Feldmanstanley2212

20; P less then 0.001; t =4.45; P less then 0.001; t= 6.18; P less then 0.001). But no significant difference found in fetal heart rate and labor outcomes in terms of duration of labor, type of delivery, baby born alive/ not and cried immediately after birth. Conclusion Warm compression was useful method to decrease the labour pain among nulliparous mothers in the first stage of labour and mothers reported satisfaction with intervention. © 2020 The Author(s).Introduction Nurses are the final safety check in the process of medication administration process to prevent errors that adversely affect life; yet death of comprehensive evidences in Ethiopia. The present study aimed to assess the pooled magnitude of MAEs (Medication Administration Errors) in Ethiopia. Methods Systematic literature search in the databases of Pub-Med, Cochrane, and Google Scholar for gray literature were performed until December 3, 2018. The quality of study was assessed using criteria adopted from similar studies. Heterogeneity test and evidence of publication bias were assessed. Moreover, sensitivity analysis was also performed. Pooled prevalence of MAE was calculated using the random effects model. Results A total of 2142 medication administrations were from observational and 681from self-reported studies were included in this systematic review and meta-analysis. The most prevalent and frequently reported type of MAEs was documentation error (52% to 87.5%) and time error (25.5% to 58.5%) respectively. Overall, the pooled magnitude of MAE was found to be 39.3% (95% CI, 29.1%-49.5%).It has no evidence of significant heterogeneity (I2 = 0%, P = 0.57) and publication bias Egger's test (P = 0.40). Conclusion Overall, more than one in four observed/perceived medication administrations had errors. Documentation error is the most prevalent type of error. Nurses are suggested to strengthen their focus on the rights of medication administration guide particularly, documentation of their activities need special attention. © 2020 The Author(s).CMV is an ancient herpesvirus that has co-evolved with its host over millions of years. Ki16198 The 236 kbp genome encodes at least 165 genes, four non-coding RNAs and 14 miRNAs. Of the protein-coding genes, 43-44 are core replication genes common to all herpesviruses, while ~30 are unique to betaherpesviruses. Many CMV genes are involved in evading detection by the host immune response, and others have roles in cell tropism. CMV replicates systemically, and thus, has adapted to various biological niches within the host. Different biological niches may place competing demands on the virus, such that genes that are favorable in some contexts are unfavorable in others. The outcome of infection is dependent on the cell type. In fibroblasts, the virus replicates lytically to produce infectious virus. In other cell types, such as myeloid progenitor cells, there is an initial burst of lytic gene expression, which is subsequently silenced through epigenetic repression, leading to establishment of latency. Latently infected ividuals. Recent studies with animal models highlight the potential for harnessing the host immune response to blunt cellular injury induced by organ transplantation, and thus, prevent reactivation of CMV and its sequelae. Copyright © 2020 Forte, Zhang, Thorp and Hummel.Acute pancreatitis (AP) is considered a cascade of immune responses triggered by acinar cell necrosis. AP involves two main processes of systemic inflammatory response syndrome and subsequent compensatory anti-inflammatory response syndrome. Although great efforts have been made regarding AP therapy, the mortality rate of AP remains high. Secondary infection acts a lethal factor in AP. Lymphocytes act as major immune mediators in immune responses in the course of this disease. However, the relationship between lymphocytes and secondary infection in AP is unclear. This review summarizes the variation of lymphocytes and infection in AP. Knowledge of the characterization of circulating lymphocyte abnormalities is relevant for understanding the pathophysiology of AP. Copyright © 2020 Ding, Yang, Li, Wang and Gao.Multiple perturbations of the immune response affecting a range of cells have been reported in Trypanosoma cruzi-infected individuals and associated to clinical manifestations of chronic Chagas disease. There is a paucity of knowledge about the role of T follicular helper (Tfh) cells in this infection. Here, we sought to characterize circulating Tfh (cTfh) cells in chronic Chagas disease patients and to identify potential associations with disease severity in humans. cTfh cells were characterized by flow cytometry in freshly isolated PBMCs from 7 T. cruzi-infected asymptomatic patients (ASYMP), 5 patients with chronic chagasic dilated cardiomyopathy (CCC) and 8 healthy controls, using antibodies against chemokine receptors CXCR5, CXCR3, CCR6, and CCR7. Our results showed significant expansion of CD4+CD45RO+CXCR5+CCR6+ cells in ASYMP and CCC patients, along with a contraction of CD4+CD45RO+CXCR5+CXCR3-CCR6- (cTfh2) cells. ASYMP patients further exhibited decreased CD4+CD45RO+CXCR5+CXCR3+CCR6- (cTfh1) cells and expanded CD4+CD45RO+CXCR5+CXCR3-CCR6+ (cTfh17) cells while CCC patients exhibited significantly increased frequencies of CD4+CD45RO+CXCR5+CCR7+ cells. Linear regression analysis revealed a positive trend of CD4+CD45RO+CXCR5+CXCR3+CCR6+ (cTfh1/17) cells and negative trends of cTfh1 and cTfh2 cells as disease was more severe. There was no correlation between the frequencies of cTfh cells and circulating CD19+IgD-IgG+ cells or serum levels of T. cruzi-specific IgG. These results demonstrate that the cTfh compartment of humans chronically infected with T. cruzi comprises expanded CCR6-expressing cells and reduced cTfh2 cells. The association of discrete phenotypic changes in cTfh subsets with different clinical forms suggests the potential contribution of T follicular helper cells to Chagas heart disease progression. Copyright © 2020 Quebrada Palacio, Fernández, Hernández-Vásquez, Petray and Postan.Verotoxin, VT (aka Shiga toxin,Stx) is produced by enterohemorrhagic E. coli (EHEC) and is the key pathogenic factor in EHEC-induced hemolytic uremic syndrome (eHUS-hemolytic anemia/thrombocytopenia/glomerular infarct) which can follow gastrointestinal EHEC infection, particularly in children. This AB5 subunit toxin family bind target cell globotriaosyl ceramide (Gb3), a glycosphingolipid (GSL) (aka CD77, pk blood group antigen) of the globoseries of neutral GSLs, initiating lipid raft-dependent plasma membrane Gb3 clustering, membrane curvature, invagination, scission, endosomal trafficking, and retrograde traffic via the TGN to the Golgi, and ER. In the ER, A/B subunits separate and the A subunit hijacks the ER reverse translocon (dislocon-used to eliminate misfolded proteins-ER associated degradation-ERAD) for cytosolic access. This property has been used to devise toxoid-based therapy to temporarily block ERAD and rescue the mutant phenotype of several genetic protein misfolding diseases. The A subunit avoids cytosolic proteosomal degradation, to block protein synthesis via its RNA glycanase activity.