Developing and Verifying an Effective Diagnostic Model Linked to Immune Infiltration in Stanford Type A Aortic Dissection.

BACKGROUND: The deadly cardiovascular condition known as Stanford type A aortic dissection (TAAD) carries a high risk of morbidity and mortality. One important step in the pathophysiology of the condition is the influx of immune cells into the aorta media, which causes medial degeneration. The purpose of this work was to investigate the potential pathogenic significance of immune cell infiltration in TAAD and to test for associated biomarkers. METHODS: The National Center for Biotechnology Information (NCBI) Gene Expression Omnibus (GEO) database provided the RNA sequencing microarray data (GSE153434, GPL20795, GSE52093). Immune cell infiltration abundance was predicted using ImmuCellAI. GEO2R was used to select differentially expressed genes (DEGs), which were then processed for Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses. Additionally, hub genes linked to immune infiltration were found using functional and pathway enrichment, least absolute shrinkage and selection operator (LASSO), weighted gene co-expression network analysis (WGCNA), and differential expression analysis. Lastly, hub genes were validated and assessed using receiver operating characteristic (ROC) curves in the microarray dataset GSE52093. The hub gene expression and its connection to immune infiltration in TAAD were confirmed using both animal models and clinic data. RESULTS: We identified the most important connections between macrophages, T helper cell 17 (Th17), iTreg cells, B cells, natural killer cells and TAAD. And screened seven hub genes associated with immune cell infiltration: ABCG2, FAM20C, ELL2, MTHFD2, ANKRD6, GLRX, and CDCP1. The diagnostic model in TAAD diagnosis with the area under ROC (AUC) was 0.996, and the sensitivity was 99.21%, the specificity was 98.67%, which demonstrated a surprisingly strong diagnostic power of TAAD in the validation datasets. The expression pattern of four hub DEGs (ABCG2, FAM20C, MTHFD2, CDCP1) in clinic samples and animal models matched bioinformatics analysis, and ABCG2, FAM20C, MTHFD2 up-regulation, and the of CDCP1 down-regulation were also linked to poor cardiovascular function. CONCLUSIONS: This study developed and verified an effective diagnostic model linked to immune infiltration in TAAD, providing new approaches to studying the potential pathogenesis of TAAD and discovering new medication intervention targets.

Association between stress hyperglycemia ratio and all-cause mortality in critically ill patients with atrial fibrillation: insights from a MIMIC-IV study.

Background: The stress hyperglycemia ratio (SHR) has emerged as a potential prognostic indicator for various critical illnesses. However, its role in determining outcomes in patients with atrial fibrillation (AF) within the intensive care unit (ICU) remains unclear. This study aimed to elucidate the association between SHR and all-cause mortality in this clinical setting. Methods: We conducted a retrospective cohort study utilizing data from a large, retrospective database. Critically ill patients with documented AF were stratified based on quartiles of SHR. The primary outcome was 365-day all-cause mortality, with secondary outcomes including 90-day and 28-day mortality. COX proportional hazards models adjusted for confounders and Kaplan-Meier curve analyses were used to explore the relationship between SHR and mortality. Results: 2,679 patients with critical AF were enrolled in the final study. Among the patients studied, those in the highest SHR quartiles exhibited an increased risk of 365-day all-cause mortality (HR:1.32, 95%CI=1.06-1.65). Notably, in subgroup analyses, the prognostic value of SHR was particularly pronounced in patients with hypertension. Sensitivity analyses confirmed the persistence of these findings after excluding cohorts with malignant tumors, and heart failure. Conclusions: Our research discerns a positive association between SHR and all-cause mortality in critically ill patients with AF, highlighting the significance of acute glycemic dysregulation on patient outcomes. Longer follow-up is still needed in the future to study the association between SHR and all-cause mortality in critically ill patients with AF.

PRELP inhibits colorectal cancer progression by suppressing epithelial-mesenchymal transition and angiogenesis via the inactivation of the FGF1/PI3K/AKT pathway.

Proline/arginine-rich end and leucine-rich protein (PRELP) is identified as a small proteoglycan in the extracellular matrix that has been tightly associated with cell adhesion. At present, the role of PRELP in colorectal cancer (CRC) remains largely unknown. PRELP expression in human CRC tissue samples was analyzed by qRT-PCR and immunochemistry. CCK-8, colony formation, transwell, and tube formation assays were utilized to determine the influences of PRELP on the malignant phenotypes of CRC cells. Mouse xenograft and tumor metastasis models were constructed to further validate the function of PRELP. Furthermore, we investigated the efficacy of PRELP combined with bevacizumab treatment in a mouse xenograft model of CRC. Additionally, RNA-seq was performed to analyze the potential signaling pathways regulated by PRELP. Immunofluorescence staining and coimmunoprecipitation were conducted to confirm the interaction between PRELP and fibroblast growth factor 1 (FGF1). In this study, we found that PRELP exerted a tumor-suppressive effect on CRC. The expression level of PRELP was significantly reduced in CRC tissues and cell lines. Both in vivo and in vitro experiments confirmed that PRELP inhibited CRC cell proliferation, promoted apoptosis, and suppressed migration and invasion via a reduction in the epithelial-mesenchymal transition and attenuated angiogenesis, thereby dampening tumor progression. In addition, PRELP markedly potentiated the efficacy of bevacizumab in a mouse xenograft model. Mechanistically, PRELP bound to FGF1 and reduced the stability of the FGF1 protein, accompanied by an increase in its degradation, which subsequently inactivated the PI3K/AKT/mTOR pathway, thereby leading to reduction in tumor angiogenesis and metastasis. Our study for the first time unveiled the tumor-suppressive role of PRELP in CRC and provided a potential effective strategy for the treatment of CRC.

Influenza vaccination for heart failure patients: a cost-effectiveness analysis from the perspective of Chinese healthcare system.

Purpose: Influenza infection induces cardiovascular events in heart failure (HF) patients, with potential risk reduction through vaccination. This study aims to evaluate the cost-effectiveness of influenza vaccination for HF patients in China. Methods: We developed a Markov model with a 3-month cycle to simulate the cost-effectiveness of administering the influenza vaccine to patients with HF over a 3-year period. Patients in the model received either the influenza vaccine or a placebo, in addition to standard HF treatment. Cost data, sourced from the China Healthcare Statistic Yearbook and other public records, and effectiveness data from the IVVE (Influenza Vaccine to Prevent Adverse Vascular Events in HF) trial, were incorporated. Specifically, the cost of the influenza vaccine was 75 Chinese Yuan (CNY) (11 USD), the cost of hospitalization for heart failure (HHF) was 9,326 CNY (1,386 USD), and the cost of treatment for pneumonia was 5,984 CNY (889 USD). The study's primary outcome, the incremental cost-effectiveness ratio (ICER), quantifies the incremental cost (CNY and USD) per incremental quality-adjusted life year (QALY). Additional outcomes included total cost, total effectiveness, incremental cost, and incremental effectiveness. We conducted one-way and probabilistic sensitivity analyses (PSA) to assess certainty and uncertainty, respectively. Scenario analysis, considering various situations, was performed to evaluate the robustness of the results. Results: In the base case analysis, influenza vaccine, compared to placebo, among Chinese HF patients, resulted in a cost increase from 21,004 CNY (3,121 USD) to 21,062 CNY (3,130 USD) and in QALYs from 1.89 to 1.92 (2.55 life years vs. 2.57 life years) per patient. The resulting ICER was 2,331 CNY (346 USD) per QALY [2,080 CNY (309 USD) per life year], falling below the willingness-to-pay threshold based on per capita GDP. One-way sensitivity analysis revealed that disparities in HHF and cardiovascular death rates between groups had the most significant impact on the ICER, while the cost of vaccines had a marginal impact. PSA and scenario analysis collectively affirmed the robustness of our findings. Conclusion: This study suggests that adding the influenza vaccine to standard treatment regimens for Chinese patients with HF may represent a highly cost-effective option. Further real-world data studies are essential to validate these findings.

Diaphragmatic dysfunction is associated with postoperative pulmonary complications in the aged patients underwent radical resection of esophageal cancer: a prospective observational study.

Background: Diaphragmatic dysfunction escalates the susceptibility to postoperative pulmonary complications (PPCs). Currently, no study reports the occurrence of diaphragmatic dysfunction correlated with PPCs following radical resection of esophageal cancer in aged patients. We aimed to diagnose diaphragmatic dysfunction via ultrasonography and analyze diaphragmatic dysfunction's relation with PPCs after radical resection of esophageal cancer surgery in aged patients. Methods: This prospective observational study comprised 86 aged patients undergoing radical resection of esophageal cancer. Patient characteristics data and intraoperative details were collected. Ultrasonography was performed before (preoperative) and after (first, third, and fifth day postoperatively) surgery. Outcome measures included PPCs within seven days postoperative, occurrence of diaphragmatic dysfunction, and short-term prognosis. Results: After excluding 14 patients, we finally analyzed clinical data from 72 patients. The prevalence of PPCs was higher in the patients with diaphragmatic dysfunction than those without (19 of 23, 83% vs. 21 of 49, 43%, P=0.004). Postoperative diaphragmatic dysfunction was positively correlated with PPCs in patients who underwent elective radical esophageal cancer surgery (r=0.37, P=0.001). Persistent diaphragmatic dysfunction, furthermore, was positively correlated with the development of multiple PPCs (r=0.43, P<0.001). The logistic regression analysis revealed that age, total open procedure, and postoperative diaphragmatic dysfunction were identified as significant risk factors for PPCs, while total open procedure was an independent risk factor for diaphragmatic dysfunction. Conclusions: Postoperative diaphragmatic dysfunction positively correlates with developing PPCs. Continuous monitoring of postoperative diaphragmatic function can screen high-risk patients with PPCs, which has specific clinical significance. Age, total open procedure, and diaphragmatic dysfunction are identified as risk factors for developing PPCs, while total open procedure specifically increases the risk for postoperative diaphragmatic dysfunction.

U-shaped association between serum Klotho and all-cause mortality in US cardiovascular patients: a prospective cohort study.

Background: Increased levels of serum Klotho have been associated with a reduced risk of several cardiovascular diseases (CVD). However, limited studies exist on the association between serum Klotho and mortality in patients with CVD. Methods: We collected data from CVD patients in the National Health and Nutrition Examination Survey (NHANES) spanning 2007 to 2016. We linked NHANES data with the National Death Index to determine the survival status of participants. Univariate and multivariable Cox regression models were used to investigate the relationship between serum Klotho levels and mortality in CVD patients. The relationship between serum Klotho quartiles and mortality in CVD patients was visualized using Kaplan-Meier (KM) curves and restricted cubic spine. Finally, subgroup analyses were used to examine the association between serum Klotho and all-cause mortality in different populations. Results: 1905 patients with CVD were finally enrolled in our study with a mean follow-up of 7.1 years. The average age of the participants was 63.4 years, with 58.40% being male. KM showed that lower Klotho levels were associated with lower survival rates. After adjusting for potential confounders, patients with higher serum Klotho levels had lower all-cause mortality (Q1: 1.00, Q2: 0.58 (0.42-0.80), Q3: 0.69 (0.47-1.01), and Q4:0.64 (0.45-0.92). However, the relationship between serum Klotho levels and cardiovascular mortality was not statistically significant. Dose-response analysis shows a U-shaped relationship between serum Klotho levels and all-cause mortality in patients with CVD (P nonlinear=0.002). Subgroup analysis indicated that participants with a history of hypertension had a higher risk of all-cause mortality in serum Klotho Q4 compared to Q1 (P trend <0.05). Conclusion: The relationship between serum Klotho levels and all-cause mortality in CVD patients exhibits a U-shaped association. The underlying mechanisms of this association need further investigation.

The association between composite dietary antioxidant index and diabetic retinopathy in type 2 diabetic patients: evidence from the NHANES.

Background: Although diabetic retinopathy (DR) is closely related to dietary patterns and oxidative stress, there is little research on the relationship between the compound dietary antioxidant index (CDAI) and DR. This study aims to fill this gap by analyzing data from the National Health and Nutrition Examination Survey (NHANES) to explore the association between CDAI and DR in patients with type 2 diabetes, in order to provide a basis for dietary guidance to prevent DR. Methods: Data for this study was obtained from NHANES conducted between 1999 and 2020. Information regarding dietary intake was collected through 24 h dietary recall interviews. Multivariate logistic regression analyses and restricted cubic splines (RCS) were employed to explore the association between CDAI and DR. Furthermore, subgroup analyses were conducted to further examine the relationship. Results: In this study, a total of 2,158 participants were included, with a mean age of 58.87 years. After adjusting for all potential confounding factors, multivariate logistic regression analyses consistently demonstrated a negative correlation between CDAI and DR (OR = 0.94, 95%CI: 0.90-0.98, p = 0.007). Specifically, individuals in the highest quartile of CDAI had a significantly reduced risk of DR compared to those in the lowest quartile (OR = 0.51, 95%CI: 0.34-0.75, p < 0.001). The RCS analyses further confirmed the linear negative correlation between CDAI and DR (non-linear p = 0.101). Additionally, subgroup analyses provided further evidence for the robustness of this association across different subpopulations. Conclusion: Our study highlights the linear negative correlation between CDAI and DR in type 2 diabetic patients. Further prospective studies are still needed in the future to confirm the role of CDAI in the risk of developing DR.

A multi-population multi-stage adaptive weighted large-scale multi-objective optimization algorithm framework.

Weighted optimization framework (WOF) achieves variable dimensionality reduction by grouping variables and optimizing weights, playing an important role in large-scale multi-objective optimization problems. However, because of possible problems such as duplicate weight vectors in the selection process and loss of population diversity, the algorithm is susceptible to local optimization. Therefore, this paper develops an algorithm framework called multi-population multi-stage adaptive weighted optimization (MPSOF) to improve the performance of WOF in two aspects. First, the method of using multi-population is employed to address the issue of insufficient algorithmic diversity, while simultaneously reducing the likelihood of converging towards local optima. Secondly, a processing stage is incorporated into MPSOF, where a certain number of individuals are adaptively selected for updating based on the weight information and evolutionary status of different subpopulations, targeting different types of weights. This approach alleviates the impact of repetitive weights on the diversity of newly generated individuals, avoids the drawback of easily converging to local optima when using a single type of weight for updating, and effectively balances the diversity and convergence of subpopulations. Experiments of three types designed on several typical function sets demonstrate that MPSOF exceeds the comparison algorithms in the three metrics for Inverse Generation Distance, Hypervolume and Spacing.

Mesenchymal stromal cells ameliorate mitochondrial dysfunction in α cells and hyperglucagonemia in type 2 diabetes via SIRT1/FoxO3a signaling.

Dysregulation of α cells results in hyperglycemia and hyperglucagonemia in type 2 diabetes mellitus (T2DM). Mesenchymal stromal cell (MSC)-based therapy increases oxygen consumption of islets and enhances insulin secretion. However, the underlying mechanism for the protective role of MSCs in α-cell mitochondrial dysfunction remains unclear. Here, human umbilical cord MSCs (hucMSCs) were used to treat 2 kinds of T2DM mice and αTC1-6 cells to explore the role of hucMSCs in improving α-cell mitochondrial dysfunction and hyperglucagonemia. Plasma and supernatant glucagon were detected by enzyme-linked immunosorbent assay (ELISA). Mitochondrial function of α cells was assessed by the Seahorse Analyzer. To investigate the underlying mechanisms, Sirtuin 1 (SIRT1), Forkhead box O3a (FoxO3a), glucose transporter type1 (GLUT1), and glucokinase (GCK) were assessed by Western blotting analysis. In vivo, hucMSC infusion improved glucose and insulin tolerance, as well as hyperglycemia and hyperglucagonemia in T2DM mice. Meanwhile, hucMSC intervention rescued the islet structure and decreased α- to ß-cell ratio. Glucagon secretion from αTC1-6 cells was consistently inhibited by hucMSCs in vitro. Meanwhile, hucMSC treatment activated intracellular SIRT1/FoxO3a signaling, promoted glucose uptake and activation, alleviated mitochondrial dysfunction, and enhanced ATP production. However, transfection of SIRT1 small interfering RNA (siRNA) or the application of SIRT1 inhibitor EX-527 weakened the therapeutic effects of hucMSCs on mitochondrial function and glucagon secretion. Our observations indicate that hucMSCs mitigate mitochondrial dysfunction and glucagon hypersecretion of α cells in T2DM via SIRT1/FoxO3a signaling, which provides novel evidence demonstrating the potential for hucMSCs in treating T2DM.

Enhanced Selective Electrosorption of Nitrate from Wastewater by Controllably Doping Nitrogen into Porous Carbon with Micropores.

The biological NO3- removal process might be accompanied by high CO2 emissions and operation costs. Capacitive deionization (CDI) has been widely studied as a very efficient method to purify water. Here, a porous carbon material with a tunable nitrogen configuration was developed. Characterization and density functional theory calculation show that nitrogenous functional groups have a higher NO3- binding energy than Cl-, SO42-, and H2PO4-. In addition, the selectivity of NO3- is improved after the introduction of micropores by using the pore template. The NO3- ion removal and selectivity of MN-C-12 are 4.57 and 3.46-5.42 times that of activated carbon (AC), respectively. The high NO3- selectivity and electrosorption properties of MN-C-12 (the highest N content and micropore area) are due to the synergistic effect of the affinity of nitrogen functional groups to NO3- and microporous ion screening. A CDI unit for the removal of nitrogen from municipal wastewater was constructed and applied to treat wastewater meeting higher discharge standards of A (N: 15 mg L-1) and B (N: 20 mg L-1) ((GB18918-2002), China). This work provides new insights into enhanced carbon materials for the selective electrosorption of wastewater by CDI technology.

Quercetin Prevents Hypertension in Dahl Salt-sensitive Rats F ed a High-salt Diet Through Balancing Endothelial Nitric Oxide Synthase and Sirtuin 1.

BACKGROUND: A high-salt diet is a leading dietary risk factor for elevated blood pressure and cardiovascular disease. Quercetin reportedly exhibits cardioprotective and antihypertensive therapeutic effects. OBJECTIVES: The objective of this study is to examine the effect of quercetin on high-salt dietinduced elevated blood pressure in Dahl salt-sensitive (SS) rats and determine the underlying molecular mechanism. MATERIALS AND METHODS: Rats of the Dahl SS and control SS-13 BN strains were separated into five groups, SS-13 BN rats fed a low-salt diet (BL group), SS-13 BN rats fed a high-salt diet (BH group), Dahl SS rats fed a low-salt diet (SL group), Dahl SS rats fed a high-salt diet (SH group), and SH rats treated with quercetin (SHQ group). Blood pressure was checked three weeks into the course of treatment, and biochemical markers in the urine and serum were examined. Additionally, western blot was done to evaluate the sirtuin 1 (SIRT1) and endothelial nitric oxide synthase (eNOS) expression levels. Immunohistochemical analysis was performed to verify SIRT1 levels. RESULTS: We demonstrated that a high-salt diet elevated blood pressure in both SS-13 BN and Dahl SS rats, and quercetin supplementation alleviated the altered blood pressure. Compared with the SH group, quercetin significantly elevated the protein expression of SIRT1 and eNOS. Immunohistochemistry results further confirmed that quercetin could improve the protein expression of SIRT1. CONCLUSION: Quercetin reduced blood pressure by enhancing the expression of SIRT1 and eNOS in Dahl SS rats fed a high-salt diet.

Gender differences in all-cause and cardiovascular mortality among US adults: from NHANES 2005-2018.

Background: Gender disparities in mortality have drawn great interest, with previous studies identifying various biological, social, and behavioral factors contributing to the observed gender differences. This study aims to identify the sources of gender disparities in mortality rates and quantify the extent to which these factors mediate the gender differences in all-cause mortality. Methods: Data from the National Health and Nutrition Examination Survey (NHANES) conducted between 2005 and 2018 were analyzed. A total of 38,924 participants were included in the study. Gender information, socioeconomic status, lifestyle factors, and baseline disease status were obtained through questionnaires. Blood samples were collected to assess serological indicators. All-cause and cardiovascular mortality were considered as primary and secondary outcomes, respectively. Results: The study with an average age of 50.1 ± 17.9 years. Among the participants, 50.7% were women, and 41.8% were non-Hispanic White. The median follow-up length was 87 months [Inter-Quartile Range (IQR): 47-128]. Men showed higher rates of all-cause and cardiovascular mortality compared to women in both the general population and the population with cardiovascular disease. After adjustment for potential confounders (age, race, marital status, socioeconomic status, lifestyle level, smoking status, cardiovascular disease, hypertension, diabetes and cancer), the men: women hazard ratios (HRs) for all-cause and cardiovascular mortality were 1.58 [95% Confidence Interval (CI): 1.48-1.68] and 1.60 (95%CI:1.43-1.80) in the general population. Among individuals with cardiovascular disease, the fully adjusted HR for all-cause mortality was 1.34 (95% CI: 1.20 to 1.51), and for cardiovascular mortality, the fully adjusted HRs was 1.52 (95% CI: 1.26 to 1.83). Mediation analysis revealed that uric acid levels significantly mediated the association between gender and all-cause mortality, accounting for 17.53% (95% CI: 11.0% to 23.7%) in the general population and 27.47% (95% CI: 9.0% to 13.6%) in the population with cardiovascular disease. Conclusions: The study highlights the complex interplay of biological and social factors contributing to gender disparities in mortality. Uric acid was identified as key mediators of the gender-mortality association. These findings can inform targeted interventions aimed at reducing gender disparities in mortality and promoting better public health outcomes.

Multi-functional composite dressings with sustained release of MSC-SLP and anti-adhesion property for accelerating wound healing.

Exudate management is of significant clinical value for the treatment of acute wound. Various wound dressings have been developed to restore the function of injured tissues and promote wound healing, but proper exploiting the healing factors inside exudate and achieving anti-adhesion wound care remains a challenge. Herein, we present a novel multi-functional composite dressing (MCD) by coupling supernatant lyophilized powder of mesenchymal stem cells (MSC-SLP) with a sandwich-structured wound dressing (SWD). The developed MCDs demonstrated unique unidirectional drainage capability, stable anti-adhesion characteristics, and improved wound healing performance. The designed SWD with both superhydrophobic inner surface and liquid-absorption ability of mid layer enables the dressings exhibit desired anti-adhesion property to neoformative granulation tissues, favorable shielding effect to exogenous bacteria, as well as appropriate exudate-retaining capability and unidirectional exudate-absorption property. The introduction of MSC-SLP in SWD was demonstrated to further improve wound healing quality. Compared to medical gauze, the synergic effect of SWD and MSC-SLP significantly accelerates wound healing rate by over 30%, avoids tissue avulsion when changing dressings, and produces a flat-smooth closure surface. More importantly, the wound treated with MCDs presents more skin accessory organs and blood vessels in regenerated tissues than other groups. In vivo/vitro biocompatibility evaluations indicated little toxicity, demonstrating the biosecurity of the developed dressings. The proposed method offers great potential in clinical applications particularly for chronic wound treatments.

Identification and functional characterization of compound heterozygous CYP11B1 gene mutations.

PURPOSE: 11ß-Hydroxylase deficiency (11ß-OHD) is the second leading cause of congenital adrenal hyperplasia (CAH), a rare autosomal recessive disease caused by mutations in the CYP11B1 gene. We previously reported the case of a male Chinese patient with typical 11ß-OHD symptoms. Sanger sequencing revealed that the patient carried a splice-site mutation, c.595+1G>A in the CYP11B1 gene. His mother and sister harbored the heterozygous mutation, c.595+1G>A. Paradoxically, Sanger sequencing did not detect any abnormality in the CYP11B1 gene of his father and brother. Therefore, in this study, we aimed to further explore the exact genetic etiology of 11ß-OHD in this pedigree and analyze the functional consequence of the c.595+1G>A mutation. METHODS: Gemomic DNA was extracted from the peripheral blood leukocytes of the family members and normal control individuals, followed by quantitative real-time polymerase chain reaction (qPCR) to detect the copy number of the target CYP11B1 gene fragment. Mutation analysis was also performed via whole-exome sequencing (WES) followed by Sanger sequencing validation. In vitro minigene assay was also performed to investigate the impact of the c.595+1G>A mutation on pre-mRNA splicing. RESULTS: qPCR results suggested a heterozygous deletion encompassing position c.595+1 along with flanking exonic and intronic sequences in the CYP11B1 gene of the patient and his father. WES followed by Sanger sequencing verified that the patient carried compound heterozygous mutations in the CYP11B1 gene, including a novel 2840-bp deletion (c.395+661_c.1121+180del) and c.595+1G>A, while his father carried the heterozygous c.395+661_c.1121+180del mutation. No other novel CYP11B1 mutations were found in the rest of the family members. Furthermore, minigene assay revealed that the c.595+1G>A mutation resulted in a 70-bp deletion of exon 3 in the mRNA, and this altered the reading frame at amino acid 176 and created a premature stop codon at amino acid 197. CONCLUSION: We identified a novel 2840-bp-sized large deletion and confirmed that the c.595+1G>A mutation disrupts normal pre-mRNA splicing. Either mutation could significantly alter the reading frame and abolish CYP11B1 enzyme activity. Therefore, our findings widen the mutation spectrum of CYP11B1 and provide an accurate diagnosis of 11ß-OHD at a molecular genetic level.

A novel entire traction method with clip-anchored nylon ring facilitating endoscopic submucosal dissection (ESD) of early gastric cancer.

A 48-year-old woman with a high-grade intraepithelial neoplasia of the gastric antrum was referred for ESD treatment.The difficulty of ESD is to expose the submucosa,especially in difficult sites and lesions with severe fibrosis.Adequate submucosal exposure is the most critical technology to reduce complications and improving efficiency.Here we report a novel entire traction method to facilitate safe and efficient ESD.

Selective electrocatalytic transformation of highly toxic phenols in wastewater to para-benzoquinone at ambient conditions.

The selective transformation of organics from wastewater to value-added chemicals is considered an upcycling process beneficial for carbon neutrality. Herein, we present an innovative electrocatalytic oxidation (ECO) system aimed at achieving the selective conversion of phenols in wastewater to para-benzoquinone (p-BQ), a valuable chemical widely utilized in the manufacturing and chemical industries. Notably, 96.4% of phenol abatement and 78.9% of p-BQ yield are synchronously obtained over a preferred carbon cloth-supported ruthenium nanoparticles (Ru/C) anode. Such unprecedented results stem from the weak Ru-O bond between the Ru active sites and generated p-BQ, which facilitates the desorption of p-BQ from the anode surface. This property not only prevents the excessive oxidation of the generated p-BQ but also reinstates the Ru active sites essential for the rapid ECO of phenol. Furthermore, this ECO system operates at ambient conditions and obviates the need for potent chemical oxidants, establishing a sustainable avenue for p-BQ production. Importantly, the system efficacy can be adaptable in actual phenol-containing coking wastewater, highlighting its potential practical application prospect. As a proof of concept, we construct an electrified Ru/C membrane for ECO of phenol, attaining phenol removal of 95.8% coupled with p-BQ selectivity of 73.1%, which demonstrates the feasibility of the ECO system in a scalable flow-through operation mode. This work provides a promising ECO strategy for realizing both phenols removal and valuable organics recovery from phenolic wastewater.

Carotid blood flow changes following a simulated end-inspiratory occlusion maneuver measured by ultrasound can predict hypotension after the induction of general anesthesia: an observational study.

BACKGROUND: The primary purpose of this study was to investigate the predictive value of alterations in cervical artery hemodynamic parameters induced by a simulated end-inspiratory occlusion test (sEIOT) measured by ultrasound for predicting postinduction hypotension (PIH) during general anesthesia. METHODS: Patients undergoing gastrointestinal tumor resection under general anesthesia were selected for this study. Ultrasound has been utilized to assess hemodynamic parameters in carotid artery blood flow before induction, specifically focusing on variations in corrected flow time (ΔFTc) and peak blood flow velocity (ΔCDPV), both before and after sEIOT. Anesthesia was induced by midazolam, sufentanil, propofol, and rocuronium, and blood pressure (BP) and heart rate (HR) were recorded within the first 10 min following endotracheal intubation. PIH was defined as fall in systolic blood pressure (SBP) or mean arterial pressure (MAP) by > 30% of baseline or MAP to < 60 mm Hg. RESULTS: The area under the receiver operating characteristic curves (AUC) for carotid artery ΔFTc was 0.88 (95%CI, 0.81 to 0.96; P < 0.001), and the optimal cutoff value was -16.57%, with a sensitivity of 91.4% and specificity of 77.60%. The gray zone for carotid artery ΔFTc was -16.34% to -15.36% and included 14% of the patients. The AUC for ΔCDPV was 0.54, with an optimal cutoff value of -1.47%. The sensitivity and specificity were calculated as 55.20% and 57.10%, respectively. CONCLUSION: The corrected blood flow time changes in the carotid artery induced by sEIOT can predict hypotension following general anesthesia-induced hypotension, wherein ΔFTc less than 16.57% is the threshold. TRIAL REGISTRATION: Chinese Clinical Trial Registry ( www.chictr.org.cn ; 20/06/2023; ChiCTR2300072632).