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Mesenchymal stem cells: A new diagnostic tool?

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World Journal of Stem Cells 2015年第5期7卷 789-792页

作者： Maria Teresa Valenti Antonio Mori Giovanni Malerba Luca Dalle Carbonare Department of medicine Section of Internal Medicine DUniversity of Verona Department of Life and Reproduction Sciences Section of Biology and GeneticsUniversity of Verona

Mesenchymal stem cells(MSCs) are progenitor cells capable of self-renewal that can differentiate in multiple tissues and, under specific and standardizedculture conditions, expand in vitro with little phenotypic alterations. In recent years, preclinical and clinical studies have focused on MSC analysis and understanding the potential use of these cells as a therapy in a wide range of pathologies, and many applications have been tested. Clinical trials using MSCs have been performed(e.g., for cardiac events, stroke, multiple sclerosis, blood diseases, auto-immune disorders, ischemia, and articular cartilage and bone pathologies), and for many genetic diseases, these cells are considered an important resource. Considering of the biology of MSCs, these cells may also be useful tools for understanding the physiopathology of different diseases, and they can be used to develop specific biomarkers for a broad range of diseases. In this editorial, we discuss the literature related to the use of MSCs for diagnostic applications and we suggest new technologies to improve their employment.

关键词： Mesenchymal stem cells Biomarkers Next generation sequencing Diagnostic tool Tumorinitiatingcells

Recent developments in the pathophysiology of irritable bowel syndrome

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World Journal of Gastroenterology 2015年第25期21卷 7621-7636页

作者： Magdy El-Salhy section for Gastroenterology Department of Medicine Stord Hospital section of Neuroendocrine Gastroenterology Division of Gastroenterology Department of Clinical MedicineUniversity of Bergen National Centre for Functional Gastrointestinal Disorders Department of Medicine Haukeland University Hospital

Irritable bowel syndrome(IBS) is a common gastrointestinal disorder, the pathophysiology of which is not completely known, although it has been shown that genetic/social learning factors, diet, intestinal microbiota, intestinal low-grade inflammation, and abnormal gastrointestinal endocrine cells play a major role. Studies of familial aggregation and on twins have confirmed the heritability of IBS. However, the proposed IBS risk genes are thus far nonvalidated hits rather than true predisposing factors. There is no convincing evidence that IBS patients suffer from food allergy/intolerance, with the effect exerted by diet seemingly caused by intake of poorly absorbed carbohydrates and fiber. Obesity is a possible comorbidity of IBS. Differences in the microbiota between IBS patients and healthy controls have been reported, but the association between IBS symptoms and specific bacterial species is uncertain. Low-grade inflammation appears to play a role in the pathophysiology of a major subset of IBS, namely postinfectious IBS. The density of intestinal endocrine cells is reduced in patients with IBS, possibly as a result of genetic factors, diet, intestinal microbiota, and low-grade inflammation interfering with the regulatory signals controlling the intestinal stem-cell clonogenic and differentiation activities. Furthermore, there is speculation that this decreased number of endocrine cells is responsible for the visceral hypersensitivity, disturbed gastrointestinal motility, and abnormal gut secretion seen in IBS patients.

关键词： Diet Endocrine cells genetic factors Lowgradeinflammation Microbiota Stem ce

Heart disease in Friedreich's ataxia

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World Journal of Cardiology 2019年第1期11卷 1-12页

作者： Emily Hanson Mark Sheldon Brenda Pacheco Mohammed Alkubeysi Veena Raizada Department of Internal medicine Cardiology Section University of New Mexico

Friedreich's ataxia(FRDA), which occurs in 1/50000 live births, is the most prevalent inherited neuromuscular disorder. Nearly all FRDA patients develop cardiomyopathy at some point in their lives. The clinical manifestations of FRDA include ataxia of the limbs and trunk, dysarthria, diabetes mellitus, and cardiac diseases. However, the broad clinical spectrum makes FRDA difficult to identify.The diagnosis of FRDA is based on the presence of suspicious clinical factors, the use of the Harding criteria and, more recently, the use of genetic testing for identifying the expansion of a triplet nucleotide sequence. FRDA is linked to a defect in the mitochondrial protein frataxin; an epigenetic alteration interferes with the folding of this protein, causing a relative deficiency of frataxin in affected patients. Frataxins are small essential proteins whose deficiency causes a range of metabolic disturbances, including oxidative stress, iron-sulfur cluster deficits, and defects in heme synthesis, sulfur amino acid metabolism, energy metabolism, stress responses, and mitochondrial function. The cardiac involvement seen in FRDA is a consequence of mitochondrial proliferation as well as the loss of contractile proteins and the subsequent development of myocardial fibrosis. The walls of the left ventricle become thickened, and different phenotypic manifestations are seen, including concentric or asymmetric hypertrophy and(less commonly) dilated cardiomyopathy. Dilated cardiomyopathy and arrhythmia are associated with mortality in patients with FRDA, whereas hypertrophic cardiomyopathy is not. Systolic function tends to be low-normal in FRDA patients, with an acute decline at the end of life.However, the literature includes only a few long-term prospective studies of cardiac progression in FRDA, and the cause of death is often attributed to heart failure and arrhythmia postmortem. Cardiomyopathy tends to be correlated with the clinical neurologic age of onset and the nucleotide triplet repeat length(i.e.,markers of phenotypi

关键词： Friedreich’s ataxia Mitochondrial disorder Nonischemic cardiomyopathy Cardiac disease

Hepatocellular carcinoma in patients with non-alcoholic fatty liver disease

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World Journal of Gastroenterology 2016年第37期22卷 8294-8303页

作者： Carrie R Wong Mindie H Nguyen Joseph K Lim Department of Internal medicine Yale University School of Medicine Division of Gastroenterology and Hepatology Stanford University School of Medicine Yale Liver Center Section of Digestive Diseases Yale University School of Medicine

Nonalcoholic fatty liver disease(NAFLD) is the most common chronic liver disease in the United States and represents an increasingly important etiology of hepatocellular carcinoma(HCC) with annual cumulative incidence rates ranging from 2% to 12% in cohorts of NAFLD cirrhosis. While the risk of progression of NAFLD to HCC remains higher among patients with fibrosis or cirrhosis, an increasing amount of literature describes NAFLD-HCC as a disease that can occur in the absence of cirrhosis. Efforts to characterize the pathogenesis of NAFLD-HCC have suggested mechanisms that strongly associate with states of hyperinsulinemia and chronic inflammation, cellular mechanisms including adaptive immune responses and hepatic progenitor cell populations, and genetic polymorphisms including mutations of PNPLA3. Current literature describes NAFLD-HCC mostly as a disease of late presentation with lower rates of receipt of curative therapy and worse prognosis. However, a growing body of evidence has reported comparable and potentially more favorable disease-free and overall survival rates among patients with NAFLD-HCC after receipt of curative treatment. This review summarizes current evidence of epidemiology, pathophysiology, disease presentation, demand and receipt of curative therapy, post-treatment outcomes, and overall survival of NAFLD-associated HCC.

关键词： Fatty liver Nonalcoholic steatohepatitis Hepatocellular carcinoma Liver cirrhosis Liver cancer

Expression quantitative trait analyses to identify causal genetic variants for type 2 diabetes susceptibility

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World Journal of Diabetes 2014年第2期5卷 97-114页

作者： Swapan Kumar Das Neeraj Kumar section on Endocrinology and Metabolism Department of Internal Medicine Wake Forest School of Medicine

Type 2 diabetes(T2D) is a common metabolic disorder which is caused by multiple genetic perturbations affecting different biological pathways. Identifying genetic factors modulating the susceptibility of this complex heterogeneous metabolic phenotype in different ethnic and racial groups remains challenging. Despite recent success, the functional role of the T2D susceptibility variants implicated by genome-wide association studies(GWAS) remains largely unknown. genetic dissection of transcript abundance or expression quantitative trait(eQTL) analysis unravels the genomic architecture of regulatory variants. Availability of eQTL information from tissues relevant for glucose homeostasis in humans opens a new avenue to prioritize GWASimplicated variants that may be involved in triggering a causal chain of events leading to T2D. In this article, we review the progress made in the field of eQTL research and knowledge gained from those studies in understanding transcription regulatory mechanisms in human subjects. We highlight several novel approaches that can integrate eQTL analysis with multiple layers of biological information to identify ethnic-specific causal variants and gene-environment interactions relevant to T2D pathogenesis. Finally, we discuss how the eQTL analysis mediated search for "missing heritability" may lead us to novel biological and molecular mechanisms involved in susceptibility to T2D.

关键词： Type 2 diabetes Single nucleotide polymorphisms Expression quantitative trait locus Expression regulatory SNPs Gene-environment interaction Genome-wide association study

Cytokines,synaptic plasticity and network dynamics:a matter of balance

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Neural Regeneration Research 2023年第12期18卷 2569-2572页

作者： Laura Bellingacci Jacopo Canonichesi Andrea Mancini Lucilla Parnetti Massimiliano Di Filippo section of Neurology Department of Medicine and SurgeryUniversity of PerugiaPerugiaItaly

The modern view of the immune system as a sensitizing and modulating machinery of the central nervous system is now well recognized.However,the specific mechanisms underlying this fine crosstalk have yet to be fully disentangled.To control cognitive function and behavior,the two systems are engaged in a subtle interacting act.In this scenario,a dual action of pro-inflammatory cytokines in the modulation of brain network connections is emerging.Pro-inflammatory cytokines are indeed required to express physiological plasticity in the hippocampal network while being detrimental when over-expressed during uncontrolled inflammatory processes.In this dynamic equilibrium,synaptic functioning and the performance of neural networks are ensured by maintaining an appropriate balance between pro-and anti-inflammatory molecules in the central nervous system microenvironment.

关键词： brain networks cognition cytokines hippocampus memory neuroimmunology neuroinflammation synaptic plasticity

Mapping of a dominantly inherited spinocerebellar ataxia with azoospermia to chromosome 7q32.3

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Mapping of a dominantly inherited spinocerebellar ataxia wit...

Colon adenoma features and their impact on risk of future advanced adenomas and colorectal cancer

中国神经科学学会第四次会员代表大会暨第八届全国学术会议

作者： Nancy J.Cox Christopher M.Gomez Section of Genetic Medicine Department of MedicineUniversity of ChicagoChicago60637USA Department of Neurology University of Chicago Medical CenterChicagoIllinois 60637USA

＜正＞The dominantly inherited spinocerebellar ataxias（SCA） are a clinically and genetically heterogeneous group of neurodegenerative disorders characterized by progressive imbalance,dysarthria and motor incoordination.Etiologically distinct SCA subtypes can only be distinguished consistently by genetic analysis.We identified a five-generation kindred of french ancestry inherited as an autosomal dominant trait that is associated with a novel form of progressive ataxia and cognitive impairment,in which all affected males are infertile.The disorder is inherited only from affected or presymptomatic females.The affected individuals including 9 females and 11 males,particularly females,have a broad range of age of onset, which is significantly much later than male patients.Detailed neuropsychological evaluations demonstrated cognitive impairment with borderline IQ scores for those with onset of ataxia before 40 years age.Brain magnetic resonance imaging demonstrates cerebellar atrophy.Affected males had testicular atrophy and azoospermia.Testicular biopsy from one sterile male demonstrated complete absence of germ cells and progenitors.After exclusion of mutations in or linkage to known SCA loci and genes,fragile X,X-linkage,Y-chromosome microdeletion,we carried out a genome-wide genetic linkage scan and located the disease locus to chromosome 7q32.3 by two-point analysis（a maximal two-point LOD score of 3.59,9=0） and haplotype-based analysis.Sequencing of one candidate disease-causing gene（transiently secret） within the region using a recombinant DNA sequencing approach including TA clone method,which carried（ATTCT）n pentanucleotide repeat units in intron 31,revealed an interesting small difference in the size of repeat between affected and normal individuals in the pedigree,for which more normal controls should be detected and confirmed for co-segregation in the disease.Identification of the gene responsible for this complex phenotype may shed additional light into the pathogenesis of ataxia,male infertility,and mental

关键词： dominantly inherited spinocerebellar ataxia kindred clinical characteristics mapping

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World Journal of Gastrointestinal Oncology 2016年第12期8卷 826-834页

作者： Audrey H Calderwood Karen E Lasser Hemant K Roy section of Gastroenterology Depart-ment of MedicineDartmouth-Hitchcock Medical Center section of General Internal medicine Depart-ment of MedicineBoston University School of Medicine section of Gastroenterology Department of MedicineBoston University School of Medicine

AIM To review the evidence on the association between specific colon adenoma features and the risk of future colonic neoplasia [adenomas and colorectal cancer(CRC)]. METHODS We performed a literature search using the National Library of medicine through Pub Med from 1/1/2003 to 5/30/2015. Specific Medical Subject Headings terms(colon, colon polyps, adenomatous polyps, epidemiology, natural history, growth, cancer screening, colonoscopy, CRC) were used in conjunction with subject headings/key words(surveillance, adenoma surveillance, polypectomy surveillance, and serrated adenoma). We defined nonadvanced adenomas as 1-2 adenomas each 25% villous histology or high-grade dysplasia. A combined endpoint of advanced neoplasia included advanced adenomas and invasive CRC.RESULTS Our search strategy identified 592 candidate articlesof which 8 met inclusion criteria and were relevant for assessment of histology(low grade vs high grade dysplasia, villous features) and adenoma size. Six of these studies met the accepted quality indicator threshold for overall adenoma detection rate > 25% among study patients. We found 254 articles of which 7 met inclusion criteria for the evaluation of multiple adenomas. Lastly, our search revealed 222 candidate articles of which 6 met inclusion criteria for evaluation of serrated polyps. Our review found that villous features, high grade dysplasia, larger adenoma size, and having ≥ 3 adenomas at baseline are associated with an increased risk of future colonic neoplasia in some but not all studies. Serrated polyps in the proximal colon are associated with an increased risk of future colonic neoplasia, comparable to having a baseline advanced adenoma.CONCLUSION Data on adenoma features and risk of future adenomas and CRC are compelling yet modest in absolute effect size. Future research should refine this risk stratification.

关键词：冒号腺瘤屏蔽的 Colorectal 癌症监视 Colonoscopy

How would preclinical Alzheimer’s disease (AD pathology) occur? An insight from a genomic instability mouse model

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Neural Regeneration Research 2021年第10期16卷 2012-2014页

作者： Chinthalapally V.Rao Hiroshi Y.Yamada Center for Cancer Prevention and Drug Development Department of MedicineHematology/Oncology SectionUniversity of Oklahoma Health Sciences Center(OUHSC)Oklahoma CityOKUSA

More than 95%of Alzheimer’s disease(AD)is late-onset,in which patients show clinical cognition/behavior symptoms after age 65.Unlike early-onset AD that comes with mutations in genes directly involved in amyloid metabolism(APP,PSEN),genetic predispositions associated with late-onset AD are harder to pinpoint,and their mechanistic links to AD development need further investigation.Although the development mechanism of late-onset AD remains controversial,amyloid-beta accumulation,initiated in middle age,is widely accepted as the triggering event for early AD pathology(Du Bois et al.,2010;Sterling et al.,2011).

关键词： clinical Alzheimer metabolism