ABSTRACT
Objective To compare the clinical efficacy of postoperative analgesia between intercostal nerve freezing and con‐trolled intravenous analgesia in patients of thoracic surgery .Methods 80 patients of thoracic surgery from January 2012 to June 2013 were randomly divided into two groups :Intercostal nerve cryotherapy group (frozen group n=40) and intravenous analgesia group(control group n=40) .Frozen group :the intercostal incision and down each one intercostal and chest tube placement of inter‐costal nerve roots were frozen before sternal closure ;control group :intravenous analgesia pump were used postoperative .According to VAS method to evaluate pain level and observe adverse reactions ,complications and analgesic drug usage of postoperative pa‐tients .Results The analgesic effect of frozen group was better than that of control group within five days after thoracotomy .Com‐pared with the control group ,the incidence of adverse reactions ,postoperative complications ,and analgesic drug usage was signifi‐cantly reduced in frozen group ,there was a significant difference between the two groups (P<0 .05) .Postoperative follow‐up dis‐play :intercostal nerve area in some patients may appear numbness ,dysesthesia ,etc .,but the above situation can return to normal gradually .Conclusion The analgesic effect of intercostal nerve cryotherapy for thoracotomy patients is excellent ,and with few side effects and good safety ,and it is worthy of promotion .
ABSTRACT
The aim of this research is to find an effective cardiomyocyte-induced method derived from porcine amniotic fluid stem cells (pAFS). For cardiac differentiation, the cells were formed embryoid bodies (EBs) firstly, then cultured in induced-medium including 5-azacytidine (5-aza) and vitamin C (Vc). We detected the specific markers of cardiomyocyte by immunocytochemistry, RT-PCR and transmission electron microscope. The results showed that some embryoid bodies beat rhythmically after 10 days of induction. Furthermore, analysis of t test revealed that the percentage of beating cardiomyocyte-like cell clusters was highest (33%) when induction using 0.1 mmol/L Vc and 5 micromol/L 5-aza. Immunocytochemistry analysis demonstrated that cardiomyocyte-like cell clusters expressed alpha-actin, Tnni3. RT-PCR analysis also illustrated that TbX5, Gata4, alpha-MHC and Tnni3 were expressed positive in cardiomyocyte-like cell clusters. Especially, we observed basic structures of myocardium, such as myofilament, glycogen granule and so on by transmission electron microscope. In conclusion, 5-azacytidine and vitamin C could promote differentiation of pAFS into myocardium.
Subject(s)
Animals , Female , Amniotic Fluid , Cell Biology , Ascorbic Acid , Pharmacology , Azacitidine , Pharmacology , Cell Differentiation , Cells, Cultured , Embryoid Bodies , Embryonic Stem Cells , Cell Biology , Myocytes, Cardiac , Cell Biology , SwineABSTRACT
Objective To investigate the protective effects of dl-3-n-butylphthalide（NBP）on amyloid β peptide 25-35（Aβ25-35）-induced apoptosis in PC-12 cells.Methods Cultured PC12 cells were divided into 6 groups：normal group,Aβ25-35 treated model group,0.1,1.0,10,100 μmol/L NBP pretreatment groups.MTT assay was employed to analyze the PC12 cell viability.The ultrastructural changes of neuronal mitochondria were viewed under transmission electron microscope.In order to observe the effects of oxidative stress,MDA and SOD activities were detected by spectrophotometry.Results NBP pretreatment could significantly prevent the cell viability induced by Aβ25-35（P 0.05）.Pretreatment with 10 μmol/L NBP could significantly inhibit the viability decrease induced by Aβ25-35（P 0.05）.Compared with the cells in the model group,the number and morphology of neuronal mitochondria changed distinctly in the NBP pretreated cells.The activity of SOD in the NBP pretreated cells was obviously higher than that of the cell in the model group,while MDA activity had opposite result.Conclusion NBP could protect the mitochondria in Aβ25-35 induced apoptosis by inhibiting the MDA activity and activating the SOD activity.