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Background: Polycystic ovarian syndrome (PCOS) is a common endocrine and metabolic disease in women. Hyperandrogenaemia (HA) and insulin resistance (IR) are the basic pathophysiological characteristics of PCOS. The aetiology of PCOS has not been fully identified and is generally believed to be related to the combined effects of genetic, metabolic, internal, and external factors. Current studies have not screened for PCOS susceptibility genes in a large population. Here, we aimed to study the effect of TGF-β1 methylation on the clinical PCOS phenotype. Methods: In this study, three generations of family members with PCOS with IR as the main characteristic were selected as research subjects. Through whole exome sequencing and bioinformatic analysis, TGF-β1 was screened as the PCOS susceptibility gene in this family. The epigenetic DNA methylation level of TGF-β1 in peripheral blood was detected by heavy sulfite sequencing in patients with PCOS clinically characterised by IR, and the correlation between the DNA methylation level of the TGF-β1 gene and IR was analysed. We explored whether the degree of methylation of this gene affects IR and whether it participates in the occurrence and development of PCOS. Results: The results of this study suggest that the hypomethylation of the CpG4 and CpG7 sites in the TGF-β1 gene promoter may be involved in the pathogenesis of PCOS IR by affecting the expression of the TGF-β1 gene. Conclusions: This study provides new insights into the aetiology and pathogenesis of PCOS. [ABSTRACT FROM AUTHOR]

Background: Patients with polycystic ovary syndrome (PCOS) exhibit a chronic inflammatory state, which is often accompanied by immune, endocrine, and metabolic disorders. Clarification of the pathogenesis of PCOS and exploration of specific biomarkers from the perspective of immunology by evaluating the local infiltration of immune cells in the follicular microenvironment may provide critical insights into disease pathogenesis. Methods: In this study, we evaluated immune cell subsets and gene expression in patients with PCOS using data from the Gene Expression Omnibus database and single-sample gene set enrichment analysis. Results: In total, 325 differentially expressed genes were identified, among which TMEM54 and PLCG2 (area under the curve = 0.922) were identified as PCOS biomarkers. Immune cell infiltration analysis showed that central memory CD4+ T cells, central memory CD8+ T cells, effector memory CD4+ T cells, γδ T cells, and type 17 T helper cells may affect the occurrence of PCOS. In addition, PLCG2 was highly correlated with γδ T cells and central memory CD4+ T cells. Conclusions: Overall, TMEM54 and PLCG2 were identified as potential PCOS biomarkers by bioinformatics analysis. These findings established a basis for further exploration of the immunological mechanisms of PCOS and the identification of therapeutic targets. [ABSTRACT FROM AUTHOR]

Lung adenocarcinoma exhibits high incidence and mortality rates, presenting a significant health concern. Concurrently, the COVID-19 pandemic has emerged as a grave global public health challenge. Existing literature suggests that T cells, pivotal components of cellular immunity, are integral to both antiviral and antitumor responses. Yet, the nuanced alterations and consequent functions of T cells across diverse disease states have not been comprehensively elucidated. We gathered transcriptomic data of peripheral blood mononuclear cells from lung adenocarcinoma patients, COVID-19 patients, and healthy controls. We followed a standardized analytical approach for quality assurance, batch effect adjustments, and preliminary data processing. We discerned distinct T cell subsets and conducted differential gene expression analysis. Potential key genes and pathways were inferred from GO and Pathway enrichment analyses. Additionally, we implemented Mendelian randomization to probe the potential links between pivotal genes and lung adenocarcinoma susceptibility. Our findings underscored a notable reduction in mature CD8 + central memory T cells in both lung adenocarcinoma and COVID-19 cohorts relative to the control group. Notably, the downregulation of specific genes, such as TRGV9, could impede the immunological efficacy of CD8 + T cells. Comprehensive multi-omics assessment highlighted genetic aberrations in genes, including TRGV9, correlating with heightened lung adenocarcinoma risk. Through rigorous single-cell transcriptomic analyses, this investigation meticulously delineated variations in T cell subsets across different pathological states and extrapolated key regulatory genes via an integrated multi-omics approach, establishing a robust groundwork for future functional inquiries. This study furnishes valuable perspectives into the etiology of multifaceted diseases and augments the progression of precision medicine. [ABSTRACT FROM AUTHOR]

Background: As biomarkers, microRNAs (miRNAs) are closely associated with the occurrence, progression, and prognosis of non-small cell lung cancer (NSCLC). However, the prognostic predictive value of miRNAs in NSCLC has rarely been explored. In this study, the value in prognosis prediction of NSCLC was mined based on data mining models using clinical data and plasma miRNAs biomarkers. Methods: A total of 69 patients were included in this prospective cohort study. After informed consent, they filled out questionnaires and had their peripheral blood collected. The expressions of plasma miRNAs were examined by quantitative polymerase chain reaction (qPCR). The Whitney U test was used to analyze non-normally distributed data. Kaplan-Meier was used to plot the survival curve, the log-rank test was used to compare with the overall survival curve, and the Cox proportional hazards model was used to screen the factors related to the prognosis of lung cancer. Data mining techniques were utilized to predict the prognostic status of patients. Results: We identified that smoking (HR = 2.406, 95% CI = 1.256–4.611), clinical stage III + IV (HR = 5.389, 95% CI = 2.290-12.684), the high expression group of miR-20a (HR = 4.420, 95% CI = 1.760–11.100), the high expression group of miR-197 (HR = 3.828, 95% CI = 1.778–8.245), the low expression group of miR-145 (HR = 0.286, 95% CI = 0.116–0.709), and the low expression group of miR-30a (HR = 0.307, 95% CI = 0.133–0.706) was associated with worse prognosis. Among the five data mining models, the decision trees (DT) C5.0 model performs the best, with accuracy and Area Under Curve (AUC) of 93.75% and 0.929 (0.685, 0.997), respectively. Conclusion: The results showed that the high expression level of miR-20a and miR-197, the low expression level of miR-145 and miR-30a were strongly associated with poorer prognosis in NSCLC patients, and the DT C5.0 model may serve as a novel, accurate, method for predicting prognosis of NSCLC. [ABSTRACT FROM AUTHOR]

Background: The strong invasiveness and rapid expansion of dengue virus (DENV) pose a great challenge to global public health. However, dengue epidemic patterns and mechanisms at a genetic scale, particularly in term of cross-border transmissions, remain poorly understood. Importation is considered as the primary driver of dengue outbreaks in China, and since 1990 a frequent occurrence of large outbreaks has been triggered by the imported cases and subsequently spread to the western and northern parts of China. Therefore, this study aims to systematically reveal the invasion and diffusion patterns of DENV-1 in Guangdong, China from 1990 to 2019. Methods: These analyses were performed on 179 newly assembled genomes from indigenous dengue cases in Guangdong, China and 5152 E gene complete sequences recorded in Chinese mainland. The genetic population structure and epidemic patterns of DENV-1 circulating in Chinese mainland were characterized by phylogenetics, phylogeography, phylodynamics based on DENV-1 E-gene-based globally unified genotyping framework. Results: Multiple serotypes of DENV were co-circulating in Chinese mainland, particularly in Guangdong and Yunnan provinces. A total of 189 transmission clusters in 38 clades belonging to 22 subgenotypes of genotype I, IV and V of DENV-1 were identified, with 7 Clades of Concern (COCs) responsible for the large outbreaks since 1990. The epidemic periodicity was inferred from the data to be approximately 3 years. Dengue transmission events mainly occurred from Great Mekong Subregion-China (GMS-China), Southeast Asia (SEA), South Asia Subcontinent (SASC), and Oceania (OCE) to coastal and land border cities respectively in southeastern and southwestern China. Specially, Guangzhou was found to be the most dominant receipting hub, where DENV-1 diffused to other cities within the province and even other parts of the country. Genome phylogeny combined with epidemiological investigation demonstrated a clear local consecutive transmission process of a 5C1 transmission cluster (5C1-CN4) of DENV-1 in Guangzhou from 2013 to 2015, while the two provinces of Guangdong and Yunnan played key roles in ongoing transition of dengue epidemic patterns. In contextualizing within Invasion Biology theories, we have proposed a derived three-stage model encompassing the stages of invasion, colonization, and dissemination, which is supposed to enhance our understanding of dengue spreading patterns. Conclusions: This study demonstrates the invasion and diffusion process of DENV-1 in Chinese mainland within a global genotyping framework, characterizing the genetic diversities of viral populations, multiple sources of importation, and periodic dynamics of the epidemic. These findings highlight the potential ongoing transition trends from epidemic to endemic status offering a valuable insight into early warning, prevention and control of rapid spreading of dengue both in China and worldwide. [ABSTRACT FROM AUTHOR]

Background: As an antifibrinolytic agent, tranexamic acid (TXA) is increasingly used in total knee arthroplasty (TKA) to reduce blood loss. The administration of intravenous and intra-articular TXA has been well explored, but the most efficient way to administer TXA remains in question. Peri-articular injection (PAI) of TXA is a recently mentioned method. A meta-analysis of the efficacy of PAI TXA in patients after TKA should be performed. Methods: A systematic search was performed within PubMed, Embase, and the Cochrane Library up to November 8, 2021. Two authors independently screened studies for eligibility and extracted data for analysis. The primary outcome was haemoglobin change. The secondary outcomes were haematocrit change, total drainage volume, thromboembolic events, and blood transfusion. Results: A total of ten studies were included in this meta-analysis. The results indicated that there was a significant decrease in haemoglobin change when using PAI TXA compared with no TXA (mean difference − 1.05; 95% CI − 1.28 to − 0.81; P < 0.00001; I2 = 0%), but it had no significant differences compared with IA and IV (mean difference − 0.01; 95% CI − 0.17 to − 0.14; P = 0.85; I2 = 39%). There were no significant differences between the TXA < 1.5 g subgroup (0.10, 95% CI − 0.27 to 0.46; P = 0.60; I2 = 0%) and the TXA ≥ 1.5 g subgroup (0.18, 95% CI − 0.12 to 0.48; P = 0.24; I2 = 74%). In addition, the combined group (PAI plus IV or IA) was superior to the IV or IA group in terms of haemoglobin change (mean difference − 0.51; 95% CI − 0.76 to − 0.27; P < 0.0001; I2 = 19%). Regarding haematocrit change, the pooled result showed it was significantly less in the PAI group than the non-TXA group. Similarly, comparing it against the IV subgroup, the result revealed a difference in favour of the PAI group, with a mean difference of − 1.89 g/dL (95% CI − 2.82 to − 0.95; P < 0.0001; I2 = 67%). For total drainage volume, the pooled result was in favour of PAI TXA over no TXA (297 ml, 95% CI − 497.26 to − 97.23; P = 0.004; I2 = 87%), but it had no significant difference compared with IA and IV (mean difference − 37.98; 95% CI − 115.68 to 39.71; P = 0.34; I2 = 95%). There was no significant difference in thromboembolic events (OR 0.74; 95% CI 0.25 to 2.21; P = 0.59; I2 = 0%). Blood transfusion was not significantly different between the PAI group and the non-TXA group (OR 0.50; 95% CI 0.23 to 1.06; P = 0.07; I2 = 21%), and there was no significant difference between PAI and the other two TXA injection methods (OR 0.72; 95% CI 0.41 to 1.25; P = 0.24; I2 = 19%). Conclusion: PAI has comparable effects to IV and IA injections. PAI is an alternative injection route of TXA for patients who have undergone TKA. [ABSTRACT FROM AUTHOR]

Background: More than half of the global population lives in areas at risk of dengue (DENV) transmission. Developing an efficient risk prediction system can help curb dengue outbreaks, but multiple variables, including mosquito-based surveillance indicators, still constrain our understanding. Mosquito or oviposition positive index (MOI) has been utilized in field surveillance to monitor the wild population density of Aedes albopictus in Guangzhou since 2005. Methods: Based on the mosquito surveillance data using Mosq-ovitrap collection and human landing collection (HLC) launched at 12 sites in Guangzhou from 2015 to 2017, we established a MOI-based model of the basic dengue reproduction number (R0) using the classical Ross-Macdonald framework combined with a linear mixed-effects model. Results: During the survey period, the mean MOI and adult mosquito density index (ADI) using HLC for Ae. albopictus were 12.96 ± 17.78 and 16.79 ± 55.92, respectively. The R0 estimated from the daily ADI (ADID) showed a significant seasonal variation. A 10-unit increase in MOI was associated with 1.08-fold (95% CI 1.05, 1.11) ADID and an increase of 0.14 (95% CI 0.05, 0.23) in the logarithmic transformation of R0. MOI-based R0 of dengue varied by month and average monthly temperature. During the active period of Ae. albopictus from April to November in Guangzhou region, a high risk of dengue outbreak was predicted by the MOI-based R0 model, especially from August to October, with the predicted R0 > 1. Meanwhile, from December to March, the estimates of MOI-based R0 were < 1. Conclusions: The present study enriched our knowledge about mosquito-based surveillance indicators and indicated that the MOI of Ae. albopictus could be valuable for application in estimating the R0 of dengue using a statistical model. The MOI-based R0 model prediction of the risk of dengue transmission varied by month and temperature in Guangzhou. Our findings lay a foundation for further development of a complex efficient dengue risk prediction system. [ABSTRACT FROM AUTHOR]

Background: This study aimed to establish and validate a novel clinical model to differentiate between benign and malignant solitary pulmonary nodules (SPNs). Methods: Records from 295 patients with SPNs in Sun Yat-sen University Cancer Center were retrospectively reviewed. The novel prediction model was established using LASSO logistic regression analysis by integrating clinical features, radiologic characteristics and laboratory test data, the calibration of model was analyzed using the Hosmer-Lemeshow test (HL test). Subsequently, the model was compared with PKUPH, Shanghai and Mayo models using receiver-operating characteristics curve (ROC), decision curve analysis (DCA), net reclassification improvement index (NRI), and integrated discrimination improvement index (IDI) with the same data. Other 101 SPNs patients in Henan Tumor Hospital were used for external validation cohort. Results: A total of 11 variables were screened out and then aggregated to generate new prediction model. The model showed good calibration with the HL test (P = 0.964). The AUC for our model was 0.768, which was higher than other three reported models. DCA also showed our model was superior to the other three reported models. In our model, sensitivity = 78.84%, specificity = 61.32%. Compared with the PKUPH, Shanghai and Mayo models, the NRI of our model increased by 0.177, 0.127, and 0.396 respectively, and the IDI changed − 0.019, -0.076, and 0.112, respectively. Furthermore, the model was significant positive correlation with PKUPH, Shanghai and Mayo models. Conclusions: The novel model in our study had a high clinical value in diagnose of MSPNs. [ABSTRACT FROM AUTHOR]

Background: Coronary artery disease (CAD) is a widespread heart condition caused by atherosclerosis and influences millions of people worldwide. Early detection of CAD is challenging due to the lack of specific biomarkers. The gut microbiota and host-microbiota interactions have been well documented to affect human health. However, investigation that reveals the role of gut microbes in CAD is still limited. This study aims to uncover the synergistic effects of host genes and gut microbes associated with CAD through integrative genomic analyses. Results: Herein, we collected 52 fecal and 50 blood samples from CAD patients and matched controls, and performed amplicon and transcriptomic sequencing on these samples, respectively. By comparing CAD patients with health controls, we found that dysregulated gut microbes were significantly associated with CAD. By leveraging the Random Forest method, we found that combining 20 bacteria and 30 gene biomarkers could distinguish CAD patients from health controls with a high performance (AUC = 0.92). We observed that there existed prominent associations of gut microbes with several clinical indices relevant to heart functions. Integration analysis revealed that CAD-relevant gut microbe genus Fusicatenibacter was associated with expression of CAD-risk genes, such as GBP2, MLKL, and CPR65, which is in line with previous evidence (Tang et al., Nat Rev Cardiol 16:137-154, 2019; Kummen et al., J Am Coll Cardiol 71:1184-1186, 2018). In addition, the upregulation of immune-related pathways in CAD patients were identified to be primarily associated with higher abundance of genus Blautia, Eubacterium, Fusicatenibacter, and Monoglobus. Conclusions: Our results highlight that dysregulated gut microbes contribute risk to CAD by interacting with host genes. These identified microbes and interacted risk genes may have high potentials as biomarkers for CAD. [ABSTRACT FROM AUTHOR]

Background: Gamma-aminobutyric acid (GABA) plays a significant role in the food and drug industries. Our previous study established an efficient fed-batch fermentation process for Lactobacillus brevis NCL912 production of GABA from monosodium l-glutamate; however, monosodium l-glutamate may not be an ideal substrate, as it can result in the rapid increase of pH due to decarboxylation. Thus, in this study, l-glutamic acid was proposed as a substrate. To evaluate its potential, key components of the fermentation medium affecting GABA synthesis were re-screened and re-optimized to enhance GABA production from L. brevis NCL912. Results: The initial fermentation medium (pH 3.3) used for optimization was: 50 g/L glucose, 25 g/L yeast extract, 10 mg/L manganese sulfate (MnSO4·H2O), 2 g/L Tween-80, and 220 g/L l-glutamic acid. Glucose, a nitrogen source, magnesium, and Tween-80 had notable effects on GABA production from the l-glutamic acid-based process; other factors showed no or marginal effects. The optimized levels of the four key components in the fermentation medium were 25 g/L glucose, 25 g/L yeast extract FM408, 25 mg/L MnSO4·H2O, and 2 g/L Tween-80. A simple and efficient fermentation process for the bioconversion of GABA by L. brevis NCL912 was subsequently developed in a 10 L fermenter as follows: fermentation medium, 5 L; glutamic acid, 295 g/L; inoculum, 10% (v/v); incubation temperature, 32 °C; and agitation, 100 rpm. After 48 h of fermentation, the final GABA concentration increased up to 205.8 ± 8.0 g/L. Conclusions: l-Glutamic acid was superior to monosodium l-glutamate as a substrate in the bioproduction of GABA. Thus, a high efficacy bioprocess with 205 g/L GABA for L. brevis NCL912 was established. This strategy may provide an alternative for increasing the bioconversion of GABA. [ABSTRACT FROM AUTHOR]

Background: Intestinal pathogen infections are widespread among impoverished populations. Enterocytozoon bieneusi is the most common pathogen of intestinal microsporidian species in humans worldwide. However, no epidemiological information is available on E. bieneusi infection in humans in Myanmar. The present study comprised the first identification and genotyping of E. bieneusi in humans conducted in Myanmar. Results: A total of 172 fecal specimens were collected from the Wa people (one each) in four villages of Pangsang Township of the Matman District of Shan State, Myanmar, and each participant completed a questionnaire. E. bieneusi was identified and genotyped using polymerase chain reaction (PCR) and sequence analysis of the internal transcribed spacer (ITS) region of the ribosomal RNA (rRNA) gene. The average prevalence of E. bieneusi was 8.72% (15/172), ranging from 3.85 to 13.89% by village. E. bieneusi infection was not related to any of the risk factors studied. Six genotypes were identified, comprising two known genotypes Peru6 (n = 10) and D (n = 1) and four novel genotypes (MMR23, MMR25, MMR86, and MMR87) (one each), and two people infected with genotype Peru6 were from the same family. A phylogenetic analysis based on a neighbor-joining tree of the ITS sequences of E. bieneusi indicated that all the six genotypes were clustered into group 1. Conclusions: This is the first identification and genotyping of E. bieneusi in humans in Myanmar. The observations that the two people infected with genotype Peru6 were from the same family, and that all six genotypes obtained in the present study fell into zoonotic group 1, showed the potential for anthropogenic and zoonotic transmissions. The present data argue for the importance of epidemiological control and prevention from medical sectors. [ABSTRACT FROM AUTHOR]

Background: TORCH (Toxoplasma gondii [TOX], Cytomegalovirus [CMV], Rubella virus [RV], and Herpes simplex virus [HSV]) represents pathogens known to traverse the maternal-fetal barrier and cause severe neonatal anomalies. We aimed to assess the prevalence of preconception TOX, CMV, and RV infections among women with fertility desire in southern China, and identify related risk factors. Methods: Data were obtained from a population-based cross-sectional study conducted as part of the National Free Preconception Health Examination Project. Women planning to conceive within the next 6 months in Guangdong Province were enrolled between 2014 and 2019. Information on sociodemographic, gynecological, and obstetric characteristics was collected. Sera were analyzed for TOX IgG, CMV IgG, and RV IgG antibodies using an enzyme-linked immunosorbent assay. Descriptive, univariate, and multivariate logistic regression analyses were performed to assess the association between TORCH infections and related factors. Results: Among 2,409,137 participants, the prevalence of IgG antibodies for TOX, CMV, and RV was 3.20% (95% CI: 3.18–3.22%), 77.67% (95% CI: 77.62–77.71%) and 76.03% (95% CI: 75.98–76.07%), respectively. Of all participants, 141,047 women (5.85%, 95% CI:5.83–5.88%) reported a history of immunization for RV. Women living in the Pearl River Delta, a more developed region, have significantly lower vaccination rates than those living in other regions. The seropositivity of TOX IgG was highest among women aged 35 years and above, with primary or lower education levels, and rural registration. Factors such as being older, having a higher educational level, and being of other ethnicities were associated with a higher prevalence of naturally acquired CMV and RV infections. Women living in the Pearl River Delta showed a higher risk of TOX, CMV, and RV infections, with aORs of 2.21, 4.45, and 1.76, respectively. A history of pregnancy, gynecological diseases, and sexually transmitted infections were potentially associated with TORCH infections, but this association varied across pathogens. Conclusion: The findings of this study update the baseline of preconception TORCH infections among women with fertility desire in southern China, helping to estimate the risk of congenital infection and guide the development and implementation of effective prevention measures for preconception TORCH infections. [ABSTRACT FROM AUTHOR]

Purpose: Myelin and lymphocyte protein 2 (MAL2) is mainly involved in endocytosis under physiological conditions and mediates the transport of materials across the membranes of cell and organelle. It has been reported that MAL2 is significantly upregulated in diverse cancers. This study aimed to investigate the role of MAL2 in breast cancer (BC). Methods: Bioinformatics analysis and Immunohistochemical assay were applied to detect the correlation between MAL2 expression in breast cancer tissues and the prognosis of breast cancer patients. Functional experiments were carried out to investigate the role of MAL2 in vitro and in vivo. The molecular mechanisms involved in MAL2-induced β-catenin and c-Myc expression and β-catenin/c-Myc-mediated enhancement of BC progression were confirmed by western blot, β-catenin inhibitor and agonist, Co-IP and immunofluorescence colocalization assays. Results: Results from the cancer genome atlas (TCGA) and clinical samples confirmed a significant upregulation of MAL2 in BC tissues than in adjacent non-tumor tissues. High expression of MAL2 was associated with worse prognosis. Functional experiments demonstrated that MAL2 knockdown reduced the migration and invasion associating with EMT, increased the apoptosis of BC cells in vitro and reduced the metastatic capacity in vivo. Mechanistically, MAL2 interacts with β-catenin in BC cells. MAL2 silencing reduced the expression of β-catenin and c-Myc, while the β-catenin agonist SKL2001 partially rescued the downregulation of c-Myc and inhibition of migration and invasion caused by MAL2 knockdown in BC cells. Conclusion: These observations provided evidence that MAL2 acted as a potential tumor promoter by regulating EMT and β-catenin/c-Myc axis, suggesting potential implications for anti-metastatic therapy for BC. [ABSTRACT FROM AUTHOR]

Background: TORCH infections are the most common prenatal infections causing congenital malformation and infant mortality, especially in developing countries. Migrant women might be vulnerable to TORCH infections, but little is known about the association between migration-related characteristics and TORCH infection risk. This study aimed to investigate the impact of migrant status, migration distance, and the spouse's migrant status on the TORCH epidemic among women of childbearing age. Methods: Based on the National Free Preconception Health Examination Project, we analyzed a representative dataset of TORCH infections among women of childbearing age (15–49 years old) in Guangdong Province of China (2014–2019, n = 2,451,297). The past and/or recent infection status of TORCH infections (Toxoplasma gondii [TOX], Cytomegalovirus [CMV], and Rubella virus [RV]) were identified. Demographic and migration-related characteristics were collected. We thoroughly assessed the prevalence of TORCH infections in both migrant and native women and estimated adjusted odd ratios (aOR) for migration-related characteristics using multivariable logistic regression after adjusting the other sociodemographic factors. Results: Among all 2,451,297 participants, 443,725 (18.1%) were migrant women. Migrant women presented a lower risk of past TOX infection (aOR: 0.89, 0.88–0.91) suggesting a healthy migrant effect (HME), but a higher risk of recent TOX infection (aOR: 1.88, 1.77–1.99), past CMV infection (aOR: 1.26, 1.25–1.28) and RV infection in natural ways (aOR: 1.05, 1.04–1.06). Compared with intra-provincial migrants, inter-provincial migrants had a lower past TOX infection (aOR: 0.88, 0.85–0.91), but a higher risk of recent TOX infection (aOR: 1.16, 1.05–1.27) and RV infection (aOR: 1.33, 1.31–1.36). In addition, having a migrant spouse was associated with a higher risk for all types of infection. Conclusion: This study reported the association of migrant status and migration distance with TORCH infections, although the significance and directionality of these associations varied between pathogens. The spouse's migrant status further amplified the infection risk for all types of pathogens. Our findings suggested interventions for preventing the spread of CMV and RV infection and new acquisition of TOX infection for migrants in southern China, to narrow the native-migrant health inequity and decrease the incidence of prenatal infections and related adverse outcomes. [ABSTRACT FROM AUTHOR]

Ocular diseases are closely related to the physiological changes in the eye sphere and its contents. Using biomechanical methods to explore the relationship between the structure and function of ocular tissue is beneficial to reveal the pathological processes. Studying the pathogenesis of various ocular diseases will be helpful for the diagnosis and treatment of ocular diseases. We provide a critical review of recent biomechanical analysis of ocular diseases including glaucoma, high myopia, and diabetes. And try to summarize the research about the biomechanical changes in ocular tissues (e.g., optic nerve head, sclera, cornea, etc.) associated with those diseases. The methods of ocular biomechanics research in vitro in recent years are also reviewed, including the measurement of biomechanics by ophthalmic equipment, finite element modeling, and biomechanical analysis methods. And the preparation and application of microfluidic eye chips that emerged in recent years were summarized. It provides new inspiration and opportunity for the pathogenesis of eye diseases and personalized and precise treatment. [ABSTRACT FROM AUTHOR]

Background: Endometriosis is a benign gynecological disease that shares some characteristics with malignant tumors and affects approximately 10% of women of reproductive age. Endometrioma refers to endometriosis that appears in the ovary. Metallopanstimulin-1 (MPS-1) is a component of the 40S subunit of ribosomes that has extra-ribosomal functions that contribute to the development of diseases. This study aimed to explore the expression pattern and role of MPS-1 in endometrioma development. Methods: Quantitative real time polymerase chain reaction, western blotting, immunohistochemistry, and enzyme-linked immunosorbent assay were used to determine the expression of MPS-1 in patients with endometrioma. Following the successful knockdown of MPS-1 by siRNA, CCK-8 assays, flow cytometry, and transwell assays were performed to detect ectopic endometrial stromal cells (EcESCs) proliferation, the rate of apoptosis, and cell cycle, migration, and invasion, respectively. Western blotting was used to explore the effect of MPS-1 knockdown on protein levels in the NF-κB signaling pathway. Results: The expression of MPS-1 was significantly higher in endometrioma and the serum of endometrioma patients than in the patients without endometriosis. In addition, the downregulation of MPS-1 expression inhibited EcESCs proliferation, migration, and invasion. This downregulation led to the arrest of the EcESCs cycle in the G0/G1 phase and apoptosis and depressed the NF-κB signaling pathway. Conclusion: MPS-1 can regulate EcESCs proliferation, motility, invasion, apoptosis, and cell cycle via the NF-κB signaling pathway in endometrioma. This may contribute to the formation or development of endometriotic foci. This study suggests the potential role of MPS-1 in the pathogenesis of endometriosis and enabled further research into the use of MPS-1 in the clinical diagnosis of endometrioma. [ABSTRACT FROM AUTHOR]

Background: Cesarean section (CS) rate has risen dramatically and stayed at a very high level in China over the past two to three decades. Given the short- and long-term adverse effects of CS, effective strategies are needed to reduce unnecessary CS. We aimed to evaluate whether a multifaceted intervention would decrease the CS rate in China.Methods: We carried out a cluster-randomized field trial with a multifaceted intervention in Shanghai, China, from 2015 to 2017. A total of 20 hospitals were randomly allocated into an intervention or a control group. The intervention consisted of more targeted health education to pregnant women, improved hospital CS policy, and training of midwives/doulas for 8 months. The study included a baseline survey, the intervention, and an evaluation survey. The primary outcome was the changes of overall CS rate from the pre-intervention to the post-intervention period. A subgroup analysis stratified by the Robson classification was also conducted to examine the CS change among women with various obstetric characteristics.Results: A total of 10,752 deliveries were randomly selected from the pre-intervention period and 10,521 from the post-intervention period. The baseline CS rates were 42.5% and 41.5% in the intervention and control groups, respectively, while the post-intervention CS rates were 43.4% and 42.4%, respectively. Compared with the control group, the intervention did not significantly reduce the CS rate (adjusted OR = 0.92; 95% CI 0.73, 1.15). Similar results were obtained in subgroup analyses stratified by the risk level of pregnancy, maternal age, number of previous CS, or parity. Scarred uterus and maternal request remained the primary reasons for CS after the interventions in both groups. The intervention did not alter the perinatal outcomes (adjusted change of risk score = - 0.06; 95%CI - 0.43, 0.31).Conclusions: A multifaceted intervention including more targeted prenatal health education, improved hospital CS policy, and training of midwives/doulas, did not significantly reduce the CS rate in Shanghai, China. However, our experience in implementing a multifaceted intervention may provide useful information to other similar areas with high CS use.Trial Registration: This trial was registered at the Chinese Clinical Trial Registry (www.chictr.org.cn) (ChiCTR-IOR-16009041) on 17 August 2016. [ABSTRACT FROM AUTHOR]

Background: Blastocystis is one of the most common intestinal parasites in humans and animals worldwide. At least 17 subtypes have been identified in mammals and birds. In China, although some studies have reported the occurrence of Blastocystis in humans and animals, our understanding of the role of animals in the transmission of human blastocystosis is only superficial due to a paucity of available molecular data. The aim of the present study was to understand infection rates of Blastocystis and the distribution and genetic diversity of subtypes in various mammal and bird species in northeastern China, as well as to assess the zoonotic potential of Blastocystis isolates. Methods: A total of 1265 fresh fecal specimens (1080 from ten mammal species and 185 from eight bird species) were collected in Heilongjiang, Liaoning and Jilin provinces of China. Each specimen was examined for the presence of Blastocystis by PCR amplification and sequence analysis of the partial SSU rRNA gene. Results: Fifty-four specimens (4.3%) were positive for Blastocystis. Birds (7.0%) had a higher infection rate of Blastocystis than mammals (3.8%). Blastocystis was found in seven mammal species, reindeer (6.7%), sika deer (14.6%), racoon dogs (7.5%), Arctic foxes (1.9%), dogs (2.9%), rats (3.7%) and rabbits (3.3%), as well as three bird species, pigeons (2.1%), chickens (13.0%) and red crowned cranes (14.0%). Eight subtypes were identified including ST1 (n = 5), ST3 (n = 3), ST4 (n = 13), ST6 (n = 8), ST7 (n = 6), ST10 (n = 13), ST13 (n = 4) and ST14 (n = 2). 64.8% (35/54) of Blastocystis isolates belonged to potentially zoonotic subtypes. Conclusions: To our knowledge, this is the first report of Blastocystis in reindeer (ST10 and ST13), rabbits (ST4), racoon dogs (ST3) and Arctic foxes (ST1, ST4 and ST7). The findings of potentially zoonotic subtypes suggest that the animals infected with Blastocystis might pose a threat to human health. These data will improve our understanding of the host range and genetic diversity of Blastocystis, and also help develop efficient control strategies to intervene with and prevent the occurrence of human blastocystosis in the investigated areas. [ABSTRACT FROM AUTHOR]

Background: A prospective study was performed to investigate the prevalence of colonization among ICU patients and to examine whether asymptomatic carriers were the source of subsequent C. difficile infection (CDI) and acquisition of toxigenic C. difficile.Methods: Rectal swabs were collected from adult patients on admission to and at discharge from a 50-bed medical ICU of a major referral hospital in western China, from August to November 2014. Stools were collected from patients who developed ICU-onset diarrhea. Both swabs and stools were screened for tcdB (toxin B gene) by PCR. Samples positive to tcdB were cultured for C. difficile and isolates recovered were screened for tcdB and the binary toxin genes by PCR. Strain typing was performed using multilocus sequence typing and isolates belonging to the same sequence type (ST) were further typed using multiple-locus variable number tandem repeat analysis (MLVA).Results: During the 4-month period, rectal swabs were collected from 360 (90.9 %) out of 396 patients who were admitted to the ICU. Among the 360 patients, 314 had stayed in the ICU more than 3 days, of which 213 (73.6 %) had a rectal swab collected within the 3 days prior to discharge from ICU. The prevalence of toxigenic C. difficile colonization was 1.7 % (6 cases) and 4.3 % (10 cases) on admission and discharge, respectively. Only four (1.1 %) out of 360 patients had CDI, corresponding to 10.7 cases per 10,000 ICU days. None of the four cases had toxigenic C. difficile either on admission or at discharge. Toxigenic C. difficile isolates were recovered from all swabs and stool samples positive for tcdB by PCR and belonged to 7 STs (ST2, 3, 6, 37, 54, 103 and 129). None of the isolates belonging to the same ST had identical MLVA patterns. Binary toxin genes were detected in one ST103 isolate that caused colonization.Conclusion: The prevalence of colonization with toxigenic C. difficile among patients on admission to ICU was low in our setting. ICU-acquired toxigenic C. difficile were not linked to those detected on admission. Active screening for toxigenic C. difficile may not be a resource-efficient measure in settings with a low prevalence of colonization. [ABSTRACT FROM AUTHOR]