Cartilage injury has a very limited capacity of recovery by itself due to the lack of blood vessel in cartilage tissues. Current studies indicate that many kinds of cytokines have the function of promoting cartilage formation or repairing the injured cartilage with cartilage-like tissues. Cell-mediated transfer of the respective genes may ideally combine the supply of a chondrogenic cell population with the production of certain factors se-creted from the lesion and to promote the repairing of the lesion, which is considered the best treatment. Gene therapy based on this technology has developed rapidly in recent years. This review aims to summarize some of the development of the research in the field.

ObjectiveTo investigate the molecular response of adult and neonate ovine articular cartilage to acute mechanical injury.MethodsAn established in vitro model was used to compare gene expression difference of ovine articular cartilage explants at different developmental stages 24 hours after mechanical injury and the gene expression was compared between these models and that of the uninjured controls by microarray analysis.Total RNA was isolated from the tissue samples,linearly amplified,and applied to a 15 208 Ovine probes cDNA microarray(Agilent).Validation for selected genes(PPARγ,GRO TNC and LDHA) was obtained by real-time polymerase chain reaction.Comparisons between groups were performed by variance analysis.ResultsThere was significant difference in gene expression in adult and neonatal ovine articular cartilage after mechanical injury.Eighty-six genes were significantly manipulated at least 2-fold following mechanical injury for neonate sheep and 83 genes for adult sheep (P＜0.05).Conclusion Our findings indicate that mechanical injury to adult and neonatal ovine articular cartilage results in the activation of a series of signaling responses.We could identify four significant genes that are up or downregulated in response to acute mechanical injury.Significant functional clusters including genes associated with wound healing,articular protection,repair integration,and energy metabolism.Of these,PPARG could be specifically identified as novel target molecules and potential chondroprotective agent involved in traumatic cartilage injury and cartilage integrated repair.

BACKGROUND:Numerous studies have focused on the clinical efficacy of alogeneic bone graft and humeral head replacement for the treatment of proximal humeral fractures, but their comparative studies are rarely reported. OBJECTIVE:To investigate the effect of alogeneic bone grafting in the treatment of proximal humeral fractures in the high risk group. METHODS:Clinical data of 120 cases of proximal humeral fractures aged≥ 60 years were retrospectively analyzed. Sixty of the 120 cases underwent alogeneic bone grafting combined with locking plate fixation as experimental group, and the other 60 cases were subjected to semi-shoulder joint replacement as control group. Al patients were folowed up for 8-24 months. Fracture healing, colodiaphyseal angle, humeral head height and shoulder joint function were observed and measured. RESULTS AND CONCLUSION:During the postoperative 8-24 months, al the fractures were healed by first intention, and there were no rejection reactions, large/smal nodules, humeral head displacement, necrosis, and screw loosening. Loss of the humeral head height at the last folow-up and the active flexion angle of the shoulder at postoperative 12 weeks were significantly higher in the experimental group than the control group (P < 0.05). Scores on forearm, shoulder and hand dysfunction were significantly lower in the experimental group than the control group (P < 0.05). However, no significant difference was observed in the colodiaphyseal angle and SF-36 scores between the two groups. These finding indicate that alogeneic bone grafting can strength the internal fixation of proximal humeral fractures in the high-risk group, and improve patient’s upper limb function.

Objective To systematically review the incidence and influencing factors of refeeding syndrome(RFS)in critically ill patients,and provide references for early identification of RFS and formulation of preventive measures.Methods Computerized searches were conducted for studies on RFS in critically ill patients in the databases of China National Knowledge Infrastructure(CNKI),Wanfang,VIP,CBM,PubMed,Embase,Web of Science,CINAHL,Cochrane Library from inception to May 29th,2024.Data analysis was performed using Stata 16.0 software.Results A total of 29 articles with 5 720 participants were included.The Meta-analysis showed that the incidence of RFS in critically ill patients was 33.68％.The subgroup analysis showed that the incidence of RFS in critically ill patients was higher in studies conducted in 2020 or later(38.22％),in the Americas(36.39％),and with only electrolyte changes as the diagnostic basis(37.51％).Risk factors for RFS in critically ill patients included higher acute physiological and chronic health evaluation Ⅱ scores(OR=1.41),higher sequential organ failure assessment scores(OR=1.29),initiation of feeding within 48 h of ICU admission(OR=3.36),age ≥60 years(OR＝2.82),diabetes mellitus(OR=3.53),pre-albumin concentration＜150 g/L(OR=5.53),albumin concentration＜30 g/L(OR=3.26),caloric intake＞25％standard calories(OR=2.86),enteral solution temperature of 36～38 ℃(OR=2.32),feeding rate＞50 ml/h(OR=3.76),fasting time ≥2 d before feeding(OR=2.46),history of alcoholism(OR=2.64).Conclusion The incidence of RFS in critically ill patients is high and there are many influencing factors.Nurses should improve their awareness and attention to RFS,accurately identify high-risk groups and risk factors,and adopt a multidisciplinary collaborative model to develop whole-course,detailed and personalized intervention measures to prevent RFS.