Axillary osmidrosis may have a negative impact on the patient's normal life and social interaction , though it has no obvious harm to health .Such factors as gene , hormone and food are involved in the occurrence and severity of axillary osmidrosis .The pathogenesis mechanism remians unclear .This paper aims to review on the research progress of the pathogenesis mechanism and related factors of axillary osmidrosis in recent years .

It is the direct and main cause of trigeminal neuralgia that responsible vessel compresses the root entry zone of sensory root of trigeminal nerve.Microvascular decompression is an effective way in treating trigeminal neuralgia with higher cure and lower recurrence,which can eradicate the common cause of trigeminal neuralgia and maintain the normal function of trigeminal nerve;At the same time it is an safe way with lower risk on the basis of skilled microsurgical technique.So it is an optimal approach to treat trigeminal neuralgia.

Objective To investigate the effect of L-N6-(1-iminoethyl) Lysine(L-NIL) on ischemia-reperfusion (I/R) -induced lung injury in a rat model of lung transplantation. Methods Pathogen free male SD rats weighing 250-350g were used as donor and recipient rats in this study. The animals were randomly divided into 3groups (n = 6 each): sham operation group (group S); lung tratsplantation group (group L) and lung transplantation + L-NIL (selective iNOS inhibitor) group (group L-NIL). In group L and L-NIL orthotopic left lung allograft transplantation was performed. In group L-NIL 3 mg/kg was injected iv at the beginning of reperfusion. The donor lungs were removed from live donor rats and placed in Euro-collins solution at 4 ℃. The lung transplantation was performed under microscope and non-suture cuff technique was used. The implanted donor lungs were ventilated and reperfused. 0.5% Evans blue 0.2 ml was injected iv during reperfusion. The donor lungs were removed after being implanted, ventilated and reperfused for 2 h for microscopic examination and determination of iNOS, endothelial NOS (eNOS) and myeloperoxidase (MPO) activity and malondialdehyde (MDA) and Evans blue content in the lung tissue and W/D lung weight ratio. Results Lung transplantation significantly inceased W/D ratio, iNOS and MPO activity, and Evans blue and MDA content in the lung tissue and decreased eNOS activity in group L as compared with group S. L-NIL iv significantly attenuated the increase in the variables mentioned above and ameliorated capillary congestion and inflammatory cell infiltration in the lung. Conclusion Intravenous L-NIL administered at the beginning of reperfusion can reduce I/R injury to the transplanted donor lungs.

Aim In order to provide the experimental basis to investigate the pathologic mechanisms and drug treatment of pulmonary fibrosis,establish the lung slice fibrosis model induced by transforming growth factor-?_1 (TGF-?_1) . Methods Lung was isolated and inflated with 0.4 % agarose solution, then was cut into slices. The lung slice viability was assessed through lactate dehydrogenase (LDH) leakage and MTT assay after incubation of 1, 3, 5, 7, 9 days. The sub-optimal time and dose of TGF-?_1- induced lung slice fibrosis were investigated via measurement of hydroxyproline (HYP), and lung slice fibrosis was examined with HE and Masson staining. Results The lung slice was viable for up to 9 days. The sub-optimal time and dose of TGF-?_1-induced lung slice fibrosis were 7 days and 2.5 ?g?L~ -1 respectively. Meanwhile, hydrocortisone did not decrease the HYP levels in lung slices of TGF-?_1-induced fibrosis. Conclusion TGF-?_1 (2.5 ?g?L~ -1 ,?7d) induced lung slice fibrosis, and hydrocortisone did not exert advantageous effect on this process.

The future war will inevitably to be in the land,the sea and the sky and so on hyperspace,and electromagnetic environment is very complex.How to eliminate interference of medical equipment under the complex electromagnetic environment,to promote the performance of the medical support,these is austerity and reality questions in current every level of medical and health organization.Only based on the existing,bold practice,independent innovation,the comprehensive medical support exercise under the complicated electromagnetic environment,to master various types of medical equipment in a complex electromagnetic environment of the characteristics and laws in order to give full play to existing health technologies and equipment performance,improve the timeliness of medical support.

Aim To investigate the protective effects of Aplysin on ethanol-induced oxidative damage in rat pri-mary hepatocytes. Methods Rat primary hepatocytes were obtained via the portal vein collagenaseⅣin situ perfusion technique followed by a Percoll density gradi-ent centrifuge. MTT test was used to determine the op-timum dose of Aplysin and ethanol, and detect the cell vitality in primary hepatocytes. Supernatants of primary hepatocytes were harvested to measure AST and LDH level, and the SOD, GSH-PX activities and MDA con-tent in primary hepatocytes were observed. Flow cy-tometry was used to detect the cell apoptosis rate. DNA damage in primary hepatocytes was detected by single-cell gel electrophoresis assay. The level of mitochon-drial membrane potential in primary hepatocytes was tested by fluorogenic probe JC-1 . The CYP2 E1 activity in primary hepatocytes was detected by colorimetry. The proteins of CYP2 E1 were detected by Western blot. Results 300 mmol·L-1 dose of ethanol and 30 mg·L-1 dose of Aplysin were the optimal dosages and were used in the subsequent experiments. Hepatocyte vitality was significantly increased in Aplysin group compared to that in ethanol group, and Aplysin inhibi-ted the release of AST and LDH(P<0. 05). For Apl-ysin treatment group, the activities of hepatocyte SOD and GSH were significantly increased, and MDA was markedly lowered as compared with those in ethanol group( P <0. 05 ) . Aplysin could alleviate hepatocyte apoptosis significantly, and hepatocyte DNA damage rates of Ⅱ ~Ⅲ level and Ⅳ level were significantly lowered in Aplysin treatment group as compared with those in ethanol group, and Aplysin had evident im-provement in alcohol induced mitochondria damage of hepatocyte. Primary hepatocyte activities and protein expression of CYP2 E1 were markedly lowered in Aply-sin treatment group as compared with those in ethanol group(P<0. 05). Conclusion Aplysin has protective effects on liver oxidative damage induced by alcohol of primary cultured rat hepatocytes by blocking CYP2 E1 activation, relieving oxidative stress, and sharpening the oxidation resistance ability.

Objective To observe the curative effect and adverse reactions of IMRT and conventional radiotherapy combined with chem-otherapy in treating patients with advanced nasopharyngeal carcinoma. Methods The patients were divided into the IMRT group (46 cases) and conventional radiotherapy combined with chemotherapy group ( 50 cases ) . Making the IMRT and conventional radiotherapy combined with chemotherapy treatment plan, and analyze the curative effect and adverse reaction of the two groups. Results Compared with the con-ventional radiotherapy combined with chemotherapy group, IMRT group has a significantly increase in complete remission rate and overall re-sponse rate, but there is no significant difference in long-term efficacy. The skin, dry mouth ( parotid) ,and oral mucositis response is lower in IMRT group, and the neutropenia incidence, prevalence of anemia, liver and kidney function damage rate is also significantly lower than conventional radiotherapy combined with chemotherapy. Conclusion The IMRT can significantly improve the curative effect in treatment of advanced nasopharyngeal carcinoma and reduce the adverse reactions compared with the conventional radiotherapy combined with chemotherapy.

Objective To construct an eukaryotic expression vector of human Par-4 gene with green fluorescent protein gene which iS named pIRES2-EGFP/Par-4 and transfect jt into K562 cell line. Methods Using pDNR/Par-4 plasmid as a template.the full length Par-4 cDNA was amplified by PCR and subsequently cloned into T-A vector.Then subcloned into pIRES2-EGFP vector.After identified by digestion of restriefive endonucleases.pIRES2-EGFP/Par-4 was further confirmed by sequencing.Then it was transfected into K562 cells with Superfect reagents.The total proteins were isolated and Par-4 was detected by Western blotting. Results The exact sequences of pIRES2-EGFP/Par-4 vector were confirmed by digestion of restrictive endonucleases and sequencing.After transfection,the expressions of green fluorescent protein were present.The protein expression of Par-4 has been detected in transfected ceils hv Western blotting.Conclusion The vector pIRES2-EGFP/Par-4 has been constructed and could Successfully express Par-4 gene in K562 cells.

Objective To explore the changes of Par-4 and WT1 genes expression during human leukemic K562 cells apoptosis induced by arsenic trioxide (As2O3). Methods After the K562 cells were treated with arsenic trioxide (2-10 μmol/L) for 24-72 hours, cell survival rate was evaluated by MTT assay and apoptosis was analyzed using flow cytometry. The expressions of mRNA and protein for par-4 and WT1 were tested by Real-time quantitative reverse transcriptase polymerase chain reaction (RQ-RT-PCR) method and Western blotting in K562 cells with various concentrations of arsenic trioxide at different time points. Results After the K562 cells were treated with As2O3 of different concentrations, arsenic trioxide could efficiently inhibit the growth of K562 cells and induce apoptosis with the increase of As2O3 concentration. The same time, the mRNA and protein expressions of Par-4 were up-regulated, while the mRNA and protein expression of WT1 were down-regulated. Conclusion Arsenic trioxide could inhibit the growth of K562 cells and induce apoptosis. Par-4 and WT1 genes could participate in the apoptosis of K562 cells induced by arsenic trioxide.