[Quality of Life and Its Influencing Factors Among Schizophrenia Patients Living in Urban and Rural Areas].

Objective: To investigate the status quo of the quality of life of schizophrenia patients in a city in Sichuan Province and to explore, thereof, the urban-rural differences in the factors influencing their quality of life. Methods: A total of 824 schizophrenia patients were selected for the study through multistage stratified cluster random sampling method. All the subjects were selected from a pool of patients covered by the Sichuan Provincial Information System for the Comprehensive Management of Severe Mental Disorders. Questionnaire surveys were conducted with the Schizophrenia Quality of Life Scale (SQLS), the Social Support Rating Scale (SSRS), the general circumstance questionnaire, and the lifestyle questionnaire. In addition, univariate and multiple linear regression models were used to analyze the influencing factors of quality of life among schizophrenia patients living in urban areas and those in rural areas. Results: Rural patients had poorer quality of life than urban patients did in all measurement domains ( P<0.05). Marital status, vocational skills, physical exercise, and social support were influencing factors of the quality of life among urban patients ( P<0.05). Age, marital status, annual household income, vocational skills, participation in community rehabilitation activities, and the time required to walk to the nearest medical institution were influencing factors of the quality of life among rural patients ( P<0.05). Conclusion: Targeted measures for the enhancement of the quality of life of schizophrenia patients should be formulated on the basis of urban and rural characteristics in terms of economic support, vocational skills training, input in mental health services, community rehabilitation services, and social support.

The rs738409 (I148M) variant of the PNPLA3 gene and cirrhosis: a meta-analysis.

The human patatin-like phospholipase domain-containing-3 (PNPLA3) gene rs738409 C>G polymorphism is associated with several types of liver disease. The aim of this meta-analysis was to assess the risk of cirrhosis on the basis of rs738409 allele frequency and genotype. Medline, the Cochrane Library, EMBASE, and Google Scholar were searched for prospective and retrospective studies assessing the effect of the rs738409 polymorphism on liver cirrhosis. Seven studies, involving 2,023 patients with cirrhosis, were included. The G allele was associated with a significantly increased risk of cirrhosis versus the C allele [pooled odds ratio (OR) = 1.86, 95% confidence interval (CI) = 1.64-2.12, Z = 9.55, P < 0.001]. Both the GC and GG genotypes were associated with a significantly increased risk of cirrhosis versus the CC genotype (GC vs. CC: pooled OR = 1.73, 95% CI = 1.51-1.98, Z = 7.86, P < 0.001; GG vs. CC: pooled OR = 3.41, 95% CI = 2.77-4.18, Z = 11.65, P < 0.001). There was no evidence of publication bias. Our findings suggest that patients at risk for liver cirrhosis may benefit from PNPLA3 genotyping and thus more intensive monitoring if the rs738409 C>G polymorphism is identified.

Success of susceptibility-guided eradication of Helicobacter pylori in a region with high secondary clarithromycin and levofloxacin resistance rates.

BACKGROUND: Resistance to clarithromycin (CLA) and levofloxacin (LFX) of Helicobacter pylori (H. pylori) is increasing in severity, and successful eradication is essential. Presently, the eradication success rate has greatly declined, leaving a large number of patients with previous treatment histories. AIM: To investigate secondary resistance rates, explore risk factors for antibiotic resistance, and assess the efficacy of susceptibility-guided therapy. METHODS: We recruited 154 subjects positive for Urea Breath Test who attended The First Affiliated Hospital of China Medical University between July 2022 and April 2023. Participants underwent a string test after an overnight fast. The gastric juice was obtained and transferred to vials containing storage solution. Subsequently, DNA extraction and the specific DNA amplification were performed using quantitative polymerase chain reaction (qPCR). Demographic information was also analyzed as part of the study. Based on these results, the participants were administered susceptibility-guided treatment. Efficacy was compared with that of the empiric treatment group. RESULTS: A total of 132 individuals tested positive for the H. pylori ureA gene by qPCR technique. CLA resistance rate reached a high level of 82.6% (n = 109), LFX resistance rate was 69.7% (n = 92) and dual resistance was 62.1% (n = 82). Gastric symptoms [odds ratio (OR) = 2.782; 95% confidence interval (95%CI): 1.076-7.194; P = 0.035] and rural residence (OR = 5.152; 95%CI: 1.407-18.861; P = 0.013) were independent risk factors for secondary resistance to CLA and LFX, respectively. A total of 102 and 100 individuals received susceptibility-guided therapies and empiric treatment, respectively. The antibiotic susceptibility-guided treatment and empiric treatment groups achieved successful eradication rates of 75.5% (77/102) and 59.0% (59/411) by the intention-to-treat (ITT) analysis and 90.6% (77/85) and 70.2% (59/84) by the per-protocol (PP) analysis, respectively. The eradication rates of these two treatment strategies were significantly different in both ITT (P = 0.001) and PP (P = 0.012) analyses. CONCLUSION: H. pylori presented high secondary resistance rates to CLA and LFX. For patients with previous treatment failures, treatments should be guided by antibiotic susceptibility tests or regional antibiotic resistance profile.

XRCC1 Arg399Gln polymorphism contributes to increased risk of colorectal cancer in Chinese population.

Previous studies investigating the association between X-ray repair cross-complementation group 1 (XRCC1) Arg399Gln polymorphism and colorectal cancer risk in Chinese provided inconsistent findings. To assess the association in Chinese population, a meta-analysis was performed. Eligible studies were searched in Pubmed, Emabse, and China National Knowledge Infrastructure databases. Odds ratios (OR) with the corresponding 95 % confidence intervals (95 %CI) were pooled to assess the association. Seven case-control studies involving a total of 2136 colorectal cancer cases and 3168 controls were finally included in the meta-analysis. Our analysis suggested that the variant genotypes of XRCC1 Arg399Gln were associated with an increased risk of colorectal cancer in Chinese population (Gln vs. Arg: random effect model OR = 1.24, 95 %CI = 1.01-1.52, P = 0.041; GlnGln vs. ArgArg: random effect model OR = 1.52, 95 %CI = 1.07-2.15, P = 0.019; and Recessive model: fixed effect model OR = 1.37, 95 %CI = 1.12-1.67, P = 0.002). There was low risk of publication bias in present meta-analysis. Our meta-analysis provides an evidence for the association between XRCC1 Arg399Gln polymorphism and colorectal cancer risk in Chinese population, and XRCC1 Arg399Gln variant genotypes contribute to increased risk of colorectal cancer in Chinese.

Laparoscopic management of second trimester ruptured cornual heterotopic pregnancy with subsequent live birth delivery: A case report and literature review.

OBJECTIVE: Heterotopic pregnancy (HP) is the coexistence of extra- and intrauterine gestation implantation sites. A rare case of a second-trimester ruptured cornual HP (CHP) treated with laparoscopic cornual resection with the primary repair is presented. Risk factors, clinical presentations, treatments, and outcomes of CHPs are also reviewed. CASE REPORT: A 35-year-old pregnant woman with CHP presented with lower abdominal pain with hemoperitoneum and her hemoglobin level dropped. Laparoscopic management of a ruptured HP was performed, leaving the surplus intrauterine fetus intact. She delivered a 2360 g male infant via cesarean section at 34 weeks' gestation due to preterm premature rupture of membranes. We found a well-healed wound over the left uterine cornua during the cesarean section. CONCLUSION: Ruptured CHP is a rare but life-threatening complication of an obstetric emergency. Although the pregnant uterus becomes congested and fragile, using reliable laparoscopic energy devices and barbed sutures, successful treatment is feasible.

High birth weight and greater gestational age at birth in singletons born after frozen compared to fresh embryo transfer.

OBJECTIVE: While many studies agree that the fetal birth weight is higher after frozen embryo transfer (FET), few studies have explored the difference in fetal weight change during such pregnancies. This cohort study was to identify the difference in fetal birth weight and gestational age at birth between singletons born following fresh ET and those born following FET. MATERIALS AND METHODS: This was a hospital-based cohort study using clinical data from the Kaohsiung Chang Gung Memorial Hospital Obstetric and Neonatal Database from January 1, 2007, to December 1, 2018. A sample of 784 eligible women who had singleton pregnancies and live-born deliveries after 428 fresh ET or 356 FET between January 2007 and December 2018. RESULTS: Compared with those in the fresh ET group, singletons in the FET group had higher birth weight (3137 g [2880-3441 g] vs. 3060 g [2710-3340 g], p < 0.05), were born later (39.0 weeks of gestation [38.0-40.0 weeks] vs. 38.0 weeks of gestation [37.0-39.0 weeks], p < 0.05), and had a lower incidence of preterm birth (10.4% vs. 15.2%, p < 0.05). The difference in birth weight was not associated with maternal body weight (BW) or body mass index, increase in maternal BW in the third trimester, but related to the total increase in maternal BW during pregnancy. CONCLUSIONS: The birthweight of singletons born following FET and fresh ET became significant in the late third trimester. The main reason is that singletons conceived from FET were at a lower relative risk of preterm delivery and had a higher gestational age at birth.

Endoscopic Ruler for varix size measurement: A multicenter pilot study.

BACKGROUND: We invented Endoscopic Ruler, a new endoscopic device to measure the size of varices in patients with cirrhosis and portal hypertension. AIM: To assess the feasibility and safety of Endoscopic Ruler, and evaluate the agreement on identifying large oesophageal varices (OV) between Endoscopic Ruler and the endoscopists, as well as the interobserver agreement on diagnosing large OV using Endoscopic Ruler. METHODS: We prospectively and consecutively enrolled patients with cirrhosis from 11 hospitals, all of whom got esophagogastroduodenoscopy (EGD) with Endoscopic Ruler. The primary study outcome was a successful measurement of the size of varices using Endoscopic Ruler. The secondary outcomes included adverse events, operation time, the agreement of identifying large OV between the objective measurement of Endoscopic Ruler and the empirical reading of endoscopists, together with the interobserver agreement on diagnosing large OV by Endoscopic Ruler. RESULTS: From November 2020 to April 2022, a total of 120 eligible patients with cirrhosis were recruited and all of them underwent EGD examinations with Endoscopic Ruler successfully without any adverse event. The median operation time of Endoscopic Ruler was 3.00 min [interquartile range (IQR): 3.00 min]. The kappa value between Endoscopic Ruler and the endoscopists while detecting large OV was 0.52, demonstrating a moderate agreement. The kappa value for diagnosing large OV using Endoscopic Ruler among the six independent observers was 0.77, demonstrating a substantial agreement. CONCLUSION: The data demonstrates that Endoscopic Ruler is feasible and safe for measuring the size of varices in patients with cirrhosis and portal hypertension. Endoscopic Ruler is potential to promote the clinical practice of the two-grade classification system of OV.

CDH1 promoter polymorphism and stomach cancer susceptibility.

The relationship of stomach cancer susceptibility and the presence of E-cadherin (CDH1) promoter -160 C/A polymorphism had been reported with conflicting results. To further explore the association of this polymorphism with stomach cancer susceptibility, we performed an extensive search of relevant studies and carried out a meta-analysis to obtain a more precise estimate. A total of 16 studies including 2,611 cases and 3,788 controls were involved in this meta-analysis. When all studies involved, the meta-analysis results suggest no statistically significant association between CDH1 -160 C/A polymorphism and stomach cancer risk (CA vs. CC: OR = 1.01, 95% CI: 0.85-1.19; AA vs. CC: OR = 1.05, 95% CI: 0.75-1.46; dominant model: OR = 1.02, 95% CI: 0.86-1.20; recessive model: OR = 1.04, 95% CI: 0.76-1.41). When subgroup analyses were performed by ethnicity, the A-allele carriers conferred a decreased stomach cancer risk in Asians (AA vs. CC: OR = 0.67, 95% CI: 0.47-0.96; dominant model: OR = 0.85, 95% CI: 0.72-0.99), but no statistically significant association was found in Caucasians. In conclusion, this meta-analysis suggests that CDH1 -160 A-allele may play a protective role of stomach cancer development in Asians but not in Caucasians.

The role of bile acid metabolism in the occurrence and development of NAFLD.

Non-alcoholic fatty liver disease (NAFLD) has become one of the important causes of cirrhosis and liver cancer, resulting in a huge medical burden worldwide. Currently, effective non-invasive diagnostic indicators and drugs for NAFLD are still lacking. With the development of metabolomics technology, the changes in metabolites during the development of NAFLD have been gradually revealed. Bile acid (BA) is the main endpoint of cholesterol metabolism in the body. In addition, it also acts as a signaling factor to regulate metabolism and inflammation in the body through the farnesyl X receptor and G protein-coupled BA receptor. Studies have shown that BA metabolism is associated with the development of NAFLD, but a large number of animal and clinical studies are still needed. BA homeostasis is maintained through multiple negative feedback loops and the enterohepatic circulation of BA. Recently, treatment of NAFLD by interfering with BA synthesis and metabolism has become a new research direction. Here, we review the changes in BA metabolism and its regulatory mechanisms during the development of NAFLD and describe the potential of studies exploring novel non-invasive diagnostic indicators and therapeutic targets for NAFLD based on BA metabolism.

Case Report: A Rare Heterozygous ATP8B1 Mutation in a BRIC1 Patient: Haploinsufficiency?

Benign recurrent intrahepatic cholestasis (BRIC) is an autosomal recessive disorder characterized by recurrent cholestasis. ATPase class I, type 8B, member 1 (ATP8B1) encodes familial intrahepatic cholestasis 1 (FIC1), which acts as a phosphatidylserine reversing enzyme in the tubule membrane of hepatocytes to mediate the inward translocation of phosphatidylserine (PS). At present, dozens of ATP8B1 pathogenic mutations have been identified that mainly cause BRIC1 and progressive familial intrahepatic cholestasis 1 (PFIC1). The diagnosis of BRIC1 is based on symptoms, laboratory tests, imaging, liver histology, and genetic testing. BRIC1 treatment seeks to prevent recurrence and reduce disease severity. At present, the main treatment methods include ursodeoxycholic acid (UDCA), rifampin, cholestyramine and haemofiltration, and endoscopic nasobiliary drainage (ENBD). Here, we report a 17-year-old patient with cholestasis who has a rare heterozygous ATP8B1 gene mutation (p.T888K). The patient was treated with UDCA, glucocorticoids and haemofiltration, after which bilirubin levels gradually returned to normal. This case was thought to be caused by an ATP8B1 heterozygous mutation, which may be related to haploinsufficiency (HI).

Validation of Non-Invasive Preimplantation Genetic Screening Using a Routine IVF Laboratory Workflow.

Embryo selection is needed to optimize the chances of pregnancy in assisted reproduction technology. This study aimed to validate non-invasive preimplantation genetic testing for aneuploidy (niPGT-A) using a routine IVF laboratory workflow. Can niPGT-A combined with time-lapse morphokinetics provide a better embryo-selection strategy? A total of 118 spent culture mediums (SCMs) from 32 couples were collected. A total of 40 SCMs and 40 corresponding trophectoderm (TE) biopsy samples (n = 29) or arrested embryos (n = 11) were assessed for concordance. All embryos were cultured to the blastocyst stage (day 5 or 6) in a single-embryo culture time-lapse incubator. The modified multiple annealing and looping-based amplification cycle (MALBAC) single-cell whole genome amplification method was used to amplify cell-free DNA (cfDNA) from the SCM, which was then sequenced on the Illumina MiSeq system. The majority of insemination methods were conventional IVF. Low cfDNA concentrations were noted in this study. The amplification niPGT-A and conventional PGT-A was 67.7%. Based on this study, performing niPGT-A without altering the daily laboratory procedures cannot provide a precise diagnosis. However, niPGT-A can be applied in clinical IVF, enabling the addition of blastocysts with a better prediction of euploidy for transfer.

Novel mechanism of hepatobiliary system damage and immunoglobulin G4 elevation caused by Clonorchis sinensis infection.

Clonorchis sinensis infection is still a major public health problem. It is estimated that more than 15 million people worldwide are infected, especially in Northeast China, Taiwan, South Korea, and North Vietnam. The detection of Clonorchis sinensis eggs in feces and bile is still the only gold standard for the diagnosis of Clonorchis sinensis infection, and new detection methods are needed to improve the detection rate. After Clonorchis sinensis invades the human body, it mainly parasitizes the hepatobiliary tract. Therefore, it is closely related to hepatobiliary diseases such as cholangitis, bile duct stones, liver fibrosis, and cholangiocarcinoma. The increase in immunoglobulin G4 (IgG4) caused by Clonorchis sinensis infection is rare and there are few reports about the relevant mechanism. It may be related to the inflammatory factors interleukin (IL)-4, IL-10, and IL-13 produced by human phagocytes, T cells, B cells, and other immune cells in the process of resisting the invasion of Clonorchis sinensis. However, this finding still needs further clarification and confirmation. This article reviews the epidemiology, clinical manifestations, serology, imaging, pathogenic mechanism, and control measures of Clonorchis sinensis infection to help establish the diagnostic process for Clonorchis sinensis. We report novel mechanisms of IgG4 elevation due to Clonorchis sinensis infection to provide more experience and a theoretical basis for clinical diagnosis and treatment of this infection.

Distinctive gut microbial dysbiosis between chronic alcoholic fatty liver disease and metabolic-associated fatty liver disease in mice.

The gut microbiota, which may affect normal physiological and biochemical functions, has an important role in the development of human liver diseases. The aim of the present study was to investigate differences in the gut microbiota between chronic alcoholic fatty liver disease (AFLD) and metabolic-associated fatty liver disease (MAFLD). AFLD was induced by chronic alcohol administration and MAFLD was induced by a Western-style diet in C57BL/6 mice. After 8 weeks, the levels of plasma alanine aminotransferase (ALT), aspartate aminotransferase (AST), triglyceride (TG), total cholesterol (TC), lipopolysaccharide (LPS), tumor necrosis factor (TNF)-α, interleukin (IL)-6, IL-1ß and IL-10 were assessed and H&E staining of mouse liver tissue was performed. High-throughput sequencing of 16S ribosomal DNA from the intestinal contents was used to analyze the different effects of AFLD and MAFLD on the gut microbiota. Differences in the gut microbiota composition were assessed by the t-test. The results revealed increases in LPS, ALT, AST, TG, IL-1ß and TNF-α in the AFLD group. Compared with those in the MAFLD control group, the MAFLD group exhibited increased plasma ALT, TG, TC, IL-6, IL-1ß and TNF-α levels and decreased plasma IL-10 levels. In addition, the α- and ß-diversities revealed that the AFLD and MAFLD groups exhibited obvious changes in the gut structure (with an increase in abundance in the AFLD group and a decrease in abundance in the MAFLD group). In comparison to the AFLD control group, Enterococcaceae were the most abundant bacteria at the family level and Enterococcus and Streptococcus were the most abundant bacteria at the genus level in the AFLD group. However, in the MAFLD group, Lachnospiraceae was the most abundant at the family level, with increases in Erysipelatoclostridium, Gordonibacter and Streptococcus at the genus level and a decrease in the genus Bifidobacterium. In conclusion, the present study confirmed that the AFLD and MAFLD groups harbored differences in the gut microbiota. The marked differences in the gut microbiota at the family and genus levels may contribute to the development process of FLD.

Eosinophilic pancreatitis: a review of the pathophysiology, diagnosis, and treatment.

Eosinophilic pancreatitis (EP) is an extremely rare disease caused by purely eosinophilic infiltration of the pancreas. EP is prone to being misdiagnosed as pancreatic cancer, causing unnecessary economic and physical harm to the patient. We report three cases of EP that were cured by steroids without relapse from 2017 to now. The clinical data of the three patients, including clinical manifestations, serological manifestations, imaging (ultrasound, computed tomography, and MRI), pathological diagnosis and treatment, and telephone follow-up of all patients, were retrospectively analysed. In addition, a literature search was conducted on the Web of Science and PubMed databases using key terms related to EP, considering case reports with no restrictions on the date of publication or language. In conclusion, we analysed 19 cases and determined the diagnostic criteria for EP. The diagnostic algorithm for EP can be used to diagnose EP easily. We hope that our standards and algorithm can reduce the rate of misdiagnosis and contribute to clinical diagnosis and treatment. In addition, we expect to evaluate more EP cases to test our diagnostic criteria and design a systematic diagnostic flow chart.

Human herpesvirus 8 viral FLICE-inhibitory protein retards cell proliferation via downregulation of Id2 and Id3 expression.

Death receptor-mediated apoptosis is potently inhibited by viral FLIP (FLICE/caspase 8 inhibitory protein) through reduced activation of procaspase 8. In this study, we show that the human herpesvirus 8-encoded vFLIP retards cell proliferation. Overexpression of vFLIP caused cell cycle arrest, with an apparent decrease of cells in the S phase. The Id (inhibitor of DNA binding) proteins are considered as dominant negative regulators of differentiation pathways, but positive regulators of cellular proliferation. The mechanisms by which Id proteins promote the cell cycle are diverse, but appear to involve affecting the expression of cell cycle regulators. RT-PCR results demonstrated that the expression of vFLIP decreased the expression levels of Id2 and Id3 as well as cyclin E and cyclin A compared with the vFLIP-null cells. These indicate that vFLIP affects cell proliferation by decreasing the expression levels of cell cycle regulatory proteins.

[The relationship of leptin and adiponectin with insulin resistance in nonalcoholic fatty liver disease].

OBJECTIVES: To investigate the serum leptin and adiponectin levels in nonalcoholic fatty liver disease (NAFLD) patients, and their relationship with insulin resistance. METHODS: A total of 120 cases were enrolled and divided into two groups: NAFLD group (n = 60) and normal control group (n = 60). The serum levels of leptin and adiponectin were measured by ELISA. The body mass index (BMI), waist-to-hip ratio (WHR), triglyceride (TG), total cholesterol (Tchol), high-density lipoprotein cholesterol (HDL-C) , aspartate aminotransferase (AST), alanine aminotransferase (ALT), gamma-glutamyl transpeptidase (GGT), fasting blood glucose (FBG) and HOMA-IR (homeostasis model assessment insulin resistance) were detected and analyzed. RESULTS: Compared with control group, the serum leptin level in NAFLD group was Significantly higher [(12.37+/-1.99) microg/L vs (5.20+/-1.03) microg/L, P less than 0.01], while the serum adiponectin level was significantly lower [(12.69+/-2.83) mg/L vs (22.83+/-4.61) mg/L, P less than 0.01]. HOMA-IR was also much higher in NAFLD group than that in control group[(4.86+/-0.63) vs (1.91+/-0.41), P less than 0.01]. Logistic regression analysis showed that leptin was positively correlated with WHR (beta value = 8.175, P less than 0.01), HOMA-IR (beta value = 0.974, P less than 0.01 ), FBG (beta value = 0.564, P less than 0.01 ). In contrast, adiponectin inversely associated with HOMA-IR (beta value = -0.495, P less than 0.01 ) and BMI (beta value = -0.314, P less than 0.01) respectively. CONCLUSION: The increased serum leptin level and decreased serum adiponectin level in NAFLD patients independently associated with HOMA-IR.

Pituitary stalk interruption syndrome and liver changes: From clinical features to mechanisms.

Pituitary stalk interruption syndrome (PSIS) is a rare congenital abnormality characterized by thinning or disappearance of the pituitary stalk, hypoplasia of the anterior pituitary and an ectopic posterior pituitary. Although the etiology of PSIS is still unclear, gene changes and perinatal adverse events such as breech delivery may play important roles in the pathogenesis of PSIS. PSIS can cause multiple hormone deficiencies, such as growth hormone, which then cause a series of changes in the human body. On the one hand, hormone changes affect growth and development, and on the other hand, they could affect human metabolism and subsequently the liver resulting in nonalcoholic fatty liver disease (NAFLD). Under the synergistic effect of multiple mechanisms, the progression of NAFLD caused by PSIS is faster than that due to other causes. Therefore, in addition to early identification of PSIS, timely hormone replacement therapy and monitoring of relevant hormone levels, clinicians should routinely assess the liver function while managing PSIS.

Pathogenesis of liver injury in Takayasu arteritis: advanced understanding leads to new horizons.

Liver injury in Takayasu arteritis (TA) is a rare phenomenon. Most symptoms are nonspecific, and the exact pathogenesis remains to be elucidated. Early diagnosis and new treatment methods are important for an improved prognosis. A summary of the clinical information and mechanistic analyses may contribute to making an early diagnosis and development of new treatment methods. A PubMed search was conducted using the specific key words "Takayasu arteritis" and "liver" or "hepatitis" or "hepatic". Symptoms and treatment of TA with an accompanying liver injury were reviewed retrospectively. Many factors are presumed to be involved in the mechanism of TA with liver injury, including the immune response, genes, infections, and gut microbiota. There are several lines of evidence indicating that immune dysfunction is the main pathogenic factor that triggers granuloma formation in TA patients. However, the role of genetics and infections has not been fully confirmed. Recently, the gut microbiota has emerged as an essential component in the process. We reviewed in detail the current concepts that support the complex pathogenesis of TA accompanied by liver injury, and we presented recent theories from the literature. Finally, we discussed future research directions of liver injury in TA.

Mesh-related complications in single-incision transvaginal mesh (TVM) and laparoscopic abdominal sacrocolpopexy (LASC).

OBJECTIVE: Few studies have investigated the long-term impact of synthetic mesh reconstructive surgery for pelvic organ prolapse (POP) on patient outcomes. This study aimed to examine the incidence and risk factors of mesh exposure and the subsequent requirement for surgical interventions due to mesh-related complications. MATERIALS AND METHODS: This retrospective study was conducted from November 2010 to April 2018. We recruited women with Pelvic Organ Prolapse Quantification (POP-Q) stage 3 or 4 who underwent mesh reconstructive surgery for POP, and enrolled 487 women who received transvaginal mesh (TVM) and 110 women who received laparoscopic abdominal sacrocolpopexy (LASC). Assessments included mesh exposure rate and mesh-related complications requiring surgical interventions in both groups. RESULTS: In the LASC group, the overall mesh-related complication rate was 8.18% over a mean follow-up period of 18 months. Concomitant laparoscopic-assisted vaginal hysterectomy was associated with mesh exposure (OR = 9.240; 95% CI = 1.752-48.728). No patients in the concurrent supracervical hysterectomy group were exposed to mesh. In the single-incision TVM group, the overall rate of mesh-related complications was 3.29% over a mean follow-up period of 19 months. Concomitant total vaginal hysterectomy was also a risk factor for mesh exposure (OR = 4.799; 95% CI = 1.313-17.359). CONCLUSION: Preserving the cervix or uterus decreased the rate of mesh exposure in those undergoing TVM and LASC surgery. The overall rate of mesh-related complications was low after up to 8 years of follow-up.

Overexpression of long non-coding RNA Rian attenuates cell apoptosis from cerebral ischemia-reperfusion injury via Rian/miR-144-3p/GATA3 signaling.

Long non-coding RNAs (lncRNAs) have been identified in cerebral ischemia-reperfusion (I/R) injury nowadays. Herein, we uncovered the function and underlying mechanism of the lncRNA Rian in cerebral I/R injury. The oxygen-glucose deprivation model in N2a cells was offered to mimic cerebral I/R injury in vitro. Trypan blue staining, reactive oxygen species (ROS) production, and caspase-3 activity were used to evaluate cell apoptosis. Then, middle cerebral artery occlusion was conducted to evaluate the function of lncRNA Rian in mice. Real-time PCR and western blotting were performed to determine the expression of lncRNA Rian, miR-144-3p, GATA binding protein 3 (GATA3), caspase-3, Bax, and Bcl-2. The results showed that both Rian and GATA3 were downregulated, and miR-144-3p was upregulated in cerebral I/R injury in vitro and in vivo. Overexpression of Rian could inhibit the cell apoptosis induced by oxygen-glucose deprivation. Furthermore, overexpression of Rian distinctly reduced the infarct size, and it also improved the neurological score. Overexpression of Rian could abolish miR-144-3p-mediated I/R injury in vitro and in vivo. Besides, GATA3 was the target of miR-144-3p and GATA3 could be regulated co-operatively by miR-144-3p and Rian. Consequently, these findings showed that the Rian/miR-144-3p/GATA3 axis is an essential signaling in cerebral I/R injury. The lncRNA Rian may serve as a potential target for novel treatment in patients with ischemic stroke.