Abstract: Objective To explore the anti-inflammatory effect of Qingre Jiedu (QRJD) formula on mice with gout and its effect on gut microbiota. Methods Forty C57BL/ 6 mice weighing 20 ~ 22 g were divided into control (CON),model (MOD), allopurinol (ALLO), and QRJD formula (QRJD)groups, and i. g. 10 g / 0. 1 mL carboxymethyl cellulose was administered to the CON every morning from 1 to 35 days. A hyperuricemia mouse model was prepared by intragastric injection of a potassium oxalic acid ( 500 mg / kg) and yeast extract ( 10 g / kg) suspension. On day 29, 50 μL sterile carboxymethyl cellulose was injected into the right ankle of mice in the CON group under isoflurane-induced anesthesia,and a gouty arthritis model was prepared by injecting the same volume of sodium urate(50 mg / mL) into the right ankle of mice in the other groups. Each group was treated with corresponding drugs every day. On day 35, samples were collected from mice that had been fasted for 6 hours without water. Blood indexes, such as uric acid, creatinine, and urea nitrogen,were assessed. Hematoxylin-eosin and saffranine O-fast green staining was performed on ankle joints. Anti-inflammatory indexes of interleukin-10 ( IL-10 ) and transforming growth factor-β1 ( TGF-β1 ) were detected by ankle joints immunohistochemical assay. The cecum contents of mice were collected, and changes in gut microbiota were analyzed by high-throughput sequencing of 16S rDNA. Results (1)After 7 days of treatment, compared with the MOD group, QRJD formula effectively reduced the blood concentrations of uric acid (P<0. 001), creatinine (P<0. 01), and urea nitrogen (P<0. 05), and effectively protected renal functions. (2)Compared with the MOD group, HE staining showed that synovial hyperplasia and inflammatory cell infiltration were reduced in the QRJD formula group after treatment. The cartilage arrangement of the compound was more orderly than before, cartilage destruction was less than that in the MOD group, and no matrix loss was observed. (3)Immunohistochemical analysis of the ankle joint indicated that IL-10 and TGF-β1 were not significantly increased in CON and MOD groups. Compared with the MOD group, IL-10 and TGF-β1 expression in the QRJD formula group were increased (P<0. 05). (4)In terms of biodiversity, the number of MOD-specific OTUs increased by 75 compared to the CON group, while the QRJD was able to reduce the number of MOD-specific OTUs to more closely resemble the CON group;no significant difference was found in α-diversity among the four groups (P<0. 05), whereas βdiversity was more similar to the CON group (p=0. 001). (5)Compared with the CON group, the MOD group exhibited increased abundances ( P<0. 05) of Ruminococcaceae spp. , Dubosiella sp. , Tyzzerella sp. , Ileibacterium sp. , and Bacteroidales spp. . In contrast to the MOD group, the QRJD formula group showed elevated abundances (P<0. 05) of Lactobacillus sp. , Ligilactobacillus sp. , and Bacteroides sp. . Furthermore, an interaction network of gut microbiota indicated mutual interactions among these microorganisms. (6)In the correlation analysis between gut microbiota and renal functions as well as anti-inflammatory factors, the relative abundances of Dubosiella sp. , Tyzzerella sp. , and Bacteroidales spp. were significantly positively correlated to SUA and SCR (P<0. 05). However, Lactobacillus sp. , Ligilactobacillus sp. , and Mitochondria spp. exhibited a positive correlation to anti-inflammatory factors IL-10 and TGF-β1 with a more significant association observed for TGF-β1 (P<0. 05). (7) COG function prediction suggested that the functions of the QRJD formula group were concentrated on inorganic ion transport and metabolism, and carbohydrate transport and metabolism. Conclusions QRJD effectively modulates immune inflammation and gut microbiota dysbiosis, thereby treating gout. Its mechanism of gout prevention and treatment may involve regulation of gut microbiota diversity and abundance, as well as the control of the abundance of differential bacterial species, such as Ruminococcaceae spp. , Dubosiella sp. , and Lactobacillus sp. , to achieve gout therapy.

Abstract: Objective To explore the mechanism of Juanxiao decoction in regulating type 3 innate lymphoid cells( ILC3s) in treating obese asthma. Methods Sixty male BALB/ c mice were randomly divided into a normal group, model group ( high-fat diet + OVA), Juanxiao decoction groups ( low, middle, and high doses of 8. 5, 17, and 34 g / kg,respectively), and dexamethasone group (1 mg / kg) with 10 mice in each group. Except for the normal group, the other groups were fed a high-fat diet for 12 weeks, and OVA sensitization by inhalation of an atomized OVA solution was used to establish the obese asthma model. From the first inhalation, the low-, medium-, and high-dose groups of Juanxiao decoction and the dexamethasone group were administered corresponding drugs by gavage, whereas normal and model groups were administered equal amounts of saline by gavage for 7 days. The state of mice and changes in typical symptoms of obese asthma were observed. At 24 hours after the last challenge, a fully automated biochemical analyzer was used to assess four blood lipids and count inflammatory cells in alveolar lavage fluid (BALF). Hematoxylin-eosin staining was used to observe morphological changes in lung tissue and abdominal fat. Enzyme-linked immunosorbent assays were used to measure the immunoglobulin E in BALF and serum, and interleukin ( IL)-1β, IL-13, and mouse thymus activation regulating chemokine (CCL17) in lung tissue. IL-17A⁺ILC3 and IL-22⁺ILC3 in lung tissue and peripheral blood were analyzed by flow cytometry. Western blot was used to detect expression of P-STAT3 protein in lung tissue. Results Compared with the normal group, model group mice showed infiltration of airway inflammatory cells and thickening of airway walls. However, compared with the model group, lung inflammation in dexamethasone and Juanxiao decoction groups was improved, especially in middle- and high-dose groups. Compared with the normal group, IL-1β, IL-17A⁺ILC3, IL-13,and CCL17 in lung tissue of the model group were significantly increased (P<0. 05), whereas the proportion of IL-22⁺ILC3 and expression of P-STAT3 were significantly decreased (P<0. 01, P<0. 05). Compared with the model group, IL1β, IL-17A⁺ILC3, IL-13, and CCL17 in lung tissue were significantly decreased and the proportion of IL-22⁺ILC3 andexpression of P-STAT3 were significantly increased in middle- and high-dose Juanxiao decoction groups ( P<0. 05, P<0. 01, P<0. 001). Conclusions Juanxiao decoction improves the inflammatory environment of obese asthmatic mice and alleviates lung inflammatory and allergic reactions. Its mechanism may be related to regulating secretion of cytokines by ILC3s.

Abstract: Objective To study the effects of radiation on the morphology, function, and NLRP3 expression of mouse salivary gland tissue, and provide new ideas to repair radiation-induced damage to salivary gland tissue. Methods We established a mouse model of radiation-induced submandibular gland injury and Recorded the weight of drinking water.The salivary flow rate was assessed, and HE staining was used to observe submandibular gland injury.Immunohistochemistry and Real-time PCR were used to assess expression of NLRP3 and Caspase-1 in the radiation-injured submandibular gland of mice at 1, 3, 7 and 14 days after radiation exposure. Results Over time, the amount of water consumed by radiation group mice was gradually increased, the salivary flow rate was decreased, and inflammatory cells in the submandibular gland continued to increase. Acinar cells gradually showed lesions, such as nuclear pyknosis and vacuolization. At 7 and 14 days after radiation exposure, expression levels of NLRP3 and Caspase-1 proteins and genes in the radiation group were significantly higher than those in the normal group (P<0. 05). Conclusions Radiation damages mouse submandibular gland tissue and activates the NLRP3 inflammasome to increase its expression level.

Abstract: Objective To assess transcriptomic differences between carbon tetrachloride ( CCl₄ )-induced and diethyl 1,4-dihydro-2, 4, 6-trimethyl-3, 5-pyridinedicarboxylate ( DDC) diet-induced mouse models of liver fibrosis to provide a framework for future research using mouse liver fibrosis models. Methods Mouse models of liver fibrosis were induced by a 10% CCl₄(2 mL/ kg) injection or a 0. 1% DDC diet. After 4 weeks of induction, serum levels of ALT, AST,and TBil were measured. HE and Sirius red staining were used to observe hepatic inflammation and collagen deposition.Jamall’ s method was used to evaluate hydroxyproline ( Hyp) content in liver tissues. Hepatic tumor necrosis factor-α (TNF-α), interleukin (IL)-6, and IL-1β were measured by ELISA. Total RNA was extracted from murine liver tissues for RNA-sequencing (RNA-seq). Differentially expressed genes of the two models were analyzed by R software and then GO and KEGG enrichment was performed. Then, genes with significant differences were verified. Results Compared with normal mice, serum levels of ALT, AST, and TBil and hepatic expression of TNF-α, IL-6, and IL-1β were significantly increased in mice that received CCl₄ and DDC, while the Alb serum level was decreased. Pathological staining showed that the structures of liver tissues were destroyed and a large number of hepatocytes around the central vein were hyalinized and necrotic in CCl₄ -treated mice. In DDC diet-treated mice, a large amount of porphyrins had been deposited in the liver and a large number of inflammatory cells had infiltrated into the portal area and bile duct. Different degrees of collagen deposition were observed in the liver tissues of the two model mice. Different genes (DEGs) of CCl₄- and DDC diet-treated mice were screened using a filter (| logFC | > 2-fold and P<0. 05). As a result , 1820 and 2373 DEGs in CCl₄- and DDC diet-treated mice were analyzed, including 1302 and 1978 upregulated genes, and 518 and 395 downregulated genes,respectively. GO annotation showed that the two models had important functions in molecular function, biological process,and cell component. KEGG analysis showed that 22 and 29 signaling pathways were activated in CCl₄- and DDC dietinduced models, respectively. Among them, 16 signaling pathways, such as extracellular matrix receptor interaction, cell cycle, protein digestion and absorption, focal adhesion, and PI3K-Akt, were significantly enriched in the two models (P<0. 05). Cluster analysis showed that Mup11, Mup15, Mup17, and Mup1 were significantly down-regulated in both models,which were identified by RT-qPCR (P<0. 05). Conclusions This study conducted a comparative analysis of the RNASeq transcriptomic features of liver fibrosis models induced by exposure to CCl₄ and a DDC diet. It examined the gene expression patterns and the pathways influenced by gene expression. The findings serve as a valuable resource for selecting appropriate animal models for future research on the pathogenesis and treatment of liver fibrosis.

Abstract: Objective To explore the effects of Shaoyao Gancao granule on hair growth, behavior, and the hypothalamic pituitary adrenal (HPA) axis in mice with alopecia areata (AA). Methods Forty-two C3H/ HeJ mice were randomly divided into control, model, Shaoyao Gancao granule high-, middle-, low-dose, corticotropin-releasing hormone receptor 1 ( CRHR1) antagonist, and compound glycyrrhizin tablet ( CGT) groups. Photography, dermoscopy, weight analysis, and behavioral measurement were performed. Corticotropin-releasing hormone ( CRH ), adrenocorticotropic hormone (ACTH), cortisol, glucocorticoid receptor ( GR), and brain-derived neurotrophic factor ( BDNF) were also assessed. Results Compared with the model group, high-dose Shaoyao Gancao granules improve hair regeneration and weight gain (P<0. 05), increased the percentage of total exercise distance and central area exercise distance in an open field test (P<0. 05), reduced the immobility time in the forced swimming and tail suspension experiments (P<0. 05),reduced peripheral blood levels of CRH, ACTH, and cortisol (P<0. 05), and increased expression of GR and BDNF in the hippocampus ( P<0. 05 ). Conclusions Shaoyao Gancao granule promotes hair growth and improves behavioral performance in mice with AA. These effects may be related to downregulating CRH, ACTH, and cortisol expression, upregulating GR and BDNF expression, and inhibiting excessive activation of the HPA axis.

Abstract: Objective To investigate the effects of acute sleep deprivation on the behavior and synaptic protein expression of rats. Methods Seventy healthy male Wistar rats were randomly divided into seven groups, a Control group and sleep deprivation groups (24, 48, 72, 96, 120 and 144 hours). The sleep deprivation rat model was established by the modified multiplatform water environment sleep deprivation method. Spatial learning and memory were assessed by the Morris water maze. Anxiety was assessed by the open field test. The morphology and quantity of hippocampal neurons were observed by Nissl staining. Western blot and Real-time PCR were used to determine the expression of synaptophysin (SYN), post-synaptic density protein-95 ( PSD-95), and brain-derived neurotrophic factor ( BDNF) in rats. Results Compared with the Control group, the numbers of standing and modification were significantly increased by prolongation of the sleep deprivation time (P<0. 05). The escape latency and path length were significantly increased in 120 and 144 h groups ( P<0. 05), whereas the number of platform crossings and the percentage of the target quadrant time were significantly decreased (P<0. 01) and negatively correlated to the sleep deprivation time. The expression levels of BDNF,SYN, and PSD-95 were significantly decreased with the prolongation of sleep deprivation time (P<0. 01). Conclusions With the increase in sleep deprivation time, cognitive dysfunction and anxiety gradually deteriorated, which may be related to decreases in the expression of synaptic biomarkers.

Abstract: Objective To investigate the mechanism of cartilage injury and inflammation in the WHBE rabbit KOA model and the effect of platelet-rich fibrin releasates (PRFr) treatment on the KOA process, we established a WHBE rabbit KOA model by excision of medial collateral and partial patellar ligaments and administered a PRFr solution. Methods Twenty-four WHBE rabbits were randomly divided into three groups: normal control ( NC) group ( n= 6),model(KOA) group(n= 12), and cure(PRFr) group ( n= 6). KOA and PRFr groups were injected with 0. 5 mL saline and PRFr into both joint cavities on 7 and 14 postoperative days, respectively. At 4 and 8 weeks of modeling, the knee joint grade scoring, X-ray imaging, and gross scoring were performed. Serum levels of IL-1β, TNF-α, and MMP-13 were measured by ELISA. At 4 weeks, 6 animals in the KOA group were euthanized, and at 8 weeks, the remaining animals in each group were euthanized. Pathological sections were prepared after decalcification, and then HE, toluidine blue, and safranin O-fast green staining and immunohistochemical analysis of TGF-β, BMP3, and NF-κB were conducted. Results The Lequesne MG behavioral score, Mankin’ s score, and Pelletier score of WHBE rabbits after the operation were significantly increased compared with the NC group (P<0. 01). Pathological observations revealed surface defects of the cartilage and partial loss of chondrocytes. These result indicated that the KOA model was established successfully. In KOA rabbits, knee joint swelling, joint pain stimulation, and movement limitation were obvious. X-rays showed a high-density soft tissue shadow, indicating more joint effusion and a rough articular surface in general. After PRFr treatment, the serum levels of proinflammatory factors IL-1β, TNF-α, and MMP-13 in KOA model rabbits were significantly reversed (P<0. 05,P<0. 01). Additionally, the cartilage surface became smooth, and most chondrocytes were neatly distributed. Expression levels of TGF-β, BMP3, and NF-κB induced by KOA were also significantly decreased (P<0. 01). Conclusions We successfully established a KOA model in WHBE rabbits, and PRFr improved the cartilage injury and inflammation of the WHBE rabbit KOA model through TGF-β/ BMP and NF-κB pathways.

Abstract: Objective To investigate the effects of ursolic acid (UA) on the TLR4 / NF-κB signaling pathway and Th17 / Treg cells in type 1 diabetes mellitus(T1DM) rats. Methods T1DM rat models were established by intraperitoneal injection of streptozotocin (STZ) and randomly divided into blank (Control), Model, metformin (MET), and UA groups.General conditions, such as body weight and blood glucose, were recorded, and peripheral blood and pancreatic tissues were collected after 6 weeks of gavage to assess insulin treatment. Immunohistochemistry was used to observe pathological changes in pancreatic tissues. Horseshoe crab reagent was used to assess changes in serum lipopolysaccharide ( LPS) content. qRT-PCR was used to measure expression of pancreatic TLR4, MyD88, IκBα, and NF-κB p65 mRNAs, and mRNA expression of transcription factors RORγt and Foxp3. Western blot was used to assess pancreatic TLR4, MyD88,IκBα, NF-κB p65, RORγt, and Foxp3. Flow cytometry was used to assess changes Th17 / Treg cell ratio in peripheral blood. ELISA were used to measure serum contents of TNF-α, IL-6, and IL-1β. Results After STZ-induced diabetic rats were treated by gavage for 6 weeks, compared with the Model group, the fasting blood glucose of rats in MET and UA groups was significantly decreased and their body weights were increased. Inflammatory infiltration of pancreatic islet βcells was reduced. Expression of TLR4, MyD88, IκBα, NF-κB p65, and RORγt mRNAs and proteins was significantly decreased. LPS content was significantly decreased. IκBα and Foxp3 mRNA and protein expression was significantly increased. The Th17 / Treg ratio was significantly decreased, and TNF-α, IL-6, and IL-1β contents were significantly decreased. Conclusions UA improves the symptoms of rats by reducing the LPS shift, inhibiting the TLR4 / NF-κB pathway, down-regulating RORγt expression, and up-regulating Foxp3 expression to correct the imbalance in the Th17 /Treg cell ratio in T1DM rats.

Abstract: Objective To explore the role of Adra1a in regulating the LPS-induced inflammation response in primary hepatocytes of lipopolysaccharide-binding protein knockout ( Lbp^{- / -}) mice. Methods Primary hepatocytes were extracted from WT and Lbp^{- / -} mice using a two-step perfusion method, and an inflammation model was established using LPS induction. Expression of Adra1a in primary hepatocytes of Lbp^{- / -} mice was suppressed by administering the inhibitor prazosin and transfection with si-Adra1a. The cells were divided into three groups under inhibitor conditions: control group A, LPS group A, and prazosin group. For siRNA transfection, cells were also divided into groups: control group B, LPS group B, si-NC group, and si-Adra1a group. WT primary hepatocytes were divided into two groups: control group (blank) and LPS group (12 h stimulation). Changes in the Adra1a response to LPS stimulation were verified by Western blot.Other method ologies, such as CCK-8, qRT-PCR, and Western blot assays, were used to confirm improvements in cell inflammation and the survival rate by prazosin and si-Adra1a. Results Significant elevation in Adra1a protein expression in Lbp^{- / -} primary hepatocytes was observed post-LPS stimulation (P<0. 01), whereas no notable change was found in the wildtype. A remarkable increase in the cell survival rate was noted in prazosin and si-Adra1a groups (P<0. 01, P<0. 05).Furthermore, prazosin and si-Adra1a groups exhibited significantly reduced expression of proinflammatory factors TNF-α and IL-1β (P<0. 01), p-p38, p-ERK, and p-JNK (P<0. 01), which are associated with cell damage and inflammation. Conclusions Following LPS stimulation, upregulation of Adra1a and proinflammatory cytokine expression was observed in Lbp^{- / -} primary hepatocytes. Specific downregulation of Adra1a expression using prazosin and si-Adra1a significantly decreased LPS-induced proinflammatory cytokines in Lbp^{- / -} primary hepatocytes. Adra1a is implicated in the regulation of the LPS-induced inflammation response in primary hepatocytes of Lbp^{- / -} mice.

Abstract: Objective To explore the effect of LIMK1 on the progression of cervical cancer (CC). Methods HeLa and C-33A human cervical cancer cells overexpressing LIMK1 were established and injected subcutaneously into nude mice. The tumor volume was measured and expression of NOX2, NOX4, p-Src, p-RUNX3, RUNX3, and MMP-9 proteins in tumor cells was detected by Western blot assays. LIMK1-overexpressing HeLa and C-33A cells were cultured in 5% O2 with antioxidants. The protein expression of LIMK1, NOX4, p-Src, p-RUNX3, RUNX3 and MMP-9 in the cells was detected by Western blot assays. Cell migration was assessed by a scratch assay. Transwell assays were used to assess cell migration and invasion. A monoclonal proliferation assay was used to assess cell proliferation. Results The tumor volume in nude mice injected with LIMK1-overexpressing HeLa cells was increased significantly, and NOX2, NOX4, p-Src, pRUNX3 and MMP-9 protein levels were increased, while RUNX3 protein expression was decreased. In LIMK1-overexpressing HeLa and C-33A cells, the protein expression of LIMK1, NOX4, p-Src, p-RUNX3, and MMP-9 was increased, RUNX3 protein expression was decreased, and cell migration, invasion, and proliferation were increased. However, after adding antioxidants, the expression levels of NOX4, p-Src, p-RUNX3, RUNX3 and MMP-9 proteins, and cell migration, invasion, and proliferation were not different from those of control cells. Conclusions LIMK1 promotes the progression of cervical cancer by enhancing the ROS / Src pathway, thereby promoting the migration, invasion, and proliferation of cervical cancer cells.

Abstract:Laboratory animal science plays a crucial role in the education and training of medical students. To ensure effective teaching of laboratory animal science in Chinese medicine institutions, the principles of Chinese medicine characteristics and innovation should be incorporated. This pedagogical approach aims to enrich traditional cultural literacy in Chinese medicine and foster the students’ capacities for innovation and critical thinking. Daily teaching of laboratory animal science should encompass various educational aspects, including inheritance, ethics, migration, exploration,inspiration, and extension education. By integrating these components and emphasizing the intersections of Chinese medicine with laboratory animal science, important areas, such as animal welfare in Chinese medicine research, the application of Chinese medicine theories in animal experiments, considerations for animal models in Chinese medicine, and the selection of experimental animal species, can be addressed. Additionally, this approach guides new research directions and effectively cultivates the students’ scientific research, innovation, and practical abilities. The primary Objective of this program is to nurture scientific innovation and practical competence among students while prioritizing the superior quality of innovative education in the context of Chinese medicine. Such efforts offer a solid foundation to advance traditional medical practices and nurture a new generation of professionals dedicated to preserving traditional medicine.

Abstract:Experimental animals as living reagents promote the development of life science and medicine, and draw public attention to the welfare ethics of experimental animals. Experimental animal welfare ethics is important for animal protection and plays an important role in protecting the rights and interests of experimental animals and promoting the rationality and morality of scientific research. However, during the evolution of animal protectionism, some extreme theories, such as extreme animal protectionism, have also emerged. This article summarizes the main theories of animal protectionism and the development of animal welfare ethics, and analyzes the main problems of extreme animal protectionism. This article expounds on the present situation and problems of experimental animal welfare ethics and puts forward some suggestions to promote the practice of experimental animal welfare ethics to provide references for our country’s experimental animal welfare ethics practice and system construction.

Abstract:Dilated cardiomyopathy (DCM) has a concealed onset with left or even whole heart enlargement as the main imaging manifestation. It is a common primary disease of heart failure and arrhythmia. With the continuous deepening of research in recent years, the intrinsic molecular mechanism of regulatory cell death (RCD) has gradually become clear. Researchers have found that the RCD mode plays a very important role in the occurrence and development of DCM. At present, the RCD modes involved in DCM mainly include apoptosis, necrotic apoptosis, pyroptosis, iron death, autophagy, and cuproptosis, and a certain correlation exists among them, which interact and regulate each other. This article provides an overview of the current research status on the mechanisms of the six RCD modes involved in DCM to provide a reference for future basic research and clinical applications.

Abstract:Astrocytes (AS) are the most abundant glial cells in the central nervous system and are involved in many physiological and pathological processes in the nervous system. Alterations in their phenotype are particularly important for the health of the CNS. Epigenetic mechanisms, including DNA methylation, histone modification, non-coding RNA regulation, and chromatin remodeling, are closely linked to alterations in AS proliferation, differentiation, inflammation, and other phenotypic features, but how these mechanisms function needs to be explored and summarized. By reviewing the recent advances in the role of epigenetic mechanisms in AS under various physiological and pathological states, we aim to provide new ideas for the understanding and treatment of related diseases.

Abstract:Immunodeficient animal models play an important role in preclinical research and are important experimental tools in modern biomedical research that are widely used in immunology, genetics, oncology, microbiology,and other research fields. Gene editing is a technology for targeted modification of biological genomes. From emergence to application, it has greatly promoted the development of biomedical research. Gene editing technology mainly includes homing endonucleases, zinc finger nucleases, transcription activator-like effector nucleases, and the CRISPR/ Cas9 system.Researchers have used these technologies to establish various types of immunodeficient animal models, each with advantages and limitations. In recent years, a large number of studies have confirmed that the human immunodeficient animal model accurately simulates the functions of cancer cells, drugs, and the human immune system, better simulates human diseases,and is widely used to study human immunobiology and the potential mechanisms of complex diseases. In this article, we review the progress in the research and application of gene editing technology to the establishment of immunodeficient animal models, discuss in depth the problems and optimization strategies of gene editing technology in the preparation of immunodeficient animal models, and present its future development prospects to provide references for researchers to select and establish immunodeficient animal models.

Abstract:Snakebite is a common clinical emergency with the characteristics of acute onset, rapid changes in condition, and high disability and mortality rates. In addition to the common systemic and local tissue damage, snake envenomation can cause significant complications, including immediate and delayed effects. These complications are the main causes of disability and even death caused by snakebites, which seriously affect the long-term prognosis and quality of life. This article summarizes the symptoms, diagnosis, and treatment of snakebite complications from the aspects of blood,nervous, motor, endocrine, and reproductive systems and other aspects to provide references for effective and precise treatment of snakebite in clinical practice.

Abstract:CRISPR/ Cas9 technology has driven the development of various fields in life science. With continuous deepening of its understanding, researchers have made multiple improvements and optimizations to adapt to various application scenarios. The optimization of CRISPR/ Cas9 technology has also provided breakthroughs in the establishment of genetically modified mouse models. This article briefly reviews the development process of CRISPR/ Cas9 technology and summarizes optimization strategies of CRISPR/ Cas9, establishment of conditional knockout / knockin gene-modified mouse models, and delivery systems for CRISPR/ Cas9 elements and HDR templates.

Abstract:Malignant tumors are a major disease threatening human health with disability and mortality rates increasing yearly. Protein tyrosine phosphatase 2 (SHP2) of Src homology 2, an important member of the protein tyrosine phosphatase family, has a wide range of functions, and its expression is elevated in a wide range of solid tumors. SHP2 plays an important regulatory role in invasion, metastasis, proliferation, apoptosis, and drug resistance. A large number of studies have shown that SHP2 plays a very important role in the genesis and development of many solid tumors, but no systematic studies have reported on the role of SHP2 in digestive system tumors. Here, we reviewed the biological functions and clinical significance of SHP2 in seven tumor types of the digestive system, explored its roles and mechanisms in cancer development stages, and summarized the development of SHP2 inhibitors to further search for potential targets for effective early diagnosis and gene therapy, which is of great significance to improvement the cancer patient survival rate.

Abstract:Inflammatory bowel disease (IBD) is a chronic intestinal disorder characterized by an immune response to factors in the intestinal environment. Dysregulation of the gut microflora ( GM) may lead to inflammation. Studies suggest that fecal microbiota transplantation, probiotics, prebiotics, and dietary treatments may reshape the GM and treat the disease. MicroRNAs (miRNAs) participate in physiological processes, including cell development, proliferation, and apoptosis. Additionally, miRNAs are important for inflammatory processes and play a role in regulating pro- and antiinflammatory pathways. MiRNA profiles may serve as diagnostic and prognostic markers for IBD. The relationship between miRNAs and GM has not been fully elucidated, and recent studies have demonstrated their roles in regulating GM and inducing ecological dysbiosis. In turn, GM regulates miRNA expression and improves intestinal homeostasis. It is important to continue exploring this relationship. Therefore, the purpose of this review is to analyze the relationship between gut microbiota and miRNAs in IBD and identify possible precision-targeted therapies for IBD.