The finite element method (FEM) is a mathematical technique using modern computer technology for stress analysis, and has been gradually used in simulating human body structures in the biomechanical field, especially more widely used in the research of thoracolumbar spine traumatology. This paper reviews the establishment of the thoracolumbar spine FEM, the verification of the FEM, and the thoracolumbar spine FEM research status in different fields, and discusses its prospects and values in forensic thoracolumbar traumatology.
Biomechanical Phenomena ; Computer Simulation ; Finite Element Analysis ; Humans ; Lumbar Vertebrae/injuries* ; Models, Theoretical ; Stress, Mechanical ; Thoracic Vertebrae/injuries* ; Traumatology

Reverse transcriptase-PCR experiments suggest that the two clusters of genes potentially involved in the oxidation of reduced sulfur compounds are organized as operons in strain of the acidophilic, chemolithoautotrophic bacterium Acidithiobacillus ferrooxidans ATCC 23270, the two clusters of genes including such the ORF of putative sulfate-thiosulfate-molybdate binding proteins, the ORF of putative thiosulfate: quinone oxidoreductase and the ORF of the rhodanese-like protein (P21). Bioinformatic analyses have predicted the possible promoters sequences and the possible +1 start site of transcription for the doxDA operons.

OBJECTIVETo construct the folic acid deficient model in zebrafish and observe the abnormal cardiac phenotypes, to find the optimal period for supplementing folic acid that can most effectively prevent the heart malformation induced by folic acid deficiency, and to investigate the possible mechanisms by which folic acid deficiency induces malformations of heart.

METHODThe folic acid deficient zebrafish model was constructed by using both the folic acid antagonist methotrexate (MTX) and knocking-down dhfr (dihydrofolate reductase gene). Exogenous tetrahydrofolic acid rescue experiment was performed. Folic acid was given to folic acid deficient groups in different periods. The percent of cardiac malformation, the cardiac phenotypes, the heart rate and the ventricular shortening fraction (VSF) were recorded. The out flow tract (OFT) was observed by using fluorescein micro-angiography. Whole-mount in situ hybridization and real-time PCR were performed to detect vmhc, amhc, tbx5 and nppa expressions.

RESULTAbout (78.00 ± 3.74)% embryos in MTX treated group and (68.00 ± 6.32)% embryos in dhfr knocking-down group had heart malformations, including the abnormal cardiac shapes, the hypogenesis of OFT and the reduced heart rate and VSF. Giving exogenous tetrahydrofolic acid rescued the above abnormalities. Given the folic acid on 8 - 12 hours post-fertilization (hpf), both the MTX treated group (20.20% ± 3.77%) and dhfr knocking-down group (43.40% ± 4.51%) showed the most significantly reduced percent of cardiac malformation and the most obviously improved cardiac development. In folic acid deficient group, the expressions of tbx5 and nppa were reduced while the expressions of vmhc and amhc appeared normal. After being given folic acid to MTX treated group and dhfr knocking-down group, the expressions of tbx5 and nppa were increased.

CONCLUSIONSThe synthesis of tetrahydrofolic acid was decreased in our folic acid deficient model. Giving folic acid in the middle period, which is the early developmental stage, can best prevent the abnormal developments of hearts induced by folic acid deficiency. Folic acid deficiency did not disrupt the differentiations of myosins in ventricle and atrium. The cardiac malformations caused by folic acid deficiency were related with the reduced expressions of tbx5 and nppa.

Animals ; Atrial Natriuretic Factor ; metabolism ; Cell Differentiation ; drug effects ; Folic Acid ; metabolism ; Folic Acid Deficiency ; genetics ; metabolism ; Gene Knockdown Techniques ; Heart ; drug effects ; embryology ; growth & development ; T-Box Domain Proteins ; metabolism ; Zebrafish ; embryology ; genetics

Objective To assess the effects of suction drainage versus nondrainage on the post-operative rehabilitation of patients receiving primary bilateral total knee arthroplasties (TKA).
Methods A prospective study including 40 patients was conducted. These patients were diagnosed with osteoarthritis and underwent primary bilateral TKA between October 2007 and September 2009 with the same operation team. A suction drainage was placed by randomization in only one knee for each patient, while the other knee as self-control. Pain visual analogue scale score, extremity swelling, wound healing, range of motion and incidence of early post-operative complications between the drained and nondrained group were compared statistically.
Results Each patient was followed up for 12 months. Placing drainage did not relieve the pain, extremity swelling, ecchymosis, or reduce the incidence of early complications (all P>0.05).
Conclusions Suction drainage in TKA does not exhibit substantial advantages in promoting post-operative rehabilitation after unsophisticated TKA, compared with nondrainage. On the other hand, it might complicate the surgical operation, and increase the incidence of post-operative hemorrhage and retrograde infection.Thus we do not recommend suction drainage in unsophisticatedTKA.

Objective：To investigate the mechanism of increased glucose uptake, the expression of myoc ardial glucose transporter1 (GLUT1) was determined after low-flow myocardial is chemia. Methods： An in vivo open-chest canine model of low -flow myocardial ischemia was used to correlate myocardial glucose uptake with the number of GLUT1. The expression of myocardial GLUT1 glucose transporter was determined by semiquantitative Northern blotting and immunoblotting. Res ults： GLUT1 mRNA and GLUT1 polypeptide expression was substantially inc reased in ischemic region from the experimental hearts when compared to normal h earts. There was no significant regional difference in GLUT1 expression in eith er normal or ischemic hearts.Conclusion：Myocardial ischemia ind uces a factor or factors which stimulate GLUT1 expression in ischemic myocardial regions. Enhanced GLUT1 expression may be an important protective mechanism by which myocardial cells enhance glucose uptake and metabolism during low-flow my ocardial ischemia.

Objective: To investigate whether there is additi ve effects of hyperinsulinemia and ischemia on expression of canine myocardial G LUT4 gene in vivo. Methods: The expression of myocardial GLU T4 was determined by semiquantitative immunoblotting.The expression of GLUT4 mRN A was determined by semiquantitative Northern blotting. Results: Dramatic changes were seen in GLUT4 mRNA and GLUT4 expression in the ischemic hearts.After infusing insulin for 8 h,regional GLUT4 mRNA and GLUT4 levels in is chemic hearts were 2.5, 2.3-fold that of expression in normal hearts(P<0.01 ). Myocardial glucose uptake in ischemic hearts was increased by 4-fold when co mpared with normal hearts(P<0.01). Conclusion: There are not only additive effects of hyperinsulinemia and low-flow ischemia on canine myoc ardial GLUT4 mRNA and GLUT4 expression in vivo, but also increase of myocar dial glucose uptake. Enhanced GLUT4 expression may be an important protective m echanism by which myocardial cells enhance glucose uptake and metabolism during low-flow ischemia.

OBJECTIVE: To determine the effect of tanshinone IIA on the growth and apoptosis in human hepatoma cell line HepG2. METHODS: The human hepatoma cell line HepG2 was treated with tanshinone IIA at various concentrations for 72 h. The inhibition of proliferation was measured by MTT assay and apoptosis-related alterations in morphology measured by cytochemical staining (HT33258). DNA fragmentation was evaluated by agarose gel electrophoresis. Apoptotic rate and cell arrest were quantified by flow cytometry (FCM). RESULTS: Tanshinone IIA inhibited the growth of HepG2 in a time- and dose- dependent manner. The semi-inhibitory concentration (IC50) value after the treatment with tanshinone IIA on HepG2 for 24, 48 and 72 h were 14.7, 7.4, and 3.9 microg/ mL, respectively. After the treatment with 0.5 - 10 microg/mL tanshinone IIA for 72 h, the formation of apoptotic bodies was observed. DNA ladder was shown in agarose gel electrophoresis, in addition to the cells treated by 1.0 microg/mL tanshinone IIA . The apoptotic rates at 0.5, 1.0, 2.0, 5.0, and 10.0 microg/mL for 72 h were 20.32%+/-2.16%, 28.0%+/-2.35%, 33.87%+/-3.43%, 46.73%+/-4.08% and 57.85%+/-3.74%, respectively, which were all significantly higher than those of the control group (P<0.05). CONCLUSION Tanshinone IIA can inhibit the proliferation of human hepatoma cell line HepG2 in a time- and dose- dependent manner, and the mechanism of growth inhibition of human hepatoma cells may be related to the induction of apoptosis.
Abietanes ; Antineoplastic Agents, Phytogenic ; pharmacology ; Apoptosis ; drug effects ; Carcinoma, Hepatocellular ; genetics ; pathology ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; DNA Fragmentation ; drug effects ; Dose-Response Relationship, Drug ; Drugs, Chinese Herbal ; pharmacology ; Flow Cytometry ; Humans ; Liver Neoplasms ; genetics ; pathology ; Microscopy, Fluorescence ; Phenanthrenes ; pharmacology ; Time Factors

OBJECTIVE: To study the effect of dhfr gene overexpression on ethanol-induced abnormal cardiac and vascular development in zebrafish embryos and underlying mechanisms. METHODS: dhfr mRNA was transcribed in vitro and microinjected into zebrafish fertilized eggs to induce the overexpression of dhfr gene, and the efficiency of overexpression was verified. Wild-type zebrafish were divided into a control group, an ethanol group, and an ethanol+dhfr overexpression group (microinjection of 6 nL dhfr mRNA). The embryonic development was observed for each group. The transgenic zebrafish Tg (cmlc2:mcherry) with heart-specific red fluorescence was used to observe atrial and ventricular development. Fluorescence microscopy was performed to observe the development of cardiac outflow tract and blood vessels. Heart rate and ventricular shortening fraction were used to assess cardiac function. Gene probes were constructed, and embryo in situ hybridization and real-time PCR were used to measure the expression of nkx2.5, tbx1, and flk-1 in the embryo. RESULTS: Compared with the ethanol group, the ethanol+dhfr overexpression group had a significant reduction in the percentage of abnormal embryonic development and a significant increase in the percentage of embryonic survival (P<0.05), with significant improvements in the abnormalities of the atrium, ventricle, outflow tract, and blood vessels and cardiac function. Compared with the control group, the ethanol group had significant reductions in the expression of nkx2.5, tbx1, and flk-1 (P<0.05), and compared with the ethanol group, the ethanol+dhfr overexpression group had significant increases in the expression of nkx2.5, tbx1, and flk-1 (P<0.05), which were still lower than their expression in the control group. CONCLUSIONS The overexpression of the dhfr gene can partially improve the abnormal development of embryonic heart and blood vessels induced by ethanol, possibly by upregulating the decreased expression of nkx2.5, tbx1, and flk-1 caused by ethanol.
Animals ; Ethanol ; Gene Expression Regulation, Developmental ; Heart ; Heart Ventricles ; Zebrafish ; Zebrafish Proteins

Objective To investigate the relationship between Wnt5a gene and E-cadherin or vimentin gene in breast cancer cell line MCF-7. Methods RT-PCR was used to detect the mRNA expression of Wnt5a, E-cadherin and vimentin in breast cancer MCF-7 cells and the normal human mammary epithelial cell line MCF-10A, respectively, and their correlation was analyzed. Results The mRNA expression levels of Wnt5a and E-cadherin in cell line MCF-7 were significantly lower than those in cell line MCF-10A [(16.93± 2.97)%vs. (27.47±2.76) %, (12.97±1.35) % vs. (20.43±2.60) %, both P<0.05]. The mRNA expression level of vimentin in cell line MCF-7 was significantly higher than that in cell line MCF-10A [(16.53±0.85)%(6.33± 2.08) %, P<0.05 ]. In cell line MCF-7, the expression of Wnt5a was positively related to E-cadherin (г=0.997, P<0.05), but it was negatively related to vimentin (г=-0.998, P<0.05). Conclusions The expression of Wnt5a in human breast cancer cell line MCF-7 is significantly lower than that in cell line MCF-10A, which indicates that Wnt5a is a cancer suppressor gene in breast cancer. The expression of Wnt5a in cell line MCF-7 is positively related with E-cadherin, and it is negatively related with vimentin. Wnt5a may cause invasion and metastasis of breast cancer cell through the breast epithelial mesenchymal transitions.

BACKGROUNDTbx1 is the major candidate gene for DiGeorge syndrome (DGS). Similar to defects observed in DGS patients, the structures disrupted in Tbx1(-/-) animal models are derived from the neural crest cells during development. Although the morphological phenotypes of some Tbx1 knock-down animal models have been well described, analysis of the cardiac performance is limited. Therefore, myocardial performance was explored in Tbx1 morpholino injected zebrafish embryos.

METHODSTo elucidate these issues, Tbx1 specific morpholino was used to reduce the function of Tbx1 in zebrafish. The differentiation of the myocardial cells was observed using whole mount in situ hybridization. Heart rates were observed and recorded under the microscope from 24 to 72 hours post fertilization (hpf). The cardiac performance was analyzed by measuring ventricular shortening fraction and atrial shortening fraction.

RESULTSTbx1 morpholino injected embryos were characterized by defects in the pharyngeal arches, otic vesicle, aortic arches and thymus. In addition, Tbx1 knock down reduced the amount of pharyngeal neural crest cells in zebrafish. Abnormal cardiac morphology was visible in nearly 20% of the Tbx1 morpholino injected embryos. The hearts in these embryos did not loop or loop incompletely. Importantly, cardiac performance and heart rate were reduced in Tbx1 morpholino injected embryos.

CONCLUSIONSTbx1 might play an essential role in the development of pharyngeal neural crest cells in zebrafish. Cardiac performance is impaired by Tbx1 knock down in zebrafish.

Animals ; Branchial Region ; cytology ; drug effects ; Heart ; drug effects ; physiology ; Heart Rate ; drug effects ; In Situ Hybridization ; Myocardium ; cytology ; Neural Crest ; cytology ; drug effects ; Oligonucleotides, Antisense ; pharmacology ; T-Box Domain Proteins ; antagonists & inhibitors ; metabolism ; Thymus Gland ; cytology ; drug effects ; Zebrafish ; embryology ; metabolism ; Zebrafish Proteins ; antagonists & inhibitors ; metabolism