Adolescent ; Child ; Diagnosis, Differential ; Dystonic Disorders ; diagnosis ; drug therapy ; physiopathology ; Female ; Humans ; Male

Background Arresting the overexpression of vascular endothelial growth factor (VEGF) will be a new approach to the inhibition of neovascularization.RNA interference (RNAi) can inhibit the expression of specific gene,and its application in eye has little interference to other gene expression.Objective This study was to investigate the effect of small interference RNA (siRNA) targeting VEGF on the expression of VEGF and retinal neovascularization in oxygen-induced retinopathy (OIR) model.Methods psi-HITM/enhanced green fluorescent protein (EGFP)/VEGF siRNA was designed and prepared in vitro.Mouse endothelioma (EOMA) were cultured in DMEM without antibiotic and divided into 5 groups.The cells were incubated in DMEM only in the blank control group;while 1 μl of LipofectamineTM 2000 + psi-HITM/EGFP,1 μl LipofectamineTM 2000 + 40,50 or 60 nmol/L of psi-HITM/EGFP/VEGF siRNA was added into DMEM in the negative control group and siRNA groups,respectively.The expression of VEGF mRNA and protein was detected by real time PCR (RT-PCR) and Western blot.The optimal effective concentration of VEGF siRNA was assessed.OIR models were established in 48 7-day-old C57BL/6J mice by raising them at an oxygen concentration of (75±2) ％ for 5 days and then to normal air.The mice were randomized into the model group,null vector group and VEGF siRNA group.1 μl of a mixture of psi-HITM/EGFP or VEGF siRNA (60 nmol/L) and LipofectamineTM 2000 was intravitreally injected,respectively,in the null vector group and VEGF siRNA group.The normal mice were used as the normal control group.Expression of VEGF mRNA and protein in the mouse retinas was detected by RT-PCR and Western blot,respectively,and FITC-dextran stretched retinal preparation was examined to evaluate the neovascularization,and retinal sections were examined to quantify the number of vascular endothelial cell nuclei extending beyond the internal limiting membrane (ILM).Results The in vitro transfection test showed that the expression of VEGF mRNA and protein in the EOMA cells was significantly different among the blank control group,negative control group and 40,50,60 nmol/L VEGF siRNA groups (F =148.890,P ＜ 0.001; F =306.960,P ＜ 0.001),and the expression of VEGF mRNA was lower in different concentrations of VEGF siRNA groups than that in the blank control group (t=73.950,119.890,156.480,all at P＜0.001).Also,the expression of VEGF protein was less in different concentrations of VEGF siRNA groups than that in the blank control group (t =15.452,23.344,42.119,all at P＜0.001).The optimal inhibitory concentration of VEGF siRNA was 60 nmol/L.In vivo study determined that compared to the model group and null vector group,the non-perfusion zones and neovascular net in the retina were decreased,and the number of vascular endothelial cell nuclei extending beyond the ILM was less in the VEGF siRNA group.The relative expression level of VEGF mRNA in the retinas was 1.23±0.18,4.02±0.16,3.98±0.19 and 1.98±0.12 in the normal control group,model group,null vector group and VEGF siRNA group,respectively,with a significant difference among them (F=369.780,P＜0.001),and the relative expression levels of VEGF mRNA in the model group and null vector group were higher than that in the normal control group (t=37.880,37.336,both P＜0.001),and the expression of VEGF mRNA in the VEGF siRNA group declined by 50.8％ (t=10.183,P＜0.001).The difference in the expression levels of VEGF protein also was assayed among the various groups (F=408.980,P＜0.001),and VEGF level in the retina was lowered by 68.0％ in the VEGF siRNA group compared to the model group (t =11.473,P＜0.001).However,VEGF level in the VEGF siRNA group remained at a high level in comparison with the normal control group (t =2.422,P＜0.001).Conclusions Intravitreal injection of VEGF siRNA can attenuate retinal neovascularization by effectively downregulate the expression VEGF mRNA and protein in the retina.

BACKGROUND:The output of computed tomography (CT) is Digital Imaging and Communications in Medicine (DICOM), whereas the input of three-dimensional (3D) printing is an object Standard Template Library model represented by a triangular mesh. The process of data handing and forrmat conversion are keys to the combination of these two techniques. OBJECTIVE:To explore how to convert CT data into a stereoscopic 3D model efficiently. METHODS:The DICOM in Medicine format data of the patients with femoral fractures were edited and produced by Mimics. We made a 3D model by adjusting the parameters of the 3D printer slicing software, and discussed the significance of 3D model in medical field, especially orthopedics. RESULTS AND CONCLUSION:Mimics software is the bridge to connect two-dimensional CT scan images and 3D images, to create a 3D model by editing the data of DICOM which comes from the CT scanner, with a 3D printing technology. The 3D Model can help doctors for routine clinical diagnosis and treatment, to improve the communication between doctors and patients and the quality of clinical medical teaching. 3D printing also makes medicine more personalized, remote, minimally invasive, and promote the development of medicine to the direction of digital medicine.

As the technologic sophistication of generation and distribution of electrical energy has grown, so has the general concern about the effects of electric fields on human health. There can be no doubt that the significance of electrical trauma will continue to grow with our increasing use of power. It is apparent that our understanding of the various forms of electric trauma must increase, while we continue to promote safety near electrical hazards and develop effective medical therapies. Tissue damage as a result of electrical injury occurs by two mechanisms which are summative in action and have a variable degree of contribute to the ultimate damage produced. Thermal tissue damage occurs as a result of heat generated within the tissue (which offer an electrical resistance) secondary to the passage of the electrical current. High temperatures can also lead to cell membrane components, e.g., phospholipids, to dissolve. Electroportation damage is the tissue damage induced secondary to the strong electric field. Transmembrane potentials caused by electrical current result in the formation of pore in the phospholipid component of the cell membrane resulting in loss of function of the cell membrane with consequent cell death.
Animals ; Electric Injuries/physiopathology* ; Heart Injuries/physiopathology* ; Hemodynamics ; Humans ; Muscle, Skeletal/injuries*

Adolescent ; Adult ; Aged ; Child ; Child, Preschool ; China ; epidemiology ; Female ; Humans ; Infant ; Infant, Newborn ; Male ; Metapneumovirus ; Middle Aged ; Paramyxoviridae Infections ; epidemiology ; pathology

OBJECTIVETo evaluate the clinical efficacy of autologous semitendinosus and gracilis tendon grafting with anchor repair for the treatment of chronic achilles tendon rupture and severe scarring.

METHODSFrom April 2010 to October 2012,26 patients with chronic achilles tendon rupture(with Myerson type III ) and severe scarring were treated with autologous semitendinosus and gracilis tendon grafting with anchor repair. There were 19 males and 7 females,with an average age of 32 years old (ranged, 22 to 47 years). The time from injury to surgery was from 3 to 12 months (7 months on average). The plantar flexion strength of all injuried feet attenuated and single heel rise test were positive in 26 cases before operation. Plaster immobilization and routine rehabilitation therapy were performed after operation. Clinical effects were evaluated by Arner-lindholm criterion and complications were observed after operation.

RESULTSAll the patients were followed up from 12 to 24 months with a mean of 16 months. No complications such as achilles tendon re-rupture, wound infection, etc were found during follow-up period. According to the Arner-Lindholm standard, 15 cases got excellent results and 11 good.

CONCLUSIONUsing autologous semitendinosus and gracilis tendon grafts with anchor repair to treat chronic achilles tendon rupture and severe scarring is a perfect surgical procedure.

Achilles Tendon ; injuries ; surgery ; Adult ; Chronic Disease ; Cicatrix ; surgery ; Female ; Follow-Up Studies ; Humans ; Male ; Middle Aged ; Rupture ; Young Adult

Objective Negative pressure aspirator clogging ( OSAC) frequently occurs in orthopedic surgery .This study was to investigate the frequency , location , and mechanisms of OSAC in China by analysis of the current status and clinical observation of OSAC so as to provide evidence for the solution of the problem . Methods Using the two-stage random sampling method , we conduc-ted a questionnaire survey on OSAC among 738 clinical orthopedists during the 16th and 17th Chinese Orthopedic Association Confer-ences.Totally, 160 out 1200 orthopedic surgeries were randomly selected in the time order of operation , including 38 cases of total hip arthroplasty ( THA) , 39 cases of total knee arthroplasty ( TKA) , 43 cases of extremity and spinal fractures surgery , and 40 cases of other orthopedic surgeries .We also obtained the satisfaction scores with the existing aspirators from related medical professionals . Results Among the 738 respondents included into the analysis , 706 (95.7%) thought that OSAC often occurred during surgery , 631 (85.5%) considered THA to be the leading cause of OSAC , and 714 (96.7%) regarded the tip and hose joint of the aspirator as the common causes . The mean satisfaction score with the existing aspirators was 7.62 ±0.74.Clinical observation showed the mean frequency of OSAC to be 2.55 ±1.62 in THA, 1.95 ±1.33 in TKA, 1.52 ±1.18 in extremity and spinal fracture surgeries , and 0.95 ± 0.68 in other orthopedic surgeries , and the satisfaction score to be 7.36 ±0.84. Conclusion OSAC has a high incidence rate during orthopedic surgeries in China , thus affecting orthopedic surgery and reducing orthopedists'satisfaction with the aspirators . The current negative pressure aspirator system demands prompt improvement .

Objective：Rat UREB1 protein coded by the gene UREB1 can specially bind to URE (upstream regulatory element) which is in the upstream of the promoter. It′ s reported that the protein of UREB1 promote the transcription of Dynorphin gene and inhibits p53 transactivation. This study was designed to clone human UREB1 gene and explore the relationship between UREB1 and the development of tumor. Methods： The artificial synthetic oligonucleotide was used as the probe to screen human brain cDNA library and human UREB1 gene was cloned. The antibody, which was produced using the recombinant UREB1 from E.coli as the antigen and immunizing the animals, was utilized for detecting the distribution of UREB1 in different tumor tissues. Results： The human UREB1 gene was cloned by using in situ hybridization for screening human brain cDNA library, and the nucleotide sequences and the deduced amino acid sequence of human UREB1 has 91％ homology with that of rat UREB1 identified previously. Western blot analysis revealed that the human UREB1 was present in all tumor tissues but the quantity of UREB1 in different tissues was not the same. Immunohistochemistry results shown that the human UREB1 distributes primarily in the cytoplasm and nuclear of tumor cells and nuclear UREB1 in carcinosarcoma is much more than that in adenoma. After analyzing the level of tyrosine phosphorylated UREB1 in a few tumor tissues, the result shown that the more malignant the tumor tissue was, the higher level the tyrosine phosphorylated of UREB1 was in that tumor tissues. Conclusion： Human UREB1 may be involved in the development of tumor and its tyrosine phosphorylation may affect the degree of tumor malignant.

OBJECTIVE: To study the distribution and proportion of neuropeptide containing nervers in the sinus node in cases of sudden manhood death syndrome (SMDS) and to explore the mechanism of SMDS. METHODS: Immunohistochemical staining and quantitative analysis of neuropeptide Y (NPY) and vasoactive intestinal peptide(VIP) in the sinus node in 6 cases of SMDS and in 12 cases of non-cardiac death(control group) were achieved by LSAB method and computerized image system. RESULTS: As for NPY positive materials, VIP positive materials and the ratio of VIP/NPY in the sinus nodes, there were no significant difference between the control group and SMDS group. CONCLUSION The mechanism of SMDS and the abnormality of autonomic nervous innervation in the sinoatrial nodes maybe incorrelation.
Adult ; Autonomic Nervous System/physiology* ; Death, Sudden/pathology* ; Humans ; Immunohistochemistry ; Male ; Myocardium/metabolism* ; Neuropeptide Y/metabolism* ; Sinoatrial Node/innervation* ; Vasoactive Intestinal Peptide/metabolism*

OBJECTIVE: To observe the changes of electrocardiogram and serum cardiac troponin I at the early stage of severe crush injury in rats. METHODS: Crush injury was produced in Sprague-Dawley rats. The changes of electrocardiogram were recorded with the standard II, the serum levels of cardiac troponin I were studied by automated chemiluminescence assay. RESULTS: The ST segment elevated considerably after crush injury and lasted 24 h, the levels of serum cTnI were much higher than those of the control groupes after 6 h of injury. CONCLUSION Cardiomyocyte injury was induced in the early phase of crush injury.
Animals ; Crush Syndrome/physiopathology* ; Electrocardiography ; Extremities/injuries* ; Female ; Heart Injuries/physiopathology* ; Male ; Rats ; Rats, Sprague-Dawley ; Troponin I/blood*