BACKGROUND:Biomimetic design of bioactive materials to restore,maintain or improve the function of tissue based on the understanding of anatomy on the function and structure of biological tissue is a research hotspot in the field of regenerative medicine at present. OBJECTIVE:To discuss the effect of mechanical properties,three-dimensional spatial structure,and biochemical activity of biomedical scaffolds on cell behavior and review the application of biomedical scaffolds in the field of tissue engineering. METHODS:The articles published in CNKI,Wanfang,Web of Science,and PubMed databases from January 2003 to April 2023 were searched by computer.The Chinese search terms were"extracellular matrix,tissue engineering,scaffolds,biomaterials,biomimetic structures,mechanical properties,three-dimensional structures,tendon-bone interface,osteochondral,neural conduits,artificial blood vessels".English search terms were"extracellular matrix,tissue engineering,scaffolds,biomimetic structures,biomaterials,tendon bone interfaces,osteochondral,neural conduits,artificial blood vessels". RESULTS AND CONCLUSION:Cells are in a complex and dynamic three-dimensional environment,so the extracellular matrix is the ultimate target of biomaterial simulation.The bionic structure of biomedical scaffolders needs to be similar to the real microenvironment,so that cells can stick to the wall,grow and migrate normally,and maintain their diverse physiological functions.Biomimetic design of extracellular matrix in terms of mechanical properties,three-dimensional spatial structure,and biochemical properties of biomedical scaffolds can play a decisive role in tissue repair,thus affecting the final result of tissue repair.Biomimetic biomedical scaffolds have been widely used in tendon-bone interface,bone cartilage interface,nerve,vascular regeneration,and other fields,providing a promising new idea in clinical practice.

Objective To summarize the pathological survey of time-zero renal biopsy (T0-RBx ) . Methods The material qualities and pathological features were analyzed retrospectively for T 0-RBx (n=176) between March 2008 and May 2016 .According to the source of donor kidney ,T0-RBx specimens were divided into living donors (LD) group (n=137) and Deceased donation (DD) group (n=39) .Furthermore , the DD group was divided into cerebral hemorrhage group (n= 10) and brain trauma group (n= 29) according to the causes of death .The inter-group differences of pathological characteristics and the effects of abnormal pathological lesions on allograft function were observed .Results All T0-RBx specimens contained cortical kidney tissue .The average microscopic length of renal tissue was (0 .39 ± 0 .23) cm and the median glomerular number 11 . The abnormal pathological lesions included glomerulosclerosis (GS ,30 .7 ％ ) , segmental glomerulosclerosis (1 .1 ％ ) ,mesangial increase (MI ,19 .3 ％ ) ,tubular atrophy (TA ,35 .2 ％ ) , acute tubular necrosis (ATN ,9 .1 ％ ) ,vacuolar degeneration of tubular epithelium (27 .3 ％ ) ,losses in tubule epithelial brush border (97 .7 ％ ) , protein cast (25 ％ ) , interstitial fibrosis (IF ,34 .1 ％ ) , inflammation (I ,42 .6 ％ ) ,arteriolar hyalinosis (AH) (26 .1 ％ ) and vascular fibrous intimal thickening (CV ,23 .3 ％ ) .Among them ,23 .9 ％ ,1 .1 ％ ,0 .55 ％ and 0 .55 ％ cases were diagnosed as IgA nephropathy ,immune complex associated with glomerular disease and focal segmental glomerulosclerosis diabetic nephropathy respectively .And the reminders were of ischemic injury .The incidence rates of TA ,IF and I were lower in DD group than those in LD group ( P< 0 .05 ) . However , ATN and vacuolar degeneration of tubular epithelium were higher (P<0 .001) .The incidence of GS was significantly higher in cerebral hemorrhage group than that in brain trauma group (P<0 .01) .No statistical difference existed in other lesions or disease constitution among the groups (P>0 .05) .Further analysis showed GS was related with allograft function at 6/12 months post-transplantation in both LD and DD groups (P<0 .05) .IF and AH were also related to short-term renal function of recipients post-transplantation in LD and DD groups (P>0 .05) .Conclusions T0-RBx may detect the abnormal lesions of donor kidney .Some differences exist in types and degree of abnormal lesions among different donor kidneys .LD group has a higher risk for chronic histological injury such as TA and IF while DD group is more susceptible to acute renal tubular interstitial injury .Thus it is valuable for predicting allograft function post-transplantation .Material quality is essential for ensuring the reliability of T 0-RBx .

OBJECTIVE To explore the pharmacodynamic related substances and mechanism of Weining San(WNS) against gastric ulcer(GU) according to fingerprint and network pharmacology. METHODS Twelve batches of WNS fingerprints were established by HPLC, and methodological investigation was carried out. Combined with reference substances, characteristic peaks were identified, pharmacodynamic related substances were screened, and network pharmacological analysis was carried out. Using TCMIP and Swiss Target Prediction database to retrieve component targets; Using OMIM, GeneCards and Drugbank databases to retrieve GU disease targets, taking the intersection targets of components and diseases, using String database to construct protein-protein interaction network diagram, and analyzing topological parameters; Using Cytoscape 3.8.2 software to construct "component-disease-target" network diagram; GO and KEGG enrichment analysis of intersection targets were carried out by Metascape website. Then the alcoholic GU mouse model was established by intragastric administration of absolute ethanol to verify the results of network pharmacology prediction. RESUITS　The precision, stability and repeatability of HPLC fingerprint method were good. By comparison and comprehensive analysis of control substances, notoginsenoside R1, ginsenoside Rg1, militarine, ginsenoside Rb1, schisandrin, schisandrol B, deoxyschizandrin and schisantherin A were identified as pharmacodynamic related substances in WNS, which may play their role by regulating core targets such as AKT1, IL-6, STAT3, TNF, IL1B and key signal pathways such as PI3K-Akt and JAK-STAT. The gastric ulcer index, ulcer inhibition rate and HE staining showed that WNS could improve gastric mucosal injury in GU mice. The results of ELISA, WST-1 and TBA showed that WNS could decrease the levels of TNF-α, IL-6, IL-1β and MDA, and increase the levels of SOD and PGE2, suggesting that the anti-GU effect of WNS was related to the inhibition of inflammatory reaction and oxidative stress mechanism, which further verified the prediction of network pharmacology. CONCLUSION This study combines fingerprint analysis, network pharmacology, and animal experimental validation to explore the pharmacodynamic related substances and mechanisms of WNS anti-GU efficacy, providing reference for quality control and clinical research of WNS.

As one of the hallmarks of cancer, metabolic reprogramming leads to cancer progression, and targeting glycolytic enzymes could be useful strategies for cancer therapy. By screening a small molecule library consisting of 1320 FDA-approved drugs, we found that penfluridol, an antipsychotic drug used to treat schizophrenia, could inhibit glycolysis and induce apoptosis in esophageal squamous cell carcinoma (ESCC). Gene profiling and Ingenuity Pathway Analysis suggested the important role of AMPK in action mechanism of penfluridol. By using drug affinity responsive target stability (DARTS) technology and proteomics, we identified phosphofructokinase, liver type (PFKL), a key enzyme in glycolysis, as a direct target of penfluridol. Penfluridol could not exhibit its anticancer property in PFKL-deficient cancer cells, illustrating that PFKL is essential for the bioactivity of penfluridol. High PFKL expression is correlated with advanced stages and poor survival of ESCC patients, and silencing of PFKL significantly suppressed tumor growth. Mechanistically, direct binding of penfluridol and PFKL inhibits glucose consumption, lactate and ATP production, leads to nuclear translocation of FOXO3a and subsequent transcriptional activation of BIM in an AMPK-dependent manner. Taken together, PFKL is a potential prognostic biomarker and therapeutic target in ESCC, and penfluridol may be a new therapeutic option for management of this lethal disease.