BACKGROUND:Neural stem cel transplantation provides an important way to treat sequela of traumatic brain injury, but the timing for treatment is inconclusive.
OBJECTIVE:To explore the clinical effect of neural stem cel transplantation in the treatment of sequela of traumatic brain injury and the choice of the best treatment time.
METHODS: Totaly 178 patients with sequela of traumatic brain injury who underwent neural stem cel transplantation were divided into three groups as per the timing for neural stem cel transplantation: group A (with 6 months after injury,n=60), group B (6-12 months after injury,n=59), and group C (over 12 months after injury,n=59). Improvement in clinical symptoms and scores on function independent measure (FIM) were recorded and compared in the three groups.
RESULTS AND CONCLUSION:The total effective rate of group A was significantly higher than that in groups B and C (P < 0.05). FIM scores were significantly improved in the three groups after cel transplantation (P < 0.05). At 3 months after the fourth transplantation, the FIM score in the group A was significantly higher than that in the other two groups, and the incidence of adverse reactions in the group A was significantly lower than that in the other two groups (P < 0.05). These findings indicate that neural stem cel transplantation at different timing can al harvest certain clinical effects, but the best timing for neural stem cel transplantation is within 6 months after injury.

Objective To investigate the expression of Beclin1,p62 and Atg5 in serous ovarian cancer and its clinical significance.Methods The expression of Beclin1,p62 and Atg5 was detected in 50 serous ovarian cancer tissues by immunohistochemical method,and the relationship between their expression levels and the clinical parameters of serous ovarian cancer patients were analyzed.Results The expression of Beclin1 and Atg5 in serous ovarian cancer tissue was significantly lower than that in normal ovarian tissue,but p62 was significantly higher than that in normal ovarian tissue,and the difference had statistically significance (P＜0.05).The expression of Beclin1 and Atg5 were correlated with degree of cell differentiation and clinical stage (P＜0.05),while the expression of p62 was associated with clinical stages and lymph node metastasis (P＜0.05).Conclusions The abnormal expression of Beclin1,p62,Atg5 in serous ovarian cancer,which can lead to reduced autophagy body formation and autophagy activity,may be involved in the occurrence and development of serous ovarian cancer.

BACKGROUND: Studies have demonstrated that platelet-rich plasma can promote osteogenesis and proliferation of bone marrow mesenchymal stem cells, adipose-derived stem cells and skeletal muscle satellite cell, but whether it can promote the proliferation and osteogenesis of human umbilical cord mesenchymal stem cells (hUC-MSCs) is unclear. OBJECTIVE: To investigate the effects of different concentrations of platelet-rich plasma on the proliferation and osteogenic differentiation of hUC-MSCs. METHODS: Passage 5 hUC-MSCs were cultured in medium containing different concentrations of platelet-rich plasma (0, 250, 500, 750, 1000, 2000 ng/L), respectively. Cell proliferation was detected at 1, 3, 5, 7 days after culture, and the best platelet-rich plasma mass concentration was screened. Afterwards, passage 5 hUC-MSCs were divided and cultured in complete medium (blank control group), optimal concentration of platelet-rich plasma (platelet rich plasma group), osteogenesis induction medium (osteogenic induction group), or the osteogenesis induction medium containing the optimal concentration of platelet-rich plasma (combined group). Cell activity of alkaline phosphatase was detected after cultivated for 3, 7, 14 days. Osteopontin, bone specific transcription factor, and osteocalcin mRNA relative expression levels were detected after cultivated for 7, 14, 21 days. Mineralization of the extracellular matrix was detected after cultivated for 21 days. RESULTS AND CONCLUSION: After 5 and 7 days of culture, the cell proliferation was higher in 500, 750, 1000 ng/L platelet-rich plasma groups than 0 ng/L group (P < 0.05), and 750 ng/L platelet-rich plasma showed the best effect on cell proliferation, which was used in the following experiments. Compared with the other groups, the combined group had significantly increased alkaline phosphatase activity (P < 0.05), and up-regulated osteopontin, bone specific transcription factor and osteocalcin mRNA relative expression levels (P < 0.05) at different culture times. In addition, the degree of extracellular matrix mineralization in the combined group was also higher than that in the other three groups (P < 0.05).To conclude, 750 ng/L platelet-rich plasma can promote hUC-MSCs proliferation and osteogenic differentiation.

Pathological cardiac hypertrophy serves as a significant foundation for cardiac dysfunction and heart failure. Recently, growing evidence has revealed that microRNAs (miRNAs) play multiple roles in biological processes and participate in cardiovascular diseases. In the present research, we investigate the impact of miRNA-34c-5p on cardiac hypertrophy and the mechanism involved. The expression of miR-34c-5p was proved to be elevated in heart tissues from isoprenaline (ISO)-infused mice. ISO also promoted miR-34c-5p level in primary cultures of neonatal rat cardiomyocytes (NRCMs). Transfection with miR-34c-5p mimic enhanced cell surface area and expression levels of foetal-type genes atrial natriuretic factor (Anf) and β-myosin heavy chain (β-Mhc) in NRCMs. In contrast, treatment with miR-34c-5p inhibitor attenuated ISO-induced hypertrophic responses. Enforced expression of miR-34c-5p by tail intravenous injection of its agomir led to cardiac dysfunction and hypertrophy in mice, whereas inhibiting miR-34c-5p by specific antagomir could protect the animals against ISO-triggered hypertrophic abnormalities. Mechanistically, miR-34c-5p suppressed autophagic flux in cardiomyocytes, which contributed to the development of hypertrophy. Furthermore, the autophagy-related gene 4B (ATG4B) was identified as a direct target of miR-34c-5p, and miR-34c-5p was certified to interact with 3' untranslated region of Atg4b mRNA by dual-luciferase reporter assay. miR-34c-5p reduced the expression of ATG4B, thereby resulting in decreased autophagy activity and induction of hypertrophy. Inhibition of miR-34c-5p abolished the detrimental effects of ISO by restoring ATG4B and increasing autophagy. In conclusion, our findings illuminate that miR-34c-5p participates in ISO-induced cardiac hypertrophy, at least partly through suppressing ATG4B and autophagy. It suggests that regulation of miR-34c-5p may offer a new way for handling hypertrophy-related cardiac dysfunction.