The purposes of the current study were to investigate the effects of a monoclonal antibody (mAb) on cytosolic phospholipase A2 alpha (cPLA2α) in mice with cerebral ischemia-reperfusion (IR) injury and to ascertain the potential mechanisms of those effects. This study evaluated whether the use of anti-cPLA2α mAb could reduce stroke injury in a mouse model of cerebral IR injury. The expression/activity of cPLA2α and cPLA2α- derived proinflammatory lipid mediators such as prostaglandin E2 (PGE2), leukotriene B4 (LTB4), lysophosphatidylcholine (LPC), and free fatty acids (FFA) was assessed. This study also evaluated neurological deficits, motor function, pathological changes, apoptosis, and the area of infarction in the injured mice. Mice treated with anti-cPLA2α mAb recovered neurological function and their condition improved, apoptosis in the brain decreased and infarct volume decreased, and expression of cPLA2α, 5-LOX, COX-2, FFA, LPC, PGE2, and LTB4 was attenuated. Our findings indicate that cPLA2α plays a key role in cerebral IR injury and that treatment with anti-cPLA2α mAb after cerebral IR injury helps to reduce levels of proinflammatory cytokines, alleviate tissue damage, and reduce levels of deleterious lipid mediators. Thus, anti-cPLA2α mAb treatment has the potential to treat ischemic brain damage.
The management of bile duct injury (BDI) remains a considerable challenge in hepatobiliary surgery. BDI is mainly iatrogenic, and mostly occurs in cholecystectomy. Laparoscopic cholecystectomy (LC) has been performed widely, however, the incidence of BDI associated with LC increases 2-3 times compared to that in open cholecystectomy (OC). BDI also occurs in robotic cholecystectomy. In China, the evidence-based Practice Guideline for Diagnosis and Treatment of BDI was published by the Biliary Surgery Group of Surgery Branch of Chinese Medical Association, with the purpose of reducing the incidence of BDI as well as promoting its optimal diagnosis and treatment. Surgery remains the mainstay of treatment for BDI and traumatic bile duct stricture. The definitive repair involves a series of procedures including exposing the proximal and distal bile duct, anastomotic bile duct tissue preparation, minimally invasive tissue anastomoses, and so on. Successful management is a surgical challenge requiring great specialized experience and precise surgical skill. The application of precision biliary surgery is recommended for promoting standardized management of BDI.
As a rare type of liver cancer, intrahepatic cholangiocarcinoma (ICC) has become an increasingly important malignancy and continues to present significant therapeutic challenges. Since coagulopathy is associated with poor prognosis in hepatocellular carcinoma (HCC), and prognostic factors of ICC after curative resection were still not clear, we aim to analyze the characteristics of ICC patients with coagulopathy and its correlation to prognosis. From January 2000 to June 2011, 541 ICC patients, after curative resection, were enrolled in our study. Survival curves were depicted by the Kaplan-Meier method and analyzed by the log-rank test. The Cox proportional hazard regression was adopted for multivariate survival analysis. Student's t test was performed to analyze the difference between the coagulopathy group and the normal group. The correlation between coagulation parameters and prognosis was also evaluated. The incidence rate of at least one coagulation parameter abnormality was 22.6% (122/541) while PT was the most common factor (8.87%, 48/541). The one-year survival rate of patients with coagulopathy was significantly lower than that of patients with normal coagulation (p < 0.01). In a univariate analysis, patients with prolonged PT was associated with shortened DFS (p < 0.05). Meanwhile, PT was negatively correlated with pre-albumin level. TNM stage, CA19-9, GGT, and pre-albumin level were independent prognostic factors of DFS in the multivariate analysis. In conclusion, the incidence rate of coagulopathy of ICC patients is lower than HCC patients. Prolonged PT, advanced TNM stage, low pre-albumin level, and high CA19-9 and GGT level were correlated with high recurrence rate and poor prognosis.
The aim of this study was to assess the prevalence of metabolic syndrome (MetS) in non-obese adults (body mass index (BMI) < 25 kg/m2) and the prevalence of obese adults (body mass index (BMI) ≥ 25 kg/m2) without MetS in Chinese Beijing urban subjects. A cross-sectional study was conducted and the subjects who came to the hospital to receive a health examination were enrolled randomly. Regardless of age stratification, men have a higher prevalence of MetS than women. Among the urban Beijing population, prevalence of metabolically obese but normal weight (MONW) is lower than metabolically healthy but obese (MHO) regardless of gender. Except for the underweight group, participants exhibit significant differences between MetS and non-MetS subgroups in all tested variables in normal weight and overweight groups, whereas MONW and MHO participants exhibit significant differences in all variables except for creatinine (CR), aspartate aminotransferase (AST), uric acid (UAC) and high-density lipoprotein cholesterol (HDL-C). Women tend to have a higher MONW prevalence but lower MHO prevalence than men. Accordingly, MetS happens more frequently among those 40-59 yr. Besides, sex, age, WC, SBP, DBP, ALT, FG, UAC, TG, HDL-C and LDL-C are risk factors for MetS after multivariate adjustment. In conclusion, the prevalence of MONW is lower than MHO regardless of gender. Women tend to have a higher MONW prevalence but lower MHO prevalence than men.
We retrospectively analyzed newborns with deafness gene mutations and summarized the relationship between genotype and phenotype to provide a basis for genetic counseling. We studied 582 subjects positive for deafness gene mutations that were treated in the otology outpatient department of Beijing Tongren Hospital, Capital Medical University, between April 2012 and April 2016. The subjects were divided into 3 categories: a diagnosed group (group A), which was further subdivided into subgroups A1 (homozygous and compound heterozygous GJB2 mutations) and A2 (homozygous and compound heterozygous SLC26A4 mutations); a drug-induced deafness group (group B, mitochondrial (Mt) gene mutations); and a mutation carrier group (group C), which was further subdivided into the subgroups C1 (GJB2 heterozygous mutations), C2 (SLC26A4 heterozygous mutations), C3 (GJB3 heterozygous mutations), and C4 (double gene mutations). Partial sequences positive for GJB2 or SLC26A4 were sequenced and analyzed for mutations. Subjects underwent otoscopic examination and comprehensive audiological evaluation, and temporal bone computerized tomography and/or inner ear magnetic resonance imaging were performed. GJB2 235delC was the most common mutation locus. The highest proportion of deafness detected during universal newborn hearing screening was for drug-induced deafness, whereas the lowest was for the diagnosed group. GJB2 gene mutations mainly resulted in flat-type, profound-to-severe sensorineural hearing loss (SNHL). SLC26A4 gene mutation was mainly associated with high-frequency drop-type and profound-severe SNHL and was closely related to enlargement of the vestibular aqueduct.
Cervical cancer is one of the most frequently diagnosed cancers and is a major cause of death from gynecologic cancers worldwide; the cancer burden from cervical cancer is especially heavy in less developed countries. Most cases of cervical cancer are caused by persistent infection with carcinogenic human papillomavirus (HPV) genotypes 16 and 18. Non-resolving inflammation caused by HPV infection provides a microenvironment that facilitates cancer development. Molecular alterations during the process of HPV-induced carcinogenesis are characterized by DNA methylation within the HPV genome, promoter hypermethylation of tumor suppressor genes in the host genome, as well as genomic instability caused by viral DNA integrating into the host genome. Catalytic polypeptide-like apolipoprotein B mRNA editing enzymes (APOBECs) normally function as part of the innate immune system. APOBEC expression is stimulated upon viral infection and plays an important role in HPV-induced cervical cancer. APOBECs catalyze the deamination of cytosine bases in nucleic acids, which leads to a conversion of target cytosine (C) to uracil (U) and consequently a change in the single-stranded DNA/RNA sequence. APOBEC proteins mediate the complex interactions between HPV and the host genome and link immunity and viral infection during HPV-driven carcinogenesis. Understanding the effects of APOBECs in HPV-induced cervical carcinogenesis will enable the development of better tools for HPV infection control and personalized prevention and treatment strategies.
Female fertility declines with age as the number of ovarian follicles decreases and aneuploidy increases. Degradation of the cohesin complex might be responsible for age-related aneuploidy. Dehydroepiandrosterone (DHEA) can improve the ovarian reserve and reduce the rate of aneuploidy, but the relationship between DHEA and cohesin levels in oocytes is still unknown. The aim of the current study was to evaluate the effect of the supplement DHEA on ovarian function, including the number of follicles and cohesin levels in oocytes. C57BL/6J mice at 3 weeks, 6 weeks, 12 weeks, 6 months, and 10 months of age were used to obtain a systematic view into follicle apoptosis and cohesin levels in oocytes. Nine-month-old C57BL/6J mice were administered saline (n = 5), 17β-estradiol (100 µg/kg per day, n = 5), or DHEA (5mg/Kg per day, n = 5). After 4 weeks, aged mice were weighed and sacrificed, and ovarian tissue samples were prepared. Anti-VASA staining and HE staining were used to count the number of follicles. Anti-γH2AX staining and TUNEL were used to measure follicle apoptosis and immunofluorescent staining was used to detect the levels of three oocyte cohesin subunits: REC8, SMC1β, and SMC3. Administration of the supplements 17β-estradiol and DHEA to aged mice increased the number of primordial and primary follicles and decreased the age-related apoptosis of follicles. Levels of the cohesin subunits REC8 and SMC1β declined with age, but DHEA and 17β-estradiol tended to delay that decline. The supplement DHEA increased the number of primordial and primary follicles in aged mice by inhibiting follicle apoptosis and tended to delay the decrease in cohesin levels in oocytes.
Respiratory Syncycial Virus (RSV) is the most important pathogen responsible for children's severe lower respiratory tract infection. So far no RSV vaccine has yet been authorized for clinical use. The main impediment that blocked development of RSV vaccine is that inactivated RSV vaccine could cause RSV vaccine-enhanced disease (RVED). The mechanism of RVED remains unclear. Recently some researchers found that insufficient activation of innate immunity, including Toll-like receptors (TLRs), might be associated with the onset of RVED. Based on the above findings, this research was conducted to further study the mechanism of RVED. We first vaccinated mice with formalin-inactivated RSV vaccine (FIRSV) and then exposed them to RSV to establish a RVED mouse model. Consequently, we found that mice previously inoculated with FIRSV showed obvious weight loss and extensive pneumonia, as well as T helper 2 cells (Th2)-biased immunity and suppressed CD8+T cell immunity after viral exposure, suggesting that we have successfully established a RVED mouse model. Then based on this model, we further added Poly(U) (TLR7/8 agonist) and CpG (TLR9 agonist) in FIRSV to see if RVED could be ameliorated. As a result, mice inoculated with FIRSV supplemented with Poly(U) and CpG had a much relieved weight loss and pneumonia, as well as suppressed Th2-biased immunity and strengthened CD8+T cell function. Thus, the insufficient stimulation of TLR7/8 and (or) TLR9 might play a role in the development of RVED, which could provide evidence for using TLR agonists as vaccine adjuvants to confer a protective immune response against RSV.
July 31, 2017 Due to the end of the Yahoo!JAPAN OpenID service, My J-STAGE will end the support of the following sign-in services with OpenID on August 26, 2017: -Sign-in with Yahoo!JAPAN ID -Sign-in with livedoor ID * After that, please sign-in with My J-STAGE ID.
July 03, 2017 There had been a service stop from Jul 2‚ 2017‚ 8:06 to Jul 2‚ 2017‚ 19:12(JST) (Jul 1‚ 2017‚ 23:06 to Jul 2‚ 2017‚ 10:12(UTC)) . The service has been back to normal.We apologize for any inconvenience this may cause you.
May 18, 2016 We have released “J-STAGE BETA site”.
May 01, 2015 Please note the "spoofing mail" that pretends to be J-STAGE.
Edited and published by : International Research and Cooperation Association for Bio & Socio-Sciences Advancement Produced and listed by : International Advancement Center for Medicine & Health Research