transcriptomic

转录组
  • 文章类型: Journal Article
    有先兆子痫(PE)病史的女性患晚年心血管疾病(CVD)的风险高达五倍。虽然已知PE和CVD具有共同的临床和分子特征,有有限的研究调查他们共同的基因组学(遗传学,表观遗传学或转录组学)随时间的变化。因此,我们试图系统地回顾文献,以确定关注PE后发生CVD的基因组进展的纵向研究.
    通过PubMed对主要来源进行文献检索,Scopus,通过OVID进行WebofScience和Embase。1980年1月1日至2023年7月28日发表的关于PE和CVD基因组学研究的研究符合纳入条件。纳入的研究是根据Cochrane系统评价指南和PRISMA2020清单进行筛选的。使用纽卡斯尔-渥太华量表进一步评估合格文章的质量。
    共筛选了9,231篇文章,14项研究接受了质量评估。经过进一步评估,6项研究被纳入最终审查.所有六项研究在CVD/危险因素作为结果方面都是异质的,基因定位方法,和不同的目标基因。相关基因为RGS2、LPA、和AQP3,与miR-122-5p一起,miR-126-3p,miR-146a-5p,还有miR-206.此外,鉴定了12个可能与PE后晚年CVD相关的差异甲基化区域。所有六项研究中唯一的共同变量是使用病例对照研究设计。
    我们的结果为研究PE后CVD的基因组研究的异质性提供了重要的见解,并强调迫切需要进行纵向研究以进一步研究PE后CVD进展的遗传变异。
    UNASSIGNED: Women with a history of preeclampsia (PE) have been shown to have up to five times the risk of developing later-life cardiovascular disease (CVD). While PE and CVD are known to share clinical and molecular characteristics, there are limited studies investigating their shared genomics (genetics, epigenetics or transcriptomics) variation over time. Therefore, we sought to systematically review the literature to identify longitudinal studies focused on the genomic progression to CVD following PE.
    UNASSIGNED: A literature search of primary sources through PubMed, Scopus, Web of Science and Embase via OVID was performed. Studies published from January 1, 1980, to July 28, 2023, that investigated genomics in PE and CVD were eligible for inclusion. Included studies were screened based on Cochrane systematic review guidelines in conjunction with the PRISMA 2020 checklist. Eligible articles were further assessed for quality using the Newcastle-Ottawa scale.
    UNASSIGNED: A total of 9,231 articles were screened, with 14 studies subjected to quality assessment. Following further evaluation, six studies were included for the final review. All six of these studies were heterogeneous in regard to CVD/risk factor as outcome, gene mapping approach, and in different targeted genes. The associated genes were RGS2, LPA, and AQP3, alongside microRNAs miR-122-5p, miR-126-3p, miR-146a-5p, and miR-206. Additionally, 12 differentially methylated regions potentially linked to later-life CVD following PE were identified. The only common variable across all six studies was the use of a case-control study design.
    UNASSIGNED: Our results provide critical insight into the heterogeneous nature of genomic studies investigating CVD following PE and highlight the urgent need for longitudinal studies to further investigate the genetic variation underlying the progression to CVD following PE.
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  • 文章类型: Systematic Review
    胰胆管和妇科腺癌需要更好的工具来预测临床结果。已经在这些癌症中鉴定了潜在的基于间充质(样)转录组的预后亚型。在这次系统审查中,我们包括对分子亚型的研究,并总结起源内和跨部位的亚型的生物学和临床特征,寻找改进分类和预测的建议。在PubMed和Embase中搜索了描述胰胆或妇科腺癌中潜在的基于间充质(样)mRNA的亚型的原始研究文章。仅限于监督聚类的研究被排除在外。有44项研究讨论了胆管癌,胆囊,壶腹,胰腺,卵巢,包括子宫内膜腺癌。在所有腺癌中,间充质(样)亚型的分子和临床特征存在重叠。包括显微解剖在内的方法更有可能识别与预后相关的亚型。最后,胰胆和妇科腺癌的分子亚型具有相同的生物学和临床特征。此外,基质和上皮信号的分离应应用于未来的胆道和妇科腺癌的研究。
    Pancreato-biliary and gynecological adenocarcinomas need better tools to predict clinical outcome. Potential prognostic mesenchymal(-like) transcriptome-based subtypes have been identified in these cancers. In this systematic review, we include studies into molecular subtyping and summarize biological and clinical features of the subtypes within and across sites of origin, searching for suggestions to improve classification and prognostication. PubMed and Embase were searched for original research articles describing potential mesenchymal(-like) mRNA-based subtypes in pancreato-biliary or gynecological adenocarcinomas. Studies limited to supervised clustering were excluded. Fourty-four studies discussing cholangiocarcinomas, gallbladder, ampullary, pancreatic, ovarian, and endometrial adenocarcinomas were included. There was overlap in molecular and clinical features in mesenchymal(-like) subtypes across all adenocarcinomas. Approaches including microdissection were more likely to identify prognosis-associated subtypes. To conclude, molecular subtypes in pancreato-biliary and gynecological adenocarcinomas share biological and clinical characteristics. Furthermore, separation of stromal and epithelial signals should be applied in future studies of biliary and gynecological adenocarcinomas.
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  • 文章类型: Journal Article
    由于高代谢和生理活性,果实在收获后容易受到品质损失和变质。在过去的四十年中,各种采后处理确保了质量的维持,通过减缓采后成熟和衰老来控制疾病或腐烂。然而,采后果实品质的变化,主要是利用物理化学特性进行探索的。考虑到果实生理代谢的复杂性,组学技术的应用可以帮助深入分析和理解采后果实品质变化。因此,这篇综述介绍了整合组学应用的最新信息(转录组学,蛋白质组学,和代谢组学)在采后研究中,概述了水果的质量和安全。强调了采后处理期间水果组学数据分析的趋势。综合组学在提高我们对自然采后进程(朝向腐烂)在储存过程中水果反应的理解中的作用,以及在诱导反应的情况下,由于生物控制的应用进行了讨论。文章最后对集成组学作为创新采后解决方案的催化剂的未来研究进行了展望。
    Fruit are susceptible to quality loss and deterioration after harvest due to high metabolic and physiological activities. Over the last four decades various postharvest treatments have ensured maintenance of quality, control of diseases or decay by slowing down the postharvest ripening and senesce. The fruit quality change during postharvest however, has been mostly explored using physicochemical characteristics. Considering the complexity of fruit physiology and metabolism, the application of omics techniques could aid the in-depth analysis and understanding of fruit quality change during postharvest treatment. Therefore, this review presents recent information on the application of integrated omics (transcriptomics, proteomics, and metabolomics) in postharvest research, with an overview on fruit quality and safety. Trends in omics data analysis for fruit during postharvest handling was highlighted. The role of integrated omics in improving our understanding of fruit response during natural postharvest progression (towards decay) during storage, as well as in case of induced responses due to the application of biocontrols was discussed. The article concluded with the outlooks of future studies on the application of integrated omics as the catalyst for innovative postharvest solutions.
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  • 文章类型: Journal Article
    CADASIL(伴有皮质下梗死和白质脑病的常染色体显性动脉病)是一种由NOTCH3突变引起的小血管疾病,该突变导致表皮生长因子(EGF)样重复结构域中的半胱氨酸数量奇数,导致蛋白质错误折叠和聚集。主要症状是偏头痛,精神疾病,复发性中风,和痴呆症。Omic技术允许对不同分子进行大规模研究,以无偏见的方式了解疾病,甚至发现靶标及其可能的治疗方法。我们分析了组学科学在理解CADASIL方面的进展。为此,我们纳入了专注于CADASIL和使用组学技术的研究,搜索书目资源,比如PubMed。我们排除了其他表型的研究,如偏头痛或脑白质营养不良。共回顾了18篇文章。由于迄今为止在基因组存储库中被认为是致病性的NOTCH3突变的高患病率,人们可以问他们是否都生产CADASIL,不同程度的疾病,或者它们是否只是小血管疾病的危险因素。此外,蛋白质组学和转录组学研究发现,CADASIL中发生显著改变的分子主要与细胞粘附,细胞骨架或细胞外基质成分,误折叠控制,自噬,血管生成,或转化生长因子β(TGFβ)信号通路。对CADASIL进行的组学研究对于理解生物学机制很有用,并且可能是寻找潜在药物靶标的关键因素。
    CADASIL (Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy) is a small vessel disease caused by mutations in NOTCH3 that lead to an odd number of cysteines in the epidermal growth factor (EGF)-like repeat domain, causing protein misfolding and aggregation. The main symptoms are migraines, psychiatric disorders, recurrent strokes, and dementia. Omic technologies allow the massive study of different molecules for understanding diseases in a non-biased manner or even for discovering targets and their possible treatments. We analyzed the progress in understanding CADASIL that has been made possible by omics sciences. For this purpose, we included studies that focused on CADASIL and used omics techniques, searching bibliographic resources, such as PubMed. We excluded studies with other phenotypes, such as migraine or leukodystrophies. A total of 18 articles were reviewed. Due to the high prevalence of NOTCH3 mutations considered pathogenic to date in genomic repositories, one can ask whether all of them produce CADASIL, different degrees of the disease, or whether they are just a risk factor for small vessel disease. Besides, proteomics and transcriptomics studies found that the molecules that are significantly altered in CADASIL are mainly related to cell adhesion, the cytoskeleton or extracellular matrix components, misfolding control, autophagia, angiogenesis, or the transforming growth factor β (TGFβ) signaling pathway. The omics studies performed on CADASIL have been useful for understanding the biological mechanisms and could be key factors for finding potential drug targets.
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  • 文章类型: Journal Article
    怀孕期间的母体免疫激活(mIA)被认为会破坏后代的神经发育并使后代易患精神分裂症等神经发育障碍。mIA的啮齿动物模型已经探索了这种范式的可能机制,并为临床前研究提供了重要工具。然而,缺乏对MIA模型中发生的分子变化的全面分析,阻碍识别稳健的临床目标。本系统综述评估了特定后代大脑区域中mIA驱动的转录组和表观基因组改变。在118项研究中,我们专注于88个候选基因,并在关键功能区显示表达的重复变化,包括炎症标志物升高,和减少髓鞘和GABA能信号蛋白。Further,这些基因中有9个基因的表观遗传标记支持mIA驱动的转录表观遗传调节。总的来说,我们的研究结果表明,目前的结局指标与假设的精神分裂症病理有直接相关性,并强调mIA模型在有助于理解mIA影响的生物学途径和发现新的药物靶点方面的重要性.
    Maternal immune activation (mIA) during pregnancy is hypothesised to disrupt offspring neurodevelopment and predispose offspring to neurodevelopmental disorders such as schizophrenia. Rodent models of mIA have explored possible mechanisms underlying this paradigm and provide a vital tool for preclinical research. However, a comprehensive analysis of the molecular changes that occur in mIA-models is lacking, hindering identification of robust clinical targets. This systematic review assesses mIA-driven transcriptomic and epigenomic alterations in specific offspring brain regions. Across 118 studies, we focus on 88 candidate genes and show replicated changes in expression in critical functional areas, including elevated inflammatory markers, and reduced myelin and GABAergic signalling proteins. Further, disturbed epigenetic markers at nine of these genes support mIA-driven epigenetic modulation of transcription. Overall, our results demonstrate that current outcome measures have direct relevance for the hypothesised pathology of schizophrenia and emphasise the importance of mIA-models in contributing to the understanding of biological pathways impacted by mIA and the discovery of new drug targets.
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  • 文章类型: Journal Article
    下一代测序(NGS)技术彻底改变了基于序列的研究。近年来,高通量测序已成为通过观察和测量转录水平变化来研究化学试剂毒性的首选方法。工程化纳米材料(ENM)毒性已成为研究的主要领域,并已采用微阵列和较新的RNA-Seq方法。最近,纳米技术已成为诊断和治疗人类多种疾病的有前途的工具。然而,由于它们的高稳定性,它们可能能够在身体和环境中长时间停留。它们的毒性机制和对我们健康的长期影响仍然知之甚少。这篇综述探讨了三种ENM的作用,包括碳纳米管(CNT),量子点(QDs),和Ag纳米颗粒(AgNPs)通过交叉检查有关这些纳米材料诱导的转录组变化的出版物。
    Next-generation sequencing (NGS) technology has revolutionized sequence-based research. In recent years, high-throughput sequencing has become the method of choice in studying the toxicity of chemical agents through observing and measuring changes in transcript levels. Engineered nanomaterial (ENM)-toxicity has become a major field of research and has adopted microarray and newer RNA-Seq methods. Recently, nanotechnology has become a promising tool in the diagnosis and treatment of several diseases in humans. However, due to their high stability, they are likely capable of remaining in the body and environment for long periods of time. Their mechanisms of toxicity and long-lasting effects on our health is still poorly understood. This review explores the effects of three ENMs including carbon nanotubes (CNTs), quantum dots (QDs), and Ag nanoparticles (AgNPs) by cross examining publications on transcriptomic changes induced by these nanomaterials.
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  • 文章类型: Journal Article
    Oral melanoma (OM) is a highly aggressive tumor of the oral cavity in humans and dogs. Here we review the phenotypic similarities between the disease in these 2 species as the basis for the view that canine OM is a good model for the corresponding human disease. Utility of the \"canine model\" has likely been hindered by a paucity of information about the extent of the molecular genetic similarities between human and canine OMs. Current knowledge of the somatic alterations that underpin human tumorigenesis and metastatic progression is relatively limited, primarily due to the rarity of the disease in humans and consequent lack of opportunity for large-scale molecular analysis. The molecular genetic comparisons between human and canine OMs that have been completed indicate some overlap between the somatic mutation profiles of canine OMs and a subset of human OMs. However, further comparative studies featuring, in particular, larger numbers of human OMs are required to provide substantive evidence that canine OMs share mechanisms of tumorigenesis with at least a subset of human OMs. Future molecular genetic investigations of both human and canine OMs should investigate how primary tumors develop a metastatic gene expression signature and the genetic and epigenetic alterations specific to metastatic sites. Such studies may identify genetic alterations and pathways specific to the metastatic disease which could be targetable by new drugs.
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  • 文章类型: Journal Article
    In recent years, numerous studies conducted on teleost fish have highlighted the contribution of transcriptomic studies in elucidating the physiological mechanisms underlying the molecular events of oogenesis and follicular atresia, enabling the identification of potential genes and molecular networks that participate in both the reproductive cycle and the process of follicular atresia. Atresia can affect the reproductive potential of females by reducing the healthy eggs that a female can spawn in both aquaculture and wild populations. The substantial diversity of reproductive strategies exhibited by teleost fish has contributed to the difficulty in identifying common genes between species, but a set of core genes has emerged as potential markers for atresia in relation to apoptosis/autophagy, lipid metabolism, oxidative metabolism and other physiological processes similar to those identified in other vertebrates, even mammals. We review the current status of the genes that have been identified in ovaries with atretic oocytes. Our primary goal is to review the current status regarding gene expression during gonadal development and follicular atresia. This information will enable us to understand the factors and expression patterns involved in the follicular atresia of teleost fish.
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  • 文章类型: Journal Article
    One-quarter of the global population, including the majority of adults in tuberculosis (TB) endemic countries, are estimated to be Mycobacterium tuberculosis (MTB) infected. An estimated 10 million new TB cases occurred in 2017. One of the biggest challenges confronting TB control is the lack of accurate diagnosis and prediction of prevalent and incident TB disease, respectively. Several host blood transcriptomic messenger RNA (mRNA) signatures that reflect the host immune response following infection with MTB and progression to TB disease in different study populations have recently been published, but these TB biomarkers have not been systematically described. We will conduct a systematic review of the performance of host blood transcriptional signatures for TB diagnosis and prediction of progression to TB disease.
    This systematic review will involve conducting a comprehensive literature search of cohort, case-control, cross-sectional and randomised-controlled studies of the performance of host blood transcriptomic signatures for TB diagnosis and prediction of progression to TB disease. We will search Medline via PubMed, Scopus, Web of Science and EBSCO libraries, complemented by a search of bibliographies of selected articles for other relevant articles. The literature search will be restricted to studies published in English from 2005 to 2018 and conducted in HIV-uninfected adults and adolescents (≥12 years old). Forest plots and a narrative synthesis of the findings will be provided. The primary outcomes will be sensitivity, specificity, as well as true/false positives and true/false negatives. Heterogeneity resulting from differences in the design, composition and structure of individual signatures will preclude meta-analysis and pooling of results.
    Ethics approval is not required for this systematic review protocol. The results of this review will be disseminated through a peer-reviewed journal as well as conference presentations.
    CRD42017073817.
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