Obiective: To compare the tissue biocompatibility of domestically manufactured NiTi alloy before and after thermal surface oxidation under 3 different temperatures. Methods: Domestically manufactured NiTi alloy was oxidized in air (group A) and subjected to 30 min heat treatment at 400°C (group B),500°C, (group C),and 600°C (group D) to form different protective oxide surface layers in presence of argon (607.95 kPa). Wire samples from A, B, C and D groups were subcutaneously implanted in guinea pigs. Guinea pigs received 317L stainless steel transplantation(group E) and sham-operation group (F) were taken as control. The order of inflammatory cell infiltration and tissue hyperplasia around implanted materials were observed 1, 2, 4, and 8 weeks after implantation. Results: The peak time of inflammatory cell infiltration and fibrous hyperplasia were at the first and fourth week after implantation. The inflammatory cell infiltration and fibrous hyperplasia were both slight and all met the GB/T 16886. 6-1997 in vivo implantation standard. The order of inflammatory cell infiltration and thickness of capsule walls from low to high was F

Objective:To compare the tissue biocompatibility of domestically manufactured NiTi alloy before and after thermal surface oxidation under 3 different temperatures.Methods:Domestically manufactured NiTi alloy was oxidized in air (group A)and subjected to 30 min heat treatment at 400℃(group B),500℃(group C),and 600℃(group D)to form different protective oxide surface layers in presence of argon(607.95 kPa).Wire samples from A,B,C and I3 groups were subcutaneously implanted in guinea pigs.Guinea pigs received 317L stainless steel transplantation(group E)and sham-operation group(F)were taken as control.The order of inflammatory cell infiltration and tissue hyperplasia around implanted materials were observed 1,2,4,and 8 weeks after implantation.Results:The peak time of inflammatory cell infiltration and fibrous hyperplasia were at the first and fourth week after implantation.The inflammatory cell infiltration and fibrous hyperplasia were both slight and all met the GB/T 16886.6-1997 in vivo implantation standard.The order of inflammatory cell infiltration and thickness of capsule walls from low to high was F

Heart Valve Diseases ; therapy ; Heart Valve Prosthesis Implantation ; methods ; Humans

OBJECTIVEFamilial left ventricular noncompaction(LVNC) is quite rare. We screened for the presence of LVNC and related clinical characteristics in a 5-generation Chinese family.

METHODSComprehensive medical history was obtained from 40 members in a 5-generation Chinese family. Systemic clinical investigations including echocardiography (UCG), routine and ambulatory electrocardiogram (ECG), X-rays were performed in 33 family members. Cardiovascular magnetic resonance image (MRI) was carried out in 2 family members.

RESULTSSudden cardiac death (including 1 occurred while following-up) was reported in 7 family members (17.5%, 7/40). LVNC was diagnosed in 10 out of the 33 family members (30.3%) and heart enlargement was evidenced in 3, heart failure in 2, complete left branch conductive block in 3, serious sick sinus syndrome (SSS) treated with permanent pacemaker implantation in 1 and paroxysmal supraventricular tachycardia treated with radiofrequency ablation procedure in 1 out of these 10 LVNC patients. Primary pedigree analysis revealed that offspring from female patients were at the highest risk to be affected by LVNC (15/18, 83.3%) while LVNC was absent in offspring of male LVNC patients (0/8). Moreover, clinical heart failure symptoms and arrhythmias were more severe in female LVNC patients than in male LVNC patients.

CONCLUSIONPrimary familial investigation reveals the matrilineal inheritance of familial LVNC in this 5-generation Chinese family, further investigations are warranted to explore the potential mutations in the mitochondrial genome responsible for LVNC in this family.

Adolescent ; Adult ; Aged ; Asian Continental Ancestry Group ; genetics ; Cardiomyopathies ; epidemiology ; genetics ; Child ; Child, Preschool ; Death, Sudden, Cardiac ; Female ; Humans ; Infant ; Male ; Middle Aged ; Mutation ; Pedigree ; Ventricular Dysfunction, Left ; Young Adult

The present study sought to investigate the anti-inflammation and immunoloregulation effect of 17 Guizhi Fuling capsule ingredients. The anti-inflammatory ingredients on LPS-induced RAW264. 7 cell injury were assessed with ELISA and immunofluorescence. The release of IL-1β, TNF-α, PGE2 were detected with ELISA and the expression of COX-2 was detected with immunofluorescence. The effects of them on promoting splenic lymphocyte proliferation were assessed with MTT and Hoechst 33342 staining method. The results showed that 15 ingredients had obviously anti-inflammatory activity on LPS- induced injury and play the immunoloregulation roles. This study suggested that the 15 ingredients may be the active ingredients on pelvic infection.
Animals ; Anti-Inflammatory Agents ; pharmacology ; Capsules ; pharmacology ; Cyclooxygenase 2 ; immunology ; Drugs, Chinese Herbal ; administration & dosage ; Immunologic Factors ; pharmacology ; Inflammation ; drug therapy ; Interleukin-1beta ; immunology ; Macrophages ; drug effects ; enzymology ; immunology ; Male ; Mice ; Mice, Inbred BALB C ; Spleen ; cytology ; drug effects ; immunology ; Tumor Necrosis Factor-alpha ; immunology

OBJECTIVETo explore cell death and apoptosis in rat hippocampal neurons at different time points after ischemia, hypoxia and reperfusion injury and to elucidate time window characteristics in ischemia neuronal injury.

METHODSHippocampal neurons were obtained from rat embryo and were cultured in vitro. The ischemia and reperfusion of cultured rat hippocampal neurons were simulated by oxygen-glucose deprivation (OGD) and recovery. OGD at different time points (0.25 h to 3.0 h) and then the same recovery (24 h) were prepared. Annexin V-PI staining and flow cytometry examined neuron death and apoptosis at different time after injury.

RESULTSAfter OGD and recovery, both necrosis and apoptosis were observed. At different times after OGD, there were statistically significant differences in neuron necrosis rate (P < 0.05), but not in apoptosis rate (P > 0.05). At recovery, survival rate of hippocampal neurons further decreased while apoptosis rate increased. Furthermore, apoptosis rates of different time differed greatly (P < 0.05). Apoptosis rate gradually increased with significant difference among those of different time points (P < 0.05). However, 2 h after ischemia, apoptosis rate decreased markedly.

CONCLUSIONSApoptosis is an important pathway of delayed neuron death. The therapeutic time window should be within 2 h after cerebral ischemia and hypoxia.

Animals ; Apoptosis ; physiology ; Brain Ischemia ; pathology ; Cell Death ; physiology ; Cell Hypoxia ; Cells, Cultured ; Disease Models, Animal ; Female ; Fetus ; cytology ; Flow Cytometry ; Hippocampus ; pathology ; Neurons ; pathology ; Pregnancy ; Pregnancy, Animal ; Probability ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury ; pathology ; Sensitivity and Specificity ; Time Factors

OBJECTIVETo construct an eukaryotic expression vector carrying rat brain-derived neurotrophic factor receptor trkB gene.

METHODSUsing the total RNA isolated from rat brain as template, the trkB gene was amplified by reverse-transcription-polymerase chain reaction (RT-PCR) with a pair of specific primers which contained the restrictive sites of EcoR I and BamH I. The amplified fragment of trkB gene was digested with EcoR I and BamH I, and then subcloned into cloning vector pMD18-T and expression vector pEGFP-C2 respectively. The recombinant plasmids were identified by restriction endonuclease enzyme analysis and PCR.

RESULTSThe amplified DNA fragment was about 1461 bp in length. Enzyme digestion and PCR analysis showed that the gene of trkB had been successfully cloned into vector pMD18-T and pEGFP-C2.

CONCLUSIONSThe trkB gene of rat has been amplified and cloned into the eukaryotic expression vector pEGFP-C2.

Animals ; Brain-Derived Neurotrophic Factor ; genetics ; pharmacology ; Cloning, Molecular ; methods ; Eukaryotic Cells ; Female ; Gene Expression Regulation ; Genetic Therapy ; methods ; Genetic Vectors ; Male ; Models, Animal ; RNA ; analysis ; Rats ; Rats, Wistar ; Receptor, trkB ; genetics ; Reverse Transcriptase Polymerase Chain Reaction ; Schwann Cells ; cytology ; Sensitivity and Specificity ; Templates, Genetic ; Transfection

It is well known that cytoskeleton system is the sensor of gravity in cells. Under microgravity condition, cytoskeleton is associated with the changes of cell shape, function, signaling and so on; but the relationship between cytoskeleton and gene expression is not fully understood. In present study, we discussed the effects of cell microfilament on the activity of collagen type I alpha 1 chain gene (COL1A1) promoter under microgravity simulated by clinostat and/or cytochalasin B as microfilament depolymerizer in the established EGFP-ROS cell line using the method of fluorescence semi-quantitative analysis and the fluorescent stain of microfilament. Compared with the normal control, the microfilament of ROS17/2.8 cell tended to disassemble, marginal distribution of fiber stress, and showed reducing stress fibers after spaceflight in Photon-M1 or clinorotation simulated microgravity, which suggested that microgravity destroyed the well-order cell cytoskeleton and induced a rearrangement. Treatment with suitable concentration of cytochalasin B in normal gravity induced disruption of microfilament, increased the activity of COL1A1 promoter and resulted in a dose-dependent increase of EGFP fluorescence. Therefore, a certain extent disruption of the microfilament system was associated with increased activity of the COL1A1 promoter. All above demonstrate that microfilament cytoskeleton system takes part in the regulation of COL1A1 promoter activity and plays an important role in the signaling of microgravity.
Actin Cytoskeleton ; pathology ; physiology ; Animals ; Bone Neoplasms ; pathology ; Cell Line, Tumor ; Collagen Type I ; genetics ; Cytoskeleton ; pathology ; physiology ; Green Fluorescent Proteins ; genetics ; Osteosarcoma ; pathology ; Promoter Regions, Genetic ; Rats ; Transfection ; Weightlessness Simulation

Objective To investigate the expressions of interleukin-8 (IL-8) mRNA and proliferating cell nuclear antigen (PCNA) protein in astrocytic tumors and their correlation with the tumor cell apoptosis. Methods The expressions of IL-8 mRNA in 64 cases of astrocytic tumor and 10 normal brain tissues were detected using RT-PCR. The expression of PCNA protein in the tumors was assayed with immunohistochemistry, and the apoptosis index (AI) of the tumor cells determined using TUNEL assay. Results The expression ofIL-8 mRNA in the astrocytic tumors was strongly correlated to the malignancy of the tumors, and both the PCNA expression and the apoptosis index increased in tumors of greater malignancies. IL-8 mRNA expression was positively correlated to the expression of PCNA (r=0.938, P<0.01) and AI (r=0.907, P<0.01) in these tumors. Conclusion IL-8 mRNA expression is positively correlated to the histological grade of the astrocytic tumors, whose proliferation is mediated by inhibition of cell apoptosis and upregulation of IL-8 transcription.

Objective To investigate the effects of Rac1 gene silencing on cell cycle and apoptosis of Daoy cell line in medulloblastoma. Methods Daoy cells were divided into Rac1-shRNA group and empty plasmid control group; Daoy cells in the former group were transfected by using Rac1-shRNA plasmid (Rac1-shRNA). RT-PCR, Western blotting and flow cytometry were used to observe the changes of cycle and apoptosis of Daoy cells after Rac1 gene silencing. Results Rac1 mRNA and protein in medulloblastoma Daoy cell lines were highly expressed; cell cycle of Daoy cells with Rac1 gene silencing were blocked at G0-G1 phases and cell percentage of G0-G1 phases significantly increased to 80.9%±4.9%; however, the proportion of cells in the S phase reduced to 11.8%± 2.3%. The apoptosis rate of Rac1-shRNA plasmid group (36.7%±3.9%) was significantly different as compared with that of empty plasmid control group (8.5% ±0.9%) (P<0.05). Conclusion RNA-interfered Rac1 gene silencing can inhibit the proliferation of Daoy cells and promote their apoptosis, indicating that Rac1 may become a new target being able to inhibit the cell proliferation and promote the apoptosis of Daoy cells in medulloblastoma.