OBJECTIVETo seek new method for the treatment of peripheral nerve injury.

METHODSIn rat model with sciatic nerve defect, chitosan-collagen film was sutured into conduit to bridge 5 mm, 10 mm nerve defects. Rats that underwent end-to-end anastomosis were taken as controls. General observation, electrophysiological study, histological study and image analysis were performed at 4, 8, 12 weeks postoperatively.

RESULTSIn 5 mm nerve defects, the quality of nerve regeneration was similar to that of the control group. For 10 mm nerve defect, nerve regeneration was inferior to that of the control group. Chitosan-collagen film obviously degraded at 12 weeks postoperatively.

CONCLUSIONSChitosan-collagen film conduit can be used to bridge peripheral nerve defect.

Animals ; Biocompatible Materials ; therapeutic use ; Chitin ; analogs & derivatives ; therapeutic use ; Chitosan ; Collagen ; therapeutic use ; Male ; Models, Animal ; Nerve Regeneration ; Rats ; Rats, Wistar ; Sciatic Nerve ; injuries ; physiology ; surgery

OBJECTIVETo explore the effective methods for the treatment of complex tibial plateau fractures.

METHODSFrom May 2008 to April 2011, 28 patients with complex tibial plateau fractures were treated indirect reduction techniques, bilateral locking plate fixation combined with autologous bone grafts. There were 21 males and 7 females, with an average age of 43 years ranging from 21 to 65. There were 11 cases in Schatzker type V, 17 in VI. The effect was evaluated by Rasmussen standard on clinical and radiological.

RESULTSAll patients were followed-up for 7 to 36 months (averaged of 21.5 months). Healing time of fracture was from 3 to 8 months (averaged 5.5 months). The results of Rasmussen scores in clinical was 4.50 +/- 1.32 in pain, 4.32 +/- 1.63 in walking ability, 4.07 +/- 1.34 in knee activity, 4.78 +/- 1.27 in stability of the knee, 4.85 +/- 1.12 in stretch knee; the results in radiation was 5.07 +/- 0.92 in articular surface collapse, 5.00 +/- 0.98 in platform widened, 5.14 +/- 0.85 in knee external varus. The effect result was excellent in 8 cases, good in 15, fair in 3 and poor in 2.

CONCLUSIONThe key for the treatment of complex tibial plateau fractures was to fully assess the damage as much as possible to protect the soft tissue, select the appropriate timing of surgery and surgical incision, application of indirect reduction techniques, limited incision and effective internal fixation to restore joint surface smooth and good limb alignment, early exercise, in order to achieve maximum recovery of joint function.

Adult ; Aged ; Bone Plates ; Bone Transplantation ; Female ; Follow-Up Studies ; Fracture Fixation, Internal ; instrumentation ; Humans ; Male ; Middle Aged ; Recovery of Function ; Retrospective Studies ; Tibial Fractures ; diagnostic imaging ; physiopathology ; surgery ; Tomography, X-Ray Computed ; Treatment Outcome ; Young Adult

BACKGROUNDTransplantation of adult bone marrow-derived mesenchymal stem cells (MSCs) has been proposed as a strategy for cardiac repair following myocardial damage. However cell transplantation strategies to replace lost myocardium are limited by the inability to deliver large numbers of cells that resist peritransplantation graft cell death. Accordingly, we set out to isolate and expand adult swine bone marrow-derived MSCs, and to engineer these cells to overexpress AKT1 (protein kinase B), to test the hypothesis that AKT1-engineered MSCs are more resistant to apoptosis and can enhance cardiac repair after transplantation into the ischemic swine heart.

METHODSThe CDS (regulation domain of AKT1) AKT1-cDNA fragment was amplified, and MSCs were transfected following synthesis with a pCDH1-AKT1 shuttling plasmid. Western blotting analysis and real-time reverse transcription-polymerase chain reaction (RT-PCR) was performed. Myocardial infarction (MI) models were constructed in Meishan pigs, and cardiac function was evaluated by magnetic resonance imaging (MRI) measurements and echocardiography 4 weeks later. All pigs were assigned to four groups: control (A), DMEM (B), MSC (C), and AKT-transfected (D). MSCs were transfected with the AKT1 gene, and autologous BrdU-labeled stem cells (1 x 10(7)/5 ml) were injected into left anterior descending coronary atery (LAD) of the infarct heart in groups C and D. In group B, DMEM was injected using the same approach. In group A, there was no injection following LAD occlusion. After 4 weeks, cardiac function and regional perfusion measurements were repeated by MRI and echocardiography, and histological characteristics of the hearts were assessed. Connecxin-43 (CX-43), BrdU, and von Willebrand factor (VWF) immunoreactivity was tested using enzyme linked immunosorbent assay (ELISA). Vascular endothelial growth factor (VEGF), transforming growth factor-beta1 (TGF-beta1) were analyzed at the same time.

RESULTSAKT1-cDNA was cloned into pCDH1-MCS1-EF1-copGFP and the sequence was confirmed. AKT mRNA expression was detected at 24 hours after transfection. AKT1 expression in MSCs remained strong after 2 weeks, according to real-time RT-PCR and Western blotting. Prior to cell implantation, end-diastolic left ventricular dimension (EDLVd) increased and stroke volume (SV) decreased in the MI hearts. MRI scans revealed significantly improved cardiac function following implantation, and implanted MSCs prevented thinning and expanding in the infarct region, as well as improved contraction and increased perfusion in all groups compared to control hearts. The left ventricular chamber size was smaller in cell-transplanted hearts than in control hearts. Moreover, group D exhibited significant improvement. The expression of CX-43, BrdU, and VWF could be found in the immunohistochemical pathological sections of group C and group D. The level of VEGF reached a high level 1 week after implanting the MSCs, but the level of TGF-beta1 decreased gradually.

CONCLUSIONSThe AKT1-expressing lentiviral vector resulted in stable over-expression of AKT1 in MSCs. MSC engraftment in host myocardium improved cardiac function by attenuating contractile dysfunction and pathological thinning of the infracted left ventricular wall, which likely resulted from myocardial regeneration and angiogenesis.

Animals ; Blotting, Western ; Disease Models, Animal ; Electrophoresis ; Genetic Vectors ; genetics ; Lentivirus ; genetics ; Mesenchymal Stem Cell Transplantation ; Mesenchymal Stromal Cells ; metabolism ; Myocardial Infarction ; metabolism ; therapy ; Proto-Oncogene Proteins c-akt ; genetics ; metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Swine ; Ventricular Remodeling ; physiology

OBJECTIVETo study the polymorphisms of cerebrovascular and cardiovascular disease genes using Taqman single nucleotide polymorphism (SNP) genotyping kits.

METHODSA total of 2000 subjects were recruited from the Guangzhou Biobank Cohort Study (GBCS), and 15 SNPs were detected using Taqman SNP genotyping kits and an ABI 7900HT real time PCR system. The data were tested for the Hardy-Weinberg equilibrium, and then compared with the data of the Chinese population from the International HapMap Project (HapMap_HCN).

RESULTS(1) All genotype data of the 15 SNPs were consistent with the Hardy-Weinberg rules. (2) The significant differences were observed among two SNPs, rs4220 and rs5368 and the HapMap_HCN (rs4220 28.2% vs 17.8%; chi(2) = 4.891, P = 0.028; rs5368 22.1% vs 32.2%, chi(2) = 5.137, P = 0.024). Comparing other gene bank data, such as AFD-CHN-PANEL, the Allele Frequency Database (ALFRED) and JBIC-allele, it would be most likely that our observations represent differences between the Northern and Southern populations in China.

CONCLUSIONSuch Biobank study provided a useful platform for the study of the role of genetic and environmental determinants on cerebrovascular and cardiovascular disease.

Asian Continental Ancestry Group ; genetics ; Biological Specimen Banks ; statistics & numerical data ; Brain Diseases ; epidemiology ; genetics ; Cardiovascular Diseases ; epidemiology ; genetics ; China ; epidemiology ; Cohort Studies ; Genetic Association Studies ; Genotype ; Humans ; Polymorphism, Single Nucleotide