AIM:To investigate the effect of intrinsic specific transforming growth factor-β(TGF-β)signaling on regeneration and repair of myofibers in acute skeletal myositismice model induced by cardiotoxin(CTX).METHODS:One hundred and eighty-six wild C57BL/6 mice and one hundred and thirty-eight mice with conditional knockout of TGF-β receptor 2(TGF-βr2)in myofibers(SM TGF-βr2-/-mice)were selected.CTX injection to anterior tibial muscle(TA)in-duced acute myoinjury in mice.Some SM TGF-βr2-/-mice were given Smad signaling agonist SRI-011381(SRI)intramus-cular injection.All mice were mainly divided into the following groups:control group,SM TGF-βr2-/-group and SM TGF-βr2-/-+SRI group.Twenty-four mice were selected in each group.RT-qPCR and immunofluorescence staining were used to detect the relative mRNA level,protein expression of inflammatory cytokines and low-density lipoprotein receptor-related protein 1(LRP1),respectively,while the relative protein expression of myosin heavy chain 3(MHY3)and embryonic myosine heavy chain(eMHC)in damaged muscle was detected by Western blot and immunofluorescence staining.In vi-tro,after being extracted from neonatal mice,myogenic precursor cells(MPCs)were cultured in an pro-inflammatory mi-lieu and treated with SRI,recombinant mouse extracellular matrix protein 1(rmECM1)alone or in combination.Hereby,they were divided into the following seven groups:control-MPCs group,control-MPCs+LPS group,TGF-βr2-/--MPCs group,TGF-βr2-/--MPCs+LPS group,TGF-βr2-/--MPCs+LPS+SRI group,TGF-βr2-/--MPCs+LPS+rmECM1 group,and TGF-βr2-/--MPCs+LPS+SRI+rmECM1 group.Six mice were selected in each group.RT-qPCR and Western blot were used to detect the relative mRNA level,protein expression of major histocompatibility complex class I molecules(MHC-I/H-2Kb),major histocompatibility complex class II molecules(MHC-II/H2-Eα),Toll-like receptor 3(TLR3),and LRP1.And the relative protein expression of MoyD and myogenin in myotubes was detected by immunofluorescence staining.RE-SULTS:In vivo,compared with control group,SM TGF-βr2-/-group showed the significant upregulation of pro-inflamma-tory cytokines(P<0.05),and the opposite trend of anti-inflammatory cytokines,LRP1,MHY3,eMHC in the injured muscle(P<0.05),with delayed regeneration and repair of myofibers.In vitro,compared with control-MPCs+LPS group,LRP1,MoyD and myogenin significantly downregulated in TGF-βr2-/--MPCs+LPS group,but the downregulation trend was corrected after giving SRI treatment(P<0.05).In addition,compared with the TGF-βr2-/--MPCs+LPS group,the combi-nation of rmECM1 and SRI significantly upregulated the protein expression of MyoD and myogenin(P<0.05).CONCLU-SION:In a mouse model of acute skeletal myositis,intrinsic TGF-β signaling specifically in myofibers regulates local im-mune behavior.It promotes the expression of LRP1 in damaged muscle via Smad2/3 signaling,and LRP1 can then fully bind to ECM1,thereby facilitating muscle regeneration and repair,and improving the prognosis of acute skeletal myositis.

To investigate the effectiveness of a self-developed intelligent medical record writing assistant in enhancing the efficiency of discharge record writing and improving the quality of discharge records, and to assess physicians' satisfaction with the assistant.

In recent years, the incidence of liver metastasis from colorectal cancer has continued to rise, posing a significant threat to human health and life.Although traditional treat-ments such as surgery and chemotherapy have shown some efficacy in certain patients, options remain limited for those who are not surgical candidates or are resistant to chemotherapy.Yttrium-90 microsphere selective internal radiation therapy, as an innovative local treatment, has fully demons-trated its effectiveness and safety in treating colorectal cancer liver metastasis patients. The authors review the research background, mechanisms, and principles of yttrium-90 microsphere selective internal radiation therapy in the field of colorectal cancer liver metastasis, and to explore its applica-tion progress in clinical practice, aiming to provide clinical doctors with more comprehensive and detailed reference information, with the goal of improving treatment outcomes and quality of life for colorectal cancer liver metastasis patients.

AIM:To investigate the effect of intrinsic specific transforming growth factor-β(TGF-β)signaling on regeneration and repair of myofibers in acute skeletal myositismice model induced by cardiotoxin(CTX).METHODS:One hundred and eighty-six wild C57BL/6 mice and one hundred and thirty-eight mice with conditional knockout of TGF-β receptor 2(TGF-βr2)in myofibers(SM TGF-βr2-/-mice)were selected.CTX injection to anterior tibial muscle(TA)in-duced acute myoinjury in mice.Some SM TGF-βr2-/-mice were given Smad signaling agonist SRI-011381(SRI)intramus-cular injection.All mice were mainly divided into the following groups:control group,SM TGF-βr2-/-group and SM TGF-βr2-/-+SRI group.Twenty-four mice were selected in each group.RT-qPCR and immunofluorescence staining were used to detect the relative mRNA level,protein expression of inflammatory cytokines and low-density lipoprotein receptor-related protein 1(LRP1),respectively,while the relative protein expression of myosin heavy chain 3(MHY3)and embryonic myosine heavy chain(eMHC)in damaged muscle was detected by Western blot and immunofluorescence staining.In vi-tro,after being extracted from neonatal mice,myogenic precursor cells(MPCs)were cultured in an pro-inflammatory mi-lieu and treated with SRI,recombinant mouse extracellular matrix protein 1(rmECM1)alone or in combination.Hereby,they were divided into the following seven groups:control-MPCs group,control-MPCs+LPS group,TGF-βr2-/--MPCs group,TGF-βr2-/--MPCs+LPS group,TGF-βr2-/--MPCs+LPS+SRI group,TGF-βr2-/--MPCs+LPS+rmECM1 group,and TGF-βr2-/--MPCs+LPS+SRI+rmECM1 group.Six mice were selected in each group.RT-qPCR and Western blot were used to detect the relative mRNA level,protein expression of major histocompatibility complex class I molecules(MHC-I/H-2Kb),major histocompatibility complex class II molecules(MHC-II/H2-Eα),Toll-like receptor 3(TLR3),and LRP1.And the relative protein expression of MoyD and myogenin in myotubes was detected by immunofluorescence staining.RE-SULTS:In vivo,compared with control group,SM TGF-βr2-/-group showed the significant upregulation of pro-inflamma-tory cytokines(P<0.05),and the opposite trend of anti-inflammatory cytokines,LRP1,MHY3,eMHC in the injured muscle(P<0.05),with delayed regeneration and repair of myofibers.In vitro,compared with control-MPCs+LPS group,LRP1,MoyD and myogenin significantly downregulated in TGF-βr2-/--MPCs+LPS group,but the downregulation trend was corrected after giving SRI treatment(P<0.05).In addition,compared with the TGF-βr2-/--MPCs+LPS group,the combi-nation of rmECM1 and SRI significantly upregulated the protein expression of MyoD and myogenin(P<0.05).CONCLU-SION:In a mouse model of acute skeletal myositis,intrinsic TGF-β signaling specifically in myofibers regulates local im-mune behavior.It promotes the expression of LRP1 in damaged muscle via Smad2/3 signaling,and LRP1 can then fully bind to ECM1,thereby facilitating muscle regeneration and repair,and improving the prognosis of acute skeletal myositis.

In recent years, the incidence of liver metastasis from colorectal cancer has continued to rise, posing a significant threat to human health and life.Although traditional treat-ments such as surgery and chemotherapy have shown some efficacy in certain patients, options remain limited for those who are not surgical candidates or are resistant to chemotherapy.Yttrium-90 microsphere selective internal radiation therapy, as an innovative local treatment, has fully demons-trated its effectiveness and safety in treating colorectal cancer liver metastasis patients. The authors review the research background, mechanisms, and principles of yttrium-90 microsphere selective internal radiation therapy in the field of colorectal cancer liver metastasis, and to explore its applica-tion progress in clinical practice, aiming to provide clinical doctors with more comprehensive and detailed reference information, with the goal of improving treatment outcomes and quality of life for colorectal cancer liver metastasis patients.

Objective To investigate the effect of E2 signaling in myofibers on muscular macrophage efferocytosis in mice with cardiotoxin-induced acute skeletal muscle injury.Methods Female wild-type C57BL/6 mice with and without ovariectomy and male C57BL/6 mice were given a CTX injection into the anterior tibial muscle to induce acute muscle injury,followed by intramuscular injection of β-estradiol(E2)or 4-hydroxytamoxifen(4-OHT).The changes in serum E2 of the mice were detected using ELISA,and the number,phenotypes,and efferocytosis of the macrophages in the inflammatory exudates and myofiber regeneration and repair were evaluated using immunofluorescence staining and flow cytometry.C2C12 cells were induced to differentiate into mature myotubes,which were treated with IFN-γ for 24 before treatment with β-Estradiol or 4-OHT.The treated myotubes were co-cultured with mouse peritoneal macrophages in a 1:2 ratio,followed by addition of PKH67-labeled apoptotic mouse mononuclear spleen cells induced by UV irradiation,and macrophage efferocytosis was observed using immunofluorescence staining and flow cytometry.Results Compared with the control mice,the female mice with ovariectomy showed significantly increased mononuclear macrophages in the inflammatory exudates,with increased M1 cell percentage,reduced M2 cell percentage and macrophage efferocytosis in the injured muscle,and obviously delayed myofiber regeneration and repair.In the cell co-culture systems,treatment of the myotubes with β-estradiol significantly increased the number and proportion of M2 macrophages and macrophage efferocytosis,while 4-OHT treatment resulted in the opposite changes.Conclusion In injured mouse skeletal muscles,myofiber E2 signaling promotes M1 to M2 transition to increase macrophage efferocytosis,thereby relieving inflammation and promoting muscle regeneration and repair.

Objective To investigate the effect of E2 signaling in myofibers on muscular macrophage efferocytosis in mice with cardiotoxin-induced acute skeletal muscle injury.Methods Female wild-type C57BL/6 mice with and without ovariectomy and male C57BL/6 mice were given a CTX injection into the anterior tibial muscle to induce acute muscle injury,followed by intramuscular injection of β-estradiol(E2)or 4-hydroxytamoxifen(4-OHT).The changes in serum E2 of the mice were detected using ELISA,and the number,phenotypes,and efferocytosis of the macrophages in the inflammatory exudates and myofiber regeneration and repair were evaluated using immunofluorescence staining and flow cytometry.C2C12 cells were induced to differentiate into mature myotubes,which were treated with IFN-γ for 24 before treatment with β-Estradiol or 4-OHT.The treated myotubes were co-cultured with mouse peritoneal macrophages in a 1:2 ratio,followed by addition of PKH67-labeled apoptotic mouse mononuclear spleen cells induced by UV irradiation,and macrophage efferocytosis was observed using immunofluorescence staining and flow cytometry.Results Compared with the control mice,the female mice with ovariectomy showed significantly increased mononuclear macrophages in the inflammatory exudates,with increased M1 cell percentage,reduced M2 cell percentage and macrophage efferocytosis in the injured muscle,and obviously delayed myofiber regeneration and repair.In the cell co-culture systems,treatment of the myotubes with β-estradiol significantly increased the number and proportion of M2 macrophages and macrophage efferocytosis,while 4-OHT treatment resulted in the opposite changes.Conclusion In injured mouse skeletal muscles,myofiber E2 signaling promotes M1 to M2 transition to increase macrophage efferocytosis,thereby relieving inflammation and promoting muscle regeneration and repair.

Paroxysmal sympathetic hyperactivity (PSH) is mainly secondary to a variety of acquired brain injuries, with the highest incidence of traumatic brain injury. Multiple symptoms such as paroxysmal tachycardia, shortness of breath, hypertension, hyperthermia and dystonia can occur simultaneously and repeatedly. The pathophysiological mechanism of PSH is complex. At present, drug treatment is mainly used to control symptoms; however, the combined use of multiple drugs will bring different degrees of toxic and side effects to multiple organs such as liver, kidney and lung while inhibiting sympathetic excitement. This paper mainly reviews the recent advance in non-drug treatment of PSH after craniocerebral injury from 4 aspects: nutritional support, hyperbaric oxygen therapy, avoidance of adverse stimulation and family support to standardize the PSH comprehensive management, and reduce episodes in order to improve prognosis and provide reference for clinical treatment.

Since 2010, the incidence of severe fever with thrombocytopenia syndrome (SFTS) has been increased. Owing the progress in diagnosis and treatment, the overall mortality of SFTS in China has decreased, while the mortality in critical SFTS patients is still high. In order to provide guidance and working procedures for clinicians to diagnose and treat critical SFTS, the National Medical Center for Major Public Health Events invited experts to discuss and formulate this consensus based on their experience and up-to-date knowledge on SFTS.

ObjectiveTo investigate epidemiological characteristics and influencing factors of non-suicidal self-injury （NSSI） behaviors among middle school students in Jiangmen. MethodsA total of 1 220 middle school students in Jiangmen were selected for the study through stratified random sampling from November to December 2020. The self-compiled general demographic questionnaire， Coping Style Scale for Middle School Students， Olweus Bully/Victim Questionnaire （BVQ）， Social Support Scale for Adolescents， and Center for Epidemiologic Studies-Depression Scale （CES-D） were used for the assessment. Then binary Logistic regression analysis was performed to screen the factors influencing NSSI behaviors in students. ResultsA total of 204 middle school students （16.72%） were found to be engaged in NSSI behaviors， of whom 67 were male and 137 were female. There were statistically significant differences between the NSSI group and the non-NSSI group in terms of gender， school period， lodging， peer relationship and academic performance （χ²=22.162， 7.247， 6.541， 45.787， 25.097， P<0.05 or 0.01）. Compared with the non-NSSI group， the NSSI group scored higher on CES-D （t=-14.240） and BVQ （t=-5.952）， lower on Social Support Scale for Adolescents （t=9.238）. Within the Coping Style Scale for Middle School Students， NSSI group had lower problem-focused coping score （t=7.148） and higher emotion-focused coping score （t=-7.038） than those of non-NSSI group. The detection rates of school bullying， verbal and relational bullying were higher in NSSI group compared with non-NSSI group （χ²=34.215， 29.785，16.465）. The differences were statistically significant （P<0.01）. Binary Logistic regression showed that depression （OR=1.090， P<0.01） and school bullying （OR=1.492， P<0.05） entered into the regression model. ConclusionThe situation of NSSI behaviors of middle school students in Jiangmen is serious， and depression and school bullying are risk factors affecting NSSI behaviors in students.