Human immunodeficiency virus(HIV)is the pathogen of acquired immune deficiency syndrome(AIDS).The vi-rus is a highly contagious and highly pathogenic disease caused by the virus attacking the human immune system,which remains a ma-jor global public health problem.Interferon(IFN)is a key cytokine with antiviral and cell-regulatory properties,involved in functions such as cell proliferation,innate and adaptive immune responses.The JAK/STAT signaling pathway is a signal transduction pathway stimulated by cytokines that is involved in many important biological processes such as cell proliferation,differentiation,apoptosis,and immune regulation.With the further in-depth research on AIDS,it has been revealed that IFN and the JAK/STAT pathway play crucial roles in the activation and replication of HIV-1 in target cells.This paper summarizes the structure,signal transduction,and regulatory mechanisms of IFN and the JAK/STAT pathway,and explores the mechanism of IFN-regulated JAK/STAT signaling path-way in HIV-1.It is expected to provide new treatment strategies for the clinical treatment of AIDS.

Human immunodeficiency virus(HIV)is the pathogen of acquired immune deficiency syndrome(AIDS).The vi-rus is a highly contagious and highly pathogenic disease caused by the virus attacking the human immune system,which remains a ma-jor global public health problem.Interferon(IFN)is a key cytokine with antiviral and cell-regulatory properties,involved in functions such as cell proliferation,innate and adaptive immune responses.The JAK/STAT signaling pathway is a signal transduction pathway stimulated by cytokines that is involved in many important biological processes such as cell proliferation,differentiation,apoptosis,and immune regulation.With the further in-depth research on AIDS,it has been revealed that IFN and the JAK/STAT pathway play crucial roles in the activation and replication of HIV-1 in target cells.This paper summarizes the structure,signal transduction,and regulatory mechanisms of IFN and the JAK/STAT pathway,and explores the mechanism of IFN-regulated JAK/STAT signaling path-way in HIV-1.It is expected to provide new treatment strategies for the clinical treatment of AIDS.

Radiation-induced rectal injury (RRI) refers to inflammatory intestinal complications of patients with pelvic cavity, abdominal cavity and retroperitoneal tumor during or after radiotherapy, presenting symptoms such as diarrhea, abdominal pain, anal distension, bloody stool, etc. In severe cases, rectovaginal fistula, intestinal obstruction, canceration can occur, adversely affecting the quality of life of patients. The clinical factors of RRI involve total radiotherapy dose, tumor volume, radiotherapy mode and patient-related risk factors. The diagnosis mainly depends on imaging examinations (such as CT, MRI and ultrasound), endoscopy and laboratory examination. The mechanism of RRI is related to intestinal epithelial cell destruction, stem cell injury, microvascular changes and microbial flora imbalance. At present, there is no gold standard for RRI treatment, and the main measures include surgical treatment, internal medicine treatment, hyperbaric oxygen therapy and fecal microbiota transplantation, etc. In this article, the latest progress in the pathogenesis, diagnosis and treatment of RRI was reviewed.

Objective:To investigate the causal relationship between type 2 diabetes mellitus (T2DM), type 1 diabetes mellitus (T1DM), body mass index (BMI) and papillary thyroid cancer using Mendelian randomization(MR) study.Methods:Publicly available genome-wide association studies (GWAS) were used as the data source to screen single nucleotide polymorphisms significantly associated with exposure factors (instrumental variables), and the inverse variance weighting (IVW), weighted median, MR-Egger analysis, simple mode, and weighted mode of two-sample MR were used to assess the causal association between T2DM, T1DM, BMI and papillary thyroid cancer. The reliability and stability of the results were assessed by heterogeneity analysis, multiple validity analysis and sensitivity analysis.Results:A total of 118 strong instrumental variables for T2DM, 76 for T1DM, and 486 for BMI were screened respectively to conduct two-sample MR analysis. Among the 5 MR analysis methods, the results of the IVW method showed that T2DM was significantly associated with papillary thyroid cancer (odds ratio ( OR)=1.147, 95% CI: 1.026-1.282; P=0.016), and the genetic effect values ( β values) of the other 4 analysis methods and IVW method were in the same direction; the results of heterogeneity analysis, multiplicity analysis and sensitivity analysis showed all P>0.05. T1DM (IVW method: OR=1.000, 95% CI: 0.952-1.051; P=0.994) and papillary thyroid cancer, BMI (IVW method: OR=1.214, 95% CI: 0.923-1.598; P=0.166) and papillary thyroid cancer were not clearly causally related. Conclusions:There is a causal association between T2DM and papillary thyroid cancer, and T2DM increases the risk of papillary thyroid cancer. There is no clear causal association between T1DM, BMI and papillary thyroid cancer.

Objective:To investigate the causal relationship between type 2 diabetes mellitus (T2DM), type 1 diabetes mellitus (T1DM), body mass index (BMI) and papillary thyroid cancer using Mendelian randomization(MR) study.Methods:Publicly available genome-wide association studies (GWAS) were used as the data source to screen single nucleotide polymorphisms significantly associated with exposure factors (instrumental variables), and the inverse variance weighting (IVW), weighted median, MR-Egger analysis, simple mode, and weighted mode of two-sample MR were used to assess the causal association between T2DM, T1DM, BMI and papillary thyroid cancer. The reliability and stability of the results were assessed by heterogeneity analysis, multiple validity analysis and sensitivity analysis.Results:A total of 118 strong instrumental variables for T2DM, 76 for T1DM, and 486 for BMI were screened respectively to conduct two-sample MR analysis. Among the 5 MR analysis methods, the results of the IVW method showed that T2DM was significantly associated with papillary thyroid cancer (odds ratio ( OR)=1.147, 95% CI: 1.026-1.282; P=0.016), and the genetic effect values ( β values) of the other 4 analysis methods and IVW method were in the same direction; the results of heterogeneity analysis, multiplicity analysis and sensitivity analysis showed all P>0.05. T1DM (IVW method: OR=1.000, 95% CI: 0.952-1.051; P=0.994) and papillary thyroid cancer, BMI (IVW method: OR=1.214, 95% CI: 0.923-1.598; P=0.166) and papillary thyroid cancer were not clearly causally related. Conclusions:There is a causal association between T2DM and papillary thyroid cancer, and T2DM increases the risk of papillary thyroid cancer. There is no clear causal association between T1DM, BMI and papillary thyroid cancer.

Radiation-induced rectal injury (RRI) refers to inflammatory intestinal complications of patients with pelvic cavity, abdominal cavity and retroperitoneal tumor during or after radiotherapy, presenting symptoms such as diarrhea, abdominal pain, anal distension, bloody stool, etc. In severe cases, rectovaginal fistula, intestinal obstruction, canceration can occur, adversely affecting the quality of life of patients. The clinical factors of RRI involve total radiotherapy dose, tumor volume, radiotherapy mode and patient-related risk factors. The diagnosis mainly depends on imaging examinations (such as CT, MRI and ultrasound), endoscopy and laboratory examination. The mechanism of RRI is related to intestinal epithelial cell destruction, stem cell injury, microvascular changes and microbial flora imbalance. At present, there is no gold standard for RRI treatment, and the main measures include surgical treatment, internal medicine treatment, hyperbaric oxygen therapy and fecal microbiota transplantation, etc. In this article, the latest progress in the pathogenesis, diagnosis and treatment of RRI was reviewed.

Objective To investigate the clinical features of of patients with Staphylococcus aureus blood-stream infection and risk factors for septic shock.Methods A total of 51 patients diagnosed with Staphylococ-cus aureus bloodstream infection in the hospital from January 2018 to March 2023 were enrolled in the study.According to whether the patients developed septic shock,they were divided into septic shock group and non-septic shock group.The clinical data of the patients were collected,and the clinical laboratory indicators were detected on the day of blood culture samples were collected.Bacteria isolated from blood culture specimens of patients were identified and tested for drug sensitivity.The clinical data and clinical laboratory test indicators of the two groups were compared.Multivariate Logistic regression was used to analyze the independent risk factors of septic shock in patients with Staphylococcus aureus bloodstream infection.The receiver operating characteristic(ROC)curve was used to analyze the predictive value of clinical laboratory test indicators for septic shock in patients with Staphylococcus aureus bloodstream infection.Results Septic shock occurred in 12 of 51 patients,with an incidence of 23.5％.The proportion of patients with diabetes,gouty arthritis,the proportion of patients with long-term glucocorticoid use,the proportion of patients with respiratory tract in-fection,the proportion of patients who died,and the hospitalization cost in the septic shock group were higher than those in the non-septic shock group,and the differences were statistically significant(P＜0.05).Long-term glucocorticoid use was an independent risk factor for septic shock in Staphylococcus aureus bloodstream infection(P＜0.05).The combination of C-reactive protein(CRP),albumin(Alb),neutrophil/lymphocyte ratio(NLR)and procalcitonin(PCT)had high value in predicting septic shock in patients with Staphylococ-cus aureus bloodstream infection,and the area under the ROC curve was 0.983.Conclusion Long-term use of glucocorticoids can lead to an increased risk of septic shock in patients with Staphylococcus aureus blood-stream infection.The combined detection of CRP,Alb,NLR and PCT has a higher predictive value than single detection for septic shock in patients with Staphylococcus aureus bloodstream infection.

Liver regeneration following injury aids the restoration of liver mass and the recovery of liver function. In the present study we investigated the contribution of megakaryocytic leukemia 1 (MKL1), a transcriptional modulator, to liver regeneration. We report that both MKL1 expression and its nuclear translocation correlated with hepatocyte proliferation in cell and animal models of liver regeneration and in liver failure patients. Mice with MKL1 deletion exhibited defective regenerative response in the liver. Transcriptomic analysis revealed that MKL1 interacted with E2F1 to program pro-regenerative transcription. MAPKAPK2 mediated phosphorylation primed MKL1 for its interaction with E2F1. Of interest, phospholipase d2 promoted MKL1 nuclear accumulation and liver regeneration by catalyzing production of phosphatidic acid (PA). PA administration stimulated hepatocyte proliferation and enhanced survival in a MKL1-dependent manner in a pre-clinical model of liver failure. Finally, PA levels was detected to be positively correlated with expression of pro-regenerative genes and inversely correlated with liver injury in liver failure patients. In conclusion, our data reveal a novel mechanism whereby MKL1 contributes to liver regeneration. Screening for small-molecule compounds boosting MKL1 activity may be considered as a reasonable approach to treat acute liver failure.

ObjectiveTo investigate the role and mechanism of action of Yinchenhao Decoction in inhibiting ferroptosis of hepatocytes in mice with autoimmune hepatitis. MethodsA total of 18 specific pathogen-free female C57BL/6 mice were selected and divided into normal group， model group， and treatment group using a random number table， with 6 mice in each group. The mice in the model group and the treatment group were injected with concanavalin A （Con A） via the caudal vein to establish a mouse model of autoimmune hepatitis， and those in the normal group were injected with normal saline. The mice in the treatment group were given prophylactic treatment with Yinchenhao Decoction （4.68 g crude drug/kg） by gavage at 14 days before modeling， and Con A was injected after the last gavage. The levels of alanine aminotransferase （ALT）， aspartate aminotransferase （AST）， interferon gamma （IFN-γ）， tumor necrosis factor-α （TNF-α）， iron ion， glutathione （GSH）， reactive oxygen species （ROS）， adenosine triphosphate （ATP）， and malondialdehyde （MDA） were measured； liver index and spleen index were calculated； the expression levels of GPX4 and SLC7A11 were measured； liver histopathological changes were compared between groups. A one-way analysis of variance was used for comparison of normally distributed continuous data between three groups， and the least significant difference t-test was used for further comparison between two groups. ResultsCompared with the normal group， the model group had significant increases in liver index， spleen index， ALT， AST， IFN-γ， TNF-α， iron ion， ROS and MDA （all P<0.05） and significant reductions in the content of GSH and ATP and the protein expression levels of GPX4 and SLC7A11 （all P<0.05）. Compared with the model group， the treatment group had significant reductions in liver index， spleen index， ALT， AST， IFN-γ， TNF-α， iron ion， ROS and MDA （all P<0.05） and significant increases in the content of GSH and ATP and the protein expression levels of GPX4 and SLC7A11 （all P<0.05）. HE staining showed that compared with the normal group， the model group showed massive hepatocyte degeneration and necrosis and inflammatory cell aggregation at the portal area， and compared with the model group， the treatment group had alleviation of liver necrosis and inflammatory infiltration. ConclusionLiver injury induced by Con A may be associated with ferroptosis. Yinchenhao Decoction can increase the protein expression levels of SLC7A11 and GPX4 protein and thus inhibit ferroptosis of hepatocytes induced by Con A.

The biological clock(also known as the circadian rhythm)is the fundamental reliance for all organisms on Earth to adapt and survive in the Earth's rotation environment.Circadian rhythm is the most basic regulatory mechanism of life activities,and plays a key role in maintaining normal physiological and biochemical homeostasis,disease occurrence and treatment.Recent studies have shown that the biologi-cal clock plays an important role in the development of oral tissues and in the occurrence and treatment of oral diseases.Since there is cur-rently no guiding literature on the research methods of biological clock in stomatology,researchers mainly conduct research based on pub-lished references,which has led to controversy about the research methods of biological clock in stomatology,and there are many confusions about how to rationally apply the research methods of circadia rhythms.In view of this,this expert consensus summarizes the characteristics of the biological clock and analyzes the shortcomings of the current biological clock research in stomatology,and organizes relevant experts to summarize and recommend 10 principles as a reference for the rational implementation of the biological clock in stomatology research.