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Extruded Mesenchymal Originate Cell Nanovesicles Tend to be Equally Powerful to be able to Natural Extracellular Vesicles throughout Heart failure Restore.
038). Our analysis showed significant differences between cases and controls in genotypic distribution of IL6-174CC (p = 0.003; OR = 7.71 CI (1.58-37.56)), TNFα - 308 AA (p = 0.004; OR = 2.95 (1.57-5.51)) and CRP + 1059 CC (p  less then  10-3; OR = 5.40 (2.30-12.68)). However, we failed to find an association between the different genotypes and the inflammatory markers levels. Our results suggest that the presence of IL-6 (- 174 G/C), TNFα (-308 A/G) and CRP (+ 1059G/C) polymorphisms, may be considered to be a risk factor for CAD in Tunisian population.Inflammatory bowel disease (IBD) is a group of chronic intestinal inflammatory disorders with a prolonged duration characterized by recurrent relapse and remission. The exact etiology of IBD remains poorly understood despite the identification of relevant risk factors, including individual genetic susceptibility, environmental triggers, and disruption of immune homeostasis. Dysbiosis of the gut microbiota is believed to exacerbate the progression of IBD. Recently, increasing evidence has also linked oral microbiota dysbiosis with the development of IBD. On the one hand, IBD patients show significantly unbalanced composition and function of the oral microbiota known as dysbiosis. On the other, overabundances of oral commensal bacteria with opportunistic pathogenicity have been found in the gut microbiota of IBD patients. Herein, we review the current information on the causative factors of IBD, especially recent evidence of IBD-associated oral microbiota dysbiosis, which has seldom been covered in the previous literature review, highlighting the pathogenic mechanisms of specific oral bacteria in the development of IBD. Ectopic colonization of several oral bacteria, including a subset of Porphyromonas gingivalis, Streptococcus mutans, Fusobacterium nucleatum, Campylobacter concisus, and Klebsiella pneumoniae, may lead to destruction of the intestinal epithelial barrier, excessive secretion of inflammatory cytokines, disruption of the host immune system, and dysbiosis of gut microbiota, consequently aggravating chronic intestinal inflammation. Studying oral microbiota dysbiosis may open future horizons for understanding IBD pathogenesis and provide novel biomarkers for IBD. check details This review also presents the current treatment and new perspectives for IBD treatment.Subcutaneous fat (SCF) and intramuscular fat (IMF) deposition is relevant to health in humans, as well as meat production and quality in pigs. In this study, we generated RNA sequence data for 122 SCF, 120 IMF, and 87 longissimus dorsi muscle (LDM) samples using 155 F6 pigs from a specially designed heterogeneous population generated by intercrossing four highly selected European commercial breeds and four indigenous Chinese pig breeds. The phenotypes including waist back fat thickness and intramuscular fat content were also measured in the 155 F6 pigs. We found that the genes in SCF and IMF differed largely in both expression levels and network connectivity, and highlighted network modules that exhibited strongest gain of connectivity in SCF and IMF, containing genes that were associated with the immune process and DNA double-strand repair, respectively. We identified 215 SCF genes related to kinase inhibitor activity, mitochondrial fission, and angiogenesis, and 90 IMF genes related to lipolysis and fat cell differentiation, displayed a tissue-specific association with back fat thickness and IMF content, respectively. We found that cis-expression QTL for trait-associated genes in the two adipose tissues tended to have tissue-dependent predictability for the two adipose traits. Alternative splicing of genes was also found to be associated with SCF or IMF deposition, but the association was much less extensive than that based on expression levels. This study provides a better understanding of SCF and IMF gene transcription and network organization and identified critical genes and network modules that displayed tissue-specific associations with subcutaneous and intramuscular fat deposition. These features are helpful for designing breeding programs to genetically improve the two adipose traits in a balanced way.Chikungunya virus (CHIKV) infection is caused by an arbovirus prevalent in various parts of the world. The virus can induce autoantibodies and rheumatic diseases, such as rheumatoid arthritis and spondylarthritis. However, until now, no case of Sjögren syndrome (SS) was described associated with CHIKV. In this article, we describe a 49-year-old female with polyarthralgia and a temporary rash on her trunk and arms. Her physical examination showed polyarthritis of her ankles and wrists. Serologies for CHIKV were interpreted as positive with IgM 6.5 (normal range  less then  0.8) and negative for IgG. Antinuclear antibodies were positive at a titer of 1640 as well as anti-Ro/SS-A. The diagnosis of subacute CHIKV infection was determined. The Schirmer test, Rose Bengal, and salivary scintigraphy were positive and the diagnosis of SS was confirmed. She was treated with hydroxychloroquine, methotrexate, and a single dose of betamethasone depot. This is the first report on CHIKV associated with SS. Sequence analysis of the CHIKV proteome versus SS autoantigens showed an extensive peptide sharing between the virus and numerous SS autoantigens, thus supporting the hypothesis that autoimmune cross-reactivity might causally link CHIKV to SS.Ex vivo expansion of human cord blood (CB) hematopoietic stem cells (HSCs) is one approach to overcome limited numbers of HSCs in single CB units. However, there is still no worldwide acceptable HSC ex vivo expansion system. A main reason is that we still have very limited knowldege regarding mechanisms underlying maintenance and expansion of CB HSCs. Here we report that retinoid X receptor (RXR) activity is of significance for CB HSC ex vivo expansion. RXR antagonist HX531 significantly promoted ex vivo expansion of CB HSCs and progenitor cells (HPCs). RXR agonist Bexarotene notably suppressed ex vivo expansion of CB HSCs. Activation of RXR by Bexarotene significantly blocked expansion of phenotypic HSCs and HPCs and expressed increased functional HPCs as assessed by colony formation induced by UM171 and SR1. In vivo transplantation experiments in immune-deficient mice demonstrated that HX531 expanded CB HSCs possess long-term reconstituting capacities, and Bexarotene treatment inhibited expansion of functional CB HSCs.
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