Abstract: Objective We investigated the effects of ICAM5 in the hippocampus on the alcohol drinking preference of mice, and the potential mechanisms. Methods An alcohol two-bottle choice model was developed in 8-week-old male C57BL/ 6J mice, which were randomly divided to two groups: water group and alcohol group. The protein expression of ICAM5 in the hippocampus, amygdala, and medial prefrontal cortex was detected. An ICAM5-overexpressing adeno-associated virus was constructed and injected into the hippocampus by stereotaxic method. The expression level of ICAM5 protein in the hippocampus was detected by immunofluorescence and Western blot. We then detected the alcohol preference and locomotor activity of mice with a conditioned place preference (CPP) experiment, open field test, and lossof-righting reflex test. Western blot analysis was used to identify the neuron F-actin / G-actin ratio. Using Golgi staining, the morphology of dendritic spines was identified. Results The expression of ICAM5 in the hippocampus of alcohol two-bottle choice model mice in the alcohol group was considerably lower than that of the water group ( P<0. 001). The specific expression of ICAM5 in the hippocampus of mice was observed by fluorescence microscopy. In the open field experiment,the staying time and moving distance of the AAV-ICAM5 group were significantly increased compared with those of the control group ( P<0. 01). In the CPP experiment, the residence time of AAV-ICAM5 mice in the alcohol-paired compartment was significantly lower than that of control mice ( P<0. 001). In the loss-of-righting reflex experiment,overexpression of ICAM5 significantly reduced sedation latency ( P<0. 01), but significantly shortened the duration of sedation (P<0. 001). Compared with AAV-mCherry +Water group, the ratio of F-actin / G-actin in the hippocampus was significantly increased after drinking ( P<0. 01 ), but after ICAM5 overexpression, their F-actin / G-actin ratio was significantly decreased (P<0. 001). Compared with AAV-mCherry + Water group, the density of dendritic spines in the hippocampal CA1 region was increased (P<0. 001), but the density of dendritic spines in the AAV-ICAM5+Alcohol group was significantly decreased (P<0. 01). Conclusions ICAM5 modulated the expression of cytoskeleton proteins to change the structural plasticity of dendritic spines, which contributed to alcohol-drinking and locomotor behavioral changes in mice.

Abstract: Objective To study the role of ubiquitin-conjugating enzyme 9 ( UBC9) in the pyroptosis of homocysteine-induced macrophages mediated by small ubiquitin-like modifier (SUMO) modification. Methods First, the effects of homocysteine at different concentrations (0 μmol / L, 50 μmol / L, 100 μmol / L, 150 μmol / L and 200 μmol / L) on the viability and pyrodeath of mouse macrophages (RAW264. 7) were detected by CCK-8 and Western blot. Western blot was used to detect the expression levels of UBC9, SUMO-1, and the inflammatory cytokine IL-1β in different groups of cells. qRT-PCR was used to detect the mRNA expression of UBC9 before and after RNA interference and the expression of UBC9, pyrogen-related protein, and SUMO-1 after RNA interference. Results After stimulation with 100 μmol / L homocysteine, the effect of macrophage activity was minimal, and NLRP3 and Caspase-1 were the proteins with the most obvious increase in expression (P<0. 05). Compared with the Control group, the Hcy group’ s expression of IL-1β and SUMO-1 was increased (P<0. 01). Compared with the Control group, the Hcy group’ s UBC9 protein and mRNA levels were increased (P<0. 05). The expression of NLRP3, Caspase-1, IL-1β, UBC9, and SUMO-1 was decreased in the siUBC9 + Hcy group compared with the si-NC+Hcy group (P<0. 01). Conclusions Homocysteine induces pyroptosis in macrophages, and its mechanism of action is related to the up-regulation of UBC9 to induce SUMO modification.

Abstract: Objective To analyze the dynamic changes to disease activity, colonic inflammation, histopathology,and serum cytokine levels in mice with chronic ulcerative colitis ( UC). Methods For UC induction, 2. 5% dextran sodium sulfate solution was provided ad libitum for 5 days, and to model remission, tap water was supplied for another 5 days in one induction cycle. Disease activity index (DAI), colon length, and pathological changes to colon tissue were determined. The levels of myeloperoxidase (MPO) in colon tissue and of cytokines such as IL-1β in serum and colon were detected. Results During the three cycles, disease activity was aggravated and colon length shortened in mice during the induction periods, both of which were relieved during the remission periods. The blood appeared was observed in the stool was earlier in cycles 2 and 3. The number of mice with stool blood increased, and their body weight decreased by a small amount briefly, then recovered rapidly. The degree of histopathological damage to the colon and MPO content in cycles 1 and 3 increased in the induction periods and decreased in the remission periods, with the magnitude of change smaller than that of the change in DAI values; and they increased in the remission period of cycle 2. During induction, the spleen index and serum levels of IL-1β, IL-6, and IL-17A increased continuously and were higher than those in the control group at the end of the experiment. Levels of TNF-α were increased in the induction periods and decreased in the remission periods,and the trend in IL-10 change was similar to that of TNF-α. TGF-β content increased and then decreased and was higher than that in the control group at the end of cycle 3. The colon contents of IL-1β, IL-6, and IL-17A showed similar trends of increasing and then decreasing, but there was no significant change in colon TNF-α. The concentration of IL-10 decreased during the induction periods and increased during the remission periods. Conclusions During the induction of chronic UC in mice, the symptoms of hematochezia and systemic inflammatory reactions gradually increased, and the mice showed an increase in tolerance and ability to resist mortality, weight loss, and histopathological injury to the colon. The onset and remission of colonic histopathological damage lags behind symptomatic changes, and there is a gradual shift in colonic inflammation to a pattern dominated by polymorphonuclear neutrophils (PMN) activation.

Abstract: Objective This aim of this review was to clarify the role of neutrophils in diabetes by summarizing the characterization studies, potential trends, and research hotspots relating to neutrophils in the diabetes research field. Methods 2998 relevant studies on neutrophils in the diabetes research field indexed in Web of Science from 2010 to 2023 were retrieved, and a visual analysis of the relevant literature was conducted using CiteSpace 6. 1. R6. Results Since 2012, the number of publications on this topic has grown rapidly. Bayat Mohammad, Liu Tong, Amini Abdollah, and Zhang Rui are high-yield authors, with seven related articles published. China and Shanghai Jiao Tong University are the country and institution with the most published papers. The most influential journal in this field is “Nature Medicine”.Literature co-citation analysis of topics related to diabetes showed that the greatest focus is currently on “extracellular trap” and “ COVID-19 patient ”. Co-occurrence analysis, clustering analysis, and keyword burst analysis indicated that “lymphocyte ratio” (13. 08) and “ neutrophil extracellular trap” ( 7. 2) are the most researched topics in the field of neutrophils and diabetes. Literature in this field mainly focuses on “ myocardial infarction”, “ endothelial”, “ oxidative stress”, and “ apoptosis”. Conclusions This article highlights the evolving trends in research into neutrophils in the diabetes field using CiteSpace, providing new insights for researchers aiming to conduct research in this area.

Abstract: Objective To construct a patient-derived pancreatic tumor organoid ( PDO) and evaluate its effectiveness. Methods We collected fresh surgical specimens from pancreatic cancer patients for PDO culture and compared the pathological and genetic characteristics of the PDO model with those of primary tumors. The PDO model was used to evaluate the efficacy of clinical chemotherapy drugs, and the effectiveness of the model was assessed. Results A PDO model of pancreatic cancer was successfully established. Histomorphological analysis indicated that the PDO model maintained the basic pathological characteristics of the primary tumor. Whole-exon sequencing showed that both the organoids and original tumor tissue remained consistent in their gene mutation type and characteristics. Drug screening tests revealed that the PDO model had good sensitivity to gemcitabine and irinotecan. Conclusions A pancreatic cancer PDO was successfully constructed that reflected the histological and genetic characteristics of the original tumor. The model was shown to be effective for drug sensitivity experiments in vitro and is expected to have implications for precision medicine assays.

Abstract: Objective To study the effect and pathological mechanisms of the neuro-immune response to viral encephalomyelitis caused by virulence reversion following the intrathalamic neurovirulence test for poliomyelitis vaccine in rhesus macaques. Methods Stock solutions (≥7000 lgCCID₅₀/ L) of inactivated polio vaccines (Vero cells) of type I,type II, and type III Sabin strains and 10-1 dilution of each type of polio vaccine were given to macaques, which were subjected to a intrathalamic neurovirulence test. Using immunohistochemical method, the pathological changes caused by polio, as determined by the distribution of CD155 and CD4⁺receptor T lymphocytes, CD20⁺B lymphocytes, and CD68+microglia, were detected. Results Lesions were observed on the virulence-reverted polio cases. Inflammatory cell infiltration, neuronal degeneration and necrosis, satellite phenomena, perivascular cuffing, and glial cell proliferation were observed in the spinal cord. The inflammatory cells in the perivascular cuffing and proliferative glial nodules were mainly CD4⁺T lymphocytes, CD20⁺B lymphocytes, and CD68⁺ microglia. There was no significant difference in the distribution of the poliovirus receptor CD155 in the neurons and glial cells of monkeys with and without polio, and no expression was observed in their vascular endothelial cells. Conclusions Polio caused by virulence reversion of the intrathalamic neurovirulence test is viral encephalomyelitis.

Abstract: Objective To establish a stable mouse model of chronic myocardial ischemia in coronary artery disease and preliminarily elucidate the electrophysiological mechanisms of T-wave flattening under ischemic conditions. Methods APOE^{- / -} mice were randomly divided into a model group and a lipid-lowering drug (LLD) group and subjected to a high-fat diet for 3 months. C57BL/ 6J mice fed a normal diet were used as the control group. Electrocardiograms were used to assess the mice before and after modeling, and cardiac perfusion was evaluated via nuclear PET/ CT scans.Hematoxylin-eosin and oil red O staining were employed to assess pathological atherosclerosis (AS) plaque formation.Mouse myocardial cells were isolated, and action potentials were recorded. Results After modeling, mice in the model group exhibited a significant increase in cholesterol ( CHO) and low-density lipoprotein C ( LDL-C), along with the appearance of lipid plaques in the aorta. Lesions in the LLD group were noticeably reduced, and no plaques formed in the control group. Myocardial nuclear scans revealed impaired blood perfusion in the hearts of the model group mice that was significantly lower than that in the LLD and control groups. The electrocardiograms indicated a significant reduction in T/QRS in both the model and LLD groups, with no significant changes observed in the control group. Myocardial cell action potential recordings revealed an accelerated repolarization rate in the inner-layer myocardial cells under ischemia, and a reduction in the inner-to-outer potential difference was identified as the primary electrophysiological mechanism underlying T-wave flattening. Conclusions APOE^{- / -} mice can be used to establish a model of chronic myocardial ischemia. The increased repolarization rate of inner-layer myocardial cells is likely to be the main cause of T-wave flattening in electrocardiograms under ischemic conditions.

Abstract: Objective This study established a model of invasive Aspergillus niger lung disease in immunosuppressed rats to provide theoretical support for the pharmacodynamic evaluation of anti-invasive pulmonary aspergillosis drugs and mechanism studies. Methods Sixty SD rats were randomly divided into a normal control group;cyclophosphamide control group, and cyclophosphamide +fungal infection low, medium, and high dose groups, with 12 animals in each group. General clinical observations were performed daily, and the serum levels of immunoglobulin (Ig)G and IgM and galactomannan (GM) were detected by ELISA on the 3rd and 7th days of modeling. Simultaneously, the ratio of CD4⁺ and CD8⁺cells, content of white blood cells (WBCs) and neutrophils (Neu) in peripheral blood, the Aspergillus niger load in alveolar lavage, and morphological changes to rat lung tissue were observed. Results Rats in the cyclophosphamide control and cyclophosphamide+fungal infection groups showed reduced voluntary activity and erect hair after modeling, and rats in the cyclophosphamide + fungal infection group also had shortness of breath and audible wet rhonchi in the lungs. Compared with the normal control group, rats in the cyclophosphamide control group showed significant reductions in the levels of CD4⁺, WBC, Neu, IgG, and IgM in the blood, and their proportion of CD8⁺cells was significantly higher ( P<0. 05, P<0. 01 ). Compared with the cyclophosphamide control group, rats in the cyclophosphamide+fungal infection medium- and high-dose groups had significantly reduced blood levels of IgG, IgM, and CD4⁺ cells (P<0. 05, P<0. 01); while the cyclophosphamide+fungal infection low-, medium-, and high-dose groups had significantly reduced blood levels of WBC and Neu (P<0. 05, P<0. 01). Additionally, rats in the cyclophosphamide+fungal infection medium- and high-dose groups had significantly increased blood CD8⁺ cells (P<0. 05, P<0. 01), Blood GM levels and the alveolar lavage Aspergillus niger load were significantly increased in rats in the cyclophosphamide + fungal infection low-, medium-, and high-dose groups compared with the cyclophosphamide control group (P<0. 05, P<0. 01). The lung tissues of the cyclophosphamide+fungal infection low-, medium-, and high-dose groups showed mycelial distribution and destruction of alveolar epithelium, increase of bronchial epithelial cup cells in the alveoli, and infiltration of inflammatory cells, and the degree of lesions was positively correlated with the modeling dose. Conclusions In this study, we used Aspergillus niger combined with cyclophosphamide immunosuppressant to construct a model of invasive Aspergillus niger lung disease. The duration of the disease was positively correlated with the concentration of bacterial fluid and modeling time, confirming that cellular immunity plays an important role in the pathogenesis of the disease. At the same time, Ig can also affect the development of invasive pulmonary aspergillosis, and it is speculated that the pathogenesis may be related to the level of Ig produced by humoral immunity.

Abstract: Objective To establish a model of long-term atrazine (ATR)-induced liver injury in mice and to evaluate the hepatotoxic effects induced by ATR. Methods C57BL/ 6-N male mice were randomly divided into a control group and 1. 5 mg / L and 150 mg / L ATR dose (ATR-L, ATR-H) groups. After 35 and 63 days, serum liver function biochemical indexes and inflammatory factors were detected, the hepatosomatic ratio was calculated, and the histopathology and ultrastructure of the liver were observed. Lipid peroxidation levels and antioxidant capacity, the activities of major phase I metabolic enzymes and phase II detoxification enzymes, and the expression of related proteins in liver tissues were detected. Results Compared with the control group, the ATR groups showed significant changes in the AST/ ALT ratio,levels of pro-inflammatory factors CCL2, TNF-α and IL-6, H2O2 content and activities of the metabolic enzymes NCR,CYT b5, and UDPGT ( P<0. 05). In the 150 mg / L ATR group, GGT content, peroxide levels ( as indicated by malondialdehyde), and CYP1A2 expression were significantly increased (P<0. 01), while GSH content was significantly decreased (P<0. 05), and hepatocyte injury and mitochondrial vacuolation were more serious when compared to control and 1. 5 mg / L groups. Conclusions In a mouse model of low-dose ATR liver injury, both 1. 5 mg / L and 150 mg / L ATR exposure induced liver injury in mice, with 150 mg / L ATR inducing the maximum metabolic toxicity in the liver after 63 days

Abstract: Objective To explore the inhibitory effect of 17-DMAG on the growth and angiogenesis of PD-1 humanized mouse liver cancer transplantation tumors. Methods 30 PD-1 humanized mice were selected, and a human HepG2 cell suspension was injected into the subcutaneous tissue of the right inguinal region to construct a human liver cancer transplant tumor model. Tumor-bearing humanized mice were randomly divided into three groups ( 10 mice per group): ① model group (injected with 10 mg / kg of physiological saline), ② 17-DMAG group (intraperitoneal injection of 17-DMAG at 25 mg / kg, 3 times/ week), and ③ cisplatin group ( intraperitoneal injection of 20 mg / kg, 2 times per week). The experiment lasted for 4 weeks. After injection, the length and shortest diameter of humanized mouse transplanted tumors were measured to calculate the volume, and tumor mass was measured to calculate the tumor inhibition rate. At the same time, immunohistochemical method were used to detect the expression of CD31 ( tumor microvessel density, MVD) and vascular endothelial growth factor (VEGF) in tumor tissue. Results The tumor volume and mass of the 17-DMAG group and cisplatin group were significantly reduced compared to those of the model group (P<0. 05), and the tumor inhibition rate of the 17-DMAG group was slightly higher than that of the cisplatin group. However, there were no significant differences in tumor mass, volume, and tumor inhibition rate between the 17-DMAG group and cisplatin group. The number of MVD-labeled microvessels and level of VEGF expression in the 17-DMAG group and cisplatin group were lower than those in the model group ( P<0. 05), and those of the 17-DMAG group were also lower than those in the cisplatin group (P<0. 05). Conclusions 17-DMAG can inhibit the growth of humanized mouse liver cancer xenografts by reducing the expression of VEGF in liver cancer xenograft tissue, thereby inhibiting the generation of tumor neovascularization.

Abstract:An animal biosafety level-3 laboratory (ABSL-3) is a high-level biosafety installation that can conduct experiments on animals infected with highly pathogenic microorganisms. In recent years, with the continuous characterization of emerging and re-emerging infectious diseases, high-level biosafety laboratories have played increasingly important roles in pathogenic mechanism and drug and vaccine research and development. The demand for ABSL-3 is increasing year by year. At the same time, there is also a growing demand for personnel who are competent in working in ABSL-3. The systematization, normalization, and standardization of pre-service training have become important to guarantee a reduction in the risks to personnel working in ABSL-3. Training of ABSL-3 staff needs to be carried out in specific simulated laboratories. Therefore, it is necessary to construct simulated ABSL-3 and establish scientific and effective operating standards and mechanisms. This paper comprehensively introduces the design, construction, operation,and functions of a simulated ABSL-3 installation

Abstract:Japan is one of the main trading partners for the import and export of experimental animals in China,and its quarantine and supervision policies for the import and export of experimental animals are very detailed and strict. This article takes experimental dogs, cats, and monkeys as examples to provide an in-depth analysis of the quarantine and supervision policies for the main experimental animals exported to Japan. At the same time, it reflects on the current laws and regulations, import and export management method, standards, biosafety, breeding and management status, as well as the import and export business status of experimental animals in China. Suggestions are provided in improving the laws and regulations, import and export management method, ensuring national biosafety, improving the management level of experimental animal breeding, and promoting the import and export trade of experimental animals, in order to provide reference for comprehensively improving the production, use, and breeding management level of experimental animals in China and strengthening the trade between China and Japan.

Abstract:Animal experiment courses are important for developing students’ practical skills in medical and life science education. They help to cultivate students’ experimental skills, scientific reasoning, and innovative thinking ability. However, the traditional teaching method used in animal experiment courses tend to focus on a single topic and have minimal student participation. Courses should aim to promote students’ active learning and innovative thinking abilities, and this paper discusses the ways teaching in animal experiment courses can be reformed. First, the paper introduces the background and significance of teaching in animal experiment courses and emphasizes the importance of cultivating the students’ abilities. Second, it puts forward the principles of improved animal experiment course teaching, including designing student-centered lessons, providing opportunities for problem solving and practical exploration, and promoting interdisciplinary integration. At the same time, we integrate an ethical review of the welfare of experimental animals in China. Then, from the aspects of course design, teaching method, and evaluation method, this paper expounds several concrete measures of teaching reform in animal experiment courses in detail. When designing a course, attention should be paid to the selection of challenging and exploratory experimental projects, and students ’ interests and professional needs should be fully considered. Using improved teaching method, students should be encouraged to actively participate in explorative and cooperative classes, be guided through problem solving tasks, and encouraged to cultivate innovative thinking. Diversified evaluation method, such as experimental reports, group discussions, and project presentations, should be used to comprehensively evaluate students’ practical and innovative thinking abilities. Finally,with practical verification and effect evaluation, the experiences and outcomes from a reform of animal experiment course teaching are summarized, and suggestions for further improvements are put forward.

Abstract:Septic cardiomyopathy ( SIC) is an organ dysfunction frequently observed in sepsis and characterized by high mortality and poor prognosis. Understanding the complex pathogenesis of SIC and developing effective therapeutic tools are critical issues that require attention. Previous studies have demonstrated the significant role of mitochondrial dysfunction in the development of SIC. In the presence of SIC, and the mitochondrial dysfunction that result, the aberrant regulation of the mitochondrial quality control system (MQC) can exacerbate cardiomyocyte injury. Recent studies have demonstrated that the MQC maintains the dynamics of mitochondrial homeostasis through its regulation of mitochondrial biogenesis, fusion / fission, and autophagy. This article provides an overview of the role of MQC in SIC pathogenesis,reviews the latest studies in the field, and analyzes MQC’s potential as a therapeutic target.

Abstract:Liver fibrosis is a key pathological process in the progression of chronic liver disease to cirrhosis and even liver cancer. The occurrence of liver fibrosis is a highly integrated and dynamic pathological process result ing from the interactions of many cells and cytokines. The Notch signaling pathway is an evolutionarily conserved intercellular signal transduction mechanism that plays important roles in regulating the development and tissue renewal of multicellular animals.Multiple studies have shown that Notch signal transduction participates in the formation of liver fibrosis in a variety of ways.Therefore, this paper reviews the role of Notch signaling in cells involved in the formation of liver fibrosis to explain the function of this signaling pathway in liver fibrosis.

Abstract:With the increase in human activity in plateau and mountainous areas in recent years, high-altitude exposure has become increasingly common. Many patients with underlying diseases are affected by hypobaric hypoxia in plateau environments, which further aggravates disease processes and even leads to cognitive disorders. Periodontitis is a common inflammatory disease that induces periodontal local inflammatory responses and even causes central nervous system inflammation. At high altitudes, the body suffers from decreased immunity and tissue hypoxia, which can promote the occurrence and development of periodontitis and may even increase the risk of periodontitis-induced central nervous system inflammation. As plateau medical research advances, the relationship between periodontitis and central nervous system inflammation in hypobaric hypoxia environments at plateau is attracting more and more attention. This work reviews the progress of research on periodontitis and central nervous system inflammation and discusses the correlation between periodontitis and central nervous system inflammation when exposed to hypobaric hypoxia in plateau environments.

Abstract:Sepsis is defined as a life-threatening organ dysfunction caused by a dysregulated host response to infection with an extremely high mortality rate, and it is the main risk factor for acute lung injury (ALI). However, the pathophysiology and pathogenesis of sepsis-associated ALI are not fully understood, and effective drugs are extremely limited. Therefore, it is urgent that we explore the pathogenesis of sepsis-associated ALI and attempt to discover effective intervention measures to improve the prognosis of sepsis-associated ALI patients. In recent years, ferroptosis has been considered closely related to the pathological and physiological processes of sepsis-associated ALI, and inhibiting related cell ferroptosis can effectively slow down the occurrence and development of the disease. In this paper, therapeutic strategies targeting ferroptosis in related cells are reviewed to provide a reference for future research on ferroptosis in sepsisassociated ALI and provide a new perspective on potential treatments.

Abstract:Henoch-Schonlein purpura (HSP) is the most common systemic vasculitis of childhood, and is called “spot toxin”, “purpura wind”, and “ grape plague” in traditional Chinese medicine (TCM). Modern medical research suggests that the disease is related to factors such as an imbalance in cellular and humoral immunity, the abnormal secretion of cytokines, and disturbances to coagulation and fibrinolysis mechanisms, but the exact pathogenesis is still unclear. The incidence of this disease is increasing year by year, and it has a high recurrence rate and a high proportion of kidney damage, which seriously affects the physical and mental health of affected children and poses a great risk to human health. Numerous studies have shown the clinical efficacy of TCM treatment for HSP, but the mechanism of action is not completely clear. In recent years, following the establishment of animal models of HSP, a large number of animal experiments have been carried out to study the efficacy and mechanisms of TCM for HSP, but there is a lack of systematic and detailed reviews. Therefore, animal experimental literature related to the treatment of HSP with TCM in the past decade was reviewed. The effects of TCM in alleviating the abnormal glycosylation of IgA1, regulating the imbalances in Th1 / Th2 and Treg / Th17 immune cells, reducing circulating immune complexes, and inhibiting inflammatory responses were compiled and summarized to provide a reference for further research on TCM for the treatment of HSP and inspire new research ideas.

Abstract:Skeletal muscle wasting refers to a loss of skeletal muscle mass and function. Mitochondrial quality control (MQC) is the basis by which normal physiological mitochondrial function is maintained and mainly involves the regulation of mitochondrial biogenesis, mitochondrial dynamics ( fission / fusion), and mitophagy. MQC maintains muscle homeostasis by regulating the relative stability of mitochondrial shape, quantity, and quality. As an economical and effective treatment for muscular atrophy, exercise interventions are widely used, but the relationship between exercise intervention and MQC is not clear. This paper discusses the role of mitochondrial biogenesis, mitochondrial dynamics, and mitophagy in skeletal muscle atrophy and related molecular targets. We thoroughly analyze the mechanisms by which MQCmediated exercise can improve the skeletal muscle atrophy caused by aging, disuse, and cancer cachexia in order to provide theoretical guidance for intervention.

Abstract:The major histocompatibility complex (MHC) is closely related to immune regulation. MHC shows distinct genetic polymorphism, and there are also species differences in MHC restriction. The human MHC is called human leukocyte antigen (HLA), and the mouse MHC is called H-2. The construction of humanized MHC transgenic mouse models is an important strategy to overcome the differences in MHC among species and simulate the characteristics of a human immune response. MHC transgenic mice are mainly divided into MHC Ⅰ or MHC Ⅱ single-transgenic mouse models and MHC Ⅰ and MHC Ⅱ double-transgenic mouse models. The development of HLA Ⅰ transgenic mouse model went through three stages, at present, the strategy of knocking out H-2K b and H-2D b or murine β2m is adopted to eliminate the competitive inhibition of HLA Ⅰ molecules by endogenous H-2 class Ⅰ molecules. In the construction of an HLA Ⅱ transgenic mouse model, the β strand of murine origin is knocked out and HLA Ⅱ class genes are inserted. With the optimization of construction strategies, MHC transgenic mouse models have been applied to epitope vaccine development,tumor treatment, and genetic disease-association studies, becoming a powerful tool for preclinical trials. In this paper, we summarize the relevant data on MHC transgenic mouse models, as well as the construction strategies used for MHC transgenic mouse models and their application in vaccine development and disease treatment.

Abstract:Respiratory diseases (e. g. , lung inflammation and pulmonary fibrosis) are a serious threat to human health. Mitochondria, organelles unique to eukaryotic cells, not only have important functions in energy production, biosynthesis, and the maintenance of intracellular homeostasis but also act as diverse signaling organelles involved in inflammation, proliferation, differentiation, cell repair, and other processes. The mitochondrial quality control system involves mitochondrial biogenesis, dynamics, and autophagy. Certain pathological mechanisms of respiratory diseases, such as oxidative stress and inflammation, are closely related to the dysregulation of mitochondrial quality control systems. This paper summarizes the progress of research into mitochondrial quality control dysregulation in respiratory diseases (chronic obstructive pulmonary disease, pulmonary fibrosis, acute lung injury, asthma, and bacterial pneumonia) to explore new ideas for the prevention and treatment of respiratory diseases.

Abstract:Pulmonary hypertension ( PH ) is a progressive disease characterized by pulmonary vascular remodeling. Current treatments for PH remain suboptimal, and there is an urgent need to better decipher the underlying pathomechanisms to identify new therapeutic targets. MicroRNA (miRNA) are key components in the post-transcriptional machinery that mediates cellular functions and mainly act by regulating the expression of downstream target genes.Numerous in vivo and in vitro studies have demonstrated the involvement of miRNA and their regulators in PH development.However, there is no unified model for the mechanism of miRNA’ s regulation of pulmonary vascular remodeling. Therefore, this article provides a review on the mechanisms of miRNA in PH characterized in recent years.