Fusobacterium periodonticum BCT protein targeting glucose metabolism to promote the epithelial-mesenchymal transition of esophageal cancer cells by lactic acid.

BACKGROUND: The cancer microbiota was considered the main risk factor for cancer progression. We had proved that Fusobacterium periodonticum (F.p) was higher abundance in Esophageal cancer(EC)tissues. Bioinformation analysis found that BCT was a key virulence protein of F.p. However, little is known about the role and mechanism of BCT in EC. This study aimed to recognize the key virulence protein of F.p and explore the mechanism of BCT in promoting EC. METHODS: We constructed a eukaryotic expression vector and purified the recombinant protein BCT. CCK8 used to analyzed the activity of EC after treated by different concentration of BCT. UPLC-MS/MS and ELISA used to detect the metabonomics and metabolites. The ability of migration and invasion was completed by transwell assay. RT-QPCR, WB used to analyze the expression of relevant genes. RESULTS: Our data showed that BCT was higher expression in EC tumor tissues (p < 0.05) and BCT in 20 µg/mL promoted the survival, invasion and migration of EC cells (EC109) (p < 0.05). Meanwhile, UPLC-MS/MS results suggested that BCT resulted in an augmentation of hypotaurine metabolism, arachidonic acid metabolism, glycolysis/gluconeogenesis, tryptophan metabolism, citrate cycle activity in EC109. The metabolic changes resulted in decreasing in glucose and pyruvate levels but increase in lactate dehydrogenase (LDH) activity and lactic acid (LA) as well as the expression of glucose transporter 1, Hexokinase 2, LDH which regulated the glycolysis were all changed (p < 0.05). The BCT treatment upregulated the expression of TLR4, Akt, HIF-1α (p < 0.05) which regulated the production of LA. Furthermore, LA stimulation promoted the expression of GPR81, Wnt, and ß-catenin (p < 0.05), thereby inducing EMT and metastasis in EC109 cells. CONCLUSION: Altogether, these findings identified that impact of BCT in regulation of glycolysis in EC109 and its involves the TLR4/Akt/HIF-1α pathway. Meanwhile, glycolysis increasing the release of LA and promote the EMT of EC109 by GPR81/Wnt/ß-catenin signaling pathway. In summary, our findings underscore the potential of targeting BCT as an innovative strategy to mitigate the development of EC.

Fast Prediction Method for Scattering Parameters of Rigid-Flex PCBs Based on ANN.

InGaAs detection systems have been increasingly used in the aerospace field, and due to the high signal-to-noise ratio requirements of short-wave infrared quantitative payloads, there is an urgent need for methods for the rapid and precise evaluation and the optimal design of these systems. The rigid-flex printed circuit board (PCB) is a vital component of InGaAs detectors, as its grid ground plane design parameters impact parasitic capacitance and thus affect weak infrared analog signals. To address the time-intensive and costly nature of design optimization achieved with simulations and experimental measurements, we propose an innovative method based on a neural network to predict the scattering parameters of rigid-flex boards for InGaAs detection links. This is the first study in which the effects of rigid-flex boards on weak infrared detection signals have been considered. We first obtained sufficient samples with software simulation. A backpropagation (BP) neural network prediction model was trained on existing sample sets and then verified on a rigid-flex board used in a crucial aerospace short-wave infrared quantitative mission. The model efficiently and accurately predicted high-speed interconnect scattering parameters under various rigid-flex board grid plane parameter conditions. The prediction error was less than 1% compared with a 3D field solver, indicating an overcoming of the iterative optimization inefficiency and showing improved design quality for InGaAs detection circuits.

Zinc deficiency drives ferroptosis resistance by lactate production in esophageal squamous cell carcinoma.

Trace metal zinc is involved in key processes of solid tumors by its antioxidant properties, while the role of zinc at the onset of esophageal squamous cell carcinoma (ESCC) remains controversial. This study aimed to determine whether zinc is associated with the ESCC and underlying molecular events involving malignant progression. Based on a case-control study, we found serum and urine zinc were decreased and correlated with ESCC progression. Thus, an in vitro model for zinc deficiency (ZD) was established, and we found that ZD contributed to the proliferation, migration, and invasion of EC109 cells. Untargeted metabolomics identified 59 upregulated metabolites and 6 downregulated metabolites, among which glycolysis and ferroptosis-related oxidation of chain fatty acids might play crucial steps in ZD-treated molecular events. Interestingly, ZD disrupted redox homeostasis and enhanced cytosolic Fe2+ of EC109 cells, while lipid peroxidation, the key marker of ferroptosis occurrence, was decreased after ZD treatment. The mechanism underlying these changes may involve ZD-enhanced ESCC glycolysis and lactate production, which confer ferroptosis resistance by inhibiting of p-AMPK and leading to the upregulation of SREBP1 and SCD1 to enhance the production of anti-ferroptosis monounsaturated fatty acids.

A critical review of advances in tumor metabolism abnormalities induced by nitrosamine disinfection by-products in drinking water.

Intensified sanitation practices amid the recent severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) outbreak might result in the increased release of chloramine disinfectants into surface water, significantly promoting the formation of nitrosamine disinfection by-products (DBPs) in drinking water. Unfortunately, these nitrosamine DBPs exhibit significant genotoxic, carcinogenic, and mutagenic properties, whereas chlorinating disinfectants remain in global practice. The current review provides valuable insights into the occurrence, identification, contamination status, exposure limits, and toxicity of the new unregulated disinfection by-products (nitrosamine DBPs) in drinking water. As a result, concentrations of nitrosamine DBPs far exceed allowable limits in drinking water, and prolonged exposure has the potential to cause metabolic disorders, a critical step in tumor initiation and progression. Importantly, based on recent research, we have concluded the role of nitrosamines DBPs in different metabolic pathways. Remarkably, nitrosamine DBPs can induce chronic inflammation and initiate tumors by activating sphingolipid and polyunsaturated fatty acid metabolism. Regarding amino acid and nucleotide metabolism, nitrosamine DBPs can inhibit tryptophan metabolism and de novo nucleotide synthesis. Moreover, inhibition of de novo nucleotide synthesis fails to repair DNA damage induced by nitrosamines. Additionally, the accumulation of lactate induced by nitrosamine DBPs may act as a pivotal signaling molecule in communication within the tumor microenvironment. However, with the advancement of tumor metabolomics, understanding the role of nitrosamine DBPs in causing cancer by inducing metabolic abnormalities significantly lags behind, and specific mechanisms of toxic effects are not clearly defined. Urgently, further studies exploring this promising area are needed.

Searching across-cohort relatives in 54,092 GWAS samples via encrypted genotype regression.

Explicitly sharing individual level data in genomics studies has many merits comparing to sharing summary statistics, including more strict QCs, common statistical analyses, relative identification and improved statistical power in GWAS, but it is hampered by privacy or ethical constraints. In this study, we developed encG-reg, a regression approach that can detect relatives of various degrees based on encrypted genomic data, which is immune of ethical constraints. The encryption properties of encG-reg are based on the random matrix theory by masking the original genotypic matrix without sacrificing precision of individual-level genotype data. We established a connection between the dimension of a random matrix, which masked genotype matrices, and the required precision of a study for encrypted genotype data. encG-reg has false positive and false negative rates equivalent to sharing original individual level data, and is computationally efficient when searching relatives. We split the UK Biobank into their respective centers, and then encrypted the genotype data. We observed that the relatives estimated using encG-reg was equivalently accurate with the estimation by KING, which is a widely used software but requires original genotype data. In a more complex application, we launched a finely devised multi-center collaboration across 5 research institutes in China, covering 9 cohorts of 54,092 GWAS samples. encG-reg again identified true relatives existing across the cohorts with even different ethnic backgrounds and genotypic qualities. Our study clearly demonstrates that encrypted genomic data can be used for data sharing without loss of information or data sharing barrier.

Genetic determinants of IgG antibody response to COVID-19 vaccination.

Human humoral immune responses to SARS-CoV-2 vaccines exhibit substantial inter-individual variability and have been linked to vaccine efficacy. To elucidate the underlying mechanism behind this variability, we conducted a genome-wide association study (GWAS) on the anti-spike IgG serostatus of UK Biobank participants who were previously uninfected by SARS-CoV-2 and had received either the first dose (n = 54,066) or the second dose (n = 46,232) of COVID-19 vaccines. Our analysis revealed significant genome-wide associations between the IgG antibody serostatus following the initial vaccine and human leukocyte antigen (HLA) class II alleles. Specifically, the HLA-DRB1∗13:02 allele (MAF = 4.0%, OR = 0.75, p = 2.34e-16) demonstrated the most statistically significant protective effect against IgG seronegativity. This protective effect was driven by an alteration from arginine (Arg) to glutamic acid (Glu) at position 71 on HLA-DRß1 (p = 1.88e-25), leading to a change in the electrostatic potential of pocket 4 of the peptide binding groove. Notably, the impact of HLA alleles on IgG responses was cell type specific, and we observed a shared genetic predisposition between IgG status and susceptibility/severity of COVID-19. These results were replicated within independent cohorts where IgG serostatus was assayed by two different antibody serology tests. Our findings provide insights into the biological mechanism underlying individual variation in responses to COVID-19 vaccines and highlight the need to consider the influence of constitutive genetics when designing vaccination strategies for optimizing protection and control of infectious disease across diverse populations.

Potato Resistant Starch Type 1 Promotes Obesity Linked with Modified Gut Microbiota in High-Fat Diet-Fed Mice.

Obesity has become a major disease that endangers human health. Studies have shown that dietary interventions can reduce the prevalence of obesity and diabetes. Resistant starch (RS) exerts anti-obesity effects, alleviates metabolic syndrome, and maintains intestinal health. However, different RS types have different physical and chemical properties. Current research on RS has focused mainly on RS types 2, 3, and 4, with few studies on RS1. Therefore, this study aimed to investigate the effect of RS1 on obesity and gut microbiota structure in mice. In this study, we investigated the effect of potato RS type 1 (PRS1) on obesity and inflammation. Mouse weights, as well as their food intake, blood glucose, and lipid indexes, were assessed, and inflammatory factors were measured in the blood and tissues of the mice. We also analyzed the expression levels of related genes using PCR, with 16S rRNA sequencing used to study intestinal microbiota changes in the mice. Finally, the level of short-chain fatty acids was determined. The results indicated that PRS1 promoted host obesity and weight gain and increased blood glucose and inflammatory cytokine levels by altering the gut microbiota structure.

Gut Microbiome and Stroke: a Bidirectional Mendelian Randomisation Study in East Asian and European Populations.

BACKGROUND AND AIMS: Observational studies have implicated the involvement of gut microbiome in stroke development. Conversely, stroke may disrupt the gut microbiome balance, potentially causing systemic infections exacerbated brain infarction. However, the causal relationship remains controversial or unknown. To investigate bidirectional causality and potential ethnic differences, we conducted a bidirectional two-sample Mendelian randomisation (MR) study in both East Asian (EAS) and European (EU) populations. METHODS: Leveraging the hitherto largest genome-wide association study (GWAS) summary data from the MiBioGen Consortium (n=18 340, EU) and BGI (n=2524, EAS) for the gut microbiome, stroke GWAS data from the GIGASTROKE Consortium(264 655 EAS and 1 308 460 EU), we conducted bidirectional MR and sensitivity analyses separately for the EAS and EU population. RESULTS: We identified nominally significant associations between 85 gut microbiomes taxa in EAS and 64 gut microbiomes taxa in EU with stroke or its subtypes. Following multiple testing, we observed that genetically determined 1 SD increase in the relative abundance of species Bacteroides pectinophilus decreased the risk of cardioembolic stroke onset by 28% (OR 0.72 (95% CI 0.62 to 0.84); p=4.22e-5), and that genetically determined 1 SD increase in class Negativicutes resulted in a 0.76% risk increase in small vessel stroke in EAS. No significant causal association was identified in the EU population and the reverse MR analysis. CONCLUSION: Our study revealed subtype-specific and population-specific causal associations between gut microbiome and stroke risk among EAS and EU populations. The identified causality holds promise for developing a new stroke prevention strategy, warrants further mechanistic validation and necessitates clinical trial studies.

Genetic basis of pregnancy-associated decreased platelet counts and gestational thrombocytopenia.

ABSTRACT: Platelet count reduction occurs throughout pregnancy, with 5% to 12% of pregnant women being diagnosed with gestational thrombocytopenia (GT), characterized by a more marked decrease in platelet count during pregnancy. However, the underlying biological mechanism behind these phenomena remains unclear. Here, we used sequencing data from noninvasive prenatal testing of 100 186 Chinese pregnant individuals and conducted, to our knowledge, the hitherto largest-scale genome-wide association studies on platelet counts during 5 periods of pregnancy (the first, second, and third trimesters, delivery, and the postpartum period) as well as 2 GT statuses (GT platelet count < 150 × 109/L and severe GT platelet count < 100 × 109/L). Our analysis revealed 138 genome-wide significant loci, explaining 10.4% to 12.1% of the observed variation. Interestingly, we identified previously unknown changes in genetic effects on platelet counts during pregnancy for variants present in PEAR1 and CBL, with PEAR1 variants specifically associated with a faster decline in platelet counts. Furthermore, we found that variants present in PEAR1 and TUBB1 increased susceptibility to GT and severe GT. Our study provides insight into the genetic basis of platelet counts and GT in pregnancy, highlighting the critical role of PEAR1 in decreasing platelet counts during pregnancy and the occurrence of GT. Those with pregnancies carrying specific variants associated with declining platelet counts may experience a more pronounced decrease, thereby elevating the risk of GT. These findings lay the groundwork for further investigation into the biological mechanisms and causal implications of GT.

Morphology of immune-mediated hepatitis: A comparison between immune checkpoint inhibitor therapy and combined immune checkpoint inhibitor/anti-angiogenic therapy.

BACKGROUND: The combination of immune checkpoint inhibitors (ICIs) with anti-angiogenic drugs has shown promising anticancer effects. However, ICIs can trigger immune-mediated hepatitis (IMH). We aimed to clarify whether the combined use of anti-angiogenic drugs and ICIs would increase the severity of IMH. METHODS: One hundred IMH patients (ICI monotherapy vs. ICI plus anti-angiogenic therapy 30 vs. 70) were retrospectively enrolled. Clinicopathological parameters were compared between the two groups. RESULTS: IMH mainly showed variable degrees of panlobular hepatitis (84 %), while some cases presented mixed cholangio-hepatitic (14 %) or cholangitic (2 %) pattern. The incidence of moderate-severe injury was not significantly different between the two groups (combination vs. monotherapy 38.6 % vs. 20.0 %, p = 0.109). Specifically, the rates of marked lobular injury and portal inflammation were higher in the combination group than in the monotherapy cohort (p < 0.005), while the frequencies of interface hepatitis, bile duct injury, histiocytosis aggregates, and endothelialitis were comparable between the two groups (p > 0.05). Compared to mild IMH cases, severe IMH cases showed higher immunostaining expression levels of PD-L1 (60.7 % vs. 19.4 %, p < 0.0001). Treatments and outcomes of IMH were not significantly different between the two groups (p > 0.05). CONCLUSIONS: Compared to ICI monotherapy, the administration of anti-angiogenic drugs in combination with ICIs was not associated with increased hepatotoxicity.

Arginine Expedites Erastin-Induced Ferroptosis through Fumarate.

Ferroptosis is a newly characterized form of programmed cell death. The fundamental biochemical feature of ferroptosis is the lethal accumulation of iron-catalyzed lipid peroxidation. It has gradually been recognized that ferroptosis is implicated in the pathogenesis of a variety of human diseases. Increasing evidence has shed light on ferroptosis regulation by amino acid metabolism. Herein, we report that arginine deprivation potently inhibits erastin-induced ferroptosis, but not RSL3-induced ferroptosis, in several types of mammalian cells. Arginine presence reduces the intracellular glutathione (GSH) level by sustaining the biosynthesis of fumarate, which functions as a reactive α,ß-unsaturated electrophilic metabolite and covalently binds to GSH to generate succinicGSH. siRNA-mediated knockdown of argininosuccinate lyase, the critical urea cycle enzyme directly catalyzing the biosynthesis of fumarate, significantly decreases cellular fumarate and thus relieves erastin-induced ferroptosis in the presence of arginine. Furthermore, fumarate is decreased during erastin exposure, suggesting that a protective mechanism exists to decelerate GSH depletion in response to pro-ferroptotic insult. Collectively, this study reveals the ferroptosis regulation by the arginine metabolism and expands the biochemical functionalities of arginine.

Longstanding smoking associated with frontal brain lobe atrophy: a 32-year follow-up study in women.

OBJECTIVE: To examine the association between midlife tobacco smoking and late-life brain atrophy and white matter lesions. METHODS: The study includes 369 women from the Prospective Population Study of Women in Gothenburg, Sweden. Cigarette smoking was reported at baseline 1968 (mean age=44 years) and at follow-up in 1974-1975 and 1980-1981. CT of the brain was conducted 32 years after baseline examination (mean age=76 years) to evaluate cortical atrophy and white matter lesions. Multiple logistic regressions estimated associations between midlife smoking and late-life brain lesions. The final analyses were adjusted for alcohol consumption and several other covariates. RESULTS: Smoking in 1968-1969 (adjusted OR 1.85; 95% CI 1.12 to 3.04), in 1974-1975 (OR 2.37; 95% CI 1.39 to 4.04) and in 1980-1981 (OR 2.47; 95% CI 1.41 to 4.33) were associated with late-life frontal lobe atrophy (2000-2001). The strongest association was observed in women who reported smoking at all three midlife examinations (OR 2.63; 95% CI 1.44 to 4.78) and in those with more frequent alcohol consumption (OR 6.02; 95% CI 1.74 to 20.84). Smoking in 1980-1981 was also associated with late-life parietal lobe atrophy (OR 1.99; 95% CI 1.10 to 3.58). There were no associations between smoking and atrophy in the temporal or occipital lobe, or with white matter lesions. CONCLUSION: Longstanding tobacco smoking was mainly associated with atrophy in the frontal lobe cortex. A long-term stimulation of nicotine receptors in the frontal neural pathway might be harmful for targeted brain cell.

Role of mast cells activation in the tumor immune microenvironment and immunotherapy of cancers.

The mast cell is an important cellular component that plays a crucial role in the crosstalk between innate and adaptive immune responses within the tumor microenvironment (TME). Recently, numerous studies have indicated that mast cells related to tumors play a dual role in regulating cancers, with conflicting results seemingly determined by the degranulation medium. As such, mast cells are an ignored but very promising potential target for cancer immunotherapy based on their immunomodulatory function. In this review, we present a comprehensive overview of the roles and mechanisms of mast cells in diverse cancer types. Firstly, we evaluated the infiltration density and location of mast cells on tumor progression. Secondly, mast cells are activated by the TME and subsequently release a range of inflammatory mediators, cytokines, chemokines, and lipid products that modulate their pro-or anti-tumor functions. Thirdly, activated mast cells engage in intercellular communication with other immune or stromal cells to modulate the immune status or promote tumor development. Finally, we deliberated on the clinical significance of targeting mast cells as a therapeutic approach to restrict tumor initiation and progression. Overall, our review aims to provide insights for future research on the role of mast cells in tumors and their potential as therapeutic targets for cancer treatment.

Smart Grid Outlier Detection Based on the Minorization-Maximization Algorithm.

Outliers can be generated in the power system due to aging system equipment, faulty sensors, incorrect line connections, etc. The existence of these outliers will pose a threat to the safe operation of the power system, reduce the quality of the data, affect the completeness and accuracy of the data, and thus affect the monitoring analysis and control of the power system. Therefore, timely identification and treatment of outliers are essential to ensure stable and reliable operation of the power system. In this paper, we consider the problem of detecting and localizing outliers in power systems. The paper proposes a Minorization-Maximization (MM) algorithm for outlier detection and localization and an estimation of unknown parameters of the Gaussian mixture model (GMM). To verify the performance of the method, we conduct simulation experiments by simulating different test scenarios in the IEEE 14-bus system. Numerical examples show that in the presence of outliers, the MM algorithm can detect outliers better than the traditional algorithm and can accurately locate outliers with a probability of more than 95%. Therefore, the algorithm provides an effective method for the handling of outliers in the power system, which helps to improve the monitoring analyzing and controlling ability of the power system and to ensure the stable and reliable operation of the power system.

Proton pump inhibitors affect sperm parameters by regulating aquaporins.

Proton pump inhibitors (PPIs) were one of the most commonly used drugs in daily life. The adverse effects of long-term use of PPIs have aroused widespread controversy. It was of great significance to explore the molecular mechanism of sperm abnormality caused by PPIs. The PPI group was given omeprazole by gavage for 28 days. After the omeprazole intervention, the caudal epididymis was dissected to obtain sperms, and the sperm was counted through the microscope, as the acrosomal integrity was observed through PNA-FITC staining. The expression of aquaporins were detected by immunofluorescence and western blot in the testis, epididymis and spermatozoa. The liver cytochrome enzyme was evaluated by immunohistochemistry and western blot. We detected the serum estrogen level by ELISA, and the level of alanine transaminase (ALT) were detected through microplate method. The sperm count in PPI group was less than control group (p < 0.05), and the sperm acrosin integrity in PPI group was lower than control group (p < 0.05). In the testis, the expression of aquaporin 3 and aquaporin 8 in PPI group was higher than control group (p < 0.05), while the expression of aquaporin 7 was lower than control group (p < 0.05). In the epididymal and sperm, the expression of aquaporin 3 and aquaporin 7 in PPI group was higher than control group (p < 0.05), while the expression of aquaporin 8 in PPI group was lower than control group (p < 0.05). Meanwhile, the liver cytochrome enzyme in PPI group were lower than control group (p < 0.05), and estrogen and ALT in PPI group were higher than control group (p < 0.05). PPI may lead to the up-regulation of estrogen by inhibiting the activity of cytochrome enzyme, and then lead to the dysfunction of sperm parameters and acrosin integrity by affecting aquaporins function.

Female BMI has an effect on oocyte gene expression pattern.

Purpose: To explore the mechanisms by which abnormal female BMI affects oocyte quality, particularly whether it involves the alteration of gene expression patterns and how these patterns may impact clinical outcomes. Methods: In Part 1, we performed a retrospective study to compare the clinical outcomes between the female BMI ≥25 kg/m2 and female BMI ≤20 kg/m2 groups. In Part 2, we performed the transcriptome analyses based on the GSE87201 dataset. Results: In Part 1, among the clinical outcomes, only the grade 1-2 embryo rate at day 3 of ICSI cycles was significantly different between the two BMI groups; the other outcomes were not. In Part 2, compared with the BMI ≤20 kg/m2 group, the oocyte gene expression pattern of the BMI ≥25 kg/m2 group seemed to result in better oocyte tolerance to exogenous stress, such as intracytoplasmic sperm injection (ICSI). It seemed to explain the result of Part 1 that the BMI ≥25 kg/m2 group had better day-3 embryo quality after ICSI than the BMI ≤20 kg/m2 group. Conclusions: Abnormal female BMI affects oocyte quality by altering the gene expression patterns of oocytes. While a female BMI ≥25 kg/m2 is known to have certain detrimental effects on ART, our findings suggest that it can also confer some benefits to oocytes.

Sulforaphane Inhibits Exhaustive Exercise-Induced Liver Injury and Transcriptome-Based Mechanism Analysis.

Exhaustive exercise (EE) induces liver injury and has recently gained much attention. Sulforaphane (SFN) can protect the liver from inflammation and oxidative stress. However, the effects of SFN on EE-induced liver injury and its underlying mechanisms are still unclear. C57BL/6J mice swimming to exhaustion for seven days were used to simulate the liver injury caused by EE. Different doses of SFN (10, 30, 90 mg/kg body weight) were gavage-fed one week before and during the exercise. SFN intervention significantly reduced the EE-induced lactate dehydrogenase (LDH), creatine kinase (CK), alanine aminotransferase (ALT), and aspartate aminotransferase (AST) in the serum, as well as attenuating liver tissue morphological abnormality, oxidative stress injury, and inflammation. Liver transcriptomic analysis showed that the differentially expressed genes altered by SFN intervention in the exercise model were mainly enriched in glucose and lipid metabolism pathways. The most altered gene by SFN intervention screened by RNA-seq and validated by qRT-PCR is Ppp1r3g, a gene involved in regulating hepatic glycogenesis, which may play a vital role in the protective effects of SFN in EE-induced liver damage. SFN can protect the liver from EE-induced damage, and glucose and lipid metabolism may be involved in the mechanism of the protective effects.

Effect of COVID-19 inactivated vaccine on peripheral blood anti-ß2-GPI antibody and outcomes in vitro fertilization-embryo transplantation.

Corona Virus Disease 2019 (COVID-19) is an acute respiratory infection and a global public health event. The level of aß2GPI is significantly up-regulated in COVID-19 patients. The impact of inactivated vaccination against COVID-19 on aß2GPI and in vitro fertilization and embryo transfer (IVF-ET) remains unknown amidst the universal administration of COVID-19 vaccines. We conducted a retrospective study to assess the impact of COVID-19 inactivated vaccination on aß2GPI levels and its effect on superovulation and pregnancy outcomes. We found aß2GPI level is significantly up-regulated after vaccination. There was no statistical difference in mature egg rate, 2PN fertilization rate, day 3 high-quality embryo rate, blastocyst formation rate, embryo implantation rate and miscarriage rate between the vaccine group and control group. Our findings showed vaccination with COVID-19 inactivated vaccine can elevate the level of aß2GPI in peripheral blood but have no effect on the outcomes of controlled ovarian hyperstimulation and pregnancy in IVF-ET.

The advantages of penehyclidine hydrochloride over atropine in acute organophosphorus pesticide poisoning: A meta-analysis.

Background: Penehyclidine hydrochloride (PHC) has been used for many years as an anticholinergic drug for the treatment of acute organophosphorus pesticide poisoning (AOPP). The purpose of this meta-analysis was to explore whether PHC has advantages over atropine in the use of anticholinergic drugs in AOPP. Methods: We searched Scopus, Embase, Cochrane, PubMed, ProQuest, Ovid, Web of Science, China Science and Technology Journal Database (VIP), Duxiu, Chinese Biomedical literature (CBM), WanFang, and Chinese National Knowledge Infrastructure (CNKI), from inception to March 2022. After all qualified randomized controlled trials (RCTs) were included, we conducted quality evaluation, data extraction, and statistical analysis. Statistics using risk ratios (RR), weighted mean difference (WMD), and standard mean difference (SMD). Results: Our meta-analysis included 20,797 subjects from 240 studies across 242 different hospitals in China. Compared with the atropine group, the PHC group showed decreased mortality rate (RR=0.20, 95% confidence intervals [CI]: 0.16-0.25, P <0.001), hospitalization time (WMD=-3.89, 95% CI: -4.37 to -3.41, P <0.001), overall incidence rate of complications (RR=0.35, 95% CI: 0.28-0.43, P <0.001), overall incidence of adverse reactions (RR=0.19, 95% CI: 0.17-0.22, P <0.001), total symptom disappearance time (SMD=-2.13, 95% CI: -2.35 to -1.90, P <0.001), time for cholinesterase activity to return to normal value 50-60% (SMD=-1.87, 95% CI: -2.03 to -1.70, P <0.001), coma time (WMD=-5.57, 95% CI: -7.20 to -3.95, P <0.001), and mechanical ventilation time (WMD=-2.16, 95% CI: -2.79 to -1.53, P <0.001). Conclusion: PHC has several advantages over atropine as an anticholinergic drug in AOPP.