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Objective:To explore the role of comprehensive first aid skills training in improving medical students' comprehensive first aid ability.Methods:Eighty-seven medical students were enrolled in this study, and received the training of comprehensive first aid skills developed by the emergency medicine teaching and research section of our hospital. The scores of individual first aid ability, emergency handling ability, team cooperation ability, organization and coordination ability and communication ability before and after the training were analyzed. At the same time, a questionnaire survey was conducted among students to understand their evaluation and recognition of the training. SPSS 10.0 was used for t test. Results:After the training, the total score of comprehensive first aid ability was increased significantly [(73.55±3.89) vs. (63.53±3.06)], and the scores of emergency handling ability [(10.11±1.43) vs. (8.01±1.16)], team cooperation ability [(11.38±1.21) vs. (8.15±0.99)], organization and coordination ability [(10.68±1.17) vs. (8.15±0.99)] and communication ability [(9.64±1.31) vs. (7.55±1.08)] were also significantly increased ( P<0.05). However, there was no significant difference in the scores of individual first aid ability mastery before and after training. In all, 80.46%-96.55% of the students think that the training of comprehensive first aid skills is conducive to the improvement of their comprehensive first aid ability, and all of the students are willing to use this training in the future. Conclusion:Comprehensive first aid skill training is beneficial to improve medical students' comprehensive first aid ability.
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This study was designed to investigate the correlation between autophagy and polarization of macrophages in atherosclerosis (AS) plaque in arteriosclerosis obliterans amputees. Femoral artery specimens from arteriosclerosis obliterans amputees were performed hematoxylin and eosin (HE) staining, oil red O and immunofluorescence staining to observe the morphology of atherosclerotic plaque, phenotype of macrophages and autophagy in plaque; using real-time quantitative RT-PCR technology to detect the mRNA level of M1 and M2 type markers in arterial tissue; to analyze polarized signal pathway and autophagy protein levels in macrophages by Western blotting. Arterial specimens staining showed obvious lipid deposition and obvious infiltration of amount of foam cells and inflammatory cells. Macrophages were mainly expression M1 type in percentage in fibrous plaque. Although both M1 and M2 macrophages were upregulated in atheromatous plaque, the increase was dominant in M2 type in percentage. The level of autophagy was significantly higher in the atheromatous plaque than that of fibrous plaque. The expression of tumor necrosis factor- α (TNF-α), monocyte chemotactic protein-1 (MCP-1), inducible nitric oxide synthase (iNOS), interleukin-6 (IL-6) and interleukin-12 (IL-12) mRNA was significantly higher in fibrous plaque than that of atheromatous plaque (P < 0.01 or 0.05), and arginase-1 (Arg-1), transforming growth factor-β (TGF-β), CD163 and interleukin-10 (IL-10) mRNA was significantly lower than that in atheromatous plaque (P < 0.01). The levels of p-STAT1 and NF-κB were significantly increased in fibrous plaque (P < 0.01), while p-STAT6 expression was significantly increased in atheromatous plaque (P < 0.01). The level of LC3-II was significantly higher in atheromatous plaque than that in fibrous plaque (P < 0.01). Macrophages in early atherosclerotic plaque were induced to M1 type through p-STAT1/NF-κB pathway and expressed moderate levels of autophagy; while macrophages in advanced plaques were induced to polarization of M2 type through p-STAT6 pathway. M2 macrophages expressed a higher level of autophagy than M1 macrophages.
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objective To investigate the effects of different sections of receptor associated protein (RAP) on the expression and distribution of TRPC6,synaptopodin and podocalyxin in passive Heymann nephritis(PHN). Methods Male Sprague-Dawley rats were injected with three kinds of antisera (anti-RAP full-length serum,anti-RAP N-terminal serum and anti-RAP C-terminal serum)to establish three kinds of PHN models.The control group was injected with normal rabbit serum.The quatitation of 24 h urinary protein,serum albumin and creatinine were taken before injection and one week after PHN model successfully induced.The histopathologic changes of renal tissues were observed by light microscopy.The expression and distribution of TRPC6,synaptopodin and podocalyxin in glomerular podocytes were observed by laser scanning confocal microscopy and analyzed by fluorescence quantitative software after indirect immunofluorescence double staining.Results The quantities of 24 h urinary protein in the three model groups were significantly higher than those of themselves before injection and control groups (P0.05).The expression of TRPC6 in podocytes was higher in the PHN model groups than that of control group.Fluorescence intensity of TRPC6 in RAP full-length group was stronger than that in RAP N-terminal or C-terminal groups.The expressions of synaptopodin and podocalyxin distributed along the glomerular basement membrane as spot,discontinuous short line and defect of some segments,and were lower in three PHN groups than those of control group.Fluorescence intensity of synaptopodin and podocalyxin among three PHN groups had no differences. Conclusions RAP full-length and N-terminal or C-terminal parts can increase the expression of podocyte TRPC6,but decrease the expressions of synaptopodin and podocalyxin,and alter their distribution,which may be associated with the proteinuria,however,their role in the PHN pathogenesis needs further study.
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Objective To investigate the expression of slit diaphragm proteins of glomerular podocyte,such as NEPH1 and Nephrin in type Ⅴ lupus nephritis (V-LN). Methods Twenty-five patients with V-LN and 18 patients with idiopathic membranous nephritis (IMN) were enrolled into the study, and 5 normal renal samples were the normal control group. Twenty-four hours urine protein excretion, serum albumin, creatinine, triglyceride, total cholesterol, serum C3, C4, urine C3 and NAG were tested respectively.Glomerular lesions were measured by light microscopy. The expressions of NEPH1 and Nephrin were determined by indirect immunofluorescent staining. The statistical treatment was used t-test. Results Compared to the IMN group, the 24 hours urine protein excretion and the concentrations of serum albumin, creatinine, urine C3 were not significantly different while the triglyceride, total cholestorel, serum C3, C4 were significantly decrease in the V-LN group (P<0.05). Urine NAG was increased in the V-LN group (P<0.01). By indirect immuno-fluorescent histochemitry examination, the glomerular expressions of NEPH1 and Nephrin were significantly decreased in both V-LN and IMN. Compared with the IMN group, the decrease of NEPH1 and Nephrin expression was more remarkable in the V-LN group. Conclusion The expression changes of NEPH1 and Nephrin may play an important pathogenic role in proteinuria of Ⅴ lupus nephritis. Renal tubular epithelial cell damage may play a role in proteinuria of V-LN.
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Objective To define the effect and mechanism of hyperkalemic solution on atrial natriuretic peptide (ANP) secretion in rabbits. Methods Eighteen rabbits were selected and the chest was opened under anes-thetization to remove the heart. The left atrium was isolated and fixed in the atrial perfusion system with proper electric stimulation for beating. The following experiments were carried out on beating rabbit atria: ①The atrium was perfused for 60 min to stabilize parameters of ANP secretion and atrial dynamics. The control period (12 min as an experimental cycle) was followed by an infusion of hyperkalemic solution (K+ concentration of hyperkalemic solution was 5.64 mmol/L and the osmolarity of hyperkalemic solution was unchanged) for three cycles, then normal K+ cancentration was recovered for two cycles;②The control period was followed by an infusion of L type Ca2+ channel blocker nifedipine (1.0 μmol/L) for three cycles;③L type Ca2+ channel inhibitor nifedipine (1.0 μmol/L) was infused for 36 rain prior (three cycles) to infusion of hyperkalemic solution. Atrial stroke volume was determined and the ANP secretion was measured by radioimmtmoaasay. Results (1)Hyperkalemic solution increased atrial ANP secretion (P<0.01) and reduced the atrial stroke volume,hut the difference was not statistically significant as compared with that of the control cycle(P>0.05). The recovery trend was to the normal level of ANP secretion and atrial stroke volume was to become normal gradually when solution level recovered to normal ,which was not significantly different from that of the control cycle (P>0.05) ;②Nifedipine (1.0 μmol/L) also increased the atrial ANP secretion (P<0.01 or P <0.05) while decreasing atrial stroke volume (P<0.01 or P < 0.05 ) ; ③Nifodipine (1.0μmol/L) completely blocked the effect of hyperkalemic solution so to increase the ANP secretion (P <0.01 ). Conclusion Hyperkalemic solution significantly increases atrial ANP secretion via extracellular high K+ competitive inhibition of extracellular Ca2+ inflow in beating rabbit atria.
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Objective To study the differentially expressed genes in the vascular tissue of diabetic gangrene toot and the possible mechanism of diabetic gangrene.Methods The differentially expressed genes in the vascular tissue of diabetic gangrene foots were screened by the functional classific gene chip.Reverse transcription polymerase chain reaction(RT-PCR) detection was used to verify the differentially expressed 3 genes.Results In the detected 113 genes,13 of the gene expression level increased more than 2 times,3 of the gene expression level decreased more than 2 times.Three genes were verified with RT-PCR detection,which were results similar to those with chip testing.Conclusions The abnormal expression in a variety of genes in tissues of vascular lesions plays an important role in the course of development and progression of diabetic gangrene.Analysis of differential gene expression can contribute to understanding of the possible mechanisms of diabetic gangrene.
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Objective To explore the role of heme oxygenase-1 (HO-1) gene expression on murine experimental abdominal aortic aneurysm (AAA).Methods Wistar rats were divided into hemin (experimental group) and saline (control group) group randomly, and experimental AAA model was established by elastase perfusion. The specimen was obtained at postoperative day 7, and the dilatation rate was calculated. In situ hybridization was applied to detect the expression of HO-1 mRNA in aortic wall, while immunohistochemical staining was used to detect the protein expression of ICAM-1 and HO-1. Results In experimental group, the aorta dilation was inhibited and aneurysm was not observed. In experimental group, HO-1 mRNA and protein expression was strengthened (P