BACKGROUND:Stress-induced damage to hippocampal neurons may underlie abnormalities in neuronal structure and function,ultimately leading to mood disorders.G protein-coupled receptors in brain tissue play an important role in mood regulation.OBJECTIVE:To analyze the mechanism of depression-like behavior in chronic social defeat stress mice based on high-throughput sequencing and bioinformatics analysis.METHODS:C57BL/6J mice were randomly divided into control group and model group.There was no special treatment in the control group,while a mouse model of chronic social defeat stress was established in the model group.Depression-like behavior was assessed through the sucrose preference test,tail suspension test,and forced swim test.Anxiety behavior was evaluated using the elevated plus-maze,while social behavior was measured through the social interaction test.Cognitive function was assessed with the Y-maze spontaneous alternation test.Immunofluorescence staining was performed to quantify microglia markers in the mouse hippocampus,and Nissl staining was used to examine neuronal damage in mice.High-throughput sequencing was used to identify differentially expressed genes and gene enrichment in the mouse hippocampus,and qPCR was used to measure the expression of G protein-coupled receptors in the mouse hippocampus.RESULTS AND CONCLUSION:(1)Compared with the control group,chronic social defeat stress mice showed significant behavioral impairments,including increased anxiety,depression,and cognitive deficits.(2)Additionally,the Nissl body light density in hippocampal neurons was significantly reduced in chronic social defeat stress mice.(3)Sequencing results revealed synaptic damage in the neurons after chronic social defeat stress.Microglia activation was also markedly increased in the hippocampus of CSDS mice.Furthermore,the expression of G protein-coupled receptors in the hippocampus was significantly higher in chronic social defeat stress mice compared with the control group.These findings suggest that chronic social defeat stress induces anxiety,depression,and cognitive deficits in mice,accompanied by neuropathological changes in the hippocampus,and that altered G protein-coupled receptors expression may play a key role in these behavioral and neuropathological changes.

BACKGROUND:Bone morphogenetic protein 7 is mainly synthesized in the kidney and is expressed at different stages of kidney development,but the spatiotemporal distribution of its expression and its relationship with kidney development have not been systematically reported.OBJECTIVE:To observe the expression of bone morphogenetic protein 7 in mice kidneys during different developmental stages and to explore its potential relationship with kidney development.METHODS:Immunohistochemical techniques combined with stereological methods and western blot analysis were used to observe and analyze the expression of bone morphogenetic protein 7 in mouse kidney tissues at embryonic days(E)12,14,16,18,and neonatal days(N)1,3,7,14,24,40,and 70.RESULTS AND CONCLUSION:(1)The results of immunohistochemistry showed that bone morphogenetic protein 7 was mainly expressed in the nephrogenic zone and immature renal corpuscles during the early stage of kidney development.Subsequently,it was located in mature renal corpuscles and the surrounding distal convoluted tubules,and the expression range gradually increased.After N40 days,bone morphogenetic protein 7 positively expressed in the renal interstitium.(2)Stereology and western blot results showed that the expression level of bone morphogenetic protein 7 gradually decreased with the development of the kidney,reached the lowest level at N7 days,and then slowly increased.To conclude,during the process of kidney development,the expression of bone morphogenetic protein 7 has significant spatiotemporal specificity,and it is hypothesized that it may be related to the development and maturation of renal corpuscles and distal convoluted tubules.

BACKGROUND:Intestinal organoids are highly attractive in tissue/organ biology,disease modeling,and clinical applications,and have become one of the frontiers of biomedical research in recent years.However,this emerging field has not yet been summarized by bibliometrics.OBJECTIVE:To summarize the research trends of intestinal organoids and explore the hot topics and frontier advances of intestinal organoids based on bibliometrics.METHODS:Relevant literature on intestinal organoids was retrieved from the Web of Science Core Collection database,spanning the period from January 1,2006 to November 6,2024.CiteSpace,VOSviewer,and Office software was utilized to conduct bibliometric and visual analyses of the retrieved literature,focusing on annual publication volume,countries,institutions,authors,journals,citations,and keywords.RESULTS AND CONCLUSION:A total of 2 135 articles were retrieved,and after rigorous screening,1 577 articles were included in the final analysis.From 2006 to 2024,there was a steady increase in global publications in the field of intestinal organoids.Molecular biology,genetics,immunology,and clinical medicine emerged as the mainstream disciplines in intestinal organoid research.The United States had the highest number of publications in the field of intestinal organoids and maintained close collaborations with countries such as China,the Netherlands,and Germany.Utrecht University in the Netherlands was the most prolific institution,while the International Journal of Molecular Sciences was the journal with the highest number of publications in the area of intestinal organoids.The article"Replication of human noroviruses in stem cell-derived human enteroids"had the highest co-citation frequency.Human intestinal organoids,stem cell niches,and the potential of organoid therapy are the frontiers and hotspots in the domain of intestinal organoids.The integration of organoids with bioengineering and material technology,as well as intestinal organoid-on-a-chip technology,represent future research priorities in this field.This article provides a comprehensive overview of intestinal organoid research using bibliometric and visualization methods.This paper will help scholars to better understand the dynamic evolution of intestinal organoids and provide guidance for future research.

BACKGROUND:Stress-induced damage to hippocampal neurons may underlie abnormalities in neuronal structure and function,ultimately leading to mood disorders.G protein-coupled receptors in brain tissue play an important role in mood regulation.OBJECTIVE:To analyze the mechanism of depression-like behavior in chronic social defeat stress mice based on high-throughput sequencing and bioinformatics analysis.METHODS:C57BL/6J mice were randomly divided into control group and model group.There was no special treatment in the control group,while a mouse model of chronic social defeat stress was established in the model group.Depression-like behavior was assessed through the sucrose preference test,tail suspension test,and forced swim test.Anxiety behavior was evaluated using the elevated plus-maze,while social behavior was measured through the social interaction test.Cognitive function was assessed with the Y-maze spontaneous alternation test.Immunofluorescence staining was performed to quantify microglia markers in the mouse hippocampus,and Nissl staining was used to examine neuronal damage in mice.High-throughput sequencing was used to identify differentially expressed genes and gene enrichment in the mouse hippocampus,and qPCR was used to measure the expression of G protein-coupled receptors in the mouse hippocampus.RESULTS AND CONCLUSION:(1)Compared with the control group,chronic social defeat stress mice showed significant behavioral impairments,including increased anxiety,depression,and cognitive deficits.(2)Additionally,the Nissl body light density in hippocampal neurons was significantly reduced in chronic social defeat stress mice.(3)Sequencing results revealed synaptic damage in the neurons after chronic social defeat stress.Microglia activation was also markedly increased in the hippocampus of CSDS mice.Furthermore,the expression of G protein-coupled receptors in the hippocampus was significantly higher in chronic social defeat stress mice compared with the control group.These findings suggest that chronic social defeat stress induces anxiety,depression,and cognitive deficits in mice,accompanied by neuropathological changes in the hippocampus,and that altered G protein-coupled receptors expression may play a key role in these behavioral and neuropathological changes.

BACKGROUND:Bone morphogenetic protein 7 is mainly synthesized in the kidney and is expressed at different stages of kidney development,but the spatiotemporal distribution of its expression and its relationship with kidney development have not been systematically reported.OBJECTIVE:To observe the expression of bone morphogenetic protein 7 in mice kidneys during different developmental stages and to explore its potential relationship with kidney development.METHODS:Immunohistochemical techniques combined with stereological methods and western blot analysis were used to observe and analyze the expression of bone morphogenetic protein 7 in mouse kidney tissues at embryonic days(E)12,14,16,18,and neonatal days(N)1,3,7,14,24,40,and 70.RESULTS AND CONCLUSION:(1)The results of immunohistochemistry showed that bone morphogenetic protein 7 was mainly expressed in the nephrogenic zone and immature renal corpuscles during the early stage of kidney development.Subsequently,it was located in mature renal corpuscles and the surrounding distal convoluted tubules,and the expression range gradually increased.After N40 days,bone morphogenetic protein 7 positively expressed in the renal interstitium.(2)Stereology and western blot results showed that the expression level of bone morphogenetic protein 7 gradually decreased with the development of the kidney,reached the lowest level at N7 days,and then slowly increased.To conclude,during the process of kidney development,the expression of bone morphogenetic protein 7 has significant spatiotemporal specificity,and it is hypothesized that it may be related to the development and maturation of renal corpuscles and distal convoluted tubules.

Systemic autoimmune diseases represent a group of disorders characterized by loss of immune tolerance to self-antigens, leading to abnormal immune responses and subsequent tissue damage. Typical examples include systemic lupus erythematosus and systemic sclerosis. These conditions are marked by multi-system involvement, chronic progression, and recurrent flares. The pancreas, as a vital digestive and endocrine organ rich in glandular tissue and vascular supply, can also be affected by autoimmune processes. Pancreatic injury often indicates active and difficult-to-control disease, posing a serious threat to patient survival. Due to its relative rarity, diverse underlying mechanisms across different autoimmune diseases, and frequently nonspecific clinical presentations, pancreatic involvement is easily overlooked, resulting in delayed diagnosis and treatment.This article focuses on the clinical features and potential pathophysiological mechanisms of pancreatic injury associated with autoimmune diseases, such as systemic lupus erythematosus, systemic sclerosis, Sjögren's syndrome, and rheumatoid arthritis, aiming to enhance clinical awareness and facilitate early recognition and diagnosis of this condition.

Objective To describe the spatiotemporal distribution characteristics of Severe Fever with Thrombocytopenia Syndrome (SFTS) in Zibo City and identify its environmental influencing factors and potential high-risk areas, and to propose targeted strategies for SFTS prevention and control. Methods Data on SFTS incidence from 2010 to 2024 were collected. Spatiotemporal scan statistics were used to identify the time and area of SFTS clustering. The maximum entropy (MaxEnt) model was used to analyze environmental influencing factors and predict high-risk areas. Results From 2010 to 2024, a total of 459 cases of SFTS were reported in Zibo. The number of SFTS cases increased yearly, with a peak incidence from April to October each year. Spatiotemporal scan statistics showed the existence of one class I cluster and one class II cluster areas in Zibo. The class I cluster was in Yiyuan District and southern Boshan District, from April to September 2024. The class II cluster was in the center of Zichuan District, from July to September 2024. The MaxEnt model showed that yearly average atmospheric pressure (PRS), yearly average evaporation (EVP), yearly average sunshine duration (SSD) and goat density (Goat) were the key factors influencing the occurrence of SFTS. The predicted risk map showed that the area of high prevalence was 1116 km2, accounting for 18.71% of the total area of the city. Conclusion The spatiotemporal distribution of SFTS exhibits heterogeneity and is influenced by multidimensional environmental factors. This should be considered as a basis for delineating SFTS risk areas and developing SFTS prevention and control measures.

ObjectiveTo investigate the effect of Huangqi jiuni decoction （HQJND） on acute liver injury in severely scalded rats and its possible molecular mechanism by animal experiments and modern pharmacological tools. MethodsFirstly， the rat model of sepsis was established and randomly divided into 4 groups. The normal saline group was given 1 mL of normal saline twice a day， and the traditional Chinese medicine group was given 1 mL of concentrated huangqi jiuni decoction twice a day. After 72 hours of shock， the samples were sacrificed， and then the serum liver function and （+）-haematoxylin eosin staining were performed to verify the efficacy of the drug. Sham Operation Group and sepsis group were fed normally without any special treatment. Then， network pharmacology was used to screen the targets of drugs and drug responses and predict the signaling pathways that might play a role in the treatment of diseases. Finally， fluorescence quantitative PCR （RT-qPCR） was performed to detect gene expression， Western blot （WB） was performed to detect tumor necrosis factor （TNF-α）， P65， phosphorylated P65 （P-P65）， and immunohistochemical （IHC） were performed assays to verify drug efficacy and explore the mechanism of drug treatment. ResultsSerum liver function and histopathology in rats showed that HQJND significantly improved liver function in severely burned rats. Network pharmacology screening was used to identify 353 disease-related marker genes and 286 drug targets. It was predicted that tumor necrosis/NF-NF-κB pathway （TNF/NF-NF-κB pathway） might be a key pathway for HQJND to treat acute liver injury after severe burns. The results of immunohistochemistry （IHC） showed that the staining of TNF-α in the liver of the sepsis group was more than that of the sham operation group and the traditional Chinese medicine group. The results of RT-qPCR and WB showed that the expression of TNF-α， TNFR1 and P65 proteins in the liver of rats in the sepsis group was significantly higher than that in the sham operation group and the traditional Chinese medicine group； on the contrary， the expression of TNF-α， TNFR1 and P65 proteins in the liver of rats in the sepsis group was significantly higher than that in the sham operation group and the traditional Chinese medicine group. The expression level of nuclear factor-kappa B（IκBα） was higher in the sham operation group and the traditional Chinese medicine group， indicating that drug treatment effectively inhibited the activation of the TNF/NF-κb signaling pathway. ConclusionAnimal experiments and network pharmacology results confirm that HQJND has a protective effect on acute liver injury in severely burned rats， which may be related to the inhibition of TNF/NF-κB signaling pathway.

OBJECTIVE To provide a basis for aligning Chinese pharmacoeconomic research on heart failure （HF） with international standards. METHODS A qualitative comparison o f domestic and global HF pharmacoeconomic studies was conducted across four dimensions： research methods and model application， research perspectives and endpoints， data sources and parameter selection， and policy translation and practical impact. RESULTS & CONCLUSIONS Global studies predominantly utilize long-term dynamic models， societal perspectives， real-world data integration， and directly inform reimbursement decisions. Conversely， domestic research often relies on short-term simplified models， a single healthcare system perspectives， literature-derived data， and individual medicine recommendations. Future domestic studies should transition to long-term dynamic modeling， develop localized disease-specific utility databases via big data， establish reimbursement-linked closed-loop mechanisms， and foster multidisciplinary collaboration to optimize healthcare resource allocation.

Objective To investigate the distribution characteristics of pathogens causing infections within 90 days after liver transplantation and the influencing factors of infection. Methods Clinical data of 176 recipients who underwent liver transplantation at the Liver Transplant Center of Beijing Friendship Hospital Affiliated to Capital Medical University from September 2021 to August 2024 were retrospectively analyzed. Patients were divided into the infection group (n=124) and the non-infection group (n=52) based on whether they developed infection within 90 days after transplantation. The distribution characteristics of pathogens in infected patients were analyzed. Univariate and multivariate logistic regression analyses were used to explore the influencing factors of infection. Results Among the 176 liver transplant recipients, 124 cases developed 243 episodes of 518 bacterial, fungal, viral or mycoplasma infections within 90 days after transplantation, with an overall infection rate of 70.5% (124/176). The composition of pathogens was mainly Gram-negative bacteria (38.6%, 200/518), followed by Gram-positive bacteria (32.2%, 167/518) and viruses (15.4%, 80/518), and fungi accounted for 13.1% (68/518). Among Gram-negative bacteria, the main pathogen was Klebsiella pneumoniae (6.8%, 35/518), and among Gram-positive bacteria, the main pathogen was Enterococcus faecalis (8.5%, 44/518). Viruses included Epstein-Barr virus (3.7%, 19/518) and cytomegalovirus (3.7%, 19/518), and fungi were mainly Candida albicans (6.8%, 35/518). The most common infection site among the 243 episodes was pulmonary infection (42.0%, 102/243), followed by abdominal infection (22.6%, 55/243) and bloodstream infection (18.1%, 44/243). The infections mainly occurred within 2 weeks after transplantation (60.9%, 148/243). Multivariate logistic regression analysis indicated that preoperative infection within 2 weeks, a high preoperative model for end-stage liver disease (MELD) score, and preoperative sarcopenia were independent risk factors for infection within 90 days after liver transplantation (all odds ratio>1, P<0.05). After multivariate correction, the levels of CD4⁺T cells and CD8⁺T cells within 90 days after surgery were independently associated with the occurrence of infection. Low levels of CD4⁺T cells and CD8⁺T cells might be related to an increased risk of infection. Conclusions The infection rate after liver transplantation is high, and the pathogens are mainly Gram-negative bacteria. The lungs are the most common infection site. Preoperative MELD score, preoperative sarcopenia and preoperative infection within 2 weeks are independent risk factors for infection within 90 days after liver transplantation. Regular monitoring of immune indicators CD4⁺T cells and CD8⁺T cells levels after transplantation is helpful to reduce the occurrence of post-transplantation infection.