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Molecular targets in the treatment of alcoholic hepatitis

World Journal of Gastroenterology 2012年第39期18卷 5504-5513页

作者： Ashwin D Dhanda richard wl lee Peter L Collins C Anne McCune Department of Liver Medicine University Hospitals Bristol NHS Foundation TrustBS2 8HW BristolUnited Kingdom Department of Cellular and Molecular Medicine School of Clinical SciencesUniversity of BristolBS9 1TD BristolUnited Kingdom

Alcohol related costs to health and society are high. One of the most serious complications of alcohol misuse to the individual is the development of alcoholic hepatitis (AH), a clinical syndrome of jaundice and progressive inflammatory liver injury in patients with a history of recent heavy alcohol use. It has a poor outcome and few existing successful therapies. The use of glucocorticoids in patients with severe AH is still controversial and there remains a group of patients with glucocorticoid-resistant disease. However, as our understanding of the pathogenesis of the condition improves there are opportunities to develop new targeted therapies with specific actions to control liver inflammation without having a detrimental effect on the immune system as a whole. In this article we review the molecular mechanisms of AH concentrating on the activation of the innate and adaptive immune response. We consider existing treatments including glucocorticoids, anti-tumor necrosis factor therapy and pentoxifylline and their limitations. Using our knowledge of the disease pathogenesis we discuss possible novel therapeutic approaches. New targets include pro-inflammatory cytokines such as interleukin (IL)-17, chemokines and their receptors (for example IL-8, CXCL9 and CXCR3) and augmentation of anti-inflam- matory molecules such as IL-10 and IL-22. And there is also future potential to consider combination therapy to selectively modulate the immune response and gain control of disease.

关键词： Alcoholic hepatitis Tumour necrosis factor-m Pentoxifylline Interleukins Chemokine receptors

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Transcriptome Analysis of Arabidopsis Wild-Type and gl3-sst sim Trichomes Identifies Four Additional Genes Required for Trichome Development

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Molecular Plant 2009年第4期2卷 803-822页

作者： M. David Marks Jonathan R Wenger Edward Gilding Ross Jilk richard A. Dixon Department of Plant Biology University of Minnesota St Paul MN 551108 USA Department of Chemistry University of Wisconsin-River Falls River Falls Wl 54022 USA Plant Biology Division Samuel Roberts Noble Foundation Ardmore OK 73401 USA

Transcriptome analyses have been performed on mature trichomes isolated from wild-type Arabidopsis leaves and on leaf trichomes isolated from the g13-sst sim double mutant, which exhibit many attributes of immature trichomes. The mature trichome profile contained many highly expressed genes involved in cell wall synthesis, protein turnover, and abiotic stress response. The most highly expressed genes in the g13-sst sim profile encoded ribosomal proteins and other proteins involved in translation. Comparative analyses showed that all but one of the genes encoding transcription factors previously found to be important for trichome formation, and many other trichome-important genes, were preferentially expressed in gl3-sst sim trichomes. The analysis of genes preferentially expressed in gl3-sst sim led to the identification of four additional genes required for normal trichome development. One of these was the HDG2 gene, which is a member of the HD-ZIP IV transcription factor gene family. Mutations in this gene did not alter trichome expansion, but did alter mature trichome cell walls. Mutations in BIT resulted in a loss of trichome branch formation. The relationship between bit and the phenotypically identical mutant, sti, was explored. Mutations in PEL3, which was previously shown to be required for development of the leaf cuticle, resulted in the occasional tangling of expanding trichomes. Mutations in another gene encoding a protein with an unknown function altered trichome branch formation.

关键词： Cell wall cell differentiation homeodomain wax trichome

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Integrative modeling of transmitted and de novo variants identifies novel risk genes for congenital heart disease

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Quantitative Biology 2021年第2期9卷 216-227页

作者： Mo Li Xue Zeng Chentian Jin Sheng Chih Jin Weilai Dong Martina Brueckner richard Lifton Qiongshi Lu Hongyu Zhao Department of Biostatistics Yale School of Public HealthNew HavenCT 06510USA Department of Genetics Yale UniversityNew HavenCT 06510USA Department of Molecular Cellular&Developmental BiologyYale UniversityCT 06510USA Department of Genetics Washington University School of MedicineSt LouisMO 63110USA Department of Pediatrics Yale UniversityNew HavenCT 06510USA Laboratory of Human Genetics and Genomics Rockefeller UniversityNew YorkNY 10065USA Department of Biostatistics and Medical Informatics University of Wisconsin-MadisonMadisonWl 53792USA Program of Computational Biology and Bioinformatics Yale UniversityNew HavenCT 06510USA

Background:Whole-exome sequencing(WES)studies have identified multiple genes enriched for de novo mutations(DNMs)in congenital heart disease(CHD)***,risk gene identification based on DNMs alone remains statistically challenging due to heterogenous etiology of CHD and low mutation rate in each ***:In this manuscript,we introduce a hierarchical Bayesian framework for gene-level association test which jointly analyzes de novo and rare transmitted *** integrative modeling of multiple types of genetic variants,gene-level annotations,and reference data from large population cohorts,our method accurately characterizes the expected frequencies of both de novo and transmitted variants and shows improved statistical power compared to analyses based on DNMs ***:Applied to WES data of 2,645 CHD proband-parent trios,our method identified 15 significant genes,half of which are novel,leading to new insights into the genetic bases of ***:These results showcase the power of integrative analysis of transmitted and de novo variants for disease gene discovery.

关键词： rare variants gene-level association test congenital heart disease de novo mutation

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Mass cytometry uncovers a distinct peripheral immune profile and upregulated CD38 expression in patients with hidradenitis suppurativa

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Cellular & Molecular Immunology 2023年第8期20卷 972-975页

作者： Peter Dimitrion Iltefat Hamzavi Congcong Yin Jugmohit Toor Kalpana Subedi Namir Khalasawi Angela Miller richard Huggins Indra Adrianto Jesse Veenstra Gautham Vellaichamy Aakash Hans Steven Daveluy Mohammad Athar Wilson Liao Henry Lim David Ozog Li Zhou Qing-Sheng Mi Center for Cutaneous Biology and Immunology Research Department of DermatologyHenry Ford Health SystemDetroitMI48202USA Immunology Research Program Henry Ford Cancer InstituteHenry Ford Health SystemDetroitMI48202USA Cancer Biology Graduate Program School of MedicineWayne State UniversityDetroitMI48202USA Center for Bioinformatics Department of Public Health SciencesHenry Ford Health SystemDetroitMI48202USA Department of Dermatology Wayne State University School of MedicineDetroitMI48202USA University of Alabama at Birmingham(UAB)Research Center of Excellence in Arsenicals Department of DermatologyUniversity of Alabama at BirminghamBirminghamALUSA Department of Dermatology University of California San FranciscoSan FranciscoCAUSA Department of Biochemistry Microbiologyand ImmunologySchool of MedicineWayne State UniversityDetroitMI48202USA

Hidradenitis suppurativa(HS)is a chronic inflammatory skin disease with a worldwide prevalence of 0.3–4.0%,wherein abscesses and dermal sinus tracts form in intertriginous skin[1].HS remains poorly treated due to a l... 详细信息

关键词： CD38 patients pathogenesis

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Mutations in a P-type ATPase gene cause axonal degeneration

Mutations in a P-type ATPase gene cause axonal degeneration

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2012全国发育生物学大会

作者： richard T.Libby Wilhelmine N.de Vries richard S.Smith Dana L.Wright Roderick T.Bronson Kevin L.Seburn Simon W.M.John The Howard Hughes Medical Institute The Jackson Laboratory600 Main StreetBar HarborMEUSA Department of Ophthalmology Tufts University of MedicineBostonMAUSA

Neuronal loss and axonal degeneration are important pathological features of many neurodegenerative diseases. The molecular mechanisms underlying the majority of axonal degeneration conditions remain *** better understand axonal degeneration,we studied a mouse mutant wabbler-Iethal(wl).Wabbler-lethal(wl) mutant mice develop progressive ataxia with pronounced neurodegeneration in the central and peripheral nervous *** studies have led to a debate of whether myelinopathy or axonopathy is the primary cause of neurodegeneration observed in wl mice. Here we provide clear evidence that wabbler lethal mutants develop an axonopathy,and that this axonopathy is modulated by wld and Bax *** addition,we have identified the gene harboring the disease-causing mutations as *** studied three wl alleles and found that all result from mutations in the Atp8a2 *** analysis shows that ATP8A2 possesses phosphatidylserine translocase activity and is involved in localization of phosphatidylserine to the inner leaflet of the plasma ***8a2 is widely expressed in the brain,the spinal cord,and *** assessed two of the mutant alleles of Atp8a2 and found they are both nonfunctional for the phosphatidylserine translocase activity. Conclusions:Our data demonstrate for the first time that mutation of a mammalian phosphatidylserine translocase causes axon degeneration and neurodegenerative disease.

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东风

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2017年

作者： (美)理查德·沃林(richard Wolin)

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