Animals ; Cardiovascular Diseases ; Cardiovascular System ; Humans ; MicroRNAs

Objective To investigate the function of middle-methoxyl pectin-Ca2+ complex in(Graduate School,Chinese Academy of Science,Beijing 100039;1 Polymer Engineering Laboratory,Changchun Institute of Applied Chemistry,Chinese Academy of Sciences,Changchun 130022,China) lowing postprandial serum glucose of normal and impaired glucose tolerance(IGT) rats.Method The experimental IGT rats models were made by injecting STZ into abdomen.Then normal and IGT rats were given test meal and their postprandial serum glucose were measured.Results The middle-methoxyl pectin-Ca2+ complex could significantly improve the glucose tolerance and weaken the peak value of postprandial serum glucose of normal and IGT rats(P

Objective:This work aims to investigate diallyl disulfide (DADS) inhibition of cell migration and invasion in human colon cancer SW480 cells through the Rac1-ADF/cofilin1 pathway. Methods:The potential of cell migration and invasion was examined by scratch healing assay and transwell membrane assay. The expression of Rac1-ADF/cofilin1 pathway was detected by RT-PCR and Western blot. Results:After the SW480 cells were treated with 40 and 50 mg·L-1 of DADS for 24 h, the number of transmembrane cells through the Matrigel obviously decreased by 57.12%and 64.59%, respectively (P<0.05). After cell treatment for 48 h, the cell migration rates were 23.23%and 12.87%, which were significantly lower compared with the control group (75.86%;P<0.05). After the cells were treated with 45 mg·L-1 of DADS for 24 and 48 h, the expression of Rac1, Rock1, PAK1, LIMK1, and destrin mRNA respectively decreased compared with the control group (P<0.05). However, no significant difference was observed in the expression of cofilin1 mRNA (P>0.05). After the treatment with 45 mg·L-1 of DADS for 6, 12, 24, and 48 h, the expression of Rac1, Rock1, PAK1, LIMK1, and Destrin proteins respectively decreased in a time-dependent manner compared with the control group (P<0.05). However, no significant differences were observed in the expression of the cofilin1 protein (P>0.05). Moreover, the expression of p-LIMK1 and p-cofilin1 notably decreased in a time-dependent manner (P<0.05). Conclusion:DADS inhibits cell migration and invasion, which is related to the down-regulation of Rac1, Rock1, PAK1, LIMK1, p-LIMK1, p-cofilin1, and destrin through the Rac1-ADF/cofilin1 pathway.

The professional quality training ofthree orientedpersonnel training mode is one of the three core, which requires medical students to have lifelong learning ability. This study mainly describes the proposed concept of lifelong learning ability, expounds the necessity of lifelong learning ability, and analyzes the connotation, objective and strategies of improving the medical students'!lifelong learning ability under the framework of three oriented medical talents training mode. The training strategy has been discussed mainly from five aspects such as strengthening medical humanistic education, creating a lifelong learning atmosphere in campus, optimizing teaching methods, reform the course of career development and employ-ment guidance, reforming the course of career development and employment guidance, reforming the teaching of medical literature retrieval course and establishing the personal growth archives.

To explore the effect of advanced glycation end-products(AGEs)on cell viability and level of reactive oxygen species(ROS)in MIN6 cells. After intervention of various concentrations(100,200, and 400 mg/L)of AGEs for some time, cell viability was detected by MTT assay. 2', 7'-dichlorofluorescein diacetate(DCFH-DA)was used as a reactive oxygen species capture agent. The fluorescent intensity of 2', 7'-dichlorofluorescein(DCF), which was the product of cellular oxidation of DCFH-DA, was detected by flow cytometry. The level of ROS and insulin secretion was thus measured. Viability of MIN6 cells was inhibited by AGEs in a dose and time dependent manner(P＜0.05).Intracellular fluorescent intensity of DCF was markedly elevated in the AGEs groups as compared with that in the control group(P＜0.05).Insulin secretion was decreased in the AGEs groups than that in the control group(P＞0.05). The results suggest that AGEs inhibit the viability and induce oxidative stress in MIN6 cells by overproduction of ROS.

ObjectiveTo investigate the D8/17 antigen expression of patients with rheumatic heart disease (RHD) in Guangdong province and study the antigen's characteristics.Methods The level of D8/17 antigen expression on B lymphocytes was determined with flow cytometry assay in 96 RHD patients and 83 unaffected controls.The percentage of B-cells expressing the D8/17 antigen having more than 10％ was considered to be positive. D8/17 antigen was extracted by immunopreeipitation,and the antigen characteristics was analyzed by tandem mass spectrometry. Results The mean percentage of B-cells expressing the D8/17 antigen was (85.36 ± 15.15)％ in the RHD patients and (82.89 ±4.55)％ in the controls,with no significant difference between the two groups ( P =0.436).Moreover,the positive rate of the D8/17 cxprcssion was 100％ in either the RHD patients or the controls.The molecular weight of D8/17 antigen was found to be 40 000-67 000,and the purified protein was most likely to match moesin or β-actin.ConclusionsB-cell antigen D8/17 is not associated with RHD in Guangdong province of China.Moesin or β-actin is the most likely protein to match D8/17 antigen.

Objective To construct a lentiviral vector containing mir-7-3 gene and green fluorescent protein (GFP) gene,and to detect the expression of mir-7-3 gene in U251 cells.Methods The fragments containing all the mir-7-3 gene were amplified by RT-PCR and were cloned into the lentivirus vectors labeled with GFP,which was transfected together with the packaging plasmids into 293T cells by CaC12.The supernatant was collected,concentrated,identified,and was transfected to U251 cells of gliomas.Fluorescent microscopy was used to observe the fluorescence in the 293T cell,and real time RT-PCR was used to examine the relative contents of mir-7-3 in U251 cells.Results Electrophores was shown that the sequence of the RT-PCR product was consistent with the data of mir-7-3 by DNA sequence analysis,indicating that the mir-7-3 gene was successfully cloned,and strong green fluorescence was observed by fluorescent microscopy.The supernatant of lentivirus-transfected 293T cells effectively infected U251 cells and the relative content of mir-7-3 was observed in the transfected U251 cells.Conclusion It is concluded that the lentiviral vector containing mir-7-3 gene was constructed successfully,which provides a basis for further study of mir-7-3 function.

Objective To evaluate the effect of high-level spinal cord injury(SCI)on the expression of mitochondrial voltage-dependent anion channel 2(VDAC2)in rat cardiomyocytes.Methods Forty-eight pathogen-free healthy adult male Sprague-Dawley rats,weighing 200-250 g,were divided into 2 groups(n=24 each)using a random number table:sham operation group(group S)and high-level SCI group(group H).The animals were anesthetized with intraperitoneal chloral hydrate and subjected to SCI using the modified Allen weight-drop method in group H.The spinal cord was only exposed in group S.At 6,12,24 and 48 h after SCI(T1-4),6 rats in each group were randomly selected and sacrificed,and myocardial specimens were collected from the cardiac apex for microscopic examination of the cell morphology(with a transmission electron microscope) and for determination of cell apoptosis(by TUNEL assay),expression of Bax,Bcl-2 and VDAC2 protein and mRNA in cardiomyocytes(by Western blot and real-time polymerase chain reaction,respectively).The apoptosis rate and ratios of Bax/Bcl-2 protein and mRNA were calculated.Results Compared with group S,the apoptosis rate and ratios of Bax/Bcl-2 protein and mRNA were significantly increased at T1-4,the expression of VDAC2 protein and mRNA was significantly down-regulated at T2-4(P<0.05 or 0.01),and the pathologic changes of cardiomyocytes were aggravated in group H.Conclusion The mechanism of myocardial damage is related to down-regulation of mitochondrial VDAC2 expression in cardiomyocytes and promotion of cell apoptosis in rats with high-level SCI.

Objective To evaluate the cause of ischemia related to myocardial bridge (MB) by using SPECT/CT MPI and CTCA.Methods A total of 294 patients with chest pain,tightness or palpitation undergoing both CTCA and MPI were retrospectively enrolled in this study from March 2008 to March 2013.Among them,49 patients (26 males,23 females,age:32-85 (55.4± 16.6) years) had MB.Locations of MB and myocardial ischemia were recorded.Fused MPI/CTCA was analyzed.If there was no mural atherosclerotic plaque-related stenosis on CAG at the same location of coronary artery where ischemic myocardium was found,then MB was considered as the ischemic cause.Myocardial ischemia rates of different MB locations were compared by x2 test.Results Among 49 patients with MB,3 cases had MB in proximal segment of LAD,34 in mid LAD,4 in distal LAD,3 in septal branch,2 in distal LCX,1 in intermedius,and 2 in mid RCA.There were 41 cases with myocardial ischemia.Myocardial ischemia in 32 cases was caused by MB,including 23 caused by MB in mid LAD.The myocardial ischemia rates of the most common MB location (mid LAD,n =34) and other locations (n =15) were not significantly different (67.6％ (23/34) vs 60.0％ (9/15),x2 =0.27,P＞0.05).Conclusions MB is commonly found in the mid LAD.The myocardial ischemia rates caused by MB is not related the MB location.Hybrid MPI/CTCA could evaluate the sites of coronary MB and myocardial ischemia simultaneously and therefore may be useful to evaluate the relationship between MB and myocardial ischemia.

Craniocerebral Trauma ; Earthquakes ; Head ; Humans