Background: Obesity and chronic pain are related in both directions, according to earlier observational research.This research aimed to analyze the causal association between obesity and chronic pain at the genetic level, as well as to assess whether common factors mediate this relationship. Methods: This study used bidirectional two sample Mendelian randomization (MR) technique to analyze the association between obesity and chronic pain. Obesity's summary genome-wide association data were obtained from European ancestry groups, as measured by body mass index (BMI), waist-to-hip ratio, waist circumference (WC), and hip circumference (HC), genome-wide association study data for chronic pain also came from the UK population, including chronic pain at three different sites (back, hip, and headache), chronic widespread pain (CWP), and multisite chronic pain (MCP). Secondly, a two-step MR and multivariate MR investigation was performed to evaluate the mediating effects of several proposed confounders. Results: The authors discovered a link between chronic pain and obesity. More specifically, a sensitivity analysis was done to confirm the associations between greater BMI, WC, and HC with an increased risk of CWP and MCP.Importantly, the intermediate MR results suggest that education levels and smoking initiation may mediate the causal relationship between BMI on CWP, with a mediation effect of 23.08% and 15.38%, respectively. Conclusions The authors’ findings demonstrate that the importance of education and smoking in understanding chronic pain’s pathogenesis, which is important for the primary prevention and prognosis of chronic pain.

Background: Obesity and chronic pain are related in both directions, according to earlier observational research.This research aimed to analyze the causal association between obesity and chronic pain at the genetic level, as well as to assess whether common factors mediate this relationship. Methods: This study used bidirectional two sample Mendelian randomization (MR) technique to analyze the association between obesity and chronic pain. Obesity's summary genome-wide association data were obtained from European ancestry groups, as measured by body mass index (BMI), waist-to-hip ratio, waist circumference (WC), and hip circumference (HC), genome-wide association study data for chronic pain also came from the UK population, including chronic pain at three different sites (back, hip, and headache), chronic widespread pain (CWP), and multisite chronic pain (MCP). Secondly, a two-step MR and multivariate MR investigation was performed to evaluate the mediating effects of several proposed confounders. Results: The authors discovered a link between chronic pain and obesity. More specifically, a sensitivity analysis was done to confirm the associations between greater BMI, WC, and HC with an increased risk of CWP and MCP.Importantly, the intermediate MR results suggest that education levels and smoking initiation may mediate the causal relationship between BMI on CWP, with a mediation effect of 23.08% and 15.38%, respectively. Conclusions The authors’ findings demonstrate that the importance of education and smoking in understanding chronic pain’s pathogenesis, which is important for the primary prevention and prognosis of chronic pain.

Background: Obesity and chronic pain are related in both directions, according to earlier observational research.This research aimed to analyze the causal association between obesity and chronic pain at the genetic level, as well as to assess whether common factors mediate this relationship. Methods: This study used bidirectional two sample Mendelian randomization (MR) technique to analyze the association between obesity and chronic pain. Obesity's summary genome-wide association data were obtained from European ancestry groups, as measured by body mass index (BMI), waist-to-hip ratio, waist circumference (WC), and hip circumference (HC), genome-wide association study data for chronic pain also came from the UK population, including chronic pain at three different sites (back, hip, and headache), chronic widespread pain (CWP), and multisite chronic pain (MCP). Secondly, a two-step MR and multivariate MR investigation was performed to evaluate the mediating effects of several proposed confounders. Results: The authors discovered a link between chronic pain and obesity. More specifically, a sensitivity analysis was done to confirm the associations between greater BMI, WC, and HC with an increased risk of CWP and MCP.Importantly, the intermediate MR results suggest that education levels and smoking initiation may mediate the causal relationship between BMI on CWP, with a mediation effect of 23.08% and 15.38%, respectively. Conclusions The authors’ findings demonstrate that the importance of education and smoking in understanding chronic pain’s pathogenesis, which is important for the primary prevention and prognosis of chronic pain.

Background: Obesity and chronic pain are related in both directions, according to earlier observational research.This research aimed to analyze the causal association between obesity and chronic pain at the genetic level, as well as to assess whether common factors mediate this relationship. Methods: This study used bidirectional two sample Mendelian randomization (MR) technique to analyze the association between obesity and chronic pain. Obesity's summary genome-wide association data were obtained from European ancestry groups, as measured by body mass index (BMI), waist-to-hip ratio, waist circumference (WC), and hip circumference (HC), genome-wide association study data for chronic pain also came from the UK population, including chronic pain at three different sites (back, hip, and headache), chronic widespread pain (CWP), and multisite chronic pain (MCP). Secondly, a two-step MR and multivariate MR investigation was performed to evaluate the mediating effects of several proposed confounders. Results: The authors discovered a link between chronic pain and obesity. More specifically, a sensitivity analysis was done to confirm the associations between greater BMI, WC, and HC with an increased risk of CWP and MCP.Importantly, the intermediate MR results suggest that education levels and smoking initiation may mediate the causal relationship between BMI on CWP, with a mediation effect of 23.08% and 15.38%, respectively. Conclusions The authors’ findings demonstrate that the importance of education and smoking in understanding chronic pain’s pathogenesis, which is important for the primary prevention and prognosis of chronic pain.

Background: Obesity and chronic pain are related in both directions, according to earlier observational research.This research aimed to analyze the causal association between obesity and chronic pain at the genetic level, as well as to assess whether common factors mediate this relationship. Methods: This study used bidirectional two sample Mendelian randomization (MR) technique to analyze the association between obesity and chronic pain. Obesity's summary genome-wide association data were obtained from European ancestry groups, as measured by body mass index (BMI), waist-to-hip ratio, waist circumference (WC), and hip circumference (HC), genome-wide association study data for chronic pain also came from the UK population, including chronic pain at three different sites (back, hip, and headache), chronic widespread pain (CWP), and multisite chronic pain (MCP). Secondly, a two-step MR and multivariate MR investigation was performed to evaluate the mediating effects of several proposed confounders. Results: The authors discovered a link between chronic pain and obesity. More specifically, a sensitivity analysis was done to confirm the associations between greater BMI, WC, and HC with an increased risk of CWP and MCP.Importantly, the intermediate MR results suggest that education levels and smoking initiation may mediate the causal relationship between BMI on CWP, with a mediation effect of 23.08% and 15.38%, respectively. Conclusions The authors’ findings demonstrate that the importance of education and smoking in understanding chronic pain’s pathogenesis, which is important for the primary prevention and prognosis of chronic pain.

Viral hepatitis is a common infectious disease caused by a variety of hepatitis viruses,mainly including types A,B,C,D and E,among which hepatitis B virus(HBV)and hepatitis C virus(HCV)infection are more common.It is one of the important causes of liver cirrhosis and hepatocellular carcinoma.In the case of pregnancy,the interaction between pregnancy and viral infection must be considered,including the impact of the virus on fetal development,the impact on maternal health,and the progression of the disease itself caused by pregnancy,among which the prevention of mother-to-child transmission is the key to reducing the global burden of chronic viral hepatitis.In September 2023,the American College of Obstetricians and Gynecologists(ACOG)published the clinical practice guidelines for viral hepatitis in pregnancy,which replaced the 2007 version.According to the Grading of Recommendations Assessment,Development and Evaluation(GRADE),the guidelines put forward six suggestions.This paper interpreted the important recommended updates of the guidelines one by one,in order to provide help for the clinical practice of viral hepatitis during pregnancy.

Breast cancer is the most common malignant tumor among women, and early diagnosis, coupled with optimized treatment strategies is crucial for improving the prognosis. In recent years, with the advancement of nanotechnology, manganese-based nanomaterials have shown potential in various aspects of early breast cancer diagnosis, drug delivery, and tumor treatment. Compared to other nanomaterials, manganese-based nanomaterials exhibit excellent biocompatibility and have become a significant focus in the research of breast cancer diagnosis and treatment.

Machine Learning ; Image Processing, Computer-Assisted/methods*

Objective:To analyze the duration of the second stage of labor without epidural anesthesia and its association with pregnancy outcome.Methods:This retrospective study involved 12 789 women who delivered without epidural anesthesia in the First Affiliated Hospital of Kunming Medical University from January 1, 2014 to December 31, 2017. These subjects were divided into primipara group (9 517 cases) and multipara group (3 272 cases). Demographic characteristics, maternal and neonatal outcomes and the duration of the second stage of labor were compared between the two groups using two independent samples t-test, Mann-Whitney U test and Chi-square test (Fisher's exact test). Differences in the maternal and neonatal outcomes were also analyzed among different subgroups in primiparae [length of second stage: <1 h group ( n=6 265), ≥1-2 h group ( n=2 305), ≥2-3 h group ( n=831) and ≥3 h group ( n=116)] and multiparae [length of second stage <1 h group ( n=3 144), ≥1-2 h group ( n=102) and ≥2 h group ( n=26)]. The association between second stage length and pregnancy outcomes was analyzed with Cramer's V. After adjusted for maternal age, gestational weeks at delivery, body mass index before pregnancy, complications during pregnancy and neonatal birth weight, the relationship between the duration of the second stage and adverse outcomes was analyzed by binary logistic regression analysis. Results:The 95 th percentile of the second-stage labor duration was 143 min for primiparae and 52 min for multiparae. The rates of vaginal delivery, forceps delivery, cesarean section in the second stage, episiotomy, third- or fourth-degree perineal laceration, postpartum hemorrhage, grade Ⅱ postpartum hemorrhage, transfusion, umbilical arterial blood gas pH<7.15 and transferring to neonatal intensive care unit (NICU) were all correlated with the duration of second stage in primiparae (Cramer's V values: 0.22, 0.23, 0.03, 0.22, 0.05, 0.10, 0.03, 0.03, 0.03 and 0.07, respectively, all P<0.05), and so did those of vaginal delivery, forceps delivery, episiotomy, postpartum hemorrhage, grade Ⅱ postpartum hemorrhage, transfusion and transferring to NICU in multiparae (Cramer's V values: 0.18, 0.19, 0.28, 0.14, 0.09, 0.13 and 0.06, respectively, all P<0.05). Logistic analysis showed that in primiparae, the duration of second stage >1 h was an independent risk factor for episiotomy, third- or fourth-degree perineum laceration, forceps delivery, postpartum hemorrhage, admission to NICU and umbilical arterial blood gas pH<7.15 [adjusted OR (95% CI): 2.080 (1.907-2.268), 1.773 (1.080-2.911), 1.625 (1.420-1.859), 1.365 (1.231- 1.514), 1.305 (1.165-1.462) and 1.246 (1.081-1.436), respectively], while second stage length >2 h was the independent risk factor for episiotomy, forceps delivery, third- or fourth-degree perineum laceration, postpartum hemorrhage, grade Ⅱ postpartum hemorrhage, blood transfusion, admission to NICU and umbilical arterial blood gas pH<7.15 [adjusted OR (95% CI): 4.844 (4.132-5.678), 4.223 (3.571-4.993), 3.289 (1.806-5.989), 1.952 (1.675-2.274), 1.781 (1.057-3.001), 1.654 (1.025-2.668), 1.682 (1.421-1.991) and 1.298 (1.039-1.620), respectively]. In multiparae, the length of second stage >1 h was an independent risk factor for episiotomy, blood transfusion, forceps delivery, postpartum hemorrhage and admission to NICU [adjusted OR (95% CI): 8.796 (5.717-13.534), 7.469 (2.874-19.411), 6.135 (3.217-11.699), 2.697 (1.624-4.477) and 1.814 (1.063-3.097), respectively], while the duration of second stage >2 h was the independent risk factor for episiotomy, third- or fourth-degree perineum laceration, blood transfusion, grade Ⅱ postpartum hemorrhage, forceps delivery and postpartum hemorrhage [adjusted OR (95% CI): 38.868 (14.948-101.063), 28.046 (2.780-282.490), 20.076 (5.384-74.866), 16.327 (3.406-78.274), 14.337 (5.351-38.411) and 9.036 (3.880-21.011), respectively]. Conclusions:The duration of the second stage of labor without epidural anesthesia is between that reported by Friedman and by Zhang. A prolonged second stage of labor may increase the risk of adverse pregnancy outcomes.

Patients with hepatocellular carcinoma (HCC) and bone metastasis (BM) suffer from greatly reduced life quality and a dismal prognosis. However, BM in HCC has long been overlooked possibly due to its relatively low prevalence in previous decades. To date, no consensus or guidelines have been reached or formulated for the prevention and management of HCC BM. Our narrative review manifests the increasing incidence of HCC BM to sound the alarm for additional attention. The risk factors, diagnosis, prognosis, and therapeutic approaches of HCC BM are detailed to provide a panoramic view of this disease to clinicians and specialists. We further delineate an informative cancer bone metastatic cascade based on evidence from recent studies and point out the main factors responsible for the tumor-associated disruption of bone homeostasis and the formation of skeletal cancer lesions. We also present the advances in the pathological and molecular mechanisms of HCC BM to shed light on translational opportunities. Dilemmas and challenges in the treatment and investigation of HCC BM are outlined and discussed to encourage further endeavors in the exploration of underlying pathogenic and molecular mechanisms, as well as the development of novel effective therapies for HCC patients with BM.
Bone Neoplasms/secondary* ; Carcinoma, Hepatocellular/therapy* ; Humans ; Liver Neoplasms/therapy* ; Prognosis