Objective To explore the prevalence of depressive symptoms in postoperative patients with ovarian cancer and to analyze its influencing factors from multiple dimensions, including clinical characteristics, psychological factors, and laboratory indicators. Methods A cross-sectional study was conducted, which enrolled 235 postoperative patients with ovarian cancer. Depressive status was assessed using the patient health questionnaire, and the demographic, pathological, and medical record data of the patients were collected using the generalized anxiety disorder scale, Pittsburgh sleep quality index, European organization for research and treatment of cancer quality of life questionnaire core 30, and ECOG performance status score. Peripheral blood tumor marker (CA125), routine blood test, lymphocyte subsets, and serum cytokine levels were measured. Univariate and multivariate binary logistic regression analysis were used for statistical analysis. Results The prevalence of depression in postoperative patients with ovarian cancer was 39.15% (92/235). Univariate analysis showed that ECOG score ≥ 2 points, pain, anxiety, poor sleep quality, low quality of life, low life satisfaction, tumor recurrence, six or more cycles of chemotherapy, as well as higher levels of CA125, NLR, and NAR, and lower hemoglobin levels were significantly associated with depression (all P<0.05). Multivariate binary Logistic regression analysis showed that anxiety (OR=1.975, 95%CI: 1.231-3.170), sleep efficiency (OR=4.181, 95%CI: 1.211-14.43), sleep latency (OR=34.806, 95%CI: 4.258-284.542), ECOG performance status score, cognitive function (OR=0.918, 95%CI: 0.868-0.97), and life satisfaction were independent risk factors for depression (all P<0.05). Laboratory indicators were not independent influencing factors in the multivariate Logistic regression model. Conclusion Depression in postoperative patients with ovarian cancer is influenced by physiological, psychological, and social factors. Clinical management should focus on patients with anxiety, sleep disorders, poor physical condition, and low life satisfaction, and a comprehensive prevention and treatment strategy centered on psychological intervention and taking into account symptom management and social support should be implemented.

Acute respiratory distress syndrome (ARDS) is a common respiratory emergency, but current clinical treatment remains at the level of symptomatic support and there is a lack of effective targeted treatment measures. Our previous study confirmed that inhalation of hydrogen gas can reduce the acute lung injury of ARDS, but the application of hydrogen has flammable and explosive safety concerns. Drinking hydrogen-rich liquid or inhaling hydrogen gas has been shown to play an important role in scavenging reactive oxygen species and maintaining mitochondrial quality control balance, thus improving ARDS in patients and animal models. Coral calcium hydrogenation (CCH) is a new solid molecular hydrogen carrier prepared from coral calcium (CC). Whether and how CCH affects acute lung injury in ARDS remains unstudied. In this study, we observed the therapeutic effect of CCH on lipopolysaccharide (LPS) induced acute lung injury in ARDS mice. The survival rate of mice treated with CCH and hydrogen inhalation was found to be comparable, demonstrating a significant improvement compared to the untreated ARDS model group. CCH treatment significantly reduced pulmonary hemorrhage and edema, and improved pulmonary function and local microcirculation in ARDS mice. CCH promoted mitochondrial peripheral division in the early course of ARDS by activating mitochondrial thioredoxin 2 (Trx2), improved lung mitochondrial dysfunction induced by LPS, and reduced oxidative stress damage. The results indicate that CCH is a highly efficient hydrogen-rich agent that can attenuate acute lung injury of ARDS by improving the mitochondrial function through Trx2 activation.

Insulin is an important protein hormone that participates in multiple metabolic pathways.Biosynthetic insulin has been widely used in the treatment of type 1 and type 2 diabetes.Currently,the number of reported cases of insulin overdose both at home and abroad is gradually increasing,and insulin homicide is no longer a means of"committing murder without leaving a trace".At present,there are no systematic protocols for the identification of insulin overdose in the field of forensic medi-cine in China.This article introduces the causes,toxicological characteristics,forensic examination,labo-ratory testing methods and indicator reference of insulin overdose.Based on the identification practice and research results and referring to relevant studies on insulin overdose at home and abroad,this pa-per aims to provide recommendations and references for the formulation of forensic identification guide-lines for insulin overdose cases.

OBJECTIVE: To explore the mechanism by which ω-3 polyunsaturated fatty acids (hereinafter referred to as "ω-3") exert antioxidant stress protection and promote osteogenic differentiation in MC3T3-E1 cells, and to reveal the relationship between ω-3 and the key antioxidant stress pathway involving nuclear factor E2-related factor 2 (Nrf2) and NAD (P) H quinone oxidoreductase 1 (NQO1) in MC3T3-E1 cells. METHODS: The optimal concentration of H ₂O ₂ (used to establish the oxidative stress model of MC3T3-E1 cells in vitro) and the optimal intervention concentrations of ω-3 were screened by cell counting kit 8. MC3T3-E1 cells were divided into blank control group, oxidative stress group (H ₂O ₂), low-dose ω-3 group (H ₂O ₂+low-dose ω-3), and high-dose ω-3 group (H ₂O ₂+high-dose ω-3). After osteoblastic differentiation for 7 or 14 days, the intracellular reactive oxygen species (ROS) level was measured by fluorescence staining and flow cytometry, and the mitochondrial morphological changes were observed by biological transmission electron microscope; the expression levels of Nrf2, NQO1, heme oxygenase 1 (HO-1), Mitofusin 1 (Mfn1), and Mfn2 were detected by Western blot to evaluate the cells' antioxidant stress capacity; the expression levels of Runt-related transcription factor 2 (RUNX2) and osteocalcin (OCN) were detected by immunofluorescence staining and Western blot; osteogenic potential of MC3T3-E1 cells was evaluated by alkaline phosphatase (ALP) staining and alizarin red staining. RESULTS: Compared with the oxidative stress group, the content of ROS in the low and high dose ω-3 groups significantly decreased, and the protein expressions of Nrf2, NQO1, and HO-1 significantly increased ( P<0.05). At the same time, the mitochondrial morphology of MC3T3-E1 cells improved, and the expressions of mitochondrial morphology-related proteins Mfn1 and Mfn2 significantly increased ( P<0.05). ALP staining and alizarin red staining showed that the low-dose and high-dose ω-3 groups showed stronger osteogenic ability, and the expressions of osteogenesis-related proteins RUNX2 and OCN significantly increased ( P<0.05). And the above results showed a dose-dependence in the two ω-3 treatment groups ( P<0.05). CONCLUSION ω-3 can enhance the antioxidant capacity of MC3T3-E1 cells under oxidative stress conditions and upregulate their osteogenic activity, possibly through the Nrf2/NQO1 signaling pathway.
Oxidative Stress/drug effects* ; NF-E2-Related Factor 2/metabolism* ; NAD(P)H Dehydrogenase (Quinone)/metabolism* ; Animals ; Mice ; Osteogenesis/drug effects* ; Cell Differentiation/drug effects* ; Fatty Acids, Omega-3/pharmacology* ; Signal Transduction/drug effects* ; Osteoblasts/drug effects* ; Reactive Oxygen Species/metabolism* ; Cell Line ; Hydrogen Peroxide/pharmacology* ; Core Binding Factor Alpha 1 Subunit/metabolism* ; Antioxidants/pharmacology* ; Heme Oxygenase-1/metabolism*

Objective:To evaluate the efficacy and immunological mechanisms of pegylated interferon α-2b (Peg-IFNα-2b) antiviral therapy in treatment-naive patients with chronic hepatitis B(CHB).Methods:A total of 166 treatment-naive CHB patients, who were treated at Department of Infectious Diseases, the Second Affiliated Hospital of Nanchang University from March 2021 to March 2023, were enrolled in this study. All the patients received Peg-IFNα-2b therapy for 48 weeks. Serum hepatitis B virus (HBV) DNA, HBV serological markers, biochemical parameters, peripheral blood lymphocyte subsets and serum cytokine levels were detected and compared before and after treatment. Chi-square test, Mann-Whitney U test and paired sample t test were used for statistical comparison. Multivariate logistic regression analysis was used to analyze the influencing factors of hepatitis B surface antigen (HBsAg) seroconversion by stepwise regression method, and the receiver operator characteristic curve (ROC curve) was used to evaluate the predictive efficacy of immune indicators on HBsAg seroconversion. Results:Among the 166 treatment-naive CHB patients, the rate of HBV DNA negativity following 48 weeks of Peg-IFNα-2b therapy was 71.08%(118/166), the rate of hepatitis B e antigen (HBeAg) negativity was 32.05%(25/78), and the rate of HBsAg negativity was 20.48%(34/166). HBsAg negativity rate was 52.17%(24/46) in patients with baseline HBsAg<200 IU/mL, 10.26%(4/39) in patients with baseline HBsAg 200 to <1 200 IU/mL, and 7.41%(6/81) in patients with baseline HBsAg≥1 200 IU/mL, and the difference was statistically significant( χ2=39.37, P<0.001). After 48 weeks of treatment, serum levels of alanine transaminase (ALT), aspartate transaminase (AST), total bilirubin (TBil), and alpha-fetoprotein (AFP) were significantly lower than those before treatment ( Z=9.33, 8.58, 5.99, 2.36, respectively, all P<0.05). lmmune indicators were detected in 58 patients, and the proportion of peripheral blood lymphocytes increased significantly post-treatment, with notable increases in CD3 + CD8 + T/CD3 + T, CD3 + CD4 + DR + /CD3 + CD4 + , CD3 + CD8 + DR + /CD3 + CD8 + , CD3 + CD8 + CD38 + /CD3 + CD8 + , CD3 + CD8 + CD28 + /CD3 + CD8 + , and CD19 + B cells, and the differences were all statistically significant ( t=-2.56, t=-8.65, Z=-3.58, t=-3.66, Z=-3.04, t=-3.62, t=-3.87, respectively, all P<0.05). Conversely, the proportion of CD3 + , CD3 + CD4 + T/CD3 + T, CD3 + CD4 + CD45RO + /CD3 + CD4 + , CD3 + CD8 + CD45RO + /CD3 + CD8 + and the CD4 + /CD8 + ratio decreased significantly post-treatment ( t=3.13, t=5.61, t=3.69, Z=3.95, Z=7.33, respectively, all P<0.05). No significant differences were observed in the proportion of CD16 + CD56 + natural killer (NK) cells, CD3 + CD4 + CD28 + /CD3 + CD4 + , CD3 + CD4 + CD38 + /CD3 + CD4 + cells before and after treatment (all P>0.05). Serum levels of interleukin(IL)-8, IL-12P70, and IL-17 significantly decreased post-treatment ( Z=2.85, 3.26, 4.12, respectively, all P<0.05), while IL-2, IL-1β, and interferon(IFN)-α levels were significantly elevated compared to baseline ( Z=-4.92, -4.85, -9.01, respectively, all P<0.001). There were no significant differences in IL-4, IL-6, and IL-10 levels before and after treatment (all P>0.05). Logistic regression analysis identified CD3 + CD8 + T/CD3 + T(odd ratios ( OR)=1.198, 95%confidence interval( CI) 1.003 to 1.432, P=0.046), CD3 + CD4 + DR + /CD3 + CD4 + ( OR=1.185, 95% CI 1.035 to 1.357, P=0.014), CD3 + CD8 + DR + /CD3 + CD8 + ( OR=0.813, 95% CI 0.690 to 0.958, P=0.013), CD3 + CD4 + CD38 + /CD3 + CD4 + ( OR=0.678, 95% CI 0.488 to 0.940, P=0.020), CD3 + CD8 + CD38 + /CD3 + CD8 + ( OR=1.272, 95% CI 1.069 to 1.512, P=0.007), CD19 + B cells( OR=0.752, 95% CI 0.582 to 0.971, P=0.029), IL-2( OR=8.568, 95% CI 1.927 to 38.087, P=0.005), and IL-17( OR=0.728, 95% CI 0.535 to 0.989, P=0.042) as independent factors influencing HBsAg seroconversion. The area under the curve (AUC) of the proportion of dCD19 + B cells (the reciprocal of CD19 + B cells) for predicting HBsAg seroconversion was 0.716, the sensitivity was 0.636, and the specificity was 0.809. The AUC of IL-2 was 0.657, the sensitivity was 0.818, and the specificity was 0.404. The AUC of dIL-17 (the reciprocal of IL-17 levels) was 0.624, the sensitivity was 0.727, and the specificity was 0.489. The AUC of IL-2 and dIL-17 as a combined predictor was 0.830, the sensitivity was 0.909, and the specificity was 0.787. Conclusions:Peg-IFNα-2b demonstrates significant antiviral, biochemical, and serological responses in treatment-naive CHB patients, with enhanced efficacy in patients exhibiting HBsAg levels <200 IU/mL. In patients with HBsAg<200 IU/mL, the rate of HBsAg negativity reached 52.17%.Peg-IFNα-2b can regulate the immune function of patients with CHB by increasing the proportion of activated T lymphocyte subsets and functional subsets. The proportion of CD19 + B cells, IL-2 levels, and IL-17 levels hold predictive value for achieving HBsAg seroconversion.

Objective To analyze the current status of occupational stress among primary and secondary school teachers, and explore the dose-response relationship between weekly work hours and occupational stress. Methods A total of 1 252 teachers from 13 primary and secondary schools in three prefecture-level cities of a central province of China were selected as the research subjects by the convenience sampling method. The Core Occupational Stress Scale was used to assess occupational stress levels of the teachers. Multivariate logistic regression analysis combined with restricted cubic spline models was applied to study the dose-response relationship between weekly work hours and occupational stress. Results The average weekly work hours were (55.3±15.9) hours, with 78.6% of teachers working more than 40.0 hours per week. The total score of occupational stress was (40.3±8.2) points, and the detection rate of occupational stress was 29.8%. Multivariate logistic regression analysis combined with restricted cubic spline models revealed a linear dose-response relationship in weekly work hours and occupational stress among teachers (P for overall trend <0.05, P for nonlinearity was 0.22). Result of age-stratified analysis showed that weekly work hours had a linear dose-response relationship with occupational stress risk in teachers aged 21-<31 and 31-<46 years (P for overall trend <0.05, P for nonlinearity was 0.71 and 0.27, respectively). However, no association was found between weekly work hours and occupational stress risk among teachers aged ≥46 years (P for overall trend =0.08, P for nonlinearity was 0.09). Conclusion There is a linear dose-response relationship between weekly work hours and occupational stress among primary and secondary school teachers in the province, with younger teachers being more susceptible to suffer occupational stress due to long working hours.

Acute respiratory distress syndrome(ARDS)is a common respiratory emergency,but current clinical treatment remains at the level of symptomatic support and there is a lack of effective targeted treatment measures.Our previous study confirmed that inhalation of hydrogen gas can reduce the acute lung injury of ARDS,but the application of hydrogen has flammable and explosive safety concerns.Drinking hydrogen-rich liquid or inhaling hydrogen gas has been shown to play an important role in scavenging reactive oxygen species and maintaining mitochondrial quality control balance,thus improving ARDS in patients and animal models.Coral calcium hydrogenation(CCH)is a new solid molecular hydrogen carrier prepared from coral calcium(CC).Whether and how CCH affects acute lung injury in ARDS re-mains unstudied.In this study,we observed the therapeutic effect of CCH on lipopolysaccharide(LPS)induced acute lung injury in ARDS mice.The survival rate of mice treated with CCH and hydrogen inhalation was found to be comparable,demonstrating a significant improvement compared to the untreated ARDS model group.CCH treatment significantly reduced pulmonary hemorrhage and edema,and improved pulmonary function and local microcirculation in ARDS mice.CCH promoted mitochon-drial peripheral division in the early course of ARDS by activating mitochondrial thioredoxin 2(Trx2),improved lung mitochondrial dysfunction induced by LPS,and reduced oxidative stress damage.The results indicate that CCH is a highly efficient hydrogen-rich agent that can attenuate acute lung injury of ARDS by improving the mitochondrial function through Trx2 activation.

Objective:To evaluate the efficacy and safety of telitacicept in the treatment of systemic lupus erythematosus (SLE) .Methods:The clinical data of 25 SLE patients who received standard therapy combined with telitacicept at the Department of Dermatology, Xiangya Second Hospital, Central South University, from 2021 to 2024 were retrospectively collected. Baseline demographic and clinical characteristics were analyzed. Changes in skin lesions, joint pain symptoms, complete blood count, and biochemical parameters at 4, 12, and 24 weeks of treatment were compared with baseline (week 0). The Wilcoxon signed-rank test was used to compare complement C3 and C4 levels before and after treatment, and univariate logistic regression analysis was performed to explore factors influencing the efficacy of telitacicept.Results:Among the 25 SLE patients, 3 were male (12.0%) and 22 were female (88.0%). Based on the SLE Disease Activity Index (SLEDAI) -2000 scores, 8 patients were mild, 13 were moderate, and 4 were severe. Of the 11 SLE patients with rashes before treatment, 6 achieved complete remission at 12 weeks. Among the 7 patients with joint pain before treatment, 4 experienced symptom resolution at 24 weeks. The proportion of patients with leukopenia at baseline and at 4, 12, and 24 weeks was 10/25 (40.0%), 0/24 (0), 1/22 (4.5%), and 2/19 (10.5%), respectively. The proportion of patients with thrombocytopenia was 6/25 (24.0%), 3/24 (12.5%), 1/22 (4.5%), and 1/19 (5.3%), respectively, and the proportion of patients with anemia was 7/25 (28.0%), 3/24 (12.5%), 1/22 (4.5%), and 1/19 (5.3%), respectively. At baseline, 11 out of 25 patients (44.0%) had proteinuria. At 12 weeks, the urinary protein quantification level (0.4 [0, 0.6] g/L) was significantly lower than at baseline (0.9 [0.8, 1.2] g/L). The SLE responder index-4 (SRI4) response rates at 4, 12, and 24 weeks were 14/18, 15/17, and 12/14, respectively. Complement C3 and C4 levels were significantly higher at 4, 12, and 24 weeks compared to baseline (all P < 0.001). Univariate logistic regression analysis showed that age, disease duration, glucocorticoid dosage, baseline complement C4 levels, antinuclear antibody titer, and SLEDAI-2K score did not significantly affect the efficacy of telitacicept (SRI4 response rate at 12 weeks) (all P > 0.05). No serious adverse reactions related to telitacicept were observed in patients. Conclusions:Telitacicept improved skin lesions, complement C3 and C4 levels, and anti-double-stranded DNA antibody levels in SLE patients. No association was found between the efficacy of telitacicept and baseline SLEDAI-2K scores, antinuclear antibody titers, or complement C4 levels, suggesting that telitacicept is an effective and safe treatment for SLE patients.

Background: s/Aims: Sarcomatoid hepatocellular carcinoma (HCC) is a rare histological subtype of HCC characterized by extremely poor prognosis; however, its molecular characterization has not been elucidated. Methods: In this study, we conducted an integrated multiomics study of whole-exome sequencing, RNA-seq, spatial transcriptome, and immunohistochemical analyses of 28 paired sarcomatoid tumor components and conventional HCC components from 10 patients with sarcomatoid HCC, in order to identify frequently altered genes, infer the tumor subclonal architectures, track the genomic evolution, and delineate the transcriptional characteristics of sarcomatoid HCCs. Results: Our results showed that the sarcomatoid HCCs had poor prognosis. The sarcomatoid tumor components and the conventional HCC components were derived from common ancestors, mostly accessing similar mutational processes. Clonal phylogenies demonstrated branched tumor evolution during sarcomatoid HCC development and progression. TP53 mutation commonly occurred at tumor initiation, whereas ARID2 mutation often occurred later. Transcriptome analyses revealed the epithelial–mesenchymal transition (EMT) and hypoxic phenotype in sarcomatoid tumor components, which were confirmed by immunohistochemical staining. Moreover, we identified ARID2 mutations in 70% (7/10) of patients with sarcomatoid HCC but only 1–5% of patients with non-sarcomatoid HCC. Biofunctional investigations revealed that inactivating mutation of ARID2 contributes to HCC growth and metastasis and induces EMT in a hypoxic microenvironment. Conclusions We offer a comprehensive description of the molecular basis for sarcomatoid HCC, and identify genomic alteration (ARID2 mutation) together with the tumor microenvironment (hypoxic microenvironment), that may contribute to the formation of the sarcomatoid tumor component through EMT, leading to sarcomatoid HCC development and progression.