Objective To improve the analysis method of the blood components of Yinchenhao decoction （YCHD） in vivo and explore its anti-hepatocellular carcinoma mechanism. Methods Ultra-high performance liquid chromatography-quadrupole-time-of-flight mass spectrometry （UPLC-Q-TOF/MS） was used to collect and analyze blood samples from mice. The mice were given a single dose of YCHD with a concentration of 0.1 g/ml and a dose of 25 ml/kg, and then the samples were collected 2 h post–administration, which was to systematically study the chemical components of YCHD in vivo. Network pharmacological methods were used to screen the components and targets of YCHD, and the targets of hepatocellular carcinoma; The common targets of YCHD and hepatocellular carcinoma were identified for GO enrichment and KEGG enrichment. Molecular docking was performed on the main targets to verify the binding ability between the active ingredients and the core targets. The relative mRNA expression levels of serine/threonine-protein kinase（AKT1） and tumor protein p53（TP53） in liver tissues were analyzed via qPCR, including the following mouse groups: mice with concanavalin A（Con-A）-induced acute liver injury without preventive administration, mice with Con-A-induced acute liver injury that received 14 d preventive oral administration of YCHD, and untreated control mice. Results ①The active ingredients of YCHD in the blood were identified by retrieving the data from the in vitro component analysis. They were chrysophanol, herniarin, aloe-emodin, and monotropein. ②The mechanism of action of the blood components against hepatocellular carcinoma （HCC） was further analyzed using network pharmacological methods, and a total of 30 components of YCHD were screened for 213 targets and 215 HCC targets. ③There were 17 intersection targets between YCHD and hepatocellular carcinoma, including AKT1, TP53, receptor tyrosine-protein kinase erbB-2 （ERBB2）, myelocytomatosis oncogene （MYC）, interleukin-1β （IL-1β）, etc. The GO enrichment results indicated that these components were primarily involved in DNA replication，chromosome segregation，leukocyte mediated immunity，leukocyte cell-cell adhesion. The KEGG enrichment results demonstrated that these components were predominantly associated with diverse cancer pathways. Additionally, the results indicated involvement in the citrate cycle （TCA cycle）, pyruvate metabolism, and p53 signaling pathway, ect. ④The results of molecular docking showed that chrysophanol, herniarin, and aloe - emodin had strong binding abilities with AKT1, TP53, ERBB2, MYC, and IL-1β. ⑤The relative expression of AKT1 and TP53 mRNA was significantly higher in the modelling group than in the control group. The relative expression of AKT1 and TP53 mRNA was significantly lower in the drug administration group than in the modelling group. Conclusion There were 4 blood components in YCHD, among which chrysophanol, herniarin, and aloe-emodin may act on AKT1, TP53, ERBB2, MYC, IL-1β and then participated in the regulation of cancer signaling pathways and p53 signaling pathway to play a role in the treatment of HCC.

Self-limited epilepsy with centrotemporal spikes(SeLECTS)is the most common idiopathic focal epilepsy in childhood with self-limited course,characterized by centrotemporal spike-slow wave discharges on electroencephalography.Children with SeLECTS often experience language dysfunction,which is closely related to abnormalities in brain structure and function.The progresses of MRI researches of language function in children with SeLECTS were reviewed in this article.

OBJECTIVE To investigate the anti-inflammatory effect of electroacupuncture in mice with chronic obstructive pul-monary disease(COPD)and its underlying mechanisms.METHODS Forty C57BL/6 mice were randomly divided into normal group,model group,electroacupuncture(EA)group,vagotomy group,and vagotomy+EA group,with 8 mice in each group.Except for the normal group,all groups were exposed to cigarette smoke for 12 weeks to establish a COPD model.After model establishment,the vagotomy group and the vagotomy+EA group underwent left cervical vagotomy before EA.EA treatment was performed at the Feishu(BL13)and Zusanli(ST36)acupoints once daily for 20 minutes for a total of 14 days.After EA,the pulmonary ventilation function of the mice was detected by a pulmonary function analysis system;lung tissue pathology was observed by HE staining;the levels of inter-leukin(IL)-6,tumor necrosis factor-α(TNF-α),IL-10,and transforming growth factor-β(TGF-β)in lung tissue were detected by ELISA;the expression of CD86 and CD206 proteins in lung tissue was detected by Western blot;the distribution of F4/80+CD86+(M1 type)and F4/80+CD206+(M2 type)cells in lung tissue was determined by flow cytometry;the expression of CD86 and CD206 in lung tissue was observed by immunofluorescence.RESULTS Compared with the normal group,the model group showed significantly decreased lung function(P<0.01),obvious lung pathological damage,increased M1 proportion,IL-6,TNF-α,CD86 content and expression(P<0.05,P<0.01),and decreased M2 proportion,IL-10,TGF-β,CD206 content and expression(P<0.01).Compared with the model group,the EA group showed varying degrees of improvement in lung function and pathology;the M1 proportion,IL-6,TNF-α,and CD86 were reduced(P<0.05,P<0.01),while the M2 proportion,IL-10,TGF-β,and CD206 were increased(P<0.05,P<0.01).The vagotomy group showed worsened lung function and pathology,increased IL-6,TNF-α,and CD86 content and expression(P<0.05,P<0.01),and decreased IL-10,TGF-β,and CD206 content and expression(P<0.05,P<0.01).Compared with the EA group,the vagotomy+EA group showed increased M1 proportion,IL-6,TNF-α,and CD86 content and expression(P<0.01),and decreased M2 proportion,IL-10,TGF-β,and CD206 content and expression(P<0.05,P<0.01).CONCLUSION EA at Feishu(BL13)and Zusanli(ST36)acupoints can improve lung function and pulmonary inflammation in COPD mice,promoting the polarization of alveolar macrophages from M1 to M2,which is mediated by the vagus nerve.

Background During urbanization, the passenger load on urban public transport systems continues to increase, exposing bus drivers to a high risk of musculoskeletal disorders (MSDs). This occupational health issue may also potentially compromise public transport safety. Objective To investigate the prevalence of MSDs among bus drivers in a first-tier city and to explore associated influencing factors. Methods A self-administered questionnaire survey was conducted from December 2024 to March 2025 among 1300 bus drivers in a bus company. Data were collected on general demographic information, occupational activities, and MSDs indicators. A total of 1268 valid questionnaires were returned, yielding a response rate of 97.5%. Descriptive statistics were used to analyze the distribution characteristics of MSDs. Pearson χ² tests were employed to examine the association between MSDs prevalence and individual/occupational characteristics. Logistic regression was performed to identify the influencing factors of MSDs. Results The survey revealed that the prevalence of MSDs among the bus drivers was 28.5%, with the highest prevalence in the 41–50 years age group (30.5%). The conditions primarily affected the cervical spine (60.5%) and lumbar spine (61.9%), with some cases involving multiple sites. The logistic regression model indicated that the following factors were associated with a higher risk of MSDs: frequent smoking (OR=1.477), poor or moderate self-reported health status (OR=4.422), 11–20 years of service (OR=1.749), daily cumulative driving time ≥361 min (OR=1.616), frequent whole-body fatigue during driving (OR=2.077), occasional whole-body fatigue during driving (OR=1.873), feeling tense during driving (OR=1.518), fatigue after work (OR=2.485), work-related stress (OR=1.882), and prolonged smartphone use with head-down posture (OR=1.671). Conversely, occasional exercise (OR=0.713)/frequent exercise (OR=0.569), driving intervals ≥21 min per round (OR=0.645), and perceiving the driving seat comfortable (OR=0.429) were associated with a lower risk of MSDs. Conclusion Physical exercise, smoking, years of service, daily cumulative driving time, driving intervals per round, prolonged smartphone use with head-down posture, self-reported health status, and psychological factors such as work-related stress are influencing factors for MSDs among bus drivers. Drivers should increase physical exercise and change unhealthy living habits. Employers should optimize working conditions, arrange reasonable driving schedules, and foster a positive work environment to reduce MSDs prevalence.

The catalytic activity of 3-mercaptopyruvate (3MP) sulfurtransferase (MPST) converts 3MP to hydrogen sulfide (H₂S). However, the regulatory mechanisms governing MPST and its impact on the brain remain largely unexplored. Our study reveals the neuroprotective role of endothelial MPST-generated H₂S, regulated by protein phosphatase 2A (PP2A). Bioinformatics analysis and RNA sequencing demonstrated that endothelial PP2A is associated with neurodegenerative disease pathways. Cerebral ischemic mice exhibited significant inactivation of endothelial PP2A, evidenced by the reduction of PP2Acα in the brain endothelium. Mice with endothelium-specific null PP2A (PP2A^EC-cKO) exhibited neuronal loss, cognitive dysfunction, and long-term potentiation deficits. Postnatal inactivation of endothelial PP2A also contributes to cognitive dysfunction and neuronal loss. However, regaining endothelial PP2A activity by overexpressing Ppp2ca rescued neuronal dysfunction. Mechanistically, PP2A deficiency is intricately linked to the MPST-H₂S signaling pathway. A robust reduction in endothelial MPST-dependent H₂S production followed PP2A deficiency. Exogenous H₂S treatment and AAV-mediated overexpression of MPST in brain endothelial cells significantly mitigated neuronal dysfunction in PP2A^EC-cKO mice. Furthermore, PP2A deficiency promotes an increase in calcium influx and calpain2 phosphorylation, subsequently leading to MPST degradation. The PP2A activator (FTY720) and MPST activator (3MP sodium) both remarkably restored endothelial MPST-dependent H₂S production, subsequently rescuing ischemia-induced neurological deficits. In conclusion, our study demonstrates that endothelial PP2A deficiency leads to MPST degradation by activating calpain2, thus damaging neuronal function.

(+)-Borneol, the main component of "Natural Borneol" in the Chinese Pharmacopoeia, is a high-end spice and precious medicine. Plant extraction cannot meet the increasing demand for (+)-borneol, while microbial biosynthesis offers a sustainable supply route. However, its production was extremely low compared with other monoterpenes, even with extensively optimizing the mevalonate pathway. We found that the key challenge is the complex and unusual dephosphorylation reaction of bornyl diphosphate (BPP), which suffers the side-reaction and the competition from the cellular dephosphorylation process, especially lipid metabolism, thus limiting (+)-borneol synthesis. Here, we systematically optimized the dephosphorylation process by identifying, characterizing phosphatases, and balancing cellular dephosphorylation metabolism. For the first time, we identified two endogenous phosphatases and seven heterologous phosphatases, which significantly increased (+)-borneol production by up to 152%. By engineering BPP dephosphorylation and optimizing the MVA pathway, the production of (+)-borneol was increased by 33.8-fold, which enabled the production of 753 mg/L under fed-batch fermentation in shake flasks, so far the highest reported in the literature. This study showed that rewiring dephosphorylation metabolism was essential for high-level production of (+)-borneol in Saccharomyces cerevisiae, and balancing cellular dephosphorylation is also helpful for efficient biosynthesis of other terpenoids since all whose biosynthesis involves the dephosphorylation procedure.

Objective: To explore the diagnosis, treatment and prognosis of primary prostatic signet ring cell carcinoma (SRCC), so as to provide reference for the clinical diagnosis and treatment. Methods: A retrospective analysis was conducted on the clinical data of 6 patients with primary prostatic SRCC treated in Nanjing Drum Tower Hospital during Nov.2020 and Sep.2024.The clinical manifestations, imaging features, treatment methods, histological characteristics and prognosis were summarized. Results: The average age of the patients was (72.00±4.28) years.Varying degrees of dysuria occurred in 4 patients. All patients underwent multi-parametric magnetic resonance imaging (mpMRI) examination before surgery, and the results indicated typical prostate cancer.Preoperative biopsies showed high-grade (Gleason 8-10) prostate acinar adenocarcinoma.Postoperative pathological diagnoses were mixed types of prostate acinar adenocarcinoma and SRCC, and no metastasis was found in the pelvic lymph nodes.All patients were followed up for 1 to 46 months after surgery and are currently alive.Robot-assisted laparoscopic radical prostatectomy only was performed in 3 cases; apalutamide and leuprolide/triptorelin was administered after surgery in 2 cases; bicalutamide + goserelin was administered after surgery in 1 case, who developed bladder metastasis of prostate cancer 24 months later, and the serum prostate-specific antigen (PSA) concentration decreased to a safe level (<0.2 ng/mL) after the use of darolutamide with radiotherapy.No recurrence or metastasis was found in the remaining patients. Conclusion: Primary prostatic SRCC is a rare and highly aggressive malignant tumor of the prostate.The diagnosis depends on pathological examinations due to lack of specific imaging features and clinical manifestations.The prognosis is poor, and there is currently no standardized treatment.The combined use of surgery, hormonotherapy and radiotherapy can help improve the survival rate of patients.