Objective To investigate the clinical distribution and antibacterial drug susceptibility of mucoid Pseudomonas aeruginosa (mPa).Methods By looking at the patients’general information,disease information and the information of anti-microbial usage,cases of 53 strains of non-repetitive mucoid Pseudomonas aeruginosa were collected from hospitalized pa-tients from Jan 2013 to Dec 2013,and drug susceptibility were analyzed.Results A total of 53 strains of mucoid Pseudo-monas aeruginosa were isolated from sputum specimen,mainly elderly patients with a mean age of 66.7±9.1 years old;50 patients had chronic history of respiratory infections,all patients were used during the hospital stay of two or more kinds of antibiotics,used jointly only 11 cases of macrolides.All strains to commonly used antimicrobial agents showed a higher sen-sitivity in vitro,in addition to ticarcillin/clavulanate (64.2%),cefepime (60.4%),other drug sensitivity was higher than 70%.Conclusion Mucoid Pseudomonas aeruginosa was susceptible to chronic respiratory infection history of the elderly,its antimicrobial susceptibility was high in vitro,the use of antimicrobial agents in clinical was combined therapy compared,but utilization rate of macrolides drugs was low.

Objective To discuss the efficacy of alprostadil and levocarnitine in treatment of chronic renal failure combined with heart failure.Methods Totally 80 patients with chronic renal failure complicated with heart failure were selected,and randomly divided into two groups.The control group (39 cases) was given alprostadil.The observation group (41 cases) was given alprostadil and levocarnitine.The efficacy of alprostadil and levocamitine in treatment of chronic renal failure combined with heart failure was evaluated by cardiac fimction indexes,renal function indexes,SF-36 scale score,and adverse reaction during the treatment.Results Before treatment,there was no statistical significance on CO,CI,MVO,and EF between two groups.After treatment,the CO,CI,and MVO were decreased and lower in the observation group (P ＜ 0.05).The EF was increased in the observation group and higher than that of the control group (P ＜ 0.05).The EF had no changes in the control group.Before treatment,there was no statistical significance on CysC,BUN,and SCr between two groups before treatment,without statistical significance.After treatment,CysC,BUN,and SCr were decreased in two groups and lower in the observation group (P ＜ 0.05).Before treatment,there was no statistical significance on SF-36 scores between two groups.After treatment,the physiological function,physical function,and general health were higher than those of the control group (P ＜ 0.05).There was no statistical significance on the rest of the scores.During treatment,there was no statistical significance on adverse reaction between two groups.Conclusion Alprostadil and levocarnitine had a good curative effect on chronic renal failure combined with heart failure.It could improve the heart function by reducing cardiac load,improve the renal function by increasing glomerular filtration rate and improve the quality of life with good safety.It is worthy of clinical application.

When the synergy medicine education training model increasingly sophisticated,the cultivation of postgraduates of Clinical Medicine research capability has become increasingly prominent.While synergy medical education reforms will train postgraduates to become qualified doctors,we must also train students to master the basic method of clinical research and have basic research capabilities.This paper mainly discusses the measures and mechanisms for cultivating the clinical degree students' research ability from the follow aspects:the construction of innovative training mode of clinical medicine graduate students' scientific research ability,establishment of a joint training mechanism of multi tutor for clinical medical students,Strengthening instructors to guide the process of quality control,strengthening the research project research proposal assessment and increasing the graduate degree thesis review and reply process supervision and so on.

AIM: To explore the characteristics of motor evoked potential(MEP) and cortical excitability in Parkinson's disease by transcranial magnetic stimulation(TMS).METHODS: 20 normal volunteers were enrolled as control(group A),with the average age of(62.3?16.7) year old ranged from 52 to 79 years including 12 males and 8 females.MEP were assessed and compared separately between left and right hemispheres.21 patients with Parkinson's disease(PD) in asymmetry symptoms were performed in this study(group B),with the average age of(63.3?16.7) year old ranged from 46 to 80 years including 12 males and 9 females.UPDRS motor scores(UPDRSⅢ) were assessed before the check of cortical excitability(MEP).Motor evoked potentials(MEP) was assessed and compared separately on the minor and the serious bodyside,compared to control group.RESULTS: The indexes of MEP from both sides of normal control had no significant diversity.Amp was increased and both rest motor threshold(RMT) and cortical latency(CL) were also decreased significantly in PD patient compared to the normal control.On the serious side of PD,RMT decreased significantly compared to the minor side.Amp,CL and central motor conduct time(CMCT) changed without significant diversity between minor and serious bodyside.CONCLUSION: The motor cortical excitability is increased in PD patients.The excitability is higher with the more serious symptom side.The character of MEP in PD patients may be helpful to make a diagnosis and evaluate the severity of symptoms.

Objective To analyze the resenilin-1 (PS-1) gene mutations in Alzheimer' s disease (AD) patients and investigate the influence of the initiation codon mutation on the mRNA expression of PS-1 and amyloid precursor protein (APP) genes and the expression of PS-1 proteins.Methods (1) All 111 AD patients were enrolled by the Department of Neurology,Second Affiliated Hospital,College of Medicine,Zhejiang University from July 2004 to June 2010.Mutations in the 13 exons and flanking regions of PS-1 gene were examined by direct sequencing.(2) cDNAs encoding full-length wild-type and mutant (c.1A ＞G) PS-1 were subcloned into enhanced green fluorescent protein.Levels of the mRNA expression of PS-1 and APP genes and PS-1 proteins expression in the transfected cells were detected by quantitative real-time PCR and Western blot,respectively.Results A new heterozygous initiation codon mutation changing from ATG to GTG in one individual was identified.Compared to the control groups,the mRNA expression of the mutant PS-1 gene in HEK293 and N2a was significantly lower than the normal PS-1 gene(116.8 ± 3.9 vs 49.5 ±3.3,t =13.27,P ＜0.01 ;69.0 ± 1.9 vs 29.5 ± 1.3,t =17.20,P ＜0.01) and the APP gene was not obviously altered.The proteins were detected by Western blot analysis in HEK293 cells but not in N2a cells.Conclusions Since we only identified one novel heterozygous initiation codon mutation (from ATG to GTG),mutations in PS-1 are likely to be rare in AD patients.Initiation codon mutation would reduce the expression of PS-1 proteins.Inactivation of some of the PS-1 proteins could be insufficient to lead to AD and could be more likelv to act as a risk factor.

Objective To evaluate the prevalence of the DJ-1 mutation in early-onset Parkinson's disease (EOPD) patients,and analyzed the association between the certain polymorphic marker g.168_185del in intron1 and Parkinson' s disease (PD).Methods We screened all 7 exons and exon-intron boundary regions of DJ-1 by PCR and direct nucleotide sequencing in 90 Chinese patients with EOPD.We also compared the allele and genotype frequencies of the g.168_185del polymorphism between EOPD patients and controls.Results We found no causative DJ-1 mutations in our cohort of Chinese EOPD patients.But we did identified 4 known polymorphic variants,including the g.168_185del in intron 1,g.5027G ＞ A (rs17523802),g.5065T ＞ C (rs226249),and g.5094C ＞ T (rs11121064) within exon 1.Del/Ins frequencies of the g.168_185 del polymorphism were 11.1％ (10/90)and 13.3％ (14/105) in EOPD group and normal group,respectively.Ins/Ins frequencies were 88.9％ (80/90) and 86.7％ (91/105),thex2 and P value of genotype frequency were 0.222 and 0.669 between EOPD patients and controls,respectively.The insert frequencies were 94.4％ (170/180)and 93.3％ (196/210) in EOPD patients and controls,the deletion frequencies were 5.6％ (10/180) and 6.7％ (14/210),thex2 and P value of allele frequency were 0.207 and 0.679 between EOPD patients and normal,respectively.Furthermore,the P value of genotype and allele frequencies were 0.736 and 0.744 between familial EOPD patients and controls,respectively;P values of genotype and allele frequencies were 0.847 and 0.852 between sporadic EOPD patients and control group,respectively.There was no statistical difference between groups.Conclusion Mutations in DJ-1 are uncommon in Chinese EOPD patients,and no association is observed between the DJ-1 intron 1 g.168_185del polymorphism and risk of PD.

Objective To construct the eukaryotic expression vector encoding IT15 gene and detect its expression in SH-SY5Y cells.Methods The exon1 of IT15 gene was amplified from genomic DNA isolated from a healthy adult and a Huntington disease patient lymphoblastoid cell lines by PCR.PCR products were subcloned into eukaryotic expression vector pEGFP-C1.The SH-SY5Y cells were transiently transfected with the recombinant plasmids and observed under fluorescence microscope.Western blot was used to detect the expression of the fusion protein.Results PCR products had approximately 170 and 310 bp specific segments.The recombinant eukaryotie expression plasmids were confirmed by restriction endonuclease analysis and sequencing.The N-terminal fragment of normal huntingtin primarily localized in the cytoplasim of SH-SY5Y cells,while the N-terminal fragment of mutant huntingtin aggregated both perinuclearly and intranuelearly.Conclusions The recombinant eukaryotic expression vectors encoding wild type and mutant IT15 gene fragments are useful for studying pathogenesis of Huntington disease.The Nterminal fragment of mutant huntingtin aggregats both perinuclearly and intranuclearly,which could be important for Huntington disease pathophysiology.

Objective:To determine the contents of paraceltamol and caffeine in New compouad Folium Isatidis Tablets simultaneously by HPLC. Methods:The determination was carried out with C 18 chemical bonded silica gel as a solid phase, methanol-water (25∶75) as a mobile phase and UV deterction wavelength at 215 nm. Results: The average recovenies of the added sample were 99.6%( RSD=0.67, n=5) for paracetamol and 99.3%(RSD=0.58, n=5) for caffine, There was a good linear relationship between the concentration and absorption area value in the rang of 1.6?g～6.4?g for paractamol or 0.16?g～0.64?g for caffeine.Conclusions: The method is simple, quick and accurate.

Objective:To express and purificate catalytic domain of murine?-1,3-galactosyltransferase and provide the feasible method in the tumor cell surface production ?-gal epitopes..Methods:This research established expression system in pET-15b to express catalytic domain of murine ?-1,3-galactosyltransferase,then identified its activity by HPLC with anion exchange column.Results:(1)Constructed successfully recombinant ?-1,3-galactosyltransferase catalytic domain with His-tag.(2)?-1,3-galactosyltransferase with His-tag in a soluble form was expressed and purificated effeciently.(3)Its activity by HPLC with anion exchange column showed.Conclusion:This research shows ?-1,3-galactosyltransferase in a soluble form has been expressed successfully.

Objective To identify a locus at chromosome coding for hereditary palmoplantar keratoderma of three Chinese pedigrees.Methods The genome scan was conducted with microsatellite markers on chromosome 12(D12S85、D12S368、D12S83、D12S345)and 17(D17S1868、D17S787、D17S1857、D17S798、D17S944、D17S949)respectively on the ABI 3100 Genetic Analyzer(Applied Biosystems).Two-point LOD score was calculated.Results The maximum two-point LOD score 6.59 and 5.96 at ?=0.1 were obtained at D17S1868 and D17S787 on chromosome 17q12～q21.It is an evidence of linkage between this disease and KRT9 which has been mapped within the region.Conclusion There is a locus responsible for this disease on chromosome 17q12～q21.