progesterone receptor (PR) were interrogated by chromatin immunoprecipitation-quantitative polymerase chain reaction (ChIP-qPCR). Small interfering RNA was used to study gene function in primary cell lines. Results: Our analyses identified secreted Frizzled-related protein 4 (sFRP4) as a key gene product functionally linked to PR activation whose expression was 2.6 times higher in leiomyomas than myometrium (n = 26, P < 0.01) and 2.5 times higher during the proliferative phase of the menstrual cycle (n = 26, P < 0.01). Direct binding between PR and sFRP4 promoter was observed by ChIP-qPCR. Robust overexpression of sFRP4 was also observed in primary cultures derived from leiomyoma. Progesterone preferentially inhibited sFRP4 expression and secretion in leiomyoma cultures in a dose-dependent manner sensitized by estradiol. Knockdown of sFRP4 inhibited proliferation and apoptosis in primary cultures of both myometrium and leiomyoma. Conclusions: Overexpression of sFRP4 is a robust, progesterone-regulated feature of leiomyomas that increases smooth muscle proliferation. More work is needed to elucidate how progesterone's ability to modulate sFRP4 expression contributes to uterine smooth muscle tumorigenesis.
Tipo de publicación:JOURNAL ARTICLE
Nombre de substancia:0 (Proto-Oncogene Proteins); 0 (RNA, Messenger); 0 (SFRP4 protein, human); 4G7DS2Q64Y (Progesterone)


  7 / 15542 MEDLINE  
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PMID:28531338
Autor:Salomon C; Guanzon D; Scholz-Romero K; Longo S; Correa P; Illanes SE; Rice GE
Dirección:Exosome Biology Laboratory, Centre for Clinical Diagnostics, The University of Queensland Centre for Clinical Research, Royal Brisbane and Women's Hospital, The University of Queensland, Brisbane, Queensland 4029, Australia.
Título:Placental Exosomes as Early Biomarker of Preeclampsia: Potential Role of Exosomal MicroRNAs Across Gestation.
Fuente:J Clin Endocrinol Metab; 102(9):3182-3194, 2017 Sep 01.
ISSN:1945-7197
País de publicación:United States
Idioma:eng
Resumen:Context: There is a need to develop strategies for early prediction of patients who will develop preeclampsia (PE) to establish preventive strategies to reduce the prevalence and severity of the disease and their associated complications. Objective: The objective of this study was to investigate whether exosomes and their microRNA cargo present in maternal circulation can be used as early biomarker for PE. Design, Setting, Patients, and Interventions: A retrospective stratified study design was used to quantify total exosomes and placenta-derived exosomes present in maternal plasma of normal (n = 32 per time point) and PE (n = 15 per time point) pregnancies. Exosomes present in maternal circulation were determined by nanoparticle tracking analysis. An Illumina TruSeq® Small RNA Library Prep Kit was used to construct a small RNA library from exosomal RNA obtained from plasma samples. Results: In presymptomatic women, who subsequently developed PE, the concentration of total exosomes and placenta-derived exosomes in maternal plasma was significantly greater than those observed in controls, throughout pregnancy. The area under the receiver operating characteristic curves for total exosome and placenta-derived exosome concentrations were 0.745 ± 0.094 and 0.829 ± 0.077, respectively. In total, over 300 microRNAs were identified in exosomes across gestation, where hsa-miR-486-1-5p and hsa-miR-486-2-5p were identified as the candidate microRNAs. Conclusions: Although the role of exosomes during PE remains to be fully elucidated, we suggest that the concentration and content of exosomes may be of diagnostic utility for women at risk for developing PE.
Tipo de publicación:JOURNAL ARTICLE
Nombre de substancia:0 (Biomarkers); 0 (MicroRNAs)


  8 / 15542 MEDLINE  
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PMID:28526302
Autor:Gousopoulos E; Proulx ST; Bachmann SB; Dieterich LC; Scholl J; Karaman S; Bianchi R; Detmar M
Dirección:Institute of Pharmaceutical Sciences, Swiss Federal Institute of Technology, ETH Zurich, Zurich, Switzerland.
Título:An Important Role of VEGF-C in Promoting Lymphedema Development.
Fuente:J Invest Dermatol; 137(9):1995-2004, 2017 Sep.
ISSN:1523-1747
País de publicación:United States
Idioma:eng
Resumen:Secondary lymphedema is a common complication after cancer treatment, but the pathomechanisms underlying the disease remain unclear. Using a mouse tail lymphedema model, we found an increase in local and systemic levels of the lymphangiogenic factor vascular endothelial growth factor (VEGF)-C and identified CD68 macrophages as a cellular source. Surprisingly, overexpression of VEGF-C in a transgenic mouse model led to aggravation of lymphedema with increased immune cell infiltration and vascular leakage compared with wild-type littermates. Conversely, blockage of VEGF-C by overexpression of soluble VEGF receptor-3 reduced edema development, diminishing inflammation and blood vascular leakage. Similar findings were obtained in a hind limb lymph node excision lymphedema model. Flow cytometry analyses and immunofluorescence stainings in lymphedematic tissue showed that VEGF receptor-3 expression was restricted to lymphatic endothelial cells. Our data suggest that endogenous VEGF-C causes blood vascular leakage and fluid influx into the tissue, thus actively contributing to edema formation. These data may provide the basis for future clinical therapeutic approaches.
Tipo de publicación:JOURNAL ARTICLE
Nombre de substancia:0 (Biomarkers); 0 (Vascular Endothelial Growth Factor C); EC 2.7.10.1 (FLT4 protein, human); EC 2.7.10.1 (Vascular Endothelial Growth Factor Receptor-3)


  9 / 15542 MEDLINE  
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PMID:28502801
Autor:Law MH; Medland SE; Zhu G; Yazar S; Viñuela A; Wallace L; Shekar SN; Duffy DL; Bataille V; Glass D; Spector TD; Wood D; Gordon SD; Barbour JM; Henders AK; Hewitt AW; Montgomery GW; Sturm RA; Mackey DA; Green AC; Martin NG; MacGregor S; MuTHER Consortium
Dirección:QIMR Berghofer Medical Research Institute, Brisbane, Australia. Electronic address: matthew.law@qimrberghofer.edu.au.
Título:Genome-Wide Association Shows that Pigmentation Genes Play a Role in Skin Aging.
Fuente:J Invest Dermatol; 137(9):1887-1894, 2017 Sep.
ISSN:1523-1747
País de publicación:United States
Idioma:eng
Resumen:Loss of fine skin patterning is a sign of both aging and photoaging. Studies investigating the genetic contribution to skin patterning offer an opportunity to better understand a trait that influences both physical appearance and risk of keratinocyte skin cancer. We undertook a meta-analysis of genome-wide association studies of a measure of skin pattern (microtopography score) damage in 1,671 twin pairs and 1,745 singletons (N = 5,087) drawn from three independent cohorts. We identified that rs185146 near SLC45A2 is associated with a skin aging trait at genome-wide significance (P = 4.1 × 10 ); to our knowledge this is previously unreported. We also confirm previously identified loci, rs12203592 near IRF4 (P = 8.8 × 10 ) and rs4268748 near MC1R (P = 1.2 × 10 ). At all three loci we highlight putative functionally relevant SNPs. There are a number of red hair/low pigmentation alleles of MC1R; we found that together these MC1R alleles explained 4.1% of variance in skin pattern damage. We also show that skin aging and reported experience of sunburns was proportional to the degree of penetrance for red hair of alleles of MC1R. Our work has uncovered genetic contributions to skin aging and confirmed previous findings, showing that pigmentation is a critical determinant of skin aging.
Tipo de publicación:JOURNAL ARTICLE; META-ANALYSIS; REVIEW
Nombre de substancia:0 (Interferon Regulatory Factors); 0 (interferon regulatory factor-4)


  10 / 15542 MEDLINE  
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PMID:28271527
Autor:Li X; Liu R; Yang J; Sun L; Zhang L; Jiang Z; Puri P; Gurley EC; Lai G; Tang Y; Huang Z; Pandak WM; Hylemon PB; Zhou H
Dirección:Jiangsu Key Laboratory of Drug Screening, China Pharmaceutical University, Nanjing, Jiangsu, China.
Título:The role of long noncoding RNA H19 in gender disparity of cholestatic liver injury in multidrug resistance 2 gene knockout mice.
Fuente:Hepatology; 66(3):869-884, 2017 Sep.
ISSN:1527-3350
País de publicación:United States
Idioma:eng
Resumen:The multidrug resistance 2 knockout (Mdr2 ) mouse is a well-established model of cholestatic cholangiopathies. Female Mdr2 mice develop more severe hepatobiliary damage than male Mdr2 mice, which is correlated with a higher proportion of taurocholate in the bile. Although estrogen has been identified as an important player in intrahepatic cholestasis, the underlying molecular mechanisms of gender-based disparity of cholestatic injury remain unclear. The long noncoding RNA H19 is an imprinted, maternally expressed, and estrogen-targeted gene, which is significantly induced in human fibrotic/cirrhotic liver and bile duct-ligated mouse liver. However, whether aberrant expression of H19 accounts for gender-based disparity of cholestatic injury in Mdr2 mice remains unknown. The current study demonstrated that H19 was markedly induced (∼200-fold) in the livers of female Mdr2 mice at advanced stages of cholestasis (100 days old) but not in age-matched male Mdr2 mice. During the early stages of cholestasis, H19 expression was minimal. We further determined that hepatic H19 was mainly expressed in cholangiocytes, not hepatocytes. Both taurocholate and estrogen significantly activated the extracellular signal-regulated kinase 1/2 signaling pathway and induced H19 expression in cholangiocytes. Knocking down H19 not only significantly reduced taurocholate/estrogen-induced expression of fibrotic genes and sphingosine 1-phosphate receptor 2 in cholangiocytes but also markedly reduced cholestatic injury in female Mdr2 mice. Furthermore, expression of small heterodimer partner was substantially inhibited at advanced stages of liver fibrosis, which was reversed by H19 short hairpin RNA in female Mdr2 mice. Similar findings were obtained in human primary sclerosing cholangitis liver samples. CONCLUSION: H19 plays a critical role in the disease progression of cholestasis and represents a key factor that causes the gender disparity of cholestatic liver injury in Mdr2 mice. (Hepatology 2017;66:869-884).
Tipo de publicación:JOURNAL ARTICLE
Nombre de substancia:0 (Estrogens); 0 (H19 long non-coding RNA); 0 (RNA, Long Noncoding); 0 (Receptors, Lysosphingolipid); 0 (sphingosine-1-phosphate receptor-2, mouse); 5E090O0G3Z (Taurocholic Acid); EC 2.7.11.24 (Mapk1 protein, mouse); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 1)



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