Retinitis pigmentosa （RP） is the most common hereditary blinding eye disease in clinical practice， with the pathogenesis remaining unclear. Patients experience progressive apoptosis of retinal photoreceptor cells， accompanied by degeneration of retinal pigment epithelium （RPE） cells. Current Western medical treatments mainly focus on gene therapy and stem cell transplantation， showing limited efficacy. In contrast， clinical observations have confirmed the therapeutic effects of traditional Chinese medicine （TCM） treatments. Establishing an RP animal model that aligns with the diagnostic features of both TCM and Western medicine could help combine the strengths of both approaches， thereby broadening the treatment options for RP. This study categorizes and summarizes the existing RP animal models in terms of classification， types， inheritance patterns， and alignment with clinical manifestations. It is found that current RP models are primarily derived from natural animal models such as RD mice and RCS rats， transgenic animal models like RPE-65 knockout mice and rhodopsin gene knockout mice， and chemically induced models such as those created by monochromatic light exposure or N-ethyl-N-nitrosourea （ENU） administration. These three categories of models focus more on detecting RP-related histopathological， molecular biological， and cellular immunological indicators， but offer limited observation of the overall characteristics of the disease and lack insight into syndrome differentiation. Although RP is a congenital genetic disease， its progression is influenced by acquired factors such as environment， constitution， emotions， and care. Current models do not fully capture the characteristics of this disease. Therefore， establishing an RP animal model based on the diagnostic features of both TCM and Western medicine will have significant implications for future experimental and clinical research.

Retinitis pigmentosa （RP） is the most common hereditary blinding eye disease in clinical practice， with the pathogenesis remaining unclear. Patients experience progressive apoptosis of retinal photoreceptor cells， accompanied by degeneration of retinal pigment epithelium （RPE） cells. Current Western medical treatments mainly focus on gene therapy and stem cell transplantation， showing limited efficacy. In contrast， clinical observations have confirmed the therapeutic effects of traditional Chinese medicine （TCM） treatments. Establishing an RP animal model that aligns with the diagnostic features of both TCM and Western medicine could help combine the strengths of both approaches， thereby broadening the treatment options for RP. This study categorizes and summarizes the existing RP animal models in terms of classification， types， inheritance patterns， and alignment with clinical manifestations. It is found that current RP models are primarily derived from natural animal models such as RD mice and RCS rats， transgenic animal models like RPE-65 knockout mice and rhodopsin gene knockout mice， and chemically induced models such as those created by monochromatic light exposure or N-ethyl-N-nitrosourea （ENU） administration. These three categories of models focus more on detecting RP-related histopathological， molecular biological， and cellular immunological indicators， but offer limited observation of the overall characteristics of the disease and lack insight into syndrome differentiation. Although RP is a congenital genetic disease， its progression is influenced by acquired factors such as environment， constitution， emotions， and care. Current models do not fully capture the characteristics of this disease. Therefore， establishing an RP animal model based on the diagnostic features of both TCM and Western medicine will have significant implications for future experimental and clinical research.

As a pivotal strategy to alleviate the shortage of organ donors, xenotransplantation has achieved remarkable advances in both pre-clinical and clinical studies in recent years, driven by continuous optimization of gene modification techniques and immunosuppressive regimens. Nevertheless, clinical translation still confronts formidable challenges, including rejection and heightened infection risks, which severely compromise long-term graft survival. Consequently, the role of immunosuppressive regimens in xenotransplantation has become increasingly prominent. This article summarizes the mechanisms underlying xenogeneic immune rejection, the latest developments in immunosuppressive regimens, cutting-edge strategies for inducing immune tolerance and the major hurdles facing clinical xenotransplantation. It delves into potential optimization strategies and directions for future clinical research, aiming to offer theoretical insights and practical guidance for the safe and effective application of clinical xenotransplantation.

Objective To systematically analyze the literature characteristics of Journal of Organ Transplantation since its inception. Methods Using the China National Knowledge Infrastructure (CNKI) academic journal full-text database as the data source, all articles published in the Journal of Organ Transplantation from January 2010 to August 2025 were retrieved. After excluding non-academic papers, a total of 1 568 research papers were included. R language 4.3.0, Bibliometrix package 3.2.1, and Citespace software were used to analyze the number of publications, publishing institutions, authors, keywords and other aspects. Results The number of publications in Journal of Organ Transplantation increased from an average of 82 articles per year in the early years after its inception to 113 articles per year in recent years, a growth of 37.8%. The geographical distribution of publishing institutions covers 32 provinces, cities and autonomous regions nationwide, mainly concentrated in the South China, East China and North China regions, and has now basically covered the central and western regions in recent years. The author collaboration network includes 45 authors distributed across 7 major collaboration clusters, forming a stable multi-level national research system centered on key university-affiliated hospitals. The high-frequency keywords are dominated by "liver transplantation" (425 times) and "kidney transplantation" (396 times). The theme evolution shows a clear three-stage characteristic: initially focusing on clinical technology application, deepening to immune mechanism exploration in the middle stage, and recently (since 2022) focusing on cutting-edge research areas such as xenotransplantation. Conclusions Journal of Organ Transplantation has witnessed the rapid development of China's organ transplantation cause, fully reflecting the research status and trends in China's organ transplantation field, and has provided an important platform for the future development and international cooperation in China's organ transplantation field.

Objective: To investigate the efficacy of magnesium-strontium co-doped hydroxyapatite mineralized collagen (MSHA/Col) in improving the bone repair microenvironment and enhancing bone regeneration capacity, providing a strategy to address the insufficient biomimetic composition and limited bioactivity of traditional hydroxyapatite mineralized collagen (HA/Col) scaffolds. Methods: A high-molecular-weight polyacrylic acid-stabilized amorphous calcium magnesium strontium phosphate precursor (HPAA/ACMSP) was prepared. Its morphology and elemental distribution were characterized by high-resolution transmission electron microscopy (TEM) and energy-dispersive spectroscopy. Recombinant collagen sponge blocks were immersed in the HPAA/ACMSP mineralization solution. Magnesium-strontium co-doped hydroxyapatite was induced to deposit within collagen fibers (experimental group: MSHA/Col; control group: HA/Col). The morphological characteristics of MSHA/Col were observed using scanning electron microscopy (SEM). Its crystal structure and chemical composition were analyzed by X-ray diffraction and Fourier transform infrared spectroscopy, respectively. The mineral phase content was evaluated by thermogravimetric analysis. The scaffold's porosity, ion release, and in vitro degradation performance were also determined. For cytological experiments, CCK-8 assay, live/dead cell staining, alkaline phosphatase staining, alizarin red S staining, RT-qPCR, and western blotting were used to evaluate the effects of the MSHA/Col scaffold on the proliferation, viability, early osteogenic differentiation activity, late mineralization capacity, and gene and protein expression levels of key osteogenic markers [runt-related transcription factor 2 (Runx2), collagen type Ⅰ (Col-Ⅰ), osteopontin (Opn), and osteocalcin (Ocn)] in mouse embryonic osteoblast precursor cells (MC3T3-E1). Results: HPAA/ACMSP appeared as amorphous spherical nanoparticles under TEM, with energy spectrum analysis showing uniform distribution of carbon, oxygen, calcium, phosphorus, magnesium, and strontium elements. SEM results of MSHA/Col indicated successful complete intrafibrillar mineralization. Elemental analysis showed the mass fractions of magnesium and strontium were 0.72% (matching the magnesium content in natural bone) and 2.89%, respectively. X-ray diffraction revealed characteristic peaks of hydroxyapatite crystals (25.86°, 31°-34°). Infrared spectroscopy results showed characteristic absorption peaks for both collagen and hydroxyapatite. Thermogravimetric analysis indicated a mineral phase content of 78.29% in the material. The scaffold porosity was 91.6% ± 1.1%, close to the level of natural bone tissue. Ion release curves demonstrated sustained release behavior for both magnesium and strontium ions. The in vitro degradation rate matched the ingrowth rate of new bone tissue. Cytological experiments showed that MSHA/Col significantly promoted MC3T3-E1 cell proliferation (130% increase in activity at 72 h, P < 0.001). MSHA/Col exhibited excellent efficacy in promoting osteogenic differentiation, significantly upregulating the expression of osteogenesis-related genes and proteins (Runx2, Col-Ⅰ, Opn, Ocn) (P < 0.01). Conclusion The MSHA/Col scaffold achieves dual biomimicry of natural bone in both composition and structure, and effectively promotes osteogenic differentiation at the genetic and protein levels, breaking through the functional limitations of pure hydroxyapatite mineralized collagen. This provides a new strategy for the development of functional bone repair materials

OBJECTIVE To investigate the effects and potential mechanism of Qiangxin decoction on mitochondrion of rats with chronic heart failure （CHF）. METHODS The CHF model was established by ligating the left anterior descending branch of the coronary artery. Modeled rats were divided into model group， Qiangxin decoction low-dose and high-dose groups （12.25， 24.50 g/kg， calculated by crude drug）， and chemical medicine group （Sacubitril valsartan sodium tablets， 10.42 mg/kg）， with 10 rats in each group； control group was set up without treatment. Each group of rats was orally administered with the corresponding medication or normal saline twice a day for 28 consecutive days. After the last medication， the contents of N-terminal pro-brain natriuretic peptide （NT-proBNP） and adenosine triphosphate （ATP） in serum and phosphatidic acid （PA） and cardiolipin （CL） in myocardial tissue were all detected； the pathological damage and collagen fibrosis of rat myocardial tissue were observed； the apoptosis of myocardial cells was determined； the ultrastructure of myocardial tissue was observed； the protein expressions of mitofusin 1 （Mfn1）， Mfn2， optic atrophy protein 1 （OPA1） and dynamin-related protein 1 （Drp1） were all detected in myocardial tissue. RESULTS Compared with control group，the serum content of NT-proBNP， apoptotic rate of myocardial cells， and relative expressions of S-OPA1 and Drp1 proteins were all increased significantly； serum content of ATP，contents of PA and CL， and relative expressions of Mfn1， Mfn2 and L-OPA1 proteins were all significantly reduced （P＜0.05）. There were abnormal membrane tissue structure in various layers of myocardial tissue， degeneration and necrosis of myocardial cells， and severe fibrosis； the mitochondria were swollen， with reduced or absent cristae， and uneven matrix density. After intervention with Qiangxin decoction， the levels of the aforementioned quantitative indicators in serum and myocardial tissue of rats （excluding CL content in the Qiangxin decoction low- dose group） were significantly reversed （P＜0.05）； the pathological damage of myocardial tissue had significantly improved， fibrosis had significantly reduced， mitochondrial morphology tended to be normal， cristae had increased， and matrix density was uniform. CONCLUSIONS Qiangxin decoction can regulate myocardial mitochondrial function and structural integrity of CHF rats， thereby improving myocardial energy metabolism and antagonizing myocardial fibrosis， the mechanism of which may be associated with activating PA/Mfn/CL signaling pathway.

OBJECTIVE To investigate the effects and potential mechanism of Qiangxin decoction on mitochondrion of rats with chronic heart failure （CHF）. METHODS The CHF model was established by ligating the left anterior descending branch of the coronary artery. Modeled rats were divided into model group， Qiangxin decoction low-dose and high-dose groups （12.25， 24.50 g/kg， calculated by crude drug）， and chemical medicine group （Sacubitril valsartan sodium tablets， 10.42 mg/kg）， with 10 rats in each group； control group was set up without treatment. Each group of rats was orally administered with the corresponding medication or normal saline twice a day for 28 consecutive days. After the last medication， the contents of N-terminal pro-brain natriuretic peptide （NT-proBNP） and adenosine triphosphate （ATP） in serum and phosphatidic acid （PA） and cardiolipin （CL） in myocardial tissue were all detected； the pathological damage and collagen fibrosis of rat myocardial tissue were observed； the apoptosis of myocardial cells was determined； the ultrastructure of myocardial tissue was observed； the protein expressions of mitofusin 1 （Mfn1）， Mfn2， optic atrophy protein 1 （OPA1） and dynamin-related protein 1 （Drp1） were all detected in myocardial tissue. RESULTS Compared with control group，the serum content of NT-proBNP， apoptotic rate of myocardial cells， and relative expressions of S-OPA1 and Drp1 proteins were all increased significantly； serum content of ATP，contents of PA and CL， and relative expressions of Mfn1， Mfn2 and L-OPA1 proteins were all significantly reduced （P＜0.05）. There were abnormal membrane tissue structure in various layers of myocardial tissue， degeneration and necrosis of myocardial cells， and severe fibrosis； the mitochondria were swollen， with reduced or absent cristae， and uneven matrix density. After intervention with Qiangxin decoction， the levels of the aforementioned quantitative indicators in serum and myocardial tissue of rats （excluding CL content in the Qiangxin decoction low- dose group） were significantly reversed （P＜0.05）； the pathological damage of myocardial tissue had significantly improved， fibrosis had significantly reduced， mitochondrial morphology tended to be normal， cristae had increased， and matrix density was uniform. CONCLUSIONS Qiangxin decoction can regulate myocardial mitochondrial function and structural integrity of CHF rats， thereby improving myocardial energy metabolism and antagonizing myocardial fibrosis， the mechanism of which may be associated with activating PA/Mfn/CL signaling pathway.

Objective To establish an individualized nomogram model and evaluate its efficacy to provide a possible evaluation basis for the prognosis of lower third and abdominal part of oesophageal adenocarcinoma (EAC). Methods Lower third and abdominal part of EAC patients from 2010 to 2015 were chosen from the SEER Research Plus Database (17 Regs, 2022nov sub). The patients were randomly allocated to the training cohort and the internal validation cohort with a ratio of 7∶3 using bootstrap resampling. The Cox proportional hazards regression analysis was used to determine significant contributors to overall survival (OS) in EAC patients, which would be elected to construct the nomogram prediction model. C-index, calibration curve and receiver operating characteristic (ROC) curve were performed to evaluate its efficacy. Finally, the efficacy to evaluate the OS of EAC patients was compared between the nomogram prediction model and TNM staging system. Results In total, 3945 patients with lower third and abdominal part of EAC were enrolled, including 3475 males and 470 females with a median age of 65 (57-72) years. The 2761 patients were allocated to the training cohort and the remaining 1184 patients to the internal validation cohort. In the training and the internal validation cohorts, the C-index of the nomogram model was 0.705 and 0.713, respectively. Meanwhile, the calibration curve also suggested that the nomogram model had a strong capability of predicting 1-, 3-, and 5-year OS rates of EAC patients. The nomogram also had a higher efficacy than the TNM staging system in predicting 1-, 3-, and 5-year OS rates of EAC patients. Conclusion This nomogram prediction model has a high efficiency for predicting OS in the patients with lower third and abdominal part of EAC, which is higher than that of the current TNM staging system.

Objective: To investigate the prevalence and influencing factors of hepatitis C virus (HCV) infection among drug users in Baoshan District, Shanghai Municipality, so as to provide insights into strengthening HCV intervention among drug users. Methods: Drug users under community management in Baoshan District from 2017 to 2023 were recruited. Demographic information, drug use behaviors, sexual behaviors and receipt of intervention service were collected through questionnaire surveys. Blood samples were collected for HCV antibody testing, and the prevalence of anti-HCV antibody was analyzed. Factors affecting the prevalence of anti-HCV antibody among drug users were analyzed using a multivariable logistic regression model. Results: A total of 2 801 drug users were surveyed, including 2 233 males (79.72%) and 568 females (20.28%). The majority of drug users were aged 40 to <60 years (1 663 drug users, 59.37%). The prevalence of anti-HCV antibody was 28.35%, showing an overall upward trend from 2017 to 2023 (P<0.05). Multivariable logistic regression analysis showed that females (OR=1.468, 95%CI: 1.169-1.844), 40 years and over (40 to <50 years, OR=2.441, 95%CI: 1.838-3.242; 50 to <60 years, OR=2.377, 95%CI: 1.787-3.161; 60 to 97 years, OR=1.637, 95%CI: 1.163-2.304), using traditional drugs (OR=2.488, 95%CI: 1.967-3.147) or mixed drugs (OR=2.950, 95%CI: 1.974-4.409), having injected drugs (not share needles, OR=3.649, 95%CI: 2.849-4.673; share needles, OR=3.532, 95%CI: 1.851-6.738) and never using condoms during sexual contacts with spouses/cohabitants in the past year (OR=1.975, 95%CI: 1.354-2.879) were associated with a higher prevalence of anti-HCV antibody; the educational level of high school/technical secondary school (OR=0.483, 95%CI: 0.280-0.835) or college and above (OR=0.280, 95%CI: 0.129-0.608) was associated with a lower prevalence of anti-HCV antibody. Conclusions The prevalence of anti-HCV antibody among drug users in Baoshan District showed an upward trend from 2017 to 2023. Gender, age, educational level, type of drugs, history of drug injection and never using condoms during sexual contacts with spouses/cohabitants were influencing factors for prevalence of anti-HCV antibody among drug users.

ObjectiveTo investigate the role and mechanism of thymic stromal lymphopoietin （TSLP） in a mouse model of acetaminophen （APAP）-induced acute liver injury. MethodsA total of 16 wild-type （WT） male C57BL/6J mice were randomly divided into control group and APAP group， with 8 mice in each group， and the mice in the APAP group were given intraperitoneal injection of APAP solution at a dose of 400 mg/kg to establish an animal model， while those in the control group were given injection of an equal volume of normal saline， with samples collected after 6 hours. An automatic chemical analyzer was used to measure the serum levels of alanine aminotransferase （ALT） and aspartate aminotransferase （AST）； quantitative real-time PCR was used to measure the mRNA expression levels of the inflammatory factors tumor necrosis factor-α （TNF-α） and interleukin-6 （IL-6） in liver tissue； the kit was used to measure the content of glutathione （GSH） in liver tissue homogenate； quantitative real-time PCR and Western blot were used to measure the transcriptional level and protein expression level of TSLP. Furthermore， 22 WT male C57BL/6J mice were randomly divided into control group with 8 mice， APAP group with 8 mice， and APAP+recombination TSLP （rTSLP） group with 6 mice； the mice in the APAP+rTSLP group were given intraperitoneal injection of rTSLP solution， while those in the control group and the APAP group were given injection of the solvent PBS； after 30 minutes， the mice in the APAP+rTSLP group and the APAP group were given injection of APAP solution， while those in the control group were given injection of an equal volume of normal saline. The serum levels of ALT and AST were measured； HE staining was used to observe the pathological changes of the liver； kits were used to measure the levels of the oxidative stress indices malondialdehyde （MDA） and superoxide dismutase （SOD） in liver tissue homogenate； Western blot was used to measure the expression levels of the autophagy-related proteins LC3‍Ⅰ/Ⅱ， Beclin1， and P62 and the molecules such as nuclear factor erythroid 2-related factor 2 （Nrf2）， protein kinase B （Akt）， phosphorylated Akt （p-Akt）， mammalian target of rapamycin （mTOR）， and phosphorylated mTOR （p-mTOR）. In addition， 16 WT male C57BL/6J mice and 16 TSLP receptor-silenced （TSLPR^-/-） mice were divided into WT mouse control group， WT mouse APAP group， TSLPR^-/- mouse control group， and TSLPR^-/- mouse APAP group， with 8 mice in each group； the mice in the WT mouse APAP group and the TSLPR^-/- mouse APAP group were used for modeling by intraperitoneal injection of APAP solution at a dose of 400 mg/kg， and those in the WT mouse control group and the TSLPR^-/- mouse control group were given injection of an equal volume of normal saline. The serum levels of ALT and AST and the content of MDA in liver tissue were measured for these four groups， and Western blot was used to measure the protein expression levels of LC3Ⅰ/Ⅱ， Akt， and p-Akt. The independent-samples t test was used for comparison of continuous data between two groups； a one-way analysis of variance was used for comparison between multiple groups， and the least significant difference t-test was used for further comparison between two groups. ResultsAfter the mouse model of APAP-induced acute liver injury was established successfully， there were significant increases in the mRNA and protein expression levels of TSLP compared with the control group （both P<0.01）. In the study of rTSLP， compared with the control group， the APAP group had significant increases in ALT and AST （both P<0.001） and radial necrosis along the central vein observed by HE staining of liver tissue， as well as significant reductions in the protein expression levels of the oxidative stress indices SOD and Nrf2 and a significant increase in the level of MDA （all P<0.01）； compared with the APAP group， the APAP+rTSLP group had significant reductions in ALT and AST， a significant reduction in necrotic area of liver tissue， significant increases in the protein expression levels of SOD and Nrf2， and a significant reduction in MDA （all P<0.05）； there were significant differences in the protein expression levels of LC3Ⅰ/Ⅱ， Beclin1， P62， p-Akt， and p-mTOR between the APAP+rTSLP group and the control group （all P<0.01）. In the study of TSLPR^-/- mice， compared with the WT mice after modeling， the TSLPR^-/- mice had significant increases in the levels of ALT， AST， and MDA and significant reductions in the expression levels of LC3Ⅰ/Ⅱ and p-Akt （all P<0.05）. ConclusionTSLP can increase autophagy， reduce oxidative stress， and thus improve acute liver injury induced by APAP overdose， possibly by activating the PI3K/Akt signaling pathway and inhibiting mTOR.