Objective To observe the effect of monochromatic infrared energy(MIRE)on diabetic periphe- ral neuropathy(DPN).Methods Seventy-four subjects with diabetic peripheral neuropathy who were tested by Semmes-Weinstein monofilaments(SWM)were randomized into 2 groups:a conventional management group and a conventional management plus MIRE group.Then the patients'sensory function and other DPN symptoms were evalu- ated by the SWME and the score of Michigan Neuropathy Screening Instrument.Results After treatments,there was a decrease(P＜0.01)in the number of the sites insensitive to SWME(grade 5.07),and MNSI scores were sig- nificantly decreased(P＜0.01).The MIRE management was more effective than conventional management.Con- clusion Monochromatic infrared energy is perhaps a safe,non-pharmaceutical and non-invasive method for the treat- ment of diabetic peripheral neuropathy.

The diagnosis of myocardial damage in systemic lupus erythematosus(SLE) is mainly based on clinical symptoms,physical examinations and electrocardiographic abnormality,echocardiographic changes,and myocardial enzymologic diversity in general.In recent years,it has been suggested that cardiac troponin I possesses high sensitivity and specificity in the diagnosis of myocardial damage.Lupus myocardial damage is diagnosed definitively depending on endomyocardial biopsy.Its treatment has been empirical,and hormone combined with immunodepressive is routine treatment.According to pathogenetic condition,there are still several therapies such as intravenous immunoglobulin therapy,blood purification and autologous hematopoietic stem cell transplantation,extracorporeal membrane oxygenation,and so on.Most often,myocardial dysfunction in SLE is of subclinical progression,and that early diagnosis and prompt treatment may play an important role in relieving patients' condition,raising quality of life and improving prognosis.

Objective To analyze the causes of medical disputes and to find an effective way to reduce medical malpractice and medical dispute.Methods The complete identification files of 251 cases of medical malpractice obtained from corresponding Offices of Technical Identification of Medical Malpractice in three cities at prefecture level in Shandong province were analyzed to compare the cause of medical malpractice identified by patients with that identified by experts.Results The main causes that identified by patients included violation(36.41%),default(35.60%),illegality(13.05%),tort(11.89%),and absence of management(3.05%).Among the litigation claims,58.53%were identified as existed factors causing disputes.Among the identified factors,72.66%should have been prevented and controlled.Conclusion Medical malpractice and medical dispute can be effectively prevented and controlled by putting management site forward,ensuring the implemention of the policies,and strengthening the substantive responsibility of the leadership.

Adolescent ; Adult ; Diabetes Mellitus, Type 1 ; blood ; complications ; genetics ; Diabetic Angiopathies ; blood ; complications ; Female ; Gene Frequency ; Genotype ; Homocysteine ; blood ; Humans ; Male ; Methylenetetrahydrofolate Reductase (NADPH2) ; genetics ; Mutation ; Polymorphism, Genetic ; Regression Analysis

Objective To clone amastin coding genes from different strains of Leishmania parasites. Methods Using amastin cDNA sequence as the reference, dbEST data base established by National Center Biotechnology Information (NCBI), USA, was searched by BLAST tool. A 309 bp DNA fragment of Leishmania major was found and used as the probe for the screening of a DNA library. The amastin gene of Leishmania major Abdou was cloned and sequenced. Specific primers were designed and amastin genes for Leishmania mexicana WR972, Leishmania brizeliensis and Leishmania amazonensis joseph were amplified by polymerase chain reaction. Results The amastin genes from 4 strains of Leishmania parasites were cloned and sequenced. It was found that all 4 amastin genes contained unique open reading frame of 552 bp and encoded amastin protein of 183 amino acid residues. Conclusion The amastin genes of 4 strains of Leishmania parasites were successfully cloned.

Polymerase chain reaction was employed to amplify the HBV X gene from plasmid pCP10, and the product was cloned into pVR1012, then transfected HepG2 cells and cotransfected HepG2 cells with reporter plasmid pSV lacZ HBx protein produced by HepG2 cells was measured by ELISA method The activity of ? galactosidase was measured by a kit, which reflected the transactivating function of HBx protein The results showed that HepG2 cells transfected by pVR1012 X could express HBx protein The expression of ? galactosidase in HepG2 cells transfected by the pVR1012 X was 3 2 fold higher as that of control plasmid It is suggested that the recombinant plasmid pVR1012 X can be expressed in mammalian cell line, and has transactivating effect on SV40 early promoter

To construct a cDNA subtractive library of genes transactivated by hepatitis C virus core protein with suppression subtractive hybridization technique. mRNA was isolated from HepG2 cells transfected with pcDNA3 1(-)-core and pcDNA3 1(-) empty vector,respectively, then cDNA was synthesized. After restriction enzyme RsaI digestion, small sized cDNA were obtained. Then tester cDNA was divided into two groups and ligated to the specific adaptor 1 and adaptor 2, respectively. After tester cDNA was hybridized with driver cDNA twice and underwent two times of nested PCR, and then it was subcloned into T/A plasmid vectors to set up the subtractive library. Amplification of the library was carried out with E.coli strain JM109. The cDNA were sequenced and analyzed in GenBank with Blast search after PCR. The subtractive library of genes transactivated by HCV core protein was constructed successfully. The amplified library contained 233 positive clones. Colony PCR product showed that 213 clones contained 100~ 1 000 bp inserts. Sequence analysis was performed in 63 clones. Six of the sequences were unknown genes before. The full length sequences were obtained with bioinformatics method,which had been accepted by GenBank. It suggested that six novel cDNA sequences might be target genes transactivated by HCV core protein.

Objective To construct a cDNA subtractive library of genes transactivated by c-terminally truncated middle surface protein of hepatitis B virus(MHBs t) with suppression subtractive hybridization technique for cloning genes associated with transactivation. Methods The mRNA was isolated from HepG2 cells transfected with pcDNA3.1(-)-Mt167 and pcDNA3.1(-) empty vectors, respectively, then cDNA was synthesized. After restriction enzyme Rsa I digestion, small-size cDNAs were obtained. Then tester cDNA was divided into two groups and ligated to the specific adaptor 1 and adaptor 2, respectively. After tester cDNA was hybridized with driver cDNA twice and underwent two times of nested PCR and then was subcloned into T/A plasmid vectors to set up the subtractive library. Amplification of the library was carried out with E. coli strain JM109. The cDNA was sequenced and analyzed in GenBank with Blast search after PCR. Results The subtractive library of genes transactivated by MHBs t was constructed successfully. The amplified library contained 94 positive clones. Colony PCR showed that these clones contained 200-800bp inserts. Sequence analysis was performed in 50 clones,and the full length sequences were obtained with bioinformatics method. 23 coding sequences were obtained in total, which consisted of 19 known and 4 unknown ones.Conclusions The obtained sequences may be target genes transactivated by MHBs t, among which some genes coding proteins may involve in cell cycle regulation, immune response and tumour genesis.

In order to screen genes transregulated by core protein of hepatitis C virus, cDNA microarray technology was employed to detect the gene expression change between HepG2 cells transfected with pcDNA3 1(-) core and the empty vector, respectively. Among 1152 genes, there were 95 genes with different expressions, of which 45 genes were upregulated and 50 genes were downregulated in HepG2 cells transfected with core protein expression plasmid. These genes transregulated by HCV core protein included human genes encoding proteins involved in cell proliferation, differentiation, apoptosis, signal transduction and immune regulation. Therefore, the results provided some new clues for further clarifying the molecular biology mechanism of pathogenesis and tumorigenesis of HCV core protein

Hepatitis C virus (HCV) non structure 3 (NS3) protein and hepatitis B virus (HBV) X protein expressing plasmids were constructed with the vector pcDNA3 1(-). The plasmids were transfected into HepG2 cells and the viral proteins expressed in HepG2 cells were identified using Western blotting methods. Then the two recombined plasmids were transfected into HepG2 cells and were cotransfected into HepG2 cells with reporter plasmid pCAT3 promoter. The activity of CAT enzyme was detected by a CAT ELISA assay kit, which reflected the transactivating function of two proteins on SV40 early promoter. The findings indicated that the expression of two viral proteins were successfully detected in soluble protein cell extracts of transiently transfected HepG2 cells. HCV NS3 protein transactivated the CAT enzyme expressed at a value 3 5 fold higher than the control, while HBX protein transactivated at a value 4 4 times. It arrived at 8 5 times when transfected with two plamids simultaneously. The activating effect was increased in relation to the amount of plasmids. It was suggested that the two kinds of viral proteins had a transactivating effect on SV40 early promoter, and they acted synergistically. These results might contribute to explaining the mechanisms of liver injury or tumorigenesis induced by HCV or/and HBV infection