Objective: To define the mechanism by which swine TRIM25 restricts vesicular stomatitis virus replication. Methods: Porcine 3D4/21 cells with TRIM25 overexpression or knockdown were infected with vesicular stomatitis virus. Viral replication was quantified by immunoblotting, quantitative reverse transcription polymerase chain reaction, and 50% tissue culture infectious dose assays. Type I interferon signaling was assessed by transcript quantification, interferon-beta and interferon-stimulated response element reporter assays, and co-immunoprecipitation.Viral RNA binding was tested by RNA immunoprecipitation. Results: TRIM25 overexpression reduced viral RNA and infectious titers, whereas TRIM25 knockdown increased replication (p < 0.01). TRIM25 increased interferon-beta and interferon-stimulated gene expression and enhanced interferon-beta and interferonstimulated response element promoter activity (p < 0.01). Mechanistically, TRIM25 promoted Lys63-linked ubiquitination of RIG-I and increased phosphorylation of TANK-binding kinase 1 and interferon regulatory factor 3. TRIM25 also bound vesicular stomatitis virus genomic RNA, and binding required the C-terminal region. Conclusions and Relevance: Porcine TRIM25 restricts vesicular stomatitis virus replication by amplifying type I interferon signaling and directly binding viral RNA.

The interplay between psychological pain and physical pain is one of the key issues in the research of non-suicidal self-injury (NSSI). Psychological pain, driven by negative self-perception and difficulties in emotional regulation, activates specific brain regions, such as the anterior cingulate gyrus and insula, areas that overlap with neural networks involved in physical pain. Physical pain can, in turn, activate distinct neural pathways that temporarily alleviate psychological pain. However, repeated self-injury may lead to increased pain tolerance over time, contributing to a vicious cycle. This paper reviews the potential neural network connections and interactions between psychological and physical pain in the context of NSSI behavior. It also summarizes current clinical interventions and their effectiveness in treating NSSI, aiming to offer new insights for future research and clinical practice in preventing and treating NSSI.

The interplay between psychological pain and physical pain is one of the key issues in the research of non-suicidal self-injury (NSSI). Psychological pain, driven by negative self-perception and difficulties in emotional regulation, activates specific brain regions, such as the anterior cingulate gyrus and insula, areas that overlap with neural networks involved in physical pain. Physical pain can, in turn, activate distinct neural pathways that temporarily alleviate psychological pain. However, repeated self-injury may lead to increased pain tolerance over time, contributing to a vicious cycle. This paper reviews the potential neural network connections and interactions between psychological and physical pain in the context of NSSI behavior. It also summarizes current clinical interventions and their effectiveness in treating NSSI, aiming to offer new insights for future research and clinical practice in preventing and treating NSSI.

Objective To observe the expressions of oxidized low density lipoprotein ( OxLDL ) receptor CD36 in kidney tissue of diabetic rats and in tubular cells incubated with OxLDL, and to explore the association of CD36 with the tubular injury and renal fibrosis in the process of diabetic nephropathy. Methods Diabetic rat model with hyperlipidemia was established by feeding with high sugar and fat diet and injection of low dose streptozotocin intraperitoneally. The expression of CD36 in kidney tissues was analyzed immunohistochemically. Meanwhile, the tubular sclerosis and fibrosis injury index were estimated and calculated. NRK-52E cells were stimulated with 50 mg/L OxLDL for 5, 10, 24, and 48 h, or 100 and 150 mg/L OxLDLs for 2 and 3 days. The protein expression of CD36 was detected by Western blot. Results The expression of CD36 in the renal tubulointerstitium of diabetic rats was increased comparing to that in control rats, and was localized mainly at tubular region. The renal tubular damage index(STI)ofdiabetesgroupwashigherthanthatincontrolgroup(5.54±1.5vs0.65±0.15,P<0.05). OxLDL stimulated CD36 expression in NRK-52E cells in a dose-and time-dependent manner. Conclusion The expression of CD36 was increased in renal tubular of diabetic rats, in consistent with STI. OxLDL increased CD36 expression in NRK-52E cells. These results suggest that the expression of CD36 is associated with renal tubular damages in experimental rat diabetes.

Objective To examine the relationship between quetiapine serum concentration,dose,therapeu-tic efficacy and side effects in male patients with schizophrenia.Methods Sixty-three male patients with schizo-phrenia were collected.They were treated openly for 8 weeks with quetiapine,the dose was adjusted according to clini-cal improvement and tolerance.The plasma quetiapine concentrations,therapeutic efficacy and adverse drug reactions were observed after the 4 -week treatment period,and at the end of the 8 weeks of the treatment.Results After 4 weeks,the serum concentration had significant correlation with age,the disease duration and education level.After 8 weeks,there was significant correlation between serum concentration and age.We found a correlation between dose and serum concentration of quetiapine,and no relationship between serum concentration and PANSS scores.Side effects were correlated with 4 weeks′serum concentrations.Conclusion Quetiapine is effective for male patients with schizophrenia.Age,quetiapine dose and side effects have significant correlations with the serum concentration.It appears that plasma quetiapine concentration has no effects on therapeutic efficacy.