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 .

A 25-year-old woman with rheumatoid arthritis was treated with prednisone,leflunomide,hydroxychloroquine,and calcium carbonate vitamin D.Her condition was controlled well.Because of her fertility requirement,the therapeutic regimen was changed to sulfasalazine 1.0 g and hydroxychloroquine 0.2 g twice daily orally.About 2 months later,the patient developed fever,sore throat,swelling of bilateral tonsils (degree Ⅱ) with purulent exudates on the surface,and bilateral cervical lymph nodes swelling.Laboratory tests showed white blood cell count 0.6 × 109/L and neutrophil count 0.01 × 109/L.The patient was diagnosed as having agranulocytosis induced by sulfasalazine accompanied by acute suppurative tonsillitis.Sulfasalazine and hydroxychloroquine were stopped and subcutaneous injection of recombinant human granulocyte colony stimulating factor 150 μg once daily were given for 6 consecutive days.Meanwhile,anti-infectious and symptomatic support treatments were given.Three weeks later,her white blood cell count and neutrophil count were returned to normal,and the clinical symptoms disappeared.Hydroxychloroquine and calcium carbonate vitamin D were given again.At 6 months of follow-up,the blood routine test results were normal and the condition of rheumatoid arthritis was stable.

A 25-year-old woman with rheumatoid arthritis was treated with prednisone,leflunomide,hydroxychloroquine,and calcium carbonate vitamin D.Her condition was controlled well.Because of her fertility requirement,the therapeutic regimen was changed to sulfasalazine 1.0 g and hydroxychloroquine 0.2 g twice daily orally.About 2 months later,the patient developed fever,sore throat,swelling of bilateral tonsils (degree Ⅱ) with purulent exudates on the surface,and bilateral cervical lymph nodes swelling.Laboratory tests showed white blood cell count 0.6 × 109/L and neutrophil count 0.01 × 109/L.The patient was diagnosed as having agranulocytosis induced by sulfasalazine accompanied by acute suppurative tonsillitis.Sulfasalazine and hydroxychloroquine were stopped and subcutaneous injection of recombinant human granulocyte colony stimulating factor 150 μg once daily were given for 6 consecutive days.Meanwhile,anti-infectious and symptomatic support treatments were given.Three weeks later,her white blood cell count and neutrophil count were returned to normal,and the clinical symptoms disappeared.Hydroxychloroquine and calcium carbonate vitamin D were given again.At 6 months of follow-up,the blood routine test results were normal and the condition of rheumatoid arthritis was stable.

A 41-year-old woman with systemic lupus erythematosus ( SLE ) took 10 mg dydrogesterone orally twice daily for 7 days for endometrial hyperplasia. Four days after dydrogesterone administration,she developed red maculopapule on her face. She took dydrogesterone at the same dosage for 14 days for second month and developed more severe rashes and generalized exanthematous pustulosis. Active SLE,infections,intoxication or tumors were excluded by lab examinations and SLE disease activity index scores and autoimmune progesterone dermatitis induced by dydrogesterone was diagnosed. Dydrogesterone was stopped and antianaphylaxis treatment was given. Two months later,her symptoms improved gradually and no skin rash was found at 3-month follow-up.

Objective To explore the factors related to ovarian injury after cyclophosphamide therapy in the patients with systemic lupus erythematosus(SLE)and Takayasu arteritis(TA). Methods Data of patients with SLE and TA hospitalized in Xuanwu Hospital of Capital Medical University from June 2012 to October 2014 were collected and a retrospective study was conducted. All patients received cyclophosphamide treatment and were followed up in the outpatient setting. The patients with SLE who used cyclophosphamide treatment were divided into SLE group and the patients with TA who used cyclophosphamide treatment were divided into TA group. The overall incidence of ovarian injury,the incidence of amenorrhea and the time after cyclophosphamide treatment and the cumulative dosage which led to ovarian injury and amenorrhea were recorded and compared. Results Sixty-three patients were enrolled,46 cases were in SLE group,ages ranged from 15 to 41years;17 cases were in TA group,ages ranged from 17 to 37 years. Two groups of patients with ovarian injury after cyclophosphamide occurred mainly from 20 to 39 years. The overall incidence of ovarian injury and incidence of amenorrhea in two groups had no statistically significant difference[60. 9%(28 / 46)vs. 35. 3%(6 / 17),19. 6%(9 / 46)vs. 5. 9%(1 / 17),all P > 0. 05]. The ovarian injury in SLE group occurred in week 6 after cyclophosphamide treatment,the average time was 13 weeks. In TA group ovarian injury occurred in week 16,the average time was 21 weeks. Ovarian injury occurred earlier in SLE group than that in TA group,the difference was statistically significant(P = 0. 021). The cumulative dose of cyclophosphamide in SLE group was lower than that the TA group[(7. 2 ± 0. 8)g vs.(8. 0 ± 0. 9)g],the difference was statistically significant(P =0. 045). The cumulative dose of cyclophosphamide and the age showed a negative correlation(SLE group r = - 0. 681,P = 0. 028;TA group r = - 0. 244,P = 0. 043). Conclusions The cumulative dose of cyclophosphamide in patients with SLE and TA is a risk factor for ovarian injury. The cumulative dose of cyclophosphamide in SLE patients was less than patients with TA. The older patient who use cyclophosphamide initially are at greater risk of ovarian injury.

A 41-year-old woman with systemic lupus erythematosus ( SLE ) took 10 mg dydrogesterone orally twice daily for 7 days for endometrial hyperplasia. Four days after dydrogesterone administration,she developed red maculopapule on her face. She took dydrogesterone at the same dosage for 14 days for second month and developed more severe rashes and generalized exanthematous pustulosis. Active SLE,infections,intoxication or tumors were excluded by lab examinations and SLE disease activity index scores and autoimmune progesterone dermatitis induced by dydrogesterone was diagnosed. Dydrogesterone was stopped and antianaphylaxis treatment was given. Two months later,her symptoms improved gradually and no skin rash was found at 3-month follow-up.

Objective To explore the factors related to ovarian injury after cyclophosphamide therapy in the patients with systemic lupus erythematosus(SLE)and Takayasu arteritis(TA). Methods Data of patients with SLE and TA hospitalized in Xuanwu Hospital of Capital Medical University from June 2012 to October 2014 were collected and a retrospective study was conducted. All patients received cyclophosphamide treatment and were followed up in the outpatient setting. The patients with SLE who used cyclophosphamide treatment were divided into SLE group and the patients with TA who used cyclophosphamide treatment were divided into TA group. The overall incidence of ovarian injury,the incidence of amenorrhea and the time after cyclophosphamide treatment and the cumulative dosage which led to ovarian injury and amenorrhea were recorded and compared. Results Sixty-three patients were enrolled,46 cases were in SLE group,ages ranged from 15 to 41years;17 cases were in TA group,ages ranged from 17 to 37 years. Two groups of patients with ovarian injury after cyclophosphamide occurred mainly from 20 to 39 years. The overall incidence of ovarian injury and incidence of amenorrhea in two groups had no statistically significant difference[60. 9%(28 / 46)vs. 35. 3%(6 / 17),19. 6%(9 / 46)vs. 5. 9%(1 / 17),all P > 0. 05]. The ovarian injury in SLE group occurred in week 6 after cyclophosphamide treatment,the average time was 13 weeks. In TA group ovarian injury occurred in week 16,the average time was 21 weeks. Ovarian injury occurred earlier in SLE group than that in TA group,the difference was statistically significant(P = 0. 021). The cumulative dose of cyclophosphamide in SLE group was lower than that the TA group[(7. 2 ± 0. 8)g vs.(8. 0 ± 0. 9)g],the difference was statistically significant(P =0. 045). The cumulative dose of cyclophosphamide and the age showed a negative correlation(SLE group r = - 0. 681,P = 0. 028;TA group r = - 0. 244,P = 0. 043). Conclusions The cumulative dose of cyclophosphamide in patients with SLE and TA is a risk factor for ovarian injury. The cumulative dose of cyclophosphamide in SLE patients was less than patients with TA. The older patient who use cyclophosphamide initially are at greater risk of ovarian injury.