polyhornal and round cells.Conclusion The AVN of rabbit was made up by different cells.The polyhornal and round cells may be pacemaker cells;the spindle cells might be transitional cells,and the triangle cells may be myocardial cells.

This study determined the levels of serum soluble intercellular adhesion molecule-1 (sICAM-1) and soluble vascular cell adhesion molecular-1 (sVCAM-1) in patients with different types of Keshan disease (KD), examined the relationship between Coxsackie B virus-specific IgM antibody (CBV-IgM) and sICAM-1 or sVCAM-1 in KD patients, and investigated the role of these adhesion molecules in the pathogenesis of KD and their clinical implications. The levels of serum sICAM-1, sVCAM-1 and CBV-IgM were measured by using enzyme-linked immunosorbent assay in 22 patients with chronic Keshan disease (CKD), 27 with latent Keshan disease (LKD) and 28 healthy controls. The subjects in different groups were adjusted for sex and age. Echocardiography was adopted to determine left ventricular ejection fraction (LVEF) in 22 patients with CKD. The results showed that CKD patients had significantly higher levels of sICAM-1 and sVCAM-1 than LKD patients and healthy controls (P<0.01 for all). And there was significant difference in the levels of the 2 adhesion molecules between LKD patients and healthy controls (P<0.05). A negative correlation was found between LVEF and sICAM-1 or sVCAM-1 in CKD patients. The percentage of CBV-specific IgM positive individuals in KD patients was significantly higher than that of healthy controls. In CVB-specific IgM positive patients, the levels of serum sICAM-1 and sVCAM-1 were significantly greater than those in CBV-specific IgM negative counterpart. It was concluded that the increase in the levels of sICAM-1 and sVCAM-1 suggests the progression of inflammation in KD. sICAM-1 and sVCAM-1 can promote the development of myocardial pathology and lead to poor myocardial function. The increased serum sICAM-1 and sVCAM-1 in KD patients may be related to CBV infection.
Cardiomyopathies/*blood ; Cardiomyopathies/etiology ; Cardiomyopathies/*virology ; Coxsackievirus Infections/*complications ; Enterovirus B, Human ; Intercellular Adhesion Molecule-1/*blood ; Selenium/blood ; Vascular Cell Adhesion Molecule-1/blood ; Young Adult

The authors give an account of their guiding ideology, implementing methods and practical experience in setting up research funds for nursing. Their experience is as follows. Establishment of the funds in their hospital has played a positive role in promoting research on nursing. Greater increase in intellectual input and creation of a sound environment for the conduction of research on nursing is an effective guarantee for the successful conduction of the work. Emphasis has been rightly put on clinical projects by orienting the research funds towards projects involving clinical nursing. And making a good job of the whole nursing procedure is the key to the proper application of the research funds for nursing. Besides, to give full play to the role of research funds for nursing, it is imperative to cultivate academic leaders in nursing able to keep abreast of the times, aim closely at the frontier research in the field and bring into effect the starting and catalytic action of research funds for nursing.

Objective To investigate the influences of 4 kinds of collagenase with different degrees of activity on the survival rate,contraction and relaxation functions of isolated rats' myocardiocytes.Methods Rats' myocardiocytes were isolated by enzymolysis with 4 kinds of collagenase with different degrees of activity.The survival rate of myocardiocytes was observed immediately after isolation(D),one hour after loading with calcium(E time point) and 10 minutes after electric stimulation(F time point).The contraction and relaxation functions of myocardiocytes,including contraction amplitude(ph),the proportionality of ph/single cardiocyte length(bl),maximal velocity of contraction(+dL/dt) and maximal velocity of relaxation(-dL/dt),were measured with IonOptix video edge tracker.Results From 203U/mg to 299U/mg,with lowering of the activity of collagenase,the isolation time became longer,the survival rate of myocardiocytes declined 1 hour after loading calcium and 10 minutes after electric stimulation(P

In order to investigate the impairment of mitochondrial membrane phospholipid localization and DNA(3867) (mtDNA(3867)) deletion and the correlation between cardiac and skeletal muscle cells in mice with viral myocarditis, 50 BALB/c mice were divided into two groups randomly. In experimental group (n=40), the mice were intraperitoneally injected with 0.1 mL Eagle liquid with CVB3(TCID50=10(8)), while in the control group (n=10), the mice were subjected to equal volume of Eagle liquid. The impairment of mitochondrial membrane phospholipid localization and mtDNA(3867) deletion rate of cardiac and skeletal muscle were detected separately at day 3, 11 and 24 after injection. The correlation of mitochondrial membrane phospholipid localization and mtDNA(3867) deletion rate between cardiac and skeletal muscle cells cells was analyzed using Spearman method. At the day 3 after injection, in both cardiac and skeletal muscle cells, mtDNA(3867) deletion rate was significantly higher in experimental group than in control group (P<0.05), but the localization of mitochondrial membrane phospholipid showed no difference between two groups (P>0.05). At day 11 after injection, the mtDNA(3867) deletion rate of both cells in experimental group was increased to the peak level (P<0.05), and the impairment of mitochondrial membrane phospholipid localization of both cells also increased markedly in experimental group as compared with control group (P>0.05). At the day 24 after injection, the impairment of mitochondrial membrane phospholipid localization and mtDNA(3867) deletion of both cells showed a recovery tendency, but still severer than those at the day 3 after injection (P<0.05). The impairment of mitochondrial membrane phospholipid localization and mtDNA(3867) deletion were consistent and synchronistic between cardiac and skeletal muscle cells, and showed good correlations (P<0.05). The impairment of mitochondria plays an important role in the pathogenesis of viral myocarditis, and the skeletal muscle cells might act as a peripheral "window" to reflect the mitochondrial damage of cardiac myocytes.

Objective:To explore the effect of multi-channel health education model by professional team on drug compliance, disease knowledge and recurrence in rate of inflammatory bowel disease (IBD) patients, so as to provide basis for formulating scientific health education measures.Methods:From February 2016 to February 2019, IBD patients visited First Affiliated Hospital of Kunming Medical University were selected. According to whether they received health education, the patients were divided into intervention group (100 cases) and control group (138 cases). Morisky medication adherence scale-8 (MMAS-8) and Chinese version of Crohn′s and colitis knowledge score (CCKNOW) were used to evaluate treatment compliance and disease knowledge. The score of MMAS-8, the proportion of poor drug compliance, CCKNOW score and recurrence rate at 48 weeks of follow-up were compared between the intervention group and control group. Two sample t test and chi-square test were used for statistical analysis. Results:The total scores of MMAS-8 and CCKNOW of the intervention group were both higher than those of the control group (5.58±1.96 vs. 4.47±1.44, 10.87±4.21 vs. 9.23±4.65), and the differences were statistically significant ( t=-5.06 and -2.79, both P<0.05). The proportion of patients with poor drug compliance and recurrence rate at 48 weeks of follow up of the intervention group were both lower than those of the control group (56.0%, 56/100 vs. 86.2%, 119/138; 20.0%, 20/100 vs. 31.9%, 44/138), and the differences were statistically significant ( χ2=38.18 and 4.17, both P<0.05). Conclusions:Multi-channel health education by professional team can effectively improve the drug compliance and disease knowledge in IBD patients, improve patient self-management ability, and reduce the recurrence rate.

Objective To study the effect of moxonidine (Mox) on the His bundle electrogram (HBE) of normal rabbits. Methods A total of 24 healthy rabbits were randomly divided into four groups: control group, small dose of Mox (0.1 mg?kg -1), medium dose of Mox (0.3 mg?kg -1) and large dose of Mox (0.9 mg?kg -1). The electrode catheter was inserted from the right carotid artery to record the HBE. The HBE and the synchronism surface ECG were recorded before and after intravenous injection. Results In normal rabbits, the R-R interphase, P-R interphase of the ECG and the H-V interphase of the HBE were prolonged in a dose-dependent manner after intravenous injection of Mox. Mox exerted no significant influence on the A-H interphase. Conclusion ① Mox decreases the heart rate of rabbits in a dose-dependent manner in vivo. ② Mox dose-dependently prolongs the P-R interphase of the surface ECG and the H-V interphase of HBE. This indicates that Mox mainly acts on the intraventricular conducting system.

Objective To investigate the effect of paeonol antagonizing peroxynitrite(ONOO~-) on osteoblast apoptosis of rat in vitro.Methods Osteoblasts of newly born rat's skull were separated and cultured by tissue mass method.ONOO~-was produced by chemical synthesis with a quenched flow reactor.ONOO~-at 1 mmol/L concentration was added to cultured osteoblast system in vitro.After incubated for 30 min,osteoblasts were continued to be cultured for 12 h with routine method.Hoechst33258 stain and TUNEL method were used to detect the osteoblast apoptosis and 0.1 mmol/L concentration of paeonol was used to eliminate the effect of ONOO~-(1 mmol/L) on osteoblast apoptosis of rat.Results ONOO~-(1 mmol/L) could lead to rat osteoblast apoptosis.Paeonol of 0.1 mmol/L concentration could antagonize rat osteoblast apoptosis induced by ONOO~-(1 mmol/L).Conclusion Paeonol(0.1 mmol/L) has the significant antagonizing effect on ONOO~-of rat osteoblast apoptosis in vitro.

AIM: To elucidate the role of mitochondrial DNA (mtDNA) deletion in the pathogenesis of viral myocarditis in mice. METHODS: 50 BALB/c mice were divided into two groups randomly. 40 were experimental group, each of them was injected 0.1 mL Eagle liquids with CVB_3 (TCID_ 50=108) intraperitoneally. Another 10 mice were given equal volume Eagle liquids as control group. Cardiac functions in vivo and mtDNA 3867 deletion rate in myocytes were detected separately at the day 3, 11 and 24 after injection. The correlation of mtDNA 3867 deletion rate to cardiac functions was analyzed using Spearman method. RESULTS: At the day 3 after injection, mtDNA 3867 deletion rate in experimental group was 8.3 times higher than that in control group [(0.01970?0.00118)% vs (0.00211?0.00032)%,P

Objective To determine whether reduction In central pressure augmentation and central systolic blood pressure by nitroglycerine (NTG) results from effects on pre-lead or is due to arterial dilation. Methods We compared effects of NTG with these of lower body negative pressure (LBNP). Hemodyunmic measurements were made at rest, during LBNP (10, 20 and 30 mmHg, each for 15 min) and after NTG (10, 30 and 100μg/min, each dose for 15 min) in ten healthy volunteers. Cardiac pre-lead, stroke volume and cardiac output were assessed by echacardiography. Central pressure an mnentation and central systolic pressure were obtained by radial tonometry using a transfer function. Results LBNP (20 mmHg) and NTG (30μg/min) reduced pre-lead (as measured by the peak velocity of the S wave in the superior vena eava) to a similar degree [by (26. 8 ± 3.8) % and (23.9 ± 3. 4) %, respectively]. Compared to LBNP, NTG reduced systemic vascular resistance [by (32. 9 ± 7.5) %, p< 0. 01], decreased peripheral and central pressure augmentation [by (20. 8 ± 3. 4)% units and (12. 9±2. 9)% units, respectively, each P< 0. 01]. Conclusion These results suggest that a reduction in pre-load does not explain reduction in pressure augmentation and central systolic blood pressure by NTG and that these effects are mediated through arterial dilation.