This paper analyses the characteristics of USB bus power.Based on the power demand of the circuits for neuromuscular rehabilitator,power voltage transformation circuits are designed for the realization of USB bus power supply.

131 I-metabolizing genes are markers for differentiation of thyroid carcinoma.The loss or down-regulation of these genes represents progression of dedifferentiation,which results in low 131 I uptake and suggests a poor prognosis.The mechanism of dedifferentiation of DTC is important for treatment.This article reviews the mechanism of dedifferentiation from 131I radiation damage,gene mutation,tumor markers and protein.

Objective To investigate the risk factors of upper gastrointestinal injury induced by non-steroidal anti-inflammatory drugs (NSAIDs).Methods A total of 1032 patients which used NSAIDs was selected.Patients were divided into two groups based on the condition of dyspepsia,peptic ulcer or upper gastrointestinal bleeding:the adverse drug reaction group (331 cases) and the control group (701 cases).Data of two groups on clinical presentation,laboratory test,medication and treatment were analyzed.Risk factors for the adverse drug reaction were identified by multivariable Logistic regression.Results The two groups had significant difference in age ＞ 65 years old,Helicobacter pylori (Hp) infection,ulcer history,drug overdose,combination with glucocorticoid,addicted to tobacco and alcohol history,non-specific inhibitor of cyclooxygenase(COX)-2,combination with anticoagulant,concomitant chronic cardiopulmonary disease (P ＜ 0.05).Logistic regression analysis by backward elimination method revealed that following variables retained,such as combination with glucocorticoid (OR =3.104,95％ CI 1.936-4.695),Hp infection (OR =2.768,95％ CI 2.047-3.742),drug overdose (OR =2.411,95％ CI 1.683-3.453),ulcer history (OR =1.781,95％ CI 1.278-2.480),age ＞ 65 years old (OR =1.659,95％ CI 1.237-2.225),non-specific inhibitor of COX-2 (OR =1.470,95％ CI 1.103-2.133),addicted to tobacco and alcohol history (OR =1.459,95％ CI 1.032-2.064),concomitant chronic cardiopulmonary disease (OR =1.357,95％ CI 1.008-2.143),P＜0.05.Conclusion Combination with glucocorticoid,Hp infection,drug overdose,ulcer history,age ＞ 65 years old,non-specific inhibitor of COX-2,addicted to tobacco and alcohol history,concomitant chronic cardiopulmonary disease are risk factors of upper gastrointestinal injury induced bv NSAIDs.

Objective To evaluate the effectiveness of using adipose-derived stromal cells (ADSCs)into a tissue-engineered peripheral nerve on bridging sciatic nerve gaps.Methods Forty-eight F344 female rats weighing 200 - 220 g were randomly divided into 6 groups of nerve grafting to repair 15 mm long asiatic nerve lesions,with 8 mrs in each group.Group A:ADSCs-laden acellular nerves;group B:differentiated ADSCs-laden acellular nerves;group C:Schwann cells-laden acellular nerves;group D:acellular nerves without cells;group E:autografts;group F:nonimplanted grafts.The effects were evaluated in terms of electrophysiulogy,Fluorogold retrograde tracing,histology and tracking studies.Results At 12 weeks after surgery,there was no graft bridging nerve gap in nonimplanted grafts.All the examinations of group A and B were better than group D,respectively (P＜0.05 or P＜0.01).But there were no statistically significant differences among group A,B,C,and D (P＞0.05).Conclusion ADSCs and differentiated ADSCs could promote nerve regeneration when used as seed cells to build tissue-engineered peripheral nerves with acellular nerve scaffolds.

Objective To investigate the histological and ultrastructural characteristics of liver graft after different warm ischemia time (WIT) in rats. Methods According to WIT, rats were randomized into 7 groups, with WIT of 0, 10, 15, 20, 30, 45, 60 minutes respectively. All specimens were investigated by light, electron microscopy, and histochemistry stain. 6, 24, and 48 hours after orthotopic liver transplantation(OLTx) ,the graft morphology was observed. Results The donor liver from non-heart-beating donors (NHBO) underwent ischemia injury both in the warm ischemia period and in the reperfusion period. Morphological changes were positively related to warm ischemia time in a time-dependent manner during the reperfusion period. There was a histocytic degeneration of different degree within 30 minutes warm ischemia. Although becoming more severe with the prolongation of warm ischemia time within this period, there was no obvious hepatocyte necrosis in any specimens. In WIT 45 min group, small focal necrosis occurred which was found in central area of hepatic lobule first. In 60 min group, patchy or diffused necrosis was observed and the area was gradually extended, while hepatic sinusoid endothelial cell obviously swelled to be bleb or balloonlike, hepatic sinusoid was obstructed and microcirculation was in disorder. Conclusion Rat liver graft undergoing warm ischemia injury is on the reversible stage within 30 minutes warm ischemia time by histological, histochemistry and ultrastructural dynamic observation. 45 min is a critical point of rat liver graft to endure warm ischemia injury, and when WIT was over 60 min, the damage is irreversible.

Adolescent ; Adult ; Antigens, CD34 ; blood ; Case-Control Studies ; Eosinophils ; Female ; Humans ; Interleukin-5 ; blood ; Leukocyte Count ; Male ; Middle Aged ; Rhinitis, Allergic, Perennial ; blood ; Young Adult

Objective To evaluate the efficacy and safety of therapeutic drug monitoring (TDM ) based vancomycin dose adjustment in patients with gram‐positive infections .Methods A cohort study was designed with 128 inpatients undergoing TDM in Huashan Hospital from January 2005 to September 2014 .The clinical data of these patients were used to analyze the efficacy and safety of vancomycin therapy by Cox model and survival analysis .Results The patients undergoing TDM‐based dose adjustment had a higher daily dose and blood trough concentration ,which may lead to better bacteriological efficacy and overall efficacy .Cox proportional hazards model analysis showed that TDM‐based dose adjustment is a protective factor .No safety‐related risk factor was found .Conclusions TDM‐based vancomycin dose adjustment is important for patients to achieve better outcomes in fighting gram‐positive infections .

Objective To investigate the role of IQ domain GTPase-activating protein 1 (IQGAP1) in angiotensin Ⅱ (Ang Ⅱ)-induced podocyte apoptosis and the underlying mechanism.Methods Differentiated mouse podocytes were exposed to Ang Ⅱ at different concentrations for 6 h or at 10-8 mol/L for variable incubation time.Podocyte apoptosis was assessed by flow cytometry.Expression of IQGAP1 was analyzed by immunofluorescence and Western blotting.IQGAP1 siRNA and MAPK pathway inhibitors(10 μmol/L SB202190,25 μmol/L SP600125,10 μmol/L U0126) were further introduced to investigate the role of IQGAP1 and MAPK signalings in the process.And coimmunoprecipitation was used to evaluate the interaction between ERK1/2 and IQGAP1.Results (1)Ang]] promoted podocyte apoptosis in a dose-and time-dependent manner.(2) IQGAP1 was located in celluar membrane and cytoplasm of cultured podocytes.Exposure to Ang Ⅱ stimulated IQGAP1expression in a dose-and time-dependent manner,and elevated phosphorylation of p38,JNK,and ERK1/2 simultaneously.(3) Pretreatment with SB202190,SP600125,or U0126 dramatically prevented Ang Ⅱ-promoted podocyte apoptosis respectively (P ＜ 0.05).However,the protein level of IQGAP1 was not altered.(4) Knockdown of IQGAP1 with siRNA obviously prevented Ang]Ⅱ-induced apoptosis of podocytes(P ＜ 0.05) and reduced Ang Ⅱ-induced phosphorylation of ERK1/2(P ＜ 0.05),but not that of p38,JNK.This was accompanied by a reduced interaction between ERK1/2 and IQGAP1(P ＜ 0.05).Conclusion IQGAP1 contributes to Ang Ⅱ-induced podocyte apoptosis by interacting with the ERK1/2 signaling protein.

Objective:To construct recombinant lentiviral vectors harboring interference RNA ( RNAi ) targetting murine TNF-αgene,so as to lay the foundation on the RNAi gene therapy.Methods: Three small interfering RNA ( siRNA) sequences targeting murine TNF-αgene ( siRNA1,siRNA2,siRNA3) and negative-control siRNA were designed and synthesized.The inhibition effects of siRNAs on TNF-α,IL-1βand IL-6 secretion of LPS-stimulated RAW264.7 macrophages were observed using real-time PCR and ELISA methods.DNA oligo was designed and synthesized according to the most effective siRNA 2 sequence.The recombinant lentiviral shuttle plasmid expressing short hairpin RNA ( shRNA) was constructed and sequenced.The lentiviral shuttle plasmids with packaging plasmids were transfected into 293T cells to produce lentiviral particles.Results: ①The TNF-αmRNA relative expression levels of siRNA1, siRNA2 and siRNA3 were 0.24±0.01,0.16±0.02,0.19±0.01 respectively,significantly lower than that of negative control (0.95± 0.02) (F=531.3,P<0.001).The inhibition rates at mRNA level were 74.26%,83.09%,79.93%,respectively comparing with negative control.No significance was observed in IL-1βor IL-6 mRNA relative expression change after TNF-αsiRNA transfection ( P>0.05).②The TNF-αprotein expression levels of siRNA1,siRNA2 and siRNA3 were (23.95±1.21),(17.27±1.46),(19.07± 1.57)ng/ml respectively,significantly lower than that of negative control (35.37±2.93)ng/ml (F=18.1,P=0.000 6<0.001).The inhibition rates of protein expression were 32.29%, 51.16%, 46.08%, respectively comparing with negative control.③The PCR product electrophoresis showed that recombinant vectors yielded 343 bp fragments,non-constructed vectors yielded 306 bp fragments.DNA sequencing partially showed insertion sequence.④Lentiviral particles were obtained by transfecting 293T cells with recombinant lentiviral shuttle plasmids and lentiviral packaging plasmids.Cells grew well during virus production with strong fluorescence expression.The titer of concentrated virus was 2×106 TU/μl.Conclusion:The lentiviral vector harboring RNAi targeting murine TNF-αgene has been successfully constructed.

Background and purpose:A pressing obstacle in clinical chemotherapy is drug resistance in breast cancer.A nano-delivery system,which has many advantages as a drug carrier,such as carrying anticancer drugs,can be used effectively to overcome drug resistance in tumors.This paper examined a new nano-delivery system,called calcium phosphate and glycerophosphocholine-mPEG(CAP/GPC-MPEG)composite nanoparticle and its influence on the cellular drug uptake of BCRP-over expressing mitoxantrone(MIT)-resistant breast cancer cell MCF-7/MIT.This paper will also examine its effect on overcoming drug resistance in the MCF-7/MIT cells.Methods:After the calcium phosphate and GPC-mPEG composite nanoparticles were designed and prepared,the entrapment efficiency and in vitro drug release of mitoxantrone-loaded nanoparticles were investigated.Quantitative comparisons were made between cellular uptake of drug-loaded nanoparticles and free drugs.Finally,a confocal laser scanning microscopy Was used to compare the subcellular distribution of drug-loaded nanoparticles and the free drugs.Results:Calcium phosphate and GPC-mPEG composite nanoparticles were nanoporous spherical particles with diameters between 50-100 mn.The MIT-loaded nanoparticles have an entrapment efficiency of(89.45±0.05)%.Although the drug-loaded nanoparticles showed an initial burst of drug release,it was followed by a more sustained release.The concentration of mitoxantrone was 1.89 times treated with MIT-loaded nanoparticles for 1 h compared to that treated with free mitoxantrone for 1 h in MCF-7/MIT cells.and which was 2.33 times in MCF-7 cells.Fluorescent red mitoxantrone appeared in the cytoplasm and nucleus of the MCF-7 and MCF-7,MIT cells treated with MlT-loaded nanoparticles whereas it is almost undetected in both cells treated with free mitoxantrone.Conclusion:Calcium phosphate and GPC-mPEG composite nanoparticles Can promote the cellular uptake and entering of mitoxantrone to the nucleus in MCF-7 and its corresponding BCRP-over expressing MIT-resistant MCF-7/MIT breast cancer cell lines.This nanoparticle is a potential nano-carrier for overcoming drug resistance in tumors.