Objective:To establish a method for isolating adipose derived stem cells(ADSCs)from resected human subcutaneous adipose tissues.Methods:ADSCs were isolated,cultured,and expanded from human subcutaneous adipose tissues.Immuno-fluorescent staining of specific molecules.FACS and multi-lineage differentiation induction were used to characterize the obtained ADSCs.Results:ADSCs obtained in this study had the characteristics of stem cells and expressed specific molecules;they also possessed a multi-lineage differentiation potential,which was genetically stable.Conclusion:ADSCs can be isolated from human subcutaneous adipose tissues,which provides a novel and abundant seeding cells for tissue engineering.

Objective To study and assess clinical application of two Nickel-Titanium(NiTi)rotary instru- ments,namely ProTaper and Hero 642,in preparation of root canals.Methods 125 teeth were divided into three groups and respectively instrumented by stainless K-files,ProTaper or Hero 642 rotary instruments.All teeth were obturated with lateral condensation method.The efficiency of preparation and obturation was analyzed with radio- graphs.Results NiTi rotary instruments were better in keeping the curvature and flow of curved canals than stain- less K files.There was no transportation,apical blockage and ledge in NiTi groups.The operative time was shorter and endodontic flare-up seldom occurred in NiTi groups.Conclusion The NiTi rotary instrumentation technique could be used to prepare curved root canals effectively and quickly.The future use of NiTi engine-driven rotary in- strument appeared to be promising.

Objective To evaluate the possible molecular pathogenesis of intractable temporal lobe epilepsy. The potassium ion channel gene KCNJ4 encodes one of the subfamilies of Kir channels, Kir2.3 subunit, which may play an important role in modulating neuronal excitation. Interference in the function or expression of this gene would cause disturbance of ionic concentrations, thus leading to seizure activity. Methods Reverse transcription polymerase chain reaction (RT-PCR) and Western-blot analysis were used to measure the expression alterations of KCNJ4 mRNA as well as its protein product Kir2.3 channel in temporal cortex samples from patients who had undergone temporal lobectomy for intractable epilepsy (n=12). Tissue from 10 subjects who did not have epilepsy served as controls. Results The expression of KCNJ4 mRNA (0.438?0.178) and its protein Kir2.3 (M 50=0.063) were significantly decreased in epileptic brain compared with the controls (P

OBJECTIVE To determine the functional role of hydrogen sulfide (H2S) in protecting against mitochondrial dysfunction in heart failure through the inhibition of Ca2 +/calmodulin-dependent protein kinaseⅡ (CaMKⅡ) using wild type and CSE knockout mouse models. METHODS Continuous subcutaneous injection isoprenaline (7.5 mg·kg-1·d-1), once a day for 4 weeks to induce heart failure in Male C57BL/6 (6-8 weeks old) mice and CSE-/- mice. 150 μmol·L-1 H2O2 was used to induce oxidative stress in H9c2 cells. Echocardiograph was used to detect cardiac parameters. H&E stain and Masson stain was to observation histopathological changes. Western blot was used to detect protein expression and activity. The siRNA was used to silence protein expression. HPLC was used to detect H2S level. Biotin assay was used to detect the level of S- sulfhydration protein. RESULTS Treatment with S-propyl-L-cysteine (SPRC) or sodium hydrosulfide (NaHS), modulators of blood H2S levels, attenuated the development of heart failure in animals, reduced lipid peroxidation, and preserved mitochondrial function. The inhibition CaMKⅡ phosphorylation by SPRC and NaHS as demonstrated using both in vivo and in vitro models corresponded with the cardioprotective effects of these compounds. Interestingly, CaMKⅡ activity was found to be elevated in CSE-/- mice as compared to wild type animals and the phosphorylation status of CaMKⅡ appeared to relate to the severity of heart failure. Importantly, in wild type mice SPRC was found to promote S-sulfhydration of CaMKII leading to reduced activity of this protein however, in CSE-/- mice S-sulfhydration was abolished following SPRC treatment. CONCLUSION A novel mechanism depicting a role of S-sulfhydration in the regulation of CaMKⅡ is presented. SPRC mediated S-sulfhydration of CaMKII was found to inhibit CaMKⅡ activity and to preserve cardiovascular homeostasis.

OBJECTIVE To determine the functional role of hydrogen sulfide (H2S) in protecting against mitochondrial dysfunction in heart failure through the inhibition of Ca2 +/calmodulin-dependent protein kinaseⅡ (CaMKⅡ) using wild type and CSE knockout mouse models. METHODS Continuous subcutaneous injection isoprenaline (7.5 mg·kg-1 per day), once a day for 4 weeks to induce heart failure in male C57BL/6 (6-8 weeks old) mice and CSE-/- mice. 150 μmol·L-1 H2O2 was used to induce oxidative stress in H9c2 cells. Echocardiograph was used to detect cardiac parameters. H&E stain and Masson stain was to observation histopathological changes. Western blot was used to detect protein expression and activity. The siRNA was used to silence protein expression. HPLC was used to detect H2S level. Biotin assay was used to detect the level of S-sulfhydration protein. RESULTS Treatment with S-propyl-L-cysteine (SPRC) or sodium hydrosulfide (NaHS), modulators of blood H2S levels, attenuated the development of heart failure in animals, reduced lipid peroxidation, and preserved mitochondrial function. The inhibition CaMKⅡ phosphorylation by SPRC and NaHS as demonstrated using both in vivo and in vitro models corresponded with the cardioprotective effects of these compounds. Interestingly, CaMKⅡ activity was found to be elevated in CSE-/- mice as compared to wild type animals and the phosphorylation status of CaMK Ⅱ appeared to relate to the severity of heart failure. Importantly, in wild type mice SPRC was found to promote S-sulfhydration of CaMKⅡ leading to reduced activity of this protein however, in CSE-/- mice S-sulfhydration was abolished following SPRC treatment. CONCLUSION A novel mechanism depicting a role of S-sulfhydration in the regulation of CaMKⅡ is presented. SPRC mediated S-sulfhydration of CaMKⅡ was found to inhibit CaMKⅡ activity and to preserve cardiovascular homeostasis.

Objective To investigate the influence of two different dose of atorvastatin on the prognosis and endothelial function in post-PCI acute coronary syndrom patients.Methods 92 post-PCI ACS patients were randomly divided into two groups,atorvastatin 20mg and atorvastatin 10 mg group.In each group the patients were treated with atorvasta- tin 20mg or 10mg respectively.After one month we add or decrease the dose of atorvastatin according to the blood lipid level.After 12 month the blood lipid level、FMD、NO、ET、NOS、UAP、AMI were compared between two groups. Results The clinical setting have no significant association between two groups before treating,After treated 1 and 12 month the TC,LDL-C level were significantly decreased as compared with the base level before treating in each group. After treated 1 month,in atorvastatin 20 mg group the TC,LDL-C level were significantly decreased and NO、NO/ET level were significantly higher than those in atorvastatin 10 mg group.During 12 month follow up the incidence of angina pectoris onset and rehospitalization were significantly higher in atorvastatin 10 mg group(P

OBJECTIVE To study the effect of polygonatum polysaccharide on zebrafish with Alzheimer disease. METHODS Zebrafish were trained in T maze for 7 d. The 40 zebrafish successfully trained were divided into 4 groups:blank group, model group, positive group and polygonatum polysaccharide group. Model group, positive group and polygonatum polysaccharide group were put in AlCl3100μg·L-1 for 6 d. The positive group was exposed to Huperzine A solution 4μg·L-1, and the polygonatum polysaccharide group was exposed to polygonatum polysaccharide solution 6 g·L-1 for 6 d. The model group was not treated, and the blank group was not treated. Each stage of zebrafish was recorded by video, and the time of each group in the EC region was analyzed. After administration, the brain tissue was taken out and the expression of N-cadherin, P38 and p-P38 protein factors was determined by Western blotting. RESULTS In behavior, the analysis of the time spent in the EC area, the blank group, the positive group and the polygonatum polysac?charide group were compared with the model group, respectively, there were statistically significant differences (P<0.05). At the protein level, compared with the model group, the P38 and p-P38 proteins in the positive group and the polygonatum polysaccharide group were down-regulated, while the N-cadherin protein was up-regulated, with statistical difference (P<0.05). CONCLUSION Polygonatum polysaccharide can improve the learning and memory ability of zebrafish with Alzheimer disease by up regulating the protein level of N-cadherin and hindering P38 phosphorylation.

OBJECTIVETo evaluate the effectiveness of open reduction and internal fixation and repair of palmar ligment in treating trans-scaphoid perilunate dislocation.

METHODSFrom June 1995 to June 2001,14 patients with trans-scaphoid perilunate dislocation were treated with open reduction and internal fixation and repair of palmar ligment. Among them,there were 13 males and 1 female,the ranging in age from 21 to 38 years,averaged 25.4 years. All patients were posterior dislocation and all operations were performed within 2 weeks after injury.

RESULTSAll patients were followed up from 24 to 60 months with an average of 28.3 months. Thirteen scaphoid fractures were primary healed and functions of wrist joint were good. Bone disunion was found in 1 case and part functions of wrist joint were limited. No found necrosis of lunate and scaphoid. According to clinical scoring system of Cooney, 9 case got excellent results, 3 good, 1 fair and 1 poor.

CONCLUSIONOpen reduction and internal fixation and repair of palmar ligament is effective in treating trans-scaphoid perilunate dislocation,which can early provide steady fixation for scaphoid,and profit to recover blood supply of lunatum and subterminal scaphoid.

Adult ; Early Diagnosis ; Female ; Humans ; Joint Dislocations ; diagnosis ; physiopathology ; surgery ; Lunate Bone ; injuries ; physiopathology ; Male ; Recovery of Function ; Scaphoid Bone ; injuries ; physiopathology ; Treatment Outcome ; Young Adult

Amnion ; cytology ; Animals ; Brain Injuries ; therapy ; Cell Transplantation ; Cells, Cultured ; Female ; Hindlimb ; physiology ; Humans ; Rats ; Rats, Sprague-Dawley ; Transplantation, Heterologous

BACKGROUND:Bone marrow stem cell transplantation can improve heart function and prevent ventricle remodeling.At present,the adult bone marrow stem cells used for transplantation primarily included bone marrow mononuclear cells (BM-MNCs) and mesenchymal stem cells (MSCs),and endothelial progenitor cells.The curative effects and precise mechanisms of transplantation of various bone marrow stem cells remain unknown.OBJECTIVE:To compare the effects of transplantation of autologous BM-MNCs and MSCs via the coronary artery on ventricle remodeling subsequent to acute myocardial infarction (AMI). DESIGN,TIME AND SETTING:Randomized controlled animal experiment performed at the Center for Clinical Research,Hebei Provincial People's Hospital,Electron Microscope Room,Hebei Medical University between March 2005 and December 2006.MATERIALS:Thirty-six male Jizhong pigs,were randomly divided into 4 groups:control group (n = 6),infarct model group (n = 10),BM-MNC group (n = 10),and MSC group (n = 10).METHODS:Porcine autologous BM-MNCs were isolated by gradient density centrifugation,and MSCs were obtained by adherence method.Prior to transplantation,both BM-MNCs and MSCs were colloidal gold labeled.Except the infract model group,pigs in the other 3 groups were developed into AMI models by oppressing the left anterior descending branch with balloon catheter.Ninety minutes after modeling,(6.0±1.3)×107 autologous BM-MNCs and (4.5±2.1)x 107 MSCs were respectively transplanted into pigs in the BM-MNC group and the MSC group via the coronary artery and cultured for 28 days.MAIN OUTCOME MEASURES:Observation of pathological changes of cardiac muscle tissue by light and electron microscope;Examination of cardiac function by ultrasonograph;Detection of the number of blood vessels and apoptotic myocardial cells,and expression of nuclear factor-κB (NF-κB) and troponin Ⅰ and its correlation to cardiac function by immunohistochemistry;Detection of mRNA expression of vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) in the cardiac tissue as well as its correlation to cardiac function by reverse transcription-polymerase chain reaction (RT-PCR).RESULTS:In the MSC group,there was proliferation of a great deal of blood vessels as well as growth of abnormal cell masses around the coronary vessels,while the BM-MNC group exhibited the "budding" of many capillary vessels.Prior to transplantation,cardiac function indices were basically similar among each group (F = 1.550,P＞0.05).Twenty-eight days after transplantation,left ventricular ejection fraction was significantly lower in the control,BM-MNC,and MSC groups than in the infarct model group (F = 5.30,P＜0.05),while endocardial fractional shortening was significantly higher (F = 10.67,P＜0.01).Compared with the infarct model group,the number of blood vessels in the infarct zone and infarct border zone was increased in the BM-MNC group (F=29.56-34.87,P＜0.01) and had no apparent change in the MSC group.In the BM-MNC and MSC groups,apoptotic myocardial cells in the infarct zone and infarct border zone were significantly reduced (F=14.31-35.34,P＜0.01 ) and troponin I expression rate was significantly increased (F=19.05,P＜0.01 ),as compared with the infarct model group.In addition,NF-κB positive rate in the infarct border zone was significantly lower in the BM-MNC and MSC groups than in the infarct model group (F=19.05,P＜0.01).VEGF gene expression level in the infarct border zone was significandy higher in the BM-MNC group than in the infarct model group and MSC group (F = 49.41,P＜0.01).bFGF gene expression level in the infarct border zone was significantly higher in the MSC group than in the infarct model and BM-MNC groups (F=4.71,P＜0.01).LVEF was negatively correlated to myocardial cell apoptosis rate and NF-κB level (r=-0.441 1,P＜0.05;r=-0.579 6,P＜0.01 ).LVEF was positively correlated to number of blood vessels,VEGF and bFGF expression (r=0.775,P＜0.01;r=0.565 1,P＜0.05;r=0.573 5,P＜0.05).CONCLUSION:Transplantation of both autologous BM-MNC and MSC via coronary artery can improve the condition of left ventricular remodeling subsequent to myocardial infarction.The improvement of cardiac functions is related to the increase of blood vessels,VEGF and bFGF expression,the decrease of myocardial cell apoptosis and NF-κ B level in cardiac muscle tissues after stem cell transplantation.BM-MNC transplantation better promotes blood vessel proliferation and VEGF expression in the cardiac tissue but produces worse effects on bFGF gene expression than MSC transplantation.