ABSTRACT
Intramuscular fat (IMF) is an important regulator that determines meat quality, and its content is closely related to flavor, tenderness, and juiciness. Many studies have used quantitative proteomic analysis to identify proteins associated with meat quality traits in livestock, however, the potential candidate proteins that influence IMF in donkey muscle are not fully understood. In this study, we performed quantitative proteomic analysis, with tandem-mass-tagged (TMT) labeling, with samples from the longissimus dorsi (LD) muscle of the donkey. A total of 585,555 spectra were identified from the six muscle samples used in this study. In total, 20,583 peptides were detected, including 15,279 unique peptides, and 2,540 proteins were identified. We analyzed differentially abundant proteins (DAPs) between LD muscles of donkeys with high (H) and low (L) IMF content. We identified 30 DAPs between the H and L IMF content groups, of which 17 were upregulated and 13 downregulated in the H IMF group. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) functional enrichment analysis of these DAPs revealed many GO terms (e.g., bone morphogenetic protein (BMP) receptor binding) and pathways (e.g., Wnt signaling pathway and Hippo signaling pathway) involved in lipid metabolism and adipogenesis. The construction of protein-protein interaction networks identified 16 DAPs involved in these networks. Our data provide a basis for future investigations into candidate proteins involved in IMF deposition and potential new approaches to improve meat quality in the donkey.
ABSTRACT
BACKGROUND: Ralstonia mannitolilytica, a newly emerging opportunistic pathogen worldwide, has been reported to be responsible for human pneumonia, septicemia and meningitis. This is the first report of a case of Ralstonia mannitolilytica sepsis after elective cesarean delivery. CASE PRESENTATION: A 25-year-old woman, gravida 1 para 0, was scheduled for an elective cesarean delivery at 39+ 1 weeks of gestation. Sudden high fever and decreased blood pressure occurred a short time after the operation. Ralstonia mannitolilytica was identified in her blood culture 5 days after the operation. Based on the presence of sepsis and septic shock, massive fluid replacement, blood transfusion, vasoactive agents, imipenem/cilastatin and cefoperazone sulbactam sodium were applied. She was discharged after intensive care without complications. CONCLUSIONS: Although the incidence of sepsis due to Ralstonia mannitolilytica is relatively low, once infection occurs in a puerpera, severe symptoms develop abruptly. Thus, prompt diagnosis and appropriate treatment are key to the cure.
Subject(s)
Cesarean Section/adverse effects , Gram-Negative Bacterial Infections/etiology , Ralstonia , Sepsis/microbiology , Adult , Cross Infection/microbiology , Elective Surgical Procedures/adverse effects , Female , Gram-Negative Bacterial Infections/therapy , Humans , Postoperative Complications , Pregnancy , Sepsis/therapy , Treatment OutcomeABSTRACT
TREM2 (triggering receptor expressed on myeloid cells 2) gene variants were reported to increase the risk of Alzheimer's disease (AD) and even other neurodegenerative diseases (frontotemporal dementia (FTD), Parkinson's disease (PD) and amyotrophic lateral sclerosis (ALS)), but so far, no definite conclusion has been drawn. The aim of our systematic review and meta-analysis was to investigate the role of TREM2 variants in neurodegenerative diseases. A total of 39 papers (including 26 case-control studies and 13 case reports) were retrieved from PubMed, MEDLINE, EMBASE, and the Cochrane library in this study. A fixed effect model was used to pool results in the analysis. Three variants in TREM2 (rs75932628 (R47H), rs2234255 (H157Y), and rs143332484 (R62H)) were significantly associated with AD risk, but the similar associations between rs104894002 (Q33X), rs2234253 (T96K), rs142232675 (D87N), rs2234256 (L211P), and AD were not proven. Rs75932628 also increased risk of PD in North Americans and FTD, but not PD in Europeans or ALS. In the systematic review, 12 biallelic TREM2 mutations (e.g., rs104894002, rs201258663 (T66M), and rs386834144, etc.) have been described to cause Polycystic Lipomembranous Osteodysplasia with Sclerosing Leukoencephalopathy (PLOSL) in 14 families. And homozygous mutations also have been reported to cause FTD without typical bone phenotypes in 7 families. This study demonstrates that multiple variants in TREM2 have association with the onset of AD, FTD, and PD in North Americans and also play a key role in the phenotypes of the rare familial genetic disorder.
