BackgroundIndividuals with schizophrenia are prone to higher rates of hospital readmission， presenting significant clinical challenges and imposing considerable social burdens within the mental health domain. In recent years， various risk prediction models have been developed to forecast readmission in patients with schizophrenia and support clinical decision-making， but their predictive performance and clinical applicability require comprehensive evaluation. ObjectiveTo systematically evaluate the risk prediction models for readmission in patients with schizophrenia， so as to provide insights for the development of high-performance and highly applicable readmission risk prediction models for patients with schizophrenia. MethodsOn July 5， 2025， a systematic literature search was conducted across multiple electronic databases， including PubMed， Embase， Cochrane Library， Web of Science， CINAHL， CNKI， China Biomedical Literature Database， Wanfang Database， and VIP Database， to identify risk prediction models for readmission in patients with schizophrenia. The search period was from the establishment of the databases to July 1， 2025. Two researchers independently performed literature screening， data extraction， risk of bias assessment， and applicability assessment. ResultsA total of 9 studies were included in this review， encompassing 18 risk prediction models for readmission in patients with schizophrenia. Among them， 4 models reported the area under the receiver operating characteristic （ROC） curve （AUC）， ranging from 0.734 to 0.820， 16 models provided AUC values of 0.642–0.879 for internal validation， and 1 model demonstrated an AUC of 0.841 for external validation. Key predictors included disease duration and the concomitant therapy of antipsychotic medications. The risk of bias was assessed as "high" in all included studies. ConclusionThe development of risk prediction models for readmission in patients with schizophrenia remains in an exploratory stage. Although the model exhibits favorable predictive performance， it is associated with a high risk of bias and insufficient performance evaluation.

Metabolic dysfunction-associated fatty liver disease is a common chronic liver disease worldwide， and its incidence rate continues to rise. The traditional “two-hit” theory has gradually been replaced by the “multiple-hit” hypothesis， which emphasizes the synergistic effect of multiple pathogenic factors. Necroptosis is an inflammatory form of death with both the morphological characteristics of necrosis and the signaling mechanism of apoptosis， and the core of necroptosis lies in the receptor-interacting protein kinase 1-receptor-interacting protein kinase 3-mixed lineage kinase domain-like pseudokinase signaling axis. This pathway directly leads to the death of hepatocytes， and it triggers an inflammatory response and promotes the fibrosis process by releasing damage-associated molecular patterns； the pathway is also closely associated with the metabolic reprogramming of the liver. This review summarizes the activation mechanism of necroptosis in metabolic dysfunction-associated fatty liver disease， analyzes its effect on liver inflammation， fibrosis， and metabolism， and explores its therapeutic strategies and application prospects.

Objective To retrieve,analyze and synthesize evidence on post-transplant diabetes mellitus(PTDM)in lung transplant patients,providing reference for clinical healthcare professionals in preventing and managing PTDM in lung transplant patients.Methods Based on the"6S"evidence model,systematic searches were conducted across guideline websites,professional associations,and Chinese/English databases regarding post-transplant diabetes mellitus(PTDM)in lung transplant patients.The search period spanned from data-base inception to January 2025.Two researchers independently completed literature screening,quality assess-ment,and evidence extraction.Results A total of 14 articles were included,comprising 1 clinical decision,2 guidelines,5 expert consensuses,2 specifications,1 evidence summary,and 3 systematic reviews.Twenty-four pieces of best evidence were synthesized from seven aspects:risk factors,diagnosis,screening,prevention,treatment,glycemic control targets,and health education.Conclusion The best evidence for preventing and managing post-transplant diabetes mellitus in lung transplant patients provides an evidence-based foundation for clinical practice among healthcare professionals.Evidence should be selected and applied according to spe-cific clinical situations and patient needs.

Childhood primary renal tubular diseases are chronic kidney diseases characterized by impaired renal tubular reabsorption. Primary renal tubular disease has diverse clinical manifestations and lacks of specificity. Laboratory tests are limited，making it prone to missed diagnosis and misdiagnosis. Based on the current knowledge of renal tubular diseases，authors propose early warning signals of renal tubular diseases such as family history of primary tubular diseases，unexplained polyhydramnios during pregnancy，polydipsia，polyuria，delayed growth and development or rickets，decreased muscle strength and tone，unexplained electrolyte disturbance，hyperuricemia，acid-base disturbance，positive urine sugar test，renal tubular proteinuria，urinary imaging examination suggesting kidney stones，calcium deposition，renal cysts and early onset of eye，ear，joint and neuron injury.Meanwhile，some universal management strategies for primary renal tubular disease are proposed，emphasizing the importance of multidisciplinary collaboration，genetic testing and individualized intervention to improve the long-term prognosis of childhood primary renal tubular diseases.

This study aims to determine the nephrotoxic effects of 3-monochloropropanel-1,2-diol(3-MCPD)on female and male SD rats.A nephrotoxicity model was established by gavage of dif-ferent doses of 3-MCPD,and 80 SD rats were randomly divided into four groups:the control group(0 mg/kg 3-MCPD),low-dose group(15 mg/kg 3-MCPD),medium-dose group(30 mg/kg 3-MCPD),high-dose group(60 mg/kg 3-MCPD),with half female and half male.The body mass and food intake of the rats were recorded weekly,and the urine and blood and kidney tissues were col-lected after 28 consecutive days of gavage,and the blood erythrocyte count(WBC),white blood cell count(RBC),hemoglobin(HGB),erythrocyte-compaction-transfer-value(HCT),creatinine(CREA),serum urea nitrogen(BUN),and the indexes of blood phosphorus(P)and calcium(Ca)were detected;the level of kidney injury molecule(KIM-1)was measured by ELISA kit;the renal pathological changes was observed by histopathology method;and transcriptome sequencing was used to analyze differential genes in female and male rats.The results showed that 3-MCPD did not significantly affect the growth of male rats,but high doses significantly reduced the weight and food intake of female rats.The high-dose group of 3-MCPD caused a significant decrease in RBC,HGB,and HCT levels in both male and female rats,resulting in a significant increase in KIM-1 and P,and a significant decrease in Ca,but only a significant increase in CREA and BUN in female rats.Histopathology showed that in the high-dose group of male rats,only mild renal tubular dilation,epithelial cell edema,and clear tubular type were observed in the kidneys,while in female rats,a large number of renal sacs,clear tubular type,and interstitial inflammatory cells with fibrosis were observed in the kidneys.Transcriptome sequencing showed 1 712 differentially expressed genes in the high-dose group of female rats and 1 153 differentially expressed genes in the high-dose group of male rats.KEGG enrichment analysis showed that both male and female rats in the high-dose group experienced oxidative stress and cell apoptosis,but 3-MCPD may also participate in the process of kidney damage in females by inhibiting autophagy and inducing iron death pathways.The above results indicate that high-dose 3-MCPD has a more significant nephrotoxic effect on fe-male rats.

Autism spectrum disorder(ASD),characterized by unknown etiology and high heterogeneity,ne-cessitates precise diagnostic and intervention strategies.Neuroimaging techniques have shown great promise in un-covering the neural mechanisms of ASD,providing a foundation for aided diagnosis and transcranial magnetic stim-ulation(TMS)interventions.This review highlights that integrating multimodal neuroimaging and developing indi-vidualized indices with developmental specificity can significantly improve the accuracy of ASD diagnosis and clas-sification.Furthermore,TMS interventions guided by functional connectivity derived from functional magnetic reso-nance imaging(fMRI)offer a personalized approach to ASD treatment.

Gastric cancer (GC) is characterized by high morbidity and mortality rates. Chinese agarwood comprises the resin-containing wood of Aquilaria sinensis (Lour.) Gilg., traditionally utilized for treating asthma, cardiac ischemia, and tumors. However, comprehensive research regarding its anti-GC effects and underlying mechanisms remains limited. In this study, Chinese agarwood petroleum ether extract (CAPEE) demonstrated potent cytotoxicity against human GC cells, with half maximal inhibitory concentration (IC₅₀) values for AGS, HGC27, and MGC803 cells of 2.89, 2.46, and 2.37 μg·mL^-1, respectively, at 48 h. CAPEE significantly induced apoptosis in these GC cells, with B-cell lymphoma-2 (BCL-2) associated X protein (BAX)/BCL-2 antagonist killer 1 (BAK) likely mediating CAPEE-induced apoptosis. Furthermore, CAPEE induced G₀/G₁ phase cell cycle arrest in human GC cells via activation of the deoxyribonucleic acid (DNA) damage-p21-cyclin D1/cyclin-dependent kinase 4 (CDK4) signaling axis, and increased Fe²⁺, lipid peroxides and reactive oxygen species (ROS) levels, thereby inducing ferroptosis. Ribonucleic acid (RNA) sequencing, real-time quantitative polymerase chain reaction (RT-qPCR), and Western blotting analyses revealed CAPEE-mediated upregulation of heme oxygenase-1 (HO-1) in human GC cells. RNA interference studies demonstrated that HO-1 knockdown reduced CAPEE sensitivity and inhibited CAPEE-induced ferroptosis in human GC cells. Additionally, CAPEE administration exhibited robust in vivo anti-GC activity without significant toxicity in nude mice while inhibiting tumor cell growth and promoting apoptosis in tumor tissues. These findings indicate that CAPEE suppresses human GC cell growth through upregulation of the DNA damage-p21-cyclin D1/CDK4 signaling axis and HO-1-mediated ferroptosis, suggesting its potential as a candidate drug for GC treatment.
Animals ; Humans ; Mice ; Antineoplastic Agents, Phytogenic ; Apoptosis/drug effects* ; Cell Line, Tumor ; Cyclin D1/genetics* ; Cyclin-Dependent Kinase 4/genetics* ; DNA Damage/drug effects* ; Drugs, Chinese Herbal/pharmacology* ; Ferroptosis/drug effects* ; G1 Phase Cell Cycle Checkpoints/drug effects* ; Heme Oxygenase-1/genetics* ; Mice, Inbred BALB C ; Mice, Nude ; Plant Extracts/pharmacology* ; Stomach Neoplasms/physiopathology* ; Thymelaeaceae/chemistry* ; Up-Regulation/drug effects*

Growth factors (GFs) are a class of peptides that facilitate cell growth by binding to specific receptors on the cell membrane. With unique properties, GFs are widely applied in the repair of injured tissue. To address the limitations associated with natural peptide-based GFs and recombinant GFs, researchers have developed diverse GF mimetics. This article offers a comprehensive review on common types of GFs and their applications in tissue repair and summarizes the features of GF mimetics currently under development. The aim is to provide valuable references for promoting the application of GFs in regenerative medicine.
Intercellular Signaling Peptides and Proteins/therapeutic use* ; Humans ; Tissue Engineering/methods* ; Regenerative Medicine/methods* ; Animals ; Wound Healing/drug effects* ; Biomimetic Materials

Peri-implant keratinized mucosa (PIKM) augmentation refers to surgical procedures aimed at increasing the width of PIKM. Consensus reports emphasize the necessity of maintaining a minimum width of PIKM to ensure long-term peri-implant health. Currently, several surgical techniques have been validated for their effectiveness in increasing PIKM. However, the selection and application of PIKM augmentation methods may present challenges for dental practitioners due to heterogeneity in surgical techniques, variations in clinical scenarios, and anatomical differences. Therefore, clear guidelines and considerations for PIKM augmentation are needed. This expert consensus focuses on the commonly employed surgical techniques for PIKM augmentation and the factors influencing their selection at second-stage surgery. It aims to establish a standardized framework for assessing, planning, and executing PIKM augmentation procedures, with the goal of offering evidence-based guidance to enhance the predictability and success of PIKM augmentation.
Humans ; Consensus ; Dental Implants ; Mouth Mucosa/surgery* ; Keratins

Objective To investigate the effect of Biejiajian Pill(BJJP)on malignant biological behavior of hepatocellular carcinoma Hep3B cells and its regulatory mechanism.Methods A total of 72 healthy SD rats were randomly divided into blank control(BC)group,low(0.55 g/kg),medium(1.10 g/kg)and high(2.20 g/kg)BJJP experimental group,and drug-containing serum was prepared.Hep3B cells were divided into BC group,normal rat serum treatment(NC)group,low dose BJJP(LBJJP)group,medium dose BJJP(MBJJP)group and high dose BJJP(HBJJP)group,empty plasmid(pcDNA3.1)group,and CKLF-like MARVEL transmembrane domain containing 6(CMTM6)overexpression(pcDNA3.1-CMTM6)group,and the NC+pcDNA3.1 group,MBJJP+pcDNA3.1 group,NC+pcDNA3.1-CMTM6 group and MBJJP+pcDNA3.1-CMTM6 group.The proliferation of hepatoma Hep3B cells was detected by CCK-8.The migration and invasion of hepatoma Hep3B cells were detected by Transwell assay.The expression levels of proliferation-related proteins proliferating cell nuclear antigen(PCNA),epithelial-mesenchymal transition(EMT)related proteins(E-cadherin,N-cadherin and Vimentin),and CMTM6 proteins in hepatoma Hep3B cells were detected by Western blotting experiments.Results Compared with those in BC group,there were no significant differences in the proliferation,migration and invasion abilities of Hep3B cells,or the expression levels of PCNA,EMT related proteins(E-cadherin,N-cadherin and Vimentin)and CMTM6 protein in NC group(P＞0.05).Compared with NC group,LBJJP,MBJJP and HBJJP drug-containing serum inhibited the proliferation,migration and invasion of Hep3B cells,downregulated the protein expression of PCNA;MBJJP and HBJJP upregulated the protein expression of E-cadherin.The protein expressions of N-cadherin,Vimentin and CMTM6 were downregulated,with significant differences(P＜0.05).Compared with pcDNA3.1 group,the protein expression of CMTM6,cell proliferation,migration,invasion,PCNA protein expression,N-cadherin protein expression,and Vimentin protein expression in Hep3B cells in pcDNA3.1-CMTM6 group were significantly upregulated,while the protein expression of E-cadherin was significantly downregulated(P＜0.05).Compared with NC+pcDNA3.1 group,the proliferation,migration and invasion abilities of Hep3B cells in MBJJP+pcDNA3.1 group were decreased,the expression levels of PCNA,Vimentin and N-cadherin protein were decreased,while the expression level of E-cadherin protein was increased.Compared with NC+pcDNA3.1-CMTM6 group,MBJJP+pcDNA3.1-CMTM6 group had the same results in the proliferation,migration and invasion abilities of Hep3B cells and the protein expression levels of PCNA,Vimentin,N-cadherin and E-cadherin.The differences were statistically significant(all P＜0.05).Conclusion BJJP may inhibit the proliferation,migration,invasion and EMT of hepatoma Hep3B cells by regulating the expression of CMTM6.