1.Neural stem cell transplantation for sequela of traumatic brain injury:the best timing for treatment
Yongli LOU ; Ping CHEN ; Yu JIANG ; Hui ZHANG ; Youhui MIN
Chinese Journal of Tissue Engineering Research 2016;20(10):1474-1480
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.
2.Diagnostic values of vaginitis five of the joint inspection kit combined with microscopic examination for vaginal disease
Xia YU ; Xiaoyan CAI ; Youhui WU ; Chenggui LIU ; Jiangyu HUANG
International Journal of Laboratory Medicine 2014;(11):1405-1406,1409
Objective To investigate the diagnostic values of vaginitis five of the joint inspection kit combined with microscopic examination for common vaginal disease.Methods The vaginal secretions samples from 4 114 outpatients were tested with LTS-V400 vaginitis five of the joint inspection kit and microscopic examination.The examination results of age groups were analyzed and compared.Results In all 4 114 cases of samples,the positive rate of trichomonad(1.95%)was significantly lower than that of fun-gi(4.74%),P <0.05.The positive rates of N-acetyl-beta-galactosamine glycosides enzyme(NAG),sialidase(SNA),and leukocyte esterase(LE)were the highest in >40-50-age group,which were 1.95%,6.10%,14.15%,10.24% and 46.34%,respectively. The positive rates of H2 O2 ,pH >4.5 and pH < 3.8 were the highest in > 50 age group,which were 85.43%,86.09%,and 0.66%,respectively.The positive rates of trichomonad,SNA,LE,H2 O2 ,pH>4.5 and pH<3.8 were statistically different a-mong the age groups(P <0.05 ).Conclusion Vaginitis five of the joint inspection kit combined with microscopic examination is suitable for the diagnosis of trichomonas vaginitis,mouldsex vaginitis,and bacterial vaginal disease .
3.Inhibitory effect and induction of apoptosis of caffeic acid Ge on growth of U14 in mice
Yueyan HUANG ; Chun XIAO ; Mingjuan WU ; Yangfan YU ; Chunhua LIU ; Youhui XU
Chinese Journal of Pathophysiology 2000;0(08):-
AIM:To evaluate the antitumor effect of caffeic acid Ge on U14 tumor bearing mice.METHODS:The tumor inhibitory ratios of caffeic acid Ge on the growth of U14 in mice was observed.Apoptosis morphological transformation of U14 cells induced by caffeic acid Ge was detected by electronic scan microscope and MG-P staining.Alteration of cell cycle was analyzed by flow cytometry.Apoptosis-related protein levels of Bax and Bcl-2 were determined by immunity histochemistry technology.MTT assay was applied to study the antitumor activities of caffeic acid Ge in U14 cell lines in vitro.RESULTS:Tumor inhibitory rates in caffeic-acid Ge groups were 38.50%,47.17% and 64.02%(from low dose to high dose)(P
4.MicroRNA-34c-5p provokes isoprenaline-induced cardiac hypertrophy by modulating autophagy via targeting ATG4B.
Yuhong ZHANG ; Yanqing DING ; Min LI ; Jing YUAN ; Youhui YU ; Xueying BI ; Huiqi HONG ; Jiantao YE ; Peiqing LIU
Acta Pharmaceutica Sinica B 2022;12(5):2374-2390
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.