Objective To understand the level of tulnor necrosis factor-α(TNF-α)and asymmetric dimethylarginine (ADMA) in serum of healthy adults and primary hypertension patients with different left ventricle,and to explore the role of TNF-α and ADMA in the pathophysiological mechanism of heart damage due to hypertension.Methods Thirty health adults were recruited as control.Based on the left ventricular mass index(LVMI)and relative wall thickness(RWT),66 patients of hypertension were divided into 4 groups:normal left ventricle group with normal LVMI and RWT,concentric remolding group with normal LVMI and incremental RWT,typical concentric hypertrophy group with incremental LVMI and RWT,eccentric left ventricular group incremental LVMI and normal RWT.TNF-α was measured by radioimmunoassay and ADMA was measured through reversed phase high-performance liquid chromatography.Resuits TNF-α and ADMA increased with the severity of the left ventricle.Each left ventricle group was significantly higher than control group (P<0.01).The differences between left ventricle groups were statistically significant (P<0.01).Conclusions TNF-α and ADMA may participate in the development of left ventricle.

Objective To evaluate the protective effect of prior ?-adrenergic blocker therapy to patients who have PCI therapy.Methods We analyzed 210 consecutive patients undergoing ?-adrenergic blocker,of whom 105 did ?-adrenergic blocker therapy,105 had not.CK-MB、E、NE were tested before PCI,and 6~8 h,16~24 h after PCI.Procedural complications in hospital and 1-year outside outcomes were evaluated.Results (1)There was no significant difference between the two groups on CK-MB、E、NE.(2)Both the in-hospital(2.1% vs 4.1%)and one year (5.5% vs 7.1%)mortality was lower in ?-group than in no-? group.Conclusion Prior ?-adrenergic blocker therapy can reduce the incidence of cardic events.

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0.05).Conclusion DTI can noninvasive detect the potential disorder of corpus eallosum in vivo,thus providing useful information to differentiate the cerebral ischemia disease from multiple sclerosis.

Objective To construct expression vectors that Renilla reniformis (Rluc) fused with neurotensin type 1 receptor (NTSR1),and to investigate the interaction between NTSR1 and other receptors,as well as intercellular signal transduction mechanism mediated by neurotensinl-R.Methods The human NTSR1 gene was amplified by PCR using the plasmid pcDNA3.1-hNTSR1 as template.The PCR product was digested,ligased with the plasmid pRluc and then be transformed into the competent cell Top10.The construct was identified by DNA sequencing.The recombinant plasmid was transiently transfected into human embryonic kidney 293 ( HEK293 )cells,and the expression of pRluc-hNTSR1-pcDNA3.1 was detected by confocal microscopy and Western blot.Results The fragment of 1257 bp was amplified by PCR,and the DNA sequences were identical with the gene in GenBank ( NM_002531 ).Western blot showed a band about 90kDa.Confocal microscopy showed that NTSR1 was expressed on the plasma membrane.Conclusion The pRluc-hNTSR1-pcDNA3.1 eukaryotic expression vector is successfully constructed,and the expression vector can be used to investigate the interaction between NTSR1 and other receptors,as well as intercellular signal transduction mechanism mediated by neurotensinl-R,which will provide new target for drug development.

Objective To survey the multi-drug resistance among the isolates of methicillinresistant Staphyloeocus from lower respiratory tract in post-cardiothoracic surgery patients and the risk factors contributing to infection aggravation.Methods The clinical data of lower respiratory tract infections were reviewed retrospectively from June 2011 to December 2012.The antimicrobial susceptibility testing was analyzed according to CLSI breakpoints 2010.Results A total of 323 clinical isolates was identified in 264 patients,including gram-positive coccus (126 strains) and gram-negative bacillus (197 strains).The prevalence of methiciIlin-resistant srtains was 88.5 ％ (54/61)in Staphylococus.Aureus (MRSA),and 77.3％ (17/22) in Staphylococcus epidermidis (MRSE).No VISA or VRSA strain was identified.One enterococcal strain was resistant to Vancomycin and teicoplanin.MRSA/MRSE were also isolated from hands and nasal vestibule of nurses,article surfae,pipeline/interface of breathing machine and ward atmosphere.Conclusions Patients after cardiothoracic operation are susceptible to lower respiratory tract infection with gram positive cocci,which should be paid more attention to airway management.Rational administration,sterile operation and antimicrobial therapy are effective ways for control of multi-durg resistance.

Objective To investigate the effects of eardiopulmonary bypass(CPB)on plasma nitric oxide (NO)and asymmetric dimethyl arginine(ADMA)concentrations in patients with congenital heart disease complicated with pulmonary hypertension undergoing open heart surgery.Methods Eighteen ASA Ⅱ or Ⅲ patients aged 11-40 yr weighing 26-59 kg undergoing open heart surgery under CPB were divided into 3 groups according to pulmonary arterial systolic pressure(PASP)(n=6 each):group Ⅰ PASP<30 mm Hg;group Ⅱ PASP 30-50 mm Hg and group Ⅲ PASP>50 mm Hg.Arterial blood samples were taken before induction of anesthesia (To,baseline),at the start and termination of CPB(T1,2)and 3,6,24 h after CPB(T3-5)for determination of plasma NO and ADMA concentrations.Results The three groups were comparable with respect to M/F sex ratio,age,body weight and CPB time.The plasma ADMA concentrations were significantly increased while NO concentrations were significantly decreased at termination of CPB(T2)and 3 and 6 h after CPB(T3,4)as compared with the baseline at T0 in group Ⅱ and Ⅲ.The plasma ADMA concentration were significantly higher and No concentrations were significantly lower at all time points in groupⅡand Ⅲthan in group Ⅰ.Conclusion CPB can increase plasma ADMA concentration and decrease plasma NO concentration in patients with congenital heart disease complicated with pulmonary hypertension undergoing open heart surgery.

Objective To explore the effects of different concentrations of fluoride, aluminum alone and in combination exposure on mice parietal bone cell subclone 14 (MC3T3-E subclone 14), and to elucidate the pathogenesis of endemic fluorosis. Methods The proliferation of MC3T3-E1 cells exposed to 10-9 -10-3 mol/L NaF alone, 50 ?mol/L NaF and 5 ?mol/L AlCl3 alone and in combination ,was measured by CCK-8, and the change of cell cycle was measured by flow cytometry after treatment with various concentrations of fluoride and aluminum. Results Fluoride alone did not promote osteoblast MC3T3-E1cells proliferation, higher concentration fluoride inhibited MC3T3-E1 cells proliferation. Fluoride and aluminum combined exposure (50 ?mol/L NaF +5 ?mol/L AlCl3) stimulated proliferation of MC3T3-E1 cells (P

Objective To develop a model of inflammatory bowel disease in rats induced by 2,4,6-trinitrobenzenesulfonic acid(TNBS).Methods Fifty Wistar rats were randomly divided into three groups:model,mock model and normal group.2% TNBS,50% ethanol and physiological saline were administered per-rectum to each of the three groups,respectively.Feces,psychosis and appetite were observed,body weight and food eaten were recorded daily.Rats were killed after 3,6 and 14 d,and the colons were isolated and histological findings were examined.Results On the first day,rats in the model group had loose and bloody stools,and the symptoms lasted for about 8 days.Body weight and food eaten were markedly decreased for 7-10 days.Obvious pathological changes in the colon were observed on third day and heavier on sixth day,characterized by mucosal necrosis and transmutable inflammation.In the mock model group,the rats had loose stools on first day,and recovered on second day.Light pathological changes were found on third day.In the normal group,no pathological changes were found in colon.Conclusion Rats treated with TNBS showed obvious characters of inflammatory bowel disease,which could be used as a model in study on etiopathogenesis and evaluation effects of medicines.

Objective This study assessed whether the best overall response rate(ORR) of cetuximab combined with oxaliplatin,leucovorin and fluorouracil/Xeloda was superior to that of this method alone as first-line treatment for metastatic colorectal cancer.The influence of KRAS mutation status was investigated.Methods Patients received cetuximab(400mg/m2 initial dose followed by 250mg/m2,wk thereafter)less than 2 times plus chemotherapy(oxaliplatin 130mg/m2 on day 1,plus leucovorin 200mg/m2 and fluorouracil as a 400mg/m2 bolus followed by a 600mg/m2 infusion during 22 hours on days 1 and 2) or chemotherapy alone.Treatment was continued until disease progression or unacceptable toxicity.KRAS mutation status was assessed in the subset of patients with assessable tumor samples.Results The confirmed ORR for cetuximab plus oxaliplatin,leucovorin and fluorouracil/Xeloda was higher than that with alone(42.86% vs 21.74%).A statistically significant increase in the odds for a response with the addition of cetuximab to oxaliplatin,leucovorin and fluorouracil/Xeloda could be established.In patients with KRAS wild-type tumors,the addition of cetuximab to oxaliplatin,leucovorin and fluorouracil/Xeloda was associated with a clinically significant increased chance of response(ORR 54.55% vs 21.74%) and a lower risk as compared with chemothrapy alone.Cetuximab plus oxaliplatin,leucovorin and fluorouracil/Xeloda was generally well tolerated.Conclusion The clinical effcacy of chemothrapy(oxaliplatin,leucovorin and fluorouracil/Xeloda) plus cetuximab is better than only chemothrapy.KRAS mutational status was shown to be a highly predictive selection criterion in the treatment decision regarding the addition of cetuximab to oxaliplatin,leucovorin and fluorouracil/Xeloda for previously untreated patients with metastatic colorectal cancer.