Formation of disinfection by-products after pre-oxidation with chlorine dioxide or ferrate

The effect of pre-oxidation with chlorine dioxide (ClO2) or ferrate (Fe(VI)) on the formation of disinfection by-products (DBPs) during chlorination or chloramination was tested with natural waters from 12 sources (9 surface waters, 1 groundwater, and 2 wastewater effluents). DBPs investigated included trihalomethanes (THM), chloral hydrate (CH), haloketones (HK), haloacetonitriles (HAN) and trichloronitromethane (TCNM), chlorite and chlorate. Chlorite and chlorate were found in the ClO2-treated waters. Application of 1 mg/L ClO2 ahead of chlorination reduced the formation potential for THM by up to 45% and the formation of HK, HAN and TCNM in most of the samples. The CH formation results were mixed. The formation of CH and HK was enhanced with low doses of Fe(VI) (1 mg/L as Fe), but was greatly reduced at higher doses (20 mg/L Fe). Fe(VI) reduced the formation of THM, HAN and TCNM in most of the samples. Reduced potential for the formation of NDMA was observed in most of the samples after both ClO2 and Fe(VI) pre-oxidation. (C) 2013 Elsevier Ltd. All rights reserved

The Role of the Notch Signaling Pathway in the Differentiation of Human Umbilical Cord-Derived Mesenchymal Stem Cells

Human umbilical cord mesenchymal stem cells (hUCMSCs) exhibit potent self-renewal and multilineage differentiation characteristics. They have garnered substantial attention within the domain of regenerative medicine owing to their therapeutic potential, such as in tissue repair, regeneration, immunomodulation, anti-inflammation, angiogenesis, wound healing, neuroprotection, and neuroregeneration. The process of fate determination is initiated by multiple signaling molecules. During development and tissue homeostasis, the Notch signaling pathway assumes a pivotal function in cell differentiation and the renewal of stem cells. A growing body of research has revealed that the Notch signaling pathwayplays a pivotal role in hUCMSC proliferation and differentiation. The latest progress concerning the crucial functions of the Notch signaling pathway in maintaining homeostasis and determining the cell fate of hUCMSCs is summarized. Furthermore, the authors also summarized the mediators related to the Notch signaling pathway in hUCMSC differentiation, as well as the pathway alterations and mechanisms involved in hUCMSC therapy

Data_Sheet_1_Genetic associations between autoimmune diseases and the risks of severe sepsis and 28-day mortality: a two-sample Mendelian randomization study.zip

BackgroundAutoimmune diseases exhibit heterogenous dysregulation of pro-inflammatory or anti-inflammatory cytokine expression, akin to the pathophysiology of sepsis. It is speculated that individuals with autoimmune diseases may have an increased likelihood of developing sepsis and face elevated mortality risks following septic events. However, current observational studies have not yielded consistent conclusions. This study aims to explore the causal relationship between autoimmune diseases and the risks of sepsis and mortality using Mendelian randomization (MR) analysis.MethodsWe conducted a two-sample MR study involving a European population, with 30 autoimmune diseases as the exposure factors. To assess causal relationships, we employed the inverse variance-weighted (IVW) method and used Cochran's Q test for heterogeneity, as well as the MR pleiotropy residual sum and outlier (MR-PRESSO) global test for potential horizontal pleiotropy.ResultsGenetically predicted Crohn's disease (β = 0.067, se = 0.034, p = 0.046, OR = 1.069, 95% CI = 1.001–1.141) and idiopathic thrombocytopenic (β = 0.069, se = 0.031, p = 0.023, OR = 1.071, 95% CI = 1.009–1.136) were positively associated with an increased risk of sepsis in critical care. Conversely, rheumatoid arthritis (β = −0.104, se = 0.047, p = 0.025, OR = 0.901, 95% CI = 0.823–0.987), ulcerative colitis (β = −0.208, se = 0.084, p = 0.013, OR = 0.812, 95% CI = 0.690–0.957), and narcolepsy (β = −0.202, se = 0.092, p = 0.028, OR = 0.818, 95% CI = 0.684–0.978) were associated with a reduced risk of sepsis in critical care. Moreover, Crohn's disease (β = 0.234, se = 0.067, p = 0.001, OR = 1.263, 95% CI = 1.108–1.440) and idiopathic thrombocytopenic (β = 0.158, se = 0.061, p = 0.009, OR = 1.171, 95% CI = 1.041–1.317) were also linked to an increased risk of 28-day mortality of sepsis in critical care. In contrast, multiple sclerosis (β = −0.261, se = 0.112, p = 0.020, OR = 0.771, 95% CI = 0.619–0.960) and narcolepsy (β = −0.536, se = 0.184, p = 0.003, OR = 0.585, 95% CI = 0.408–0.838) were linked to a decreased risk of 28-day mortality of sepsis in critical care.ConclusionThis MR study identified causal associations between certain autoimmune diseases and risks of sepsis in critical care, and 28-day mortality in the European population. These findings suggest that exploring the mechanisms underlying autoimmune diseases may offer new diagnostic and therapeutic strategies for sepsis prevention and treatment.</p