BACKGROUND: Cardiac fibrosis, which results from the loss of balance between synthesis and degradation of cardiac matrix component, is the structural foundation of the stiffness of damaged myocardial tissues. Astragalus membranaceus, a traditional Chinese herb, has multiple functions such as exerting a tonic effect on the heart to induce diuresis. However,the effect of astragaloside Ⅳ on cardiac collagen is poorly known in practice.OBJECTIVE: To observe the effects of astragaloside Ⅳ on myocardial collagen and cardiac function in ischemic rats and to investigate the dosage and time effects of astragaloside Ⅳ.DESIGN: A completely randomized grouping design and randomized controlled trial.SETTING: Department of Pediatrics, the Affiliated Hospital of Medical College of Qingdao University.MATERIALS: The study was conducted in the Encephalopathy Research Institute, Medical College of Qingdao University, from July 2003 to February 2004. Totally 132 Wistar rats of cleaning grade were randomized into three groups: control group (n=11), ischemic group (n=10) and astragaloside Ⅳ group (n=121).METHODS: Rats in control group had thoracotomy, but did not have their left anterior descending coronary artery ligated; rats in ischemic group had thoracotomy and had their left anterior descending coronary artery ligated to establish acute myocardial infarction model; rats in astragaloside Ⅳ group were given astragaloside Ⅳ after surgical ligature of left anterior descending coronary artery. The changes in hemodynamic parameters, cardiac function and myocardial collagen were determined. The dosage and time effects of astragaloside Ⅳ on myocardial collagen and cardiac function were observed.MAIN OUTCOME MEASURES: ① The dosage and time effect of astragaloside Ⅳ on the content of myocardial collagen in the left ventricle of rats with myocardial infarction; ② The dosage and time effects of astragaloside Ⅳ on hemodynamics and cardiac function of rats with myocardial infarction.RESULTS: One hundred rats entered the results analysis. There were 10 in control group and ischemic group, respectively, and 80 in astragaloside Ⅳ group. The five dosage groups of astragaloside Ⅳ [2.5, 5.0, 10.0, 15.0 and 20.0 mg/(kg·d)] and the five postoperative time points (3, 7, 14, 21 and 28 days) had eight rats for each. Astragaloside Ⅳ at a dose of 15.0 mg/kg per day was found to have the most marked effect on ischemic myocardium, so this dose was chosen for observing time effect. ① After administration of astragaloside Ⅳ, the content of collagen in myocardial tissues of the infarcted area of left ventricle, the serum concentration of carboxyterminal procollagen type Ⅰ propeptide and aminoterminal procollagen type Ⅲ propeptide decreased gradually with the increased dose of astragaloside Ⅳ and with the prolonged action time of astragaloside Ⅳ [15 mg/(kg·d)] (P ＜ 0.05-0.01). The serum concentration of carboxyterminal procollagen type 1 propeptide and aminoterminal procollagen type Ⅲ propeptide returned to the level of control at a dose of 10 mg·kg-1per day and at 21 days after astragaloside Ⅳ administration, respectively. The content of collagen in myocardial tissues of the infarcted area of left ventricle was higher than that of non-infarcted area (P＜ 0.01); there were no significant changes in the content of cardiac collagen of right ventricle and non-infarcted area of left ventricle before and after astragaloside Ⅳ administration. ② The cardiac function of ischemic rats significantly improved after astragaloside Ⅳ administration (P ＜ 0.05-0.01); cardiac output, heart rate, stroke volume,mean aortic pressure, systolic aortic pressure, and the stroke work of left ventricle gradually returned to the level of control with the increased dose of astragaloside Ⅳ and with the prolonged action time of astragaloside Ⅳ.CONCLUSION: Astragaloside Ⅳ can inhibit the proliferation of cardiac collagen and improve cardiac function in rats with myocardial infarction.The content of myocardial collagen gradually decreases and cardiac function gradually improves with the increased dose of astragaloside Ⅳ and the prolonged action time of astragaloside Ⅳ.

The spindle assembly checkpoint ( SAC) is an important monitoring mechanism to monitor the connection between centromeres and microtubules and to ensure proper chromosome separation in human .Mitotic arrest defective protein(Mad)family,as an important part of SAC,plays a crucial role in the process of mitosis. Mutations or altered expressions of Mad may lead to abnormal separations of chromosomes and play a partial role in tumorigenesis ,poor prognosis and chemotherapy drug resistance .

Objective To evaluate the relationship between calmodulin protein kinase Ⅱ (CaMK Ⅱ) and levosimendan against arrhythmias induced by myocardial ischemia-reperfusion (I/R) in rats in vitro.Methods Thirty male Wistar rats,weighing 250-300 g,were randomly divided into 3 groups (n =10 each) using a random number table:control group (group C),I/R group and levosimendan group (group L).Their hearts were rapidly excised and perfused in a langendorff apparatus with K-H solution saturated with 95％ O2-5％ CO2 at 36.5-37.5 ℃.At 20 min of equilibration,the hearts were perfused with K-H solution for 60 min in group C.The hearts were subjected to 30 min of ischemia followed by 30 min reperfusion with K-H solution in group I/R.The hearts were subjected to 30 min of ischemia followed by 30 min reperfusion with K-H solution containing 300 nmol/L levosimendan in group L.Left ventricle developed pressure (LVDP),left ventricle end-diastolic pressure (LVEDP),+ dP/dt-dP/dtmax and heart rate (HR) were recorded immediately before ischemia and at 15 and 30 min of reperfusion.Arrhythmia was recorded during reperfusion and scored.Specimens were obtained from the apex of heart at 30 min of reperfusion for determination of the intracellular calcium concentration ([Ca2 +] i).Myocardial specimens were obtained from the left ventricle at 30 min of reperfusion to detect CaMK Ⅱ activity.Results Compared with group C,arrhythmia score,[Ca2+]i and CaMK [Ⅱ activity were significantly increased,and LVDP,+ dP/dtmax,-dP/dtmax and HR were decreased,and LVEDP was increased at 15 and 30 min of reperfusion in group I/R.Compared with group I/R,the number of ventricular premature beat,arrhythmia score,[Ca2+] i and CaMK Ⅱ activity were significantly decreased,and LVDP,+ dP/dtmax,-dP/dtmax and HR were increased,and LVEDP was decreased at 15 and 30 min of reperfusion in group L.Conclusion Inhibition of CaMK Ⅱ activity is involved in the mechanism by which levosimendan decreases the development of arrhythmias induced by myocardial I/R in rats.

Objective To assess peritonitis rate in peritoneal dialysis. Methods The peritonitis rate from 1999 Aug. 1st to 2004 Jun 30th in Renji Peritoneal Dialysis Center was analyzed retrospectively. Various methods including cohort-specific peritonitis incidence, negative binomial distribution model, median subject-specific peritonitis incidence and peritonitis-free survival were used for the analysis. Results Cohort-specific peritonitis incidence was 1756. 14 patient-month, the mean peritonitis rate estimated using the negative binomial model was 1/49.58 patient-month, median subject-specific peritonitis rate was 0, mean peritonitis-free survival time was 39. 71 months, the peritonitis-free time was inversely correlated with subject-specific peritonitis rate(P

OBJECTIVEThe glucocorticoid dexamethasone (DEX) can induce palatal cleft; however, the mechanism involved remains unclear. E-cadherin is an important cell adhesion molecule, and it can significantly affect cell fate and embryonic development. Recent studies have indicated that E-cadherin expression in palatal epithelial cells is suppressed in normal palate fusion. This study aimed to determine whether the change in E-cadherin expression is related to the incidence of cleft palate in DEX-induced mice.

METHODSMice were divided into the experimental group and the control group. Pregnant mice were injected with DEX on E10.0-E12.0, whereas mice in the control group were injected with normal saline. Hematoxylin and eosin (HE) staining, immunohistochemistry, and real-time quantitative polymerase chain reaction were employed to evaluate the effect of DEX on fetal mouse palatal processes, particularly the changes in E-cadherin and β-catenin expression levels in the phases of the experimental and control groups.

RESULTSData indicated that the incidence of cleft palate in the DEX group was 43.59% (17/39), whereas that in the control group was only 3.03% (1/33). The results of HE staining showed that the obviously shortened palatal processes could not contact and fuse with one another in the DEX-treated mice model compared with those in the control group. The ectopic expression of E-cadherin in embryonic palatal mesenchymal cells was also analyzed. The expression levels of E-cadherin and β-catenin in the experimental group were higher than those in the control group.

CONCLUSIONThese findings indicated that DEX could induce E-cadherin gene upregulation and ectopic expression, as well as high β-catenin expression, thereby inhibiting the growth of mesenchyme cells and cleft palate.

Animals ; Cadherins ; genetics ; metabolism ; Cleft Palate ; chemically induced ; embryology ; Dexamethasone ; adverse effects ; Disease Models, Animal ; Epithelial Cells ; Female ; Glucocorticoids ; Immunohistochemistry ; Mice ; Pregnancy ; beta Catenin ; metabolism

Objective To know the mastery degree of percutaneous coronary intervention (PCI) preoperative nursing knowledge in nurses who are working in emergency department and cardiac ward. Methods 158 cases of nurses who came from three different class Ⅲ grade hospitals with qualification for emergency PCI surgery of the Guizhou province were surveyed with self-made questionnaire. The survey was conducted in nurses who were working in different departments, and the educational background, age, title, category, the cognitive situation of the PCI preoperative nursing knowledge and necessity of preoperative preparations were investigated in nurses. Results The whole pass rate was 48.10%; high qualification, high education, higher title of nurses for the nursing knowledge of the emergency PCI were better; the emergency PCI preoperative preparations for the necessity of cognitive about nurses were on the low side. Conclusion The cognition of the nursing knowledge and the necessity of emergency PCI in preoperative preparations as whole are on the low level, so specialized training should be strengthened to enhance the ability of specialized nursing.

Objective To study the protective effect of lipoic acid (LA) on H9c2 cardiomyocytes hypoxia/reoxygenation injury model, and explore its relevant mechanism. Methods Eight strains of H9c2 cardiomyocytes, passaged after cultured to a full view, were divided into 3 groups:normoxia group, hypoxia/reoxygenation group and LA group. The cell survival rate, lactate dehydrogenase (LDH) activity, malondialdehyde (MDA) and heme oxygenase-1 (HO-1) levels were detected and compared. Results The cell survival rates of H9c2 cardiomyocytes in hypoxia/reoxygenation group and LA group were significantly lower than those in normoxia group:(52.86 ± 6.39)％, (69.25 ± 7.63)％vs. (92.31 ± 7.82)％, while the cell survival rate of H9c2 cardiomyocytes in LA group was significantly higher than that in hypoxia/reoxygenation group, and there were statistical differences (P<0.01). The LDH activity and MDA in hypoxia/reoxygenation group and LA group were significantly higher than those in normoxia group:(286.37 ± 27.49), (209.72 ± 25.63) U/L vs. (126.32 ± 18.94) U/L, and (1.72 ± 0.06), (1.13 ± 0.07)μmol/L vs. (0.68 ± 0.06) μmol/L, while those data in LA group were significantly lower than those in hypoxia/reoxygenation group, and there were statistical differences (P<0.01). The HO-1 in hypoxia/reoxygenation group and LA group were significantly higher than that in normoxia group:(213.71 ± 18.94)％, (367.26 ± 23.07)％vs. (87.92 ± 19.23)％, and HO-1 in LA group was significantly higher than that in hypoxia/reoxygenation group, and there were statistical differences (P<0.01). Conclusions The LA plays a protective role on myocardial cell with hypoxia/reoxygenation injurythough increasing the level of HO-1 against oxidative stress.

Long non-coding RNA plays an increasingly important role in transcriptional, post-transcriptional and epigenetic levels. In ischemic heart disease, most studies on long non-coding RNA focused on myocardial infarction, hypertrophy and fibrosis, and a few of reports directly focused on the pathological process of myocardial reperfusion injury. Thus, the purpose of this review is to introduce the processes of long non-coding RNA in myocardial reperfusion injury field, aiming to provide a novel research and theraputic method for exploring the mechanism and molecular regulation network involed with reperfusion injury.

Objective: To assess the relationships between nutritional risks, nutritional support, and doctors' knowledge related to nutritional risks. Methods: 217 pre-operative patients and 41 doctors in the same general surgical wards were surveyed by using NRS2002 and self-developed questionnaires in a Beijing hospital. Results: The overall prevalence of pre-operative nutritional risks was 15.7%. Patients with gastrointestinal and/or malignant diseases had higher risks than others(P values were both less than 0.001). The nutritional support rates were 14.7% among patients with nutritional risks, and 2.2% among those without risks. The EN: PN ratio was 1∶ 2. A majority of doctors had misconceptions in nutritional risk screening and the effectiveness of nutritional supports. Their clinical practices were not consistent with their knowledge. Related trainings were required. Conclusions: Patients with gastrointestinal and/or malignant diseases have higher possibilities of nutritional risks. The nutritional supports rates are generally low. Doctors' knowledge related to nutritional risk screening is insufficient. More training opportunities are suggested to enhance the application of NRS2002 and appropriate nutritional supports.

Objective To study the antidepressant-like effect of Butanol Extract from Stevia (BEFS) and its possible corresponding mechanisms.Methods Forty-five mice were randomly divided into control group,model group,model + Fluoxetine group,model + BEFS-3 g/kg group and model + BEFS-6 g/kg group.The chronic unpredictable mild stress(CUMS) for 3 weeks was used to make up depressive animal model.It was based on body weight,crossing numbers,rearing numbers and sucrose preference to assess whether the model was a success.After continuous lavage giving BEFS and fluoxetine for 2 weeks and subsequent behavioral test,the mRNA transcription of Single immunoglobulin interleukin-1 receptor-related molecule (SIGIRR) and nuclear factor kappa-B (NF-κB) in liver tissue of mice were detected by using quantitative real time-PCR.Results Three weeks after CUMS,behavior parameters were significantly decreased in mice exposed to CUMS compared with control group[(17.28 ±0.49) g vs (22.47 ± 0.82) g,P =0.000;(43.35 ± 1.68) scores vs (125.25 ± 3.07) scores,P =0.000;(3.92 ± 0.18) scores vs (15.92 ± 1.78) scores,P =0.000;(49.39 ± 2.05) ％ vs (67.18 ± 4.46) ％,P =0.001].However,2 weeks after dosing,body weight,crossing numbers,rearing numbers and sucrose preference were (19.03 ± 0.44) g,(70.50 ± 6.56) scores,(3.08 ± 0.77) scores and (41.27 ± 7.59) ％,respectively in model group.Compared to model group,behavior parameters of BEFS (3 and 6 g/kg BEFS) groups were significantly increased [BEFS-6 g/kg group:(24.42 ± 1.46) g,(99.75 ± 5.07) scores,(13.08 ± 1.60) scores,(64.31 ± 1.92) ％,all P ＜ 0.05;BEFS-3 g/kg group:(23.82 ± 1.72) g,(91.67 ± 5.69) scores,(6.92 ± 1.05) scores,(59.56 ± 5.31) ％,respectively,all P ＜ 0.05].Correspondingly,BEFS could reverse the mRNA expression of SIGIRR lowering and NF-κB rising in the liver of mice exposed to CUMS(BEFS-6 g/kg group:1.208 1 ± 0.102 2,1.437 7 ± 0.352 9;BEFS-3 g/kg group:0.768 0 ± 0.108 6,2.186 2 ± 0.203 8,all P ＜ 0.05).Conclusions BEFS can remarkably improve depression-like behaviors in CUMS mice and its antidepressant activity is mediated,at least in part,by upregulating SIGIRR and downregulating NF-κB in the liver.