Xiaoaiping (XAP) Injection demonstrates the anti-prostate cancer (PCa) effects, yet the underlying mechanism remains unclear. This study aims to investigate the impact of XAP on PCa and elucidate its mechanism of action. PCa cell proliferation was evaluated using a cell counting kit-8 (CCK-8) assay. Cell apoptosis was assessed through Hoechst staining and Western blotting assays. Proteomics technology was employed to identify key molecules and significant signaling pathways modulated by XAP in PCa cells. To further validate potential key genes and important pathways, a series of assays were conducted, including acridine orange (AO) staining, transmission electron microscopy, and immunofluorescence assays. The molecular mechanism of XAP against PCa in vivo was examined using a PC3 xenograft mouse model. Results demonstrated that XAP significantly inhibited cell proliferation in multiple PCa cell lines. In C4-2 and prostate cancer cell line-3 (PC3) cells, XAP induced cellular apoptosis, evidenced by reduced B-cell lymphoma 2 (Bcl-2) levels and elevated Bcl-2-associated X (Bax) levels. Proteomic, immunofluorescence, and quantitative reverse transcription-polymerase chain reaction (qRT-PCR) investigations revealed a strong correlation between forkhead box O3a (FoxO3a) autophagic degradation and the anti-PCa action of XAP. XAP hindered autophagy by reducing the expression levels of autophagy-related protein 5 (Atg5)/autophagy-related protein 12 (Atg12) and enhancing FoxO3a expression and nuclear translocation. Furthermore, XAP exhibited potent anti-PCa action in PC3 xenograft mice and triggered FoxO3a nuclear translocation in tumor tissue. These findings suggest that XAP induces PCa apoptosis via inhibition of FoxO3a autophagic degradation, potentially offering a novel perspective on XAP injection as an effective anticancer therapy for PCa.
Male ; Humans ; Prostatic Neoplasms/physiopathology* ; Autophagy/drug effects* ; Animals ; Drugs, Chinese Herbal/pharmacology* ; Proteomics ; Mice ; Apoptosis/drug effects* ; Cell Line, Tumor ; Cell Proliferation/drug effects* ; Forkhead Box Protein O3/genetics* ; Xenograft Model Antitumor Assays ; Mice, Nude ; Mice, Inbred BALB C

Objective:To analyze the clinical manifestations, risk factors and risk of recurrence in patients with primary antiphospholipid syndrome (PAPS) complicated with cerebral infarction.Methods:Inpatients diagnosed with PAPS was recruited between 2010 and 2020. Clinical characteristics,laboratory results and adjusted global antiphospholipid syndrome score (aGAPSS) were compared between patients with cerebral infarction and without cerebral infarction by χ2 test, t test or Mann-Whitney U test. Univariate and multivariate Logistic analysis were performed to identify the risk factors associated with cerebral infarction. Results:In 145 PAPS patients [median age 44.0 (34.0, 51.5) years, 66.2% female], 46 (31.7%) patients had cerebral infarction. Patients with cerebral infarction had higher rates of transient ischemic attack (TIA) (50.0% and 20.2%, χ2=13.37, P<0.001), cardiac valvular anomalies (32.6% and 11.1%, χ2=9.86, P=0.002), lupus anticoagulant (LA) (87.0% and 42.4%, χ2=25.35, P<0.001) and triple antiphospholipid antibodies (aPL) positivity (50.0% and 11.1%, χ2=26.64, P<0.001). The aGAPSS value was significantly higher in patients with cerebral infarction compared to those without [13(11, 14) and 9(7, 13), U=934.50, P<0.001]. The independent risk factors for PAPS-associated cerebral infarction were TIA [ OR (95% CI)= 3.612 (1.387, 9.403), P=0.009]、triple aPL positivity[ OR(95% CI)=8.904 (3.169, 25.019), P<0.001], higher aGAPSS[ OR(95% CI)=1.421(1.209, 1.670), P<0.001]. Conclusion:Patients with cerebral infarction may have a higher risk of thrombus recurrence. TIA, triple aPL positivity and higher aGAPSS are independent risk factors for PAPS patients with cerebral infarction.

Incentive system is an indispensable means in the process of standardized residency training, which plays an important role in improving the work efficiency and service quality of residents, teachers and other participants. Based on the analysis of the problems existing in the holistic incentive system, we have implemented a set of personalized incentive measures for the training of residents in department rotation and achieved preliminary results, which provides ideas for exploring personalized incentive system for standardized residency training.

Knee osteoarthritis (KOA ) is a common chronic degenerative disease in the elderly population .It is character-ized by knee-joint pain ,swelling ,morning stiffness and seriously affects the patients′motor function and physical health .So far ,there is no early diagnosis and effective treatment for it .This paper outlined the recent researches on knee osteoarthritis and inflammatory cytokines to discuss the relationship between knee osteoarthritis and inflammatory factors such as IL-1β,IL-6 ,TNF-α,TGF-β,IL-10 ,IL-17 and IL-37 ,and provide the theoretical basis for the diagnosis and treatment of knee osteoar-thritis .

Objective To explore the effects of intraventricular administration of insulin on the expressions of Bcl-2,Bax mRNA and neuronal hippocampus apoptosis in rats after cardiopulmonary resuscitation (CPR).Methods This experiment was implemented in the animal Laboratory center of Xuanwu Hospital of Capital Medical University.Thirty male SD rats were randomly (random number)divided into three groups:control group (n=6),CPR group (n=12),insulin treated group ( n =12).CPR was performed at 6 minutes after ventricular fibrillation induced by transesophageal overdrive pacing.Resuscitation procedures lasted until restoration of spontaneous circulation (ROSC).ROSC was defined as the recovery of the supraventricular heart rates and the increase of mean arterial pressure (MAP) ＞ 60mmHg for more than 10 minutes.Ten minutes after ROSC in rats,12.5 μL ( 1 U) regular insulin was injected into the left ventricle in the insulin group,and 12.5 μL isotonic saline was injected the control and CPR groups at least 10 minutes.Real-time PCR was used to observe the expressions of Bcl-2,Bax mRNA in hippocampus CAI after reperfusion 24 h and 72 h.TUNEL staining was used to observe the neuronal apoptosis in all groups after reperfusion 7 days.Blood glucose was monitored in rats before and after CPR.Results ① The Bcl-2mRNA in insulin groups were significantly higher than those in the CPR group after 24 h and 72 h (P ＜0.01 ).The expression of Bcl-2 mRNA in 24 h insulin group were significantly higher than those in 72 h insulin group ( P ＜ 0.01 ) ; There were no significantly different in the Bax mRNA between insulin groups and the CPR and the control group after 24 h and 72 h ( P ＞ 0.05 ) ; ②After CPR 7 d,the apoptotic neurons of hippocampal CA1 area in the CPR group ( 124.75 ± 17.35 ) were significantly higher than those in the control group (5.12 ± 3.26) ( P ＜ 0.01 ) and the insulin group (92.79 ± 7.35 )(P ＜0.01 ); the apoptotic neurons in the insulin group were higher than those in the control group (P ＜0.0l ),and the differences were statistically significant.③There were no significant difference in venous blood glucose in the CPR and insulin groups (P ＞ 0.05).Conclusions Insulin may regulate Bcl-2mRNA expression in hippocampus,inhibit neuronal apoptosis and protect neurons after CPR in rats.