Objective To study the protective effect of lipoic acid (LA) on H9c2 cardiomyocytes hypoxia/reoxygenation injury model, and explore its relevant mechanism. Methods Eight strains of H9c2 cardiomyocytes, passaged after cultured to a full view, were divided into 3 groups:normoxia group, hypoxia/reoxygenation group and LA group. The cell survival rate, lactate dehydrogenase (LDH) activity, malondialdehyde (MDA) and heme oxygenase-1 (HO-1) levels were detected and compared. Results The cell survival rates of H9c2 cardiomyocytes in hypoxia/reoxygenation group and LA group were significantly lower than those in normoxia group:(52.86 ± 6.39)％, (69.25 ± 7.63)％vs. (92.31 ± 7.82)％, while the cell survival rate of H9c2 cardiomyocytes in LA group was significantly higher than that in hypoxia/reoxygenation group, and there were statistical differences (P<0.01). The LDH activity and MDA in hypoxia/reoxygenation group and LA group were significantly higher than those in normoxia group:(286.37 ± 27.49), (209.72 ± 25.63) U/L vs. (126.32 ± 18.94) U/L, and (1.72 ± 0.06), (1.13 ± 0.07)μmol/L vs. (0.68 ± 0.06) μmol/L, while those data in LA group were significantly lower than those in hypoxia/reoxygenation group, and there were statistical differences (P<0.01). The HO-1 in hypoxia/reoxygenation group and LA group were significantly higher than that in normoxia group:(213.71 ± 18.94)％, (367.26 ± 23.07)％vs. (87.92 ± 19.23)％, and HO-1 in LA group was significantly higher than that in hypoxia/reoxygenation group, and there were statistical differences (P<0.01). Conclusions The LA plays a protective role on myocardial cell with hypoxia/reoxygenation injurythough increasing the level of HO-1 against oxidative stress.

Objective To observe the spatiotemporal characteristics of the micro-structural injury in a rat model of diffuse axonal injury (DAI) and quantitatively assess the axonal injury severity in the vulnerable areas. Methods The 7.0 T MRI was performed in rats in DAI group (n =20) and control group ( n = 15 ) to synthesize the diffusion tensor imaging ( DTI) parameter map and calculate the parameter value of the vulnerable areas. Immunohistochemistry was used to detect β-APP expression in the vulnerable areas and the IPP software to quantitatively assess the axonal injury severity. Results Compared with the control group, FA and AD maps showed local signal defection or reduction in the corpus callosum and their values decreased significantly in the brain stem and corpus callosum in the DAI group (P ＜0.01 ). The integrated optical density (IOD) value of the vulnerable areas in the DAI group was significantly higher than that of the control group ( P ＜ 0. 01 ) , with the highest level in the brain stem (P＜0.05). The normalized FA, AD and ADC in the vulnerable areas were correlated negatively with the IOD (P ＜ 0.05). Conclusion DTI can detect invisible micro-structural injury in the vulnerable areas and quantitatively assess the axonal injury severity in vivo in the early stage.

OBJECTIVE To identify the pop strain of Staphylococcus aureus hospital acquired infection by random amplification of polymorphic DNA(RAPD),and to study the molecular mechanism of antibiotic(resistance),so as to reduce the occurrence of drug resistance and infection acquired in hospital.METHODS 1.DNA from 21 strains of S.aureus were extracted by the phenol-chloroform method and analyzed by using arbitrary(primer) polymerase chain reaction(AP-PCR).2.Amplifying mecA,GyrA and GrlA by PCR,and testing the(variation) of these genes by using Hinf Ⅰ-digested analysis.RESULTS Twenty one S.aureus strains were divided into 3(genetic) types.Type Ⅰ is the pop strain in our hospital which including 12 strains.Fourteen from 17 clinical stains were resistant to meticillin and quinolones,of which 13 strains had mecA except isolate 13064.And they all had(variation) in(GyrA) and/or GrlA.CONCLUSIONS RAPD provides markers for the typing of clinical strains and is suitable for(molecular) epidemiologic studies with high type ability,powerful discrimination,simplicity and(rapidness). Type Ⅰ is the pop S.aureus strain in hospital-acquired infection of our hospital.The majority of these strains are multi-(resistant) to meticillin,quinolones and other antibiotics.

OBJECTIVE To study the molecular mechanism of antibiotic resistance in hospital acquired(Staphylococcus) epidermidis infection,so as to reduce the occurrence of drug resistance and infection(acquired) in hospital.METHODS DNA from 18 strains of S.epidermidis were extracted by the phenol-chloroform method,and mecA,gyrA and grlA were amplified by PCR,then the variation of gyrA and grlA was tested by Hinf Ⅰ-(digested)(analysis).RESULTS Fifteen from 18 S.epidermidis strains were resistant to meticillin,and all of them had mecA gene. Eleven from 18 S.epidermidis strains were resistant to meticillin,quinolones and other(antibiotics).And they all had a mutant in gyrA and/or grlA.The mutated spots were gyrA Ser84(TCA→TTA) and GrlA Ser80(TCC→TTC).CONCLUSIONS The majority of hospital acquired S.epidermidis strains are multi-resistant to meticillin,quinolones and other antibiotics,which are caused by acquirement of drug-resistance gene or(mutation) of drug-targeting genes.Medical institutions must strictly standardize the application of antibiotics to(reduce)(development) of drug resistance.

Objective:To assess the value of spiral CT in diagnosis and treatment of chronic otitis media.Methods:The spiral CT findings of 74 cases including 93 ears proved by operation and pathology were studied.Results:The lesions such as the disruption of the ossicular chain showed in spiral CT or three-dimensional image were in accord with those seen in the operation,the accuracy was 95.7%,the disruption of the ossicular chain and bony erosion in the tympanic cavity and antrum were severe in the typeⅢ chronic otitis media.Conclusion:Spiral CT is helpful to diagnose and definite the chronic otitis media,three-dimensional image can provide valuable information for surgery.

OBJECTIVETo investigate the genotypes of hepatitis E viruses (HEV) detected in sera of patients from different regions of China.

METHODSThe partial genome (nt6461-6860, nt5994-6294) of open reading frame 2 (ORF2) of 45 HEV strains detected from 14 cities of China was amplified and sequenced using polymerase chain reaction (PCR) and direct sequencing.

RESULTSForty-one of 45 strains (91%) share the same genotype with HEV Burma strain (B), with nucleotide identities higher than 98% with the representative HEV Chinese strain. Only 4 HEV strains are significantly divergent from the 3 prototype strains of HEV, with nucleotide identities of 77%-80% with HEV Burmese/Chinese strain, 74%-76% with Mexican strain and 74%-77% with the newly discovered HEV US/swine strain, respectively. Phylogenetic analysis suggests that these 4 strains may represent 2 different subtypes that belong to a novel genotype of HEV, which is significantly divergent from the prototype Mexico, Burmese and US/swine strains.

CONCLUSIONAmong patients with hepatitis E in China, most are infected by the Chinese prototype HEV, and only a small part by the new genotype HEV.

Base Sequence ; Genotype ; Hepatitis E ; virology ; Hepatitis E virus ; classification ; genetics ; Humans ; Open Reading Frames ; Phylogeny ; RNA, Viral ; blood ; chemistry

Purpose: Temozolomide is used in first-line treatment for glioblastoma. However, chemoresistance to temozolomide is common in glioma patients. In addition, mechanisms for the anti-tumor effects of temozolomide are largely unknown. Ferroptosis is a form of programmed cell death triggered by disturbed redox homeostasis, overloaded iron, and increased lipid peroxidation. The present study was performed to elucidate the involvement of ferroptosis in the anti-tumor mechanisms of temozolomide. Materials and Methods: We utilized the CCK8 assay to evaluate cytotoxicity. Levels of lactate dehydrogenase (LDH), malondialdehyde (MDA), iron, and glutathione (GSH) were measured. Flow cytometry and fluorescence microscope were used to detect the production of reactive oxygen species (ROS). Western blotting, RT-PCR and siRNA transfection were used to investigate molecular mechanisms. Results: Temozolomide increased the levels of LDH, MDA, and iron and reduced GSH levels in TG905 cells. Furthermore, we found that ROS levels and DMT1 expression were elevated in TG905 cells treated with temozolomide and were accompanied by a decrease in the expression of glutathione peroxidase 4, indicating an iron-dependent cell death, ferroptosis. Our results also showed that temozolomide-induced ferroptosis is associated with regulation of the Nrf2/HO-1 pathway. Conversely, DMT1 knockdown by siRNA evidently blocked temozolomide-induced ferroptosis in TG905 cells. Conclusion Taken together, our findings indicate that temozolomide may suppress cell growth partly by inducing ferroptosis by targeting DMT1 expression in glioblastoma cells.

Purpose: Temozolomide is used in first-line treatment for glioblastoma. However, chemoresistance to temozolomide is common in glioma patients. In addition, mechanisms for the anti-tumor effects of temozolomide are largely unknown. Ferroptosis is a form of programmed cell death triggered by disturbed redox homeostasis, overloaded iron, and increased lipid peroxidation. The present study was performed to elucidate the involvement of ferroptosis in the anti-tumor mechanisms of temozolomide. Materials and Methods: We utilized the CCK8 assay to evaluate cytotoxicity. Levels of lactate dehydrogenase (LDH), malondialdehyde (MDA), iron, and glutathione (GSH) were measured. Flow cytometry and fluorescence microscope were used to detect the production of reactive oxygen species (ROS). Western blotting, RT-PCR and siRNA transfection were used to investigate molecular mechanisms. Results: Temozolomide increased the levels of LDH, MDA, and iron and reduced GSH levels in TG905 cells. Furthermore, we found that ROS levels and DMT1 expression were elevated in TG905 cells treated with temozolomide and were accompanied by a decrease in the expression of glutathione peroxidase 4, indicating an iron-dependent cell death, ferroptosis. Our results also showed that temozolomide-induced ferroptosis is associated with regulation of the Nrf2/HO-1 pathway. Conversely, DMT1 knockdown by siRNA evidently blocked temozolomide-induced ferroptosis in TG905 cells. Conclusion Taken together, our findings indicate that temozolomide may suppress cell growth partly by inducing ferroptosis by targeting DMT1 expression in glioblastoma cells.

Kashin-Beck disease (KBD) is a chronic endemic bone and joint disease, with severe cases of short stature, joint deformities, and significantly reduced quality of life. Its etiology is currently unclear. Matrix metalloproteinases (MMPs) are endopeptidases that can degrade the extracellular matrix of articular cartilage cells, and are closely related to the occurrence and development of bone and joint diseases. At present, some scholars have found that MMPs can cause cartilage damage in KBD patients and promote the progression of KBD, but its specific mechanism of action is still unclear. This article reviews the research progress on the etiology of KBD, MMPs and its related genes, and their relationship with KBD cartilage injury both domestically and internationally. In order to provide theoretical support for in-depth research on the pathogenesis of KBD and to improve and update its treatment methods.