BACKGROUND:Acute liver injury can result from a variety of causes,and if not treated in time,it will develop into acute liver failure and seriously affect the life safety of patients.As the liver is the largest immune organ and metabolic organ,there is no optimal treatment for acute liver injury.The adipose tissue-derived mesenchymal stem cell has multi-differentiation potential and immunomodulatory activity,so it has been gradually becoming an effective tool for the treatment of acute liver injury.OBJECTIVE:To review the progress and molecular mechanism of adipose tissue-derived mesenchymal stem cell and its modification in different ways in the treatment of acute liver injury.METHODS:Relevant articles published from 2000 to 2023 were retrieved from PubMed,Web of Science,and CNKI databases.English search terms were"acute liver injury,liver injury,adipose tissue-derived mesenchymal stem cell,liver injury repair,stem cell transplantation,stem cell repair,cell surface engineering,stem cell modification."Chinese search terms were"acute liver injury,liver injury,adipose tissue-derived mesenchymal stem cell,liver injury repair,stem cell transplantation,stem cell repair,stem cell modification."Totally 62 articles of the latest research progress in this field were summarized and analyzed.RESULTS AND CONCLUSION:(1)Adipose tissue-derived mesenchymal stem cell as a potential stem cell with multi-directional differentiation has biological advantages in the treatment of acute liver injury.Compared with the other two major types of mesenchymal stem cell that is bone marrow mesenchymal stem cell and umbilical cord mesenchymal stem cell,they are more widely sourced,easily accessible and have fewer ethical issues,and more self-renewal than bone marrow mesenchymal stem cell.(2)Adipose tissue-derived mesenchymal stem cell may play a therapeutic role in acute liver injury by regulating immune responses,differentiating into hepatocytes,and secreting growth factors and exosomes.It can reduce the expression of inflammatory factors in serum and the infiltration of inflammatory cells in liver tissue,also can inhibit the pyroptosis and autophagy levels to promote regeneration of sinusoidal endothelial cells and hepatocyte,and ultimately improve liver damage.At present,no studies have shown which mechanism is the best mechanism for adipose tissue-derived mesenchymal stem cells to treat acute liver injury,and most opinions believe that these molecular mechanisms interact with each other to play a synergistic role in treatment.(3)Biomaterials modification and drug pretreatment can improve the efficacy of adipose tissue-derived mesenchymal stem cell in the treatment of acute liver injury.On the one hand,biomaterials and drug modifications can enhance the functions of adipose tissue-derived mesenchymal stem cell,such as enhancing the ability of proliferation and migration,increasing the level of growth factors secreted,and enhancing the anti-inflammatory ability and promoting the survival of adipose mesenchymal stem cells at the injury site.On the other hand,biomaterials and drug modifications can inhibit the activation of inflammatory cells at the injured site and promote the growth of blood to improve the success rate of transplantation.(4)In summary,adipose tissue-derived mesenchymal stem cell plays an important role in the treatment of acute liver injury by secreting growth factors and exosomes,regulating the immune response,and promoting liver regeneration.With the development of science and technology,biomaterials and drug modification can enhance the self-renewal ability of adipose tissue-derived mesenchymal stem cell and improve the local microenvironment of acute liver injury.It provides a new way to promote the clinical application of adipose tissue-derived mesenchymal stem cell in the treatment of acute liver injury.

Objective:To explore the effect of inhibiting miR-203a-3p gene expression on proliferation and apoptosis of rheu-matoid arthritis(RA)synovial fibroblasts.Methods:Divided fibroblast-like synovial cells MH7A into Control group(untransfected cells),anti-miR-NC group(transfected with anti-miR-NC),anti-miR-203a-3p group(transfected with anti-miR-203a-3p),anti-miR-203a-3p+LiCl group(transfected with anti-miR-203a-3p+signal pathway activator LiCl).qRT-PCR was used to detect expression level of miR-203a-3p;clone formation experiment,MTT experiment were used to detect cell proliferation;flow cytometry was used to de-tect cell apoptosis;Western blot was used to detect protein expressions of PCNA,Bcl-2,Bax,Wnt1,β-catenin.Results:Transfec-tion of miR-203a-3p reduced the number of clones and survival rate of MH7A cells,increased rate of apoptosis,reduced expression levels of PCNA,Bcl-2,Wnt1,β-catenin protein,increased expression level of Bax protein.The signaling pathway activator LiCl in-creases the number of clones and survival rate of MH7A cells transfected with miR-203a-3p,reduces the rate of apoptosis,increases the expression level of Wnt1,β-catenin,PCNA,Bcl-2 protein,and reduces expression level of Bax protein.Conclusion:miR-203a-3p may promote proliferation of RA synovial fibroblasts and inhibit cell apoptosis by activating Wnt/β-catenin.

Objective:To explore the effect of inhibiting miR-203a-3p gene expression on proliferation and apoptosis of rheu-matoid arthritis(RA)synovial fibroblasts.Methods:Divided fibroblast-like synovial cells MH7A into Control group(untransfected cells),anti-miR-NC group(transfected with anti-miR-NC),anti-miR-203a-3p group(transfected with anti-miR-203a-3p),anti-miR-203a-3p+LiCl group(transfected with anti-miR-203a-3p+signal pathway activator LiCl).qRT-PCR was used to detect expression level of miR-203a-3p;clone formation experiment,MTT experiment were used to detect cell proliferation;flow cytometry was used to de-tect cell apoptosis;Western blot was used to detect protein expressions of PCNA,Bcl-2,Bax,Wnt1,β-catenin.Results:Transfec-tion of miR-203a-3p reduced the number of clones and survival rate of MH7A cells,increased rate of apoptosis,reduced expression levels of PCNA,Bcl-2,Wnt1,β-catenin protein,increased expression level of Bax protein.The signaling pathway activator LiCl in-creases the number of clones and survival rate of MH7A cells transfected with miR-203a-3p,reduces the rate of apoptosis,increases the expression level of Wnt1,β-catenin,PCNA,Bcl-2 protein,and reduces expression level of Bax protein.Conclusion:miR-203a-3p may promote proliferation of RA synovial fibroblasts and inhibit cell apoptosis by activating Wnt/β-catenin.

BACKGROUND:Acute liver injury can result from a variety of causes,and if not treated in time,it will develop into acute liver failure and seriously affect the life safety of patients.As the liver is the largest immune organ and metabolic organ,there is no optimal treatment for acute liver injury.The adipose tissue-derived mesenchymal stem cell has multi-differentiation potential and immunomodulatory activity,so it has been gradually becoming an effective tool for the treatment of acute liver injury.OBJECTIVE:To review the progress and molecular mechanism of adipose tissue-derived mesenchymal stem cell and its modification in different ways in the treatment of acute liver injury.METHODS:Relevant articles published from 2000 to 2023 were retrieved from PubMed,Web of Science,and CNKI databases.English search terms were"acute liver injury,liver injury,adipose tissue-derived mesenchymal stem cell,liver injury repair,stem cell transplantation,stem cell repair,cell surface engineering,stem cell modification."Chinese search terms were"acute liver injury,liver injury,adipose tissue-derived mesenchymal stem cell,liver injury repair,stem cell transplantation,stem cell repair,stem cell modification."Totally 62 articles of the latest research progress in this field were summarized and analyzed.RESULTS AND CONCLUSION:(1)Adipose tissue-derived mesenchymal stem cell as a potential stem cell with multi-directional differentiation has biological advantages in the treatment of acute liver injury.Compared with the other two major types of mesenchymal stem cell that is bone marrow mesenchymal stem cell and umbilical cord mesenchymal stem cell,they are more widely sourced,easily accessible and have fewer ethical issues,and more self-renewal than bone marrow mesenchymal stem cell.(2)Adipose tissue-derived mesenchymal stem cell may play a therapeutic role in acute liver injury by regulating immune responses,differentiating into hepatocytes,and secreting growth factors and exosomes.It can reduce the expression of inflammatory factors in serum and the infiltration of inflammatory cells in liver tissue,also can inhibit the pyroptosis and autophagy levels to promote regeneration of sinusoidal endothelial cells and hepatocyte,and ultimately improve liver damage.At present,no studies have shown which mechanism is the best mechanism for adipose tissue-derived mesenchymal stem cells to treat acute liver injury,and most opinions believe that these molecular mechanisms interact with each other to play a synergistic role in treatment.(3)Biomaterials modification and drug pretreatment can improve the efficacy of adipose tissue-derived mesenchymal stem cell in the treatment of acute liver injury.On the one hand,biomaterials and drug modifications can enhance the functions of adipose tissue-derived mesenchymal stem cell,such as enhancing the ability of proliferation and migration,increasing the level of growth factors secreted,and enhancing the anti-inflammatory ability and promoting the survival of adipose mesenchymal stem cells at the injury site.On the other hand,biomaterials and drug modifications can inhibit the activation of inflammatory cells at the injured site and promote the growth of blood to improve the success rate of transplantation.(4)In summary,adipose tissue-derived mesenchymal stem cell plays an important role in the treatment of acute liver injury by secreting growth factors and exosomes,regulating the immune response,and promoting liver regeneration.With the development of science and technology,biomaterials and drug modification can enhance the self-renewal ability of adipose tissue-derived mesenchymal stem cell and improve the local microenvironment of acute liver injury.It provides a new way to promote the clinical application of adipose tissue-derived mesenchymal stem cell in the treatment of acute liver injury.

Home rehabilitation is the main rehabilitation model for elderly patients with hip fractures in China, and the application of digital health technology shows great potential in improving the quality of home rehabilitation for this population. This paper describes the concept of digital health technology, the current application status of different types of digital health technology in home rehabilitation for elderly patients with hip fractures, and discusses existing issues and future prospects, aiming to provide a reference for digital home rehabilitation nursing for elderly hip fracture patients.

Home rehabilitation is the main rehabilitation model for elderly patients with hip fractures in China, and the application of digital health technology shows great potential in improving the quality of home rehabilitation for this population. This paper describes the concept of digital health technology, the current application status of different types of digital health technology in home rehabilitation for elderly patients with hip fractures, and discusses existing issues and future prospects, aiming to provide a reference for digital home rehabilitation nursing for elderly hip fracture patients.

Endoplasmic reticulum stress(ERS)plays a crucial role in cellular self-protection.In response to environmental changes,cells activate the unfolded protein response(UPR)and endoplasmic reticulum-associated protein degradation pathways to restore homeostasis.Increasing experimental evidence indicates that hypoxia and inflammation negatively impact synoviocytes in rheumatoid arthritis(RA),leading to the activation of three key endoplasmic reticulum transmembrane proteins:inositol-requiring enzyme 1,protein kinase R-like endoplasmic reticulum kinase,and activating transcription factor 6.These proteins mediate UPR pathways that are implicated in the pathological progression of RA.Targeting ERS-related molecules has emerged as a promising therapeutic strategy for RA.This article reviews the impact of ERS on the pathogenesis of RA and discusses drugs that modulate ERS as potential treatments for the disease.

Objective:To investigate the level of occupational health literacy (OHL) among workers in the electronic manufacturing industry, analyze the influencing factors, and provide a scientific basis for occupational health promotion work.Methods:From July to September 2022, a stratified cluster random sampling method was adopted, and 870 workers from 20 large, medium, small and micro electronic manufacturing enterprises in Guangdong Province were selected as the research subjects. The OHL level of workers was investigated by using the "Personal Questionnaire for Monitoring and Surveying Occupational Health Literacy of National Key Populations", and the influencing factors were analyzed by binary logistic regression.Results:The OHL level of workers in electronic manufacturing industry was 36.09% (314/870). The OHL levels in the four dimensions of occupational health legal knowledge, basic knowledge of occupational health protection, healthy work methods and behaviors, and basic skills of occupational health protection were 39.08% (340/870), 78.97% (687/870), 56.55% (492/870), and 22.41% (195/870), respectively. logistic regression analysis showed that junior high school, senior high school/vocational high school/technical secondary school education, and average monthly income of 5000-6999 yuan and ≥7000 yuan were protective factors for high OHL levels among workers ( P<0.05) . Conclusion:The OHL level of workers in the electronic manufacturing industry is relatively low, and the promotion and intervention of OHL should be actively carried out to effectively improve the health literacy level of workers, focusing on workers with low education and low income.

Objective: To investigate the influencing factors for delay in healthcare-seeking, definitive diagnosis and identification in patients with pulmonary tuberculosis (PTB) in Minhang District, Shanghai Municipality, so as to provide the basis for effectively reducing delay in PTB patients. Methods: Data of PTB patients in Minhang District from 2017 to 2022 were collected from the Infectious Disease Reporting Information System of Chinese Disease Prevention and Control Information System. The prevalence rates of delay in healthcare-seeking, definitive diagnosis and identification were analyzed, and factors affecting delay in healthcare-seeking, definitive diagnosis and identification were identified using multivariable logistic regression models. Results: A total of 4 214 PTB patients were reported in Minhang District from 2017 to 2022, including 2 802 males and 1 412 females, with a male-to-female ratio of 1.98∶1. The majority of patients were aged 25 to <45 years (1 664 cases, 39.49%). The prevalence rates of delay in healthcare-seeking, definitive diagnosis and identification were 36.81%, 30.21% and 38.09%, respectively. Delay in healthcare-seeking was associated with the year (2018, OR=0.708; 2019, OR=0.549; 2020, OR=0.670; 2021, OR=0.682), gender (female, OR=1.199), occupation (worker, OR=1.379; housekeeping service/housework/unemployed, OR=1.481), case identification route (symptom-based consultation, OR=11.159), and level of the first-diagnosed hospital (city-level, OR=1.528). Delay in definitive diagnosis was associated with age (45 to <65 years, OR=1.476), occupation (commercial service, OR=0.687; housekeeping service/housework/unemployed, OR=0.672), household registration (non-local, OR=0.820), case identification route (symptom-based consultation, OR=0.616), pathogen test result (negative/not tested, OR=1.903), and the level of the first-diagnosed hospital (city-level, OR=0.311). Delay in identification was associated with the year (2018, OR=0.785; 2019, OR=0.647; 2020, OR=0.790; 2021, OR=0.710), occupation (commercial service, OR=0.687), household registration (non-local, OR=0.848) and level of the first-diagnosed hospital (city-level, OR=0.560) Conclusions Year, gender, occupation, case identification route and level of the first-diagnosed hospital are influencing factors for delay in healthcare-seeking in PTB patients. Age, occupation, household registration, case identification route, pathogen test result and level of the first-diagnosed hospital are influencing factors for delay in definitive diagnosis. Year, occupation, household registration and level of the first-diagnosed hospital are influencing factors for delay in identification.

BACKGROUND:Rheumatoid arthritis is an inflammatory disease.Many studies have shown that wogonin has a good anti-inflammatory effect on rheumatoid arthritis,but its exact efficacy and specific mechanism of action remain to be clarified. OBJECTIVE:To investigate the mechanism of wogonin ameliorating joint inflammation by regulating endoplasmic reticulum stress pathway in rats with collagen-induced arthritis. METHODS:(1)At the animal level:Female Wistar rats were divided into healthy control group,arthritis model group and wogonin treatment group.Rat models of arthritis in the latter two groups were established by subcutaneous injection of bovine type Ⅱ collagen and adjuvant.In the wogonin group,wogonin was given by gavage for 28 consecutive days after modeling.During this period,the rats in each group were weighed,and arthritis score and ankle swelling were measured every 7 days.After the experiment,the pathological changes of the joint were observed,the mRNA and protein levels of endoplasmic reticulum stress pathway GRP78 and CHOP were detected by qRT-PCR,western blot,and immunohistochemistry.(2)At the cellular level,cell counting kit-8 was used to detect the cytotoxic effect of wogonin on fibroblast-like synoviocytes from rats with collagen-induced arthritis.The fibroblast-like synoviocytes induced by thapsigargin were treated with different concentrations of wogonin.The levels of interleukin-1β and tumor necrosis factor-α in the cell supernatant were detected by ELISA,and the intracellular reactive oxygen species in each group were determined by DCFH-DA probe method.The mRNA and protein levels of GRP78,IRE1α,XBP1s and CHOP were detected by qRT-PCR and western blot,respectively. RESULTS AND CONCLUSION:Compared with the healthy control group,arthritis index score and ankle swelling degree in the arthritis model group were increased(P<0.01),synovial hyperplasia,inflammatory cell infiltration,cartilage destruction and bone erosion were observed in pathological sections,and the mRNA and protein expressions of GRP78 and CHOP in the ankle were significantly increased(P<0.01),which were mainly located in synovial tissue and articular surface.Compared with the arthritis model group,the arthritis index score and ankle swelling degree in the wogonin treatment group were decreased(P<0.05),synovial hyperplasia and the number of inflammatory cells were decreased,cartilage destruction and bone erosion were alleviated,the mRNA and protein expression levels of GRP78 and CHOP in the ankle were decreased(P<0.05),particularly in synovial tissue and on the articular surface.There was no significant difference in body mass among the three groups(P>0.05).In the cell experiment,200 μmol/L wogonin significantly reduced the survival rate of fibroblast-like synoviocytes(P<0.01).Compared with the blank control group,the levels of interleukin-1β,tumor necrosis factor-α,content of reactive oxygen species,and mRNA and protein expression of GRP78,IRE1α,XBP1s,and CHOP in the thapsigargin group were significantly increased(P<0.05);compared with the thapsigargin group,50 and 100 μmol/L wogonin significantly reduced the levels of interleukin-1β and tumor necrosis factor-α in the cell supernatant(P<0.05,P<0.01),and 100 μmol/L wogonin significantly reduced the content of reactive oxygen species(P<0.01)and down-regulated the mRNA and protein expression levels of GRP78,IRE1α,XBP1s and CHOP(all P<0.05).These results suggest that wogonin can effectively alleviate joint inflammatory responses in rats with collagen-induced arthritis,and the endoplasmic reticulum stress pathway may be the key target of its intervention.