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OBJECTIVE@#To investigate the effect of inhibitor of growth protein-2 (Ing2) silencing on angiotensin Ⅱ (AngⅡ)-induced cardiac remodeling in mice and explore the underlying mechanism.@*METHODS@#An adenoviral vector carrying Ing2 shRNA or empty adenoviral vector was injected into the tail vein of mice, followed 48 h later by infusion of 1000 ng · kg-1 · min-1 Ang Ⅱ or saline using a mini-osmotic pump for 42 consecutive days. Transthoracic echocardiography was used to assess cardiac geometry and function and the level of cardiac hypertrophy in the mice. Masson and WGA staining were used to detect myocardial fibrosis and cross-sectional area of cardiomyocytes, and myocardial cell apoptosis was detected with TUNEL assay. Western blotting was performed to detect myocardial expressions of cleaved caspase 3, ING2, collagen Ⅰ, Ac-p53(Lys382) and p-p53 (Ser15); Ing2 mRNA expression was detected using real-time PCR. Mitochondrial biogenesis, as measured by mitochondrial ROS content, ATP content, citrate synthase activity and calcium storage, was determined using commercial assay kits.@*RESULTS@#The expression levels of Ing2 mRNA and protein were significantly higher in the mice with chronic Ang Ⅱ infusion than in saline-infused mice. Chronic infusion of AngⅡ significantly increased the left ventricular end-systolic diameter (LVESD) and left ventricular end-diastolic diameter (LVEDD) and reduced left ventricular ejection fraction (LVEF) and left ventricular fractional shortening (LVFS) in the mice. Ing2 silencing obviously alleviated AngⅡ-induced cardiac function decline, as shown by decreased LVEDD and LVESD and increased LVEF and LVFS, improved myocardial mitochondrial damage and myocardial hypertrophy and fibrosis, and inhibited cardiomyocyte apoptosis. Chronic AngⅡ infusion significantly increased myocardial expression levels of Ac-p53(Lys382) and p-p53(Ser15) in the mice, and Ing2 silencing prior to AngⅡ infusion lessened AngⅡ- induced increase of Ac-p53(Lys382) without affecting p53 (ser15) expression.@*CONCLUSION@#Ing2 silencing can inhibit AngⅡ-induced cardiac remodeling and dysfunction in mice by reducing p53 acetylation.
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Animals , Mice , Angiotensin II , Tumor Suppressor Protein p53 , Acetylation , Stroke Volume , Ventricular Remodeling , Ventricular Function, Left , Myocytes, CardiacABSTRACT
Objective To analyze the antimicrobial resistance profile of clinical isolates in Shanghai Xinhua Hospital Chongming Branch affiliated to Shanghai Jiaotong University School of Medicine , a member of China Antimicrobial Resistance Surveillance System, during 2015, for the purpose to facilitate rational antimicrobial therapy. Methods Strain identification?and?susceptibility?testing?were?carried?out?for?the?clinical?isolates?using?MicroScan?WalkAway?96?Automated?Systems and Kirby-Bauer method. Results In 2015, a total of 1815 isolates were collected, including gram-negative bacteria (73.2 %) and gram-positive bacteria (26.8 %). The top three frequently isolated species were Escherichia coli, Klebsiella pneumoniae, and Pseudomonas aeruginosa. ESBL-producing strains were found in 36.3 % of the Escherichia coli isolates, 12.6 % of the Klebsiella (K. pneumoniae and K. oxytoca) isolates, and 28.0 % of the Proteus mirabilis isolates. The prevalence of carbapenem-resistant strains was 0.69 % in Enterobacteriaceae isolates. The prevalence of methicillin-resistant strain was 29.1 % in S. aureus, and 61.4 % in coagulase-negative Staphylococcus isolates. No more than 15 % of the Enterobacteriaceae isolates and no more than 20 % of the P. aeruginosa and Acinetobacter isolates were resistant to carbapenems. No vancomycin-or linezolid-resistant strains were found in Enterococcus or Staphylococcus. Conclusions Antibiotic-resistant clinical isolates are a serious threat for clinical antimicrobial treatment. We should pay more attention to such urgent situation and rational use of antibiotics.
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Objective To observe the influence of optimized nursing process on the clinical effect and quality of life of patients with cerebral infarction received intravenous thrombolysis.Methods Sixty-two cerebral infarction patients with thrombolytic therapy in Panzhihua Central Hospital were treated as control group from January 2013 to June 2014,74 cases cerebral infarction patients with thrombolytic therapy as the observation group from July 2014 to October 2015.The control group received routine nursing,the observation group were given optimized nursing process on the basis of routine nursing.The clinical effect and quality of life were compared between the two groups.Results The triage time,referral time and hospital stay time of the observation group were significantly shorter than the control group,the differences were statistically significant (P ＜0.05).The effective rate in the control group was 70.97％,that of the observation group was 87.84％,the effective rate in observation group was significantly better than that of the control group,the difference was statistically significant (P ＜0.05).Compared with before treatment,the life quality of two groups were significantly improved after treatment,the difference was statistically significant (P＜0.05);after treatment,the quality of life in observation groups were better than that of the control groups,the difference is statistically significant (P＜0.05).Conclusion Nursing process optimization can effectively improve the therapeutic effect for the patients with cerebral infarction intravenous thrombolytic therapy,shorten the treatment time and hospitalization time,and can significantly improve the patient' s quality of life.It is valuable for clinical application.
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Objective: To explore the effects of fosinopril on oxidative stress and vascular function in experimental rats with spontaneous hypertension. Methods: The rats were divided into 3 groups: Control group, with normal healthy rats (n=15), Spontaneous hypertension (SH) group (n=15), SH rats received intragastric administration of normal saline and Treatment group (n=15), SH rats received intragastric administration of fosinopril 10mg/(kg?d). All animals were treated for 7 weeks. Caudal artery systolic blood pressure (SBP) was measured at each week. blood levels of superoxide dismutase (SOD), reactive oxygen species (ROS), malonaldehyde (MDA) and NO2-/NO3- were determined in different groups respectively after 7 weeks. Moreover, thoracic aorta was taken to examine its diastolic reactive rate by acetylcholine (Ach)/sodium nitroprusside (SNP) induction. Results: From the 1st week until the end of experiment, compared with SH group, Treatment group had decreased SBP,P<0.05. With 7 weeks treatment, compared with Control group, SH group had decreased SOD activity, while increased protein levels of MDA and ROS, allP<0.05; compared with SH group, Treatment group showed elevated SOD activity (P=0.010), while reduced protein levels of MDA (P=0.021) and ROS (P=0.009). Compared with Control group, SH group had the lower content of NO2-/NO3-(P<0.001); both SH group and Treatment group had decreased diastolic rates by Ach/SNP induction,P<0.05. Compared with SH group, Treatment group presented the higher content of NO2-/NO3- and higher diastolic rate by Ach induction, allP<0.001. Conclusion: Fosinopril could improve vascular diastolic function via anti-oxidative stress in experimental SH rats, which might be one of its anti-hypertensive mechanisms.
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Objective:To investigate the anti-inflammation effects by activation of the cholinergic anti-inflammatory pathway and its mechanisms in non-alcoholic steatohepatitis (NASH)model mice.Me-thods:6-week-old male C57BL/6J (B6)mice were randomly divided into four groups:the first group was normal mice,injected with saline;the second group was normal mice,injected with nicotine;the third group was NASH model mice,injected with saline;the fourth group was NASH model mice,injec-ted with nicotine.The experimental mice were fed with either standard chow (SC)or high-fat and high-fructose (HFHF)for 17 weeks to generate an NASH model mice.The mice received injection once daily for 3 weeks [nicotine dose,400 μg/kg].Then,their pathological characteristics and function of the liver were assessed.The expressions of interleukin-6 (IL-6)and tumor necrosis factor-α(TNF-α)in se-rum were analyzed by enzyme linked immunosorbent assay (ELISA).The expressions of alpha 7 nicotinic acetylcholine receptors (α7nAChR),Toll-like receptors-4 (TLR-4)and nuclear factor κB of phosphory-lation (p-NF-κB)in Kupffer cells were determined by Western blot and immunofluorescence assays.Re-sults:We successfully generated NASH model mice by imitating the high-fat and high-fructose dietary style of NASH patients.The results of our investigation demonstrated that nicotine could reduce signifi-cantly the levels of IL-6,and TNF-αin serum (P <0.05).The expression of p-NF-κB protein in the group which was NASH model mice injected with nicotine declined significantly as compared with the group which was NASH model mice injected with saline (P <0.05).And the expression of α7nAChR protein elevated significantly conversely (P <0.05 ).Conclusion:Activation of the cholinergic anti-inflammatory pathway could inhibit the release of inflammatory factors as TNF-αand IL-6 in NASH model mice,and the mechanism for the inhibition of inflammatory was mediated by NF-κB pathway.
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OBJECTIVE To approach pathogens and precaution strategy of nosocomial pneumonia in patients with myasthenia gravis.METHODS Forty cases of myasthenia gravis from Jan 2003 to Dec 2006 in a certain hospital were involved in the retrospective review.Patients with myasthenia gravis and nosocomial pneumonia were selected out in accordance with diagnostic criteria of nosocomial pneumonia.Risk factors and pathogens of infection were analyzed.Precaution strategy was formulated.RESULTS There were 26 patients with nosocomial pneumonia among 40 cases of myasthenia gravis.Pathogens isolated from sputum culture were all drug resistant strains.Gram-negative bacteria such as Klebsiella pneumoniae,Pseudomonas aeruginosa,Escherichia coli,etc were the most,accounted for 51.85%(84 strains).The next was Gram-positive bacteria,accounted for 33.33%(54 strains).Fungi ranked the third,accounted for 14.81%(24 strains).CONCLUSIONS Precaution and cure measurement should be adopted to prevent and control the occurrence of nosocomial pneumonia in patients with myasthenia gravis.
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Objective To explore the molecular mechanism of bilirubin in the hippocampus of the newborn rats with hyperbilirubinemia. Methods Hyperbilirubinemia model was established. The expression levels of Fas protein and N methyl D aspartate (NMDA) receptor and the apoptosis rate of nerve cells in rat hippocampus were detected with immunochemistry, TUNEL method and cytometry. Results Histological changes of nerve cells were found in hippocampal area of rats with hyperbilirubinemia. Significantly increased expression levels of Fas protein and NMDA receptor and apoptosis rate of nerve cells were positively correlated with the bilirubin level in rat brain tissues. Conclusion The bilirubin neurotoxicity is mediated by the excessive activation of NMDA receptor and participation of Fas system, which induces the apoptosis of nerve cells.