Association of mental disorders with sepsis: a bidirectional Mendelian randomization study.

Background: Substantial research evidence supports the correlation between mental disorders and sepsis. Nevertheless, the causal connection between a particular psychological disorder and sepsis remains unclear. Methods: For investigating the causal relationships between mental disorders and sepsis, genetic variants correlated with mental disorders, including anorexia nervosa (AN), attention-deficit hyperactivity disorder (ADHD), autism spectrum disorder (ASD), bipolar disorder (BD), major depressive disorder (MDD), obsessive-compulsive disorder (OCD), panic disorder (PD), posttraumatic stress disorder (PTSD), schizophrenia (SCZ), and tourette syndrome (TS), were all extracted from the Psychiatric Genomics Consortium (PGC). The causal estimates and direction between these mental disorders and sepsis were evaluated employing a two-sample bidirectional MR strategy. The inverse variance weighted (IVW) method was the primary approach utilized. Various sensitivity analyses were performed to confirm the validity of the causal effect. Meta-analysis, multivariable MR, and mediation MR were conducted to ensure the credibility and depth of this research. Results: The presence of AN was in relation to a greater likelihood of sepsis (OR 1.08, 95% CI 1.02-1.14; p = 0.013). A meta-analysis including validation cohorts supported this observation (OR 1.06, 95% CI 1.02-1.09). None of the investigated mental disorders appeared to be impacted when sepsis was set as the exposure factor. Even after adjusting for confounding factors, AN remained statistically significant (OR 1.08, 95% CI 1.02-1.15; p = 0.013). Mediation analysis indicated N-formylmethionine levels (with a mediated proportion of 7.47%), cystatin D levels (2.97%), ketogluconate Metabolism (17.41%) and N10-formyl-tetrahydrofolate biosynthesis (20.06%) might serve as mediators in the pathogenesis of AN-sepsis. Conclusion: At the gene prediction level, two-sample bidirectional MR analysis revealed that mental disorder AN had a causal association with an increased likelihood of sepsis. In addition, N-formylmethionine levels, cystatin D levels, ketogluconate metabolism and N10-formyl-tetrahydrofolate biosynthesis may function as potential mediators in the pathophysiology of AN-sepsis. Our research may contribute to the investigation of novel therapeutic strategies for mental illness and sepsis.

Insights into the enhanced mechanism of selenium-doped iron nitride carbon catalysts for elemental mercury removal in flue gas.

This study developed a novel selenium-doped metal nitride carbon, Fe-NC-Se, via pyrolysis and impregnated hydrothermal methods for elemental mercury removal from coal-fired flue gas. The Fe-NC-Se demonstrated a remarkable mercury removal performance, achieving an average efficiency of 96.98% within 60 min at an optimal Se/Fe ratio of 2:1 and temperature of 110 °C, which was 2.5 times higher than that of the pristine Fe-NC (iron nitride carbon). Notably, Fe-NC-Se maintained an 84% efficiency in a high SO2 environment (1600 ppm), indicating strong resistance to SO2 poisoning. Long-term testing over 24 h showed a consistent removal efficiency of 84.75%, suggesting potential for recyclability. Advanced characterization techniques, including TEM (transmission electron microscopy) and XPS (X-ray photoelectron spectrometer), along with Density Functional Theory calculations, were employed to explore the removal mechanism. Results indicated that selenium doping enhanced surface charge transfer and the reactivity of surface atoms, facilitating mercury oxidation and sequestration. The oxidized Hg2+ was anchored by Se and partially stabilized by C, N, and Fe atoms, enhancing the catalyst's effectiveness. This work not only advances the design of mercury abatement catalysts but also supports the industrial applicability of Fe-NC-Se in flue gas treatment.

Knockdown of membrane-bound complement regulatory proteins suppresses colon cancer growth in mice through inducing tumor cell apoptosis.

CD46, CD55 and CD59 are membrane-bound complement regulatory proteins (mCRPs) and highly expressed in many tumor tissues. Our analysis by RNA sequencing and qRT-PCR revealed that the expression of mCRPs was significantly elevated in cancer tissues of 15 patients with colon cancer. To further investigate the role of mCRPs in the development of colon cancer, we suppressed the expression of mCRPs by CD46-shRNA, CD55-shRNA and CD59-shRNA in colon cancer cell lines, SW620 and HT-29 cells. The results indicated that CD46-shRNA, CD55-shRNA and CD59-shRNA effectively reduced the expression of mCRPs, accompanied with the increased LDH release and the percentage of Annexin V + 7-AAD- early phase of apoptotic cells. The similar cytotoxic effects were also observed in the cells treated with CD46 neutralizing antibody (aCD46), associated with the increased C5b-9 deposition, cleaved caspase-3 and Bax expression in the treated cells. The cytotoxic effects by mCRPs knock-down were potentiated in the cells co-treated with doxorubicin (Dox). In addition, STAT3, STAT6, and p38 MAPK inhibitors, including C188-9, AS1517499 and SB203580 effectively reduced the expression of CD46 in the treated colon cells, associated with increased cell apoptosis and LDH release. Further study with mouse model revealed that mCRPs knockdown by mCRPs-shRNA significantly reduced colon cancer growth, associated with increased expression of Bax, cleaved caspase-3 and C5b-9 deposition, but reduced expression of Bcl-2, IL-6 and IL-1beta in tumor tissues of nude mice transplanted with SW620 cells. Thereby, mCRPs expression in human colon cancer cells were upregulated by STAT3/STAT6/p38 MAPK signaling and mCRPs knockdown reduced colon cancer growth in mice through inducing tumor cell apoptosis.

Appraising the Accuracy of Ischaemia-Modified Albumin in Diagnosing Stroke: A Systematic Review and Meta-Analysis.

INTRODUCTION: Ischaemia-modified albumin (IMA) is a new, sensitive marker of ischaemic diseases that has been approved for diagnosing myocardial ischaemia. However, the accuracy of IMA in the diagnosis of stroke remains to be clarified. The study's purpose is to assess the potential role of IMA as a diagnostic indicator in stroke. METHODS: We carried out a systematic search in Medline, the Cochrane Library, Embase, Scopus, Science Direct, ISI Web of Knowledge, and the reference lists of relevant articles from the databases' inception to September 1, 2019. Studies that appraised the diagnostic accuracy of IMA for acute stroke patients were included in our study. Two reviewers extracted data independently and assessed the quality of the retrieved studies, and disagreements were resolved through discussions with a third reviewer. Sensitivities and specificities were pooled by using bivariate diagnostic meta-analysis. We calculated I2 to test the heterogeneity and used meta-regression to identify potential sources of heterogeneity. This systematic review and meta-analysis is registered in international prospective register of systematic reviews (number CRD42020149174). RESULTS: Six studies with 605 patients were eligible for inclusion. Our meta-analysis produced the following outcomes: the mean sensitivity of IMA in diagnosing acute stroke was 0.80 (95% confidence interval [CI], 0.69-0.88) and the specificity was 0.80 (95% CI, 0.71-0.87). The area under the receiver operating characteristic curve was 0.86 (95% CI, 0.83-0.89), and the pooled diagnostic odds ratio was 16 (95% CI, 8-33). There was obvious heterogeneity between studies (I2 = 78%, 95% CI, 53-100). Sensitivity analysis and meta-regression could account for the heterogeneity. CONCLUSION: IMA is a helpful marker for consideration in the early diagnosis of stroke.