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Objective:To develop a learning scale of scientific methods for medical students and to evaluate the reliability and validity of the scale.Methods:Based on the principles of planned behavior theory, the original scale was developed through literature analysis, pre-interview and experts' consultation. A preliminary survey was conducted among 105 medical undergraduates with random cluster sampling, and the primary scale was formed by exploratory factor analysis. Then, 851 undergraduates were selected as the objects of formal survey, and the formal scale was finally determined by the reliability and validity evaluation and confirmatory factor analysis. SPSS 22.0 and AMOS 22.0 softwares were used for statistical analysis of the measurement data.Results:The formal scale was composed of 5 latent variables, 9 observed variables and 51 items. The overall Cronbach’s α coefficient and the overall retest reliability were 0.97 and 0.89, respectively. Composite reliability and KMO values of each latent variable were more than 0.80, and the values of average variance extraction were over 0.50. The fitness test ( P=0.155) showed acceptable fitting quality with the main fit indices of χ2/ df=1.41, RMR=0.04, RMSEA=0.02, etc. Conclusion:The learning scale of scientific methods shows satisfactory reliability, validity and fitness, which can be applied as a measuring tool to evaluate the learning behavior of scientific methods for medical students.
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Objective:To develop a learning scale of scientific methods for medical students and to evaluate the reliability and validity of the scale.Methods:Based on the principles of planned behavior theory, the original scale was developed through literature analysis, pre-interview and experts’ consultation. A preliminary survey was conducted among 105 medical undergraduates with random cluster sampling, and the primary scale was formed by exploratory factor analysis. Then, 851 undergraduates were selected as the objects of formal survey, and the formal scale was finally determined by the reliability and validity evaluation and confirmatory factor analysis.Results:The formal scale was composed of 5 latent variables, 9 observed variables and 51 items. The overall Cronbach’s α coefficient and the overall retest reliability were 0.970 and 0.887, respectively. Composite reliability and KMO values of each latent variable were more than 0.8, and the values of average variance extraction were over 0.5. The fitness test ( P=0.155) showed acceptable fitting quality with the main fit indices of χ2/ df=1.405, RMR=0.039, RMSEA=0.022, etc. Conclusion:The learning scale of scientific methods shows satisfactory reliability, validity and fitness, which can be applied as a measuring tool to evaluate the learning behavior of scientific methods for medical students.
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Objective To investigate the impact of glucose metabolism-related protein 1 (GMRP1) on the regulation of c-Myc gene transcription, to establish GMRP1 gene knockout mouse model, and to study the influence of GMRP1 on glucose metabolism. Methods Chromatin immunoprecipitation-PCR (ChIP-PCR) was utilized to screen out the genes transcriptionally regulated by GMRP1. Luciferase reporter system was applied to assay the regulation of c-Myc promoter activity by GMRP1. GMRP1 knockout mice were constructed and validated by PCR and western blotting. Body weight and random blood glucose were measured in both knockout and wild type mice fed with either chow diet or high-fat diet. The levels of glucose metabolism in mice of 20 or 28 weeks old were evaluated by intraperitoneal glucose tolerance test. Results GMRP1 was capable of binding to the promoter of c-Myc gene and activating the expression of c-Myc gene. There were no significant differences in body weight, random blood glucose or glucose tolerance between GMRP1-deficient and wild type mice fed with either chow diet or high-fat diet (all P > 0.05). Conclusion GMRP1 may activate the transcription of c-Myc gene. GMRP1 deficiency exerted no significant effects on mouse glucose metabolism.
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@#The discovery of microRNAs (miRNAs) in mammalian cells has renewed the focus on posttranscriptional regulatory mechanisms during pathogenesis. The studies have showed that miRNAs play a key role in atherosclerosis development and progress, and were reviewed in this paper.
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Objective To explore the activity and its possible neural mechanism of brain default mode network by using resting state functional magnetic resonance imaging (fMRI) in patients with mild cognitive impairment (MCI). Methods The 20 amnestic MCI patients and 25 healthy controls were included in this study, and all subjects underwent mini-mental state examination (MMSE), auditory verbal learning test (AVLT) and fMRI. The data were analyzed by amplitude of low frequency fluctuation (ALFF), and the enhanced and weakened regions of ALFF were observed and compared in both MCI patients and healthy controls. Results MMSE and AVLT tests showed that the memory function was seriously impaired in MCI patients compared with healthy controls, which is based on the short and long delayed episodic memory impairment (2.4±1.7 vs. 6.6±1.4, t=3.70, P＜0.01; 2.1±1.6 vs. 6.7±1.5, t=4.16, P＜0.01). The resting state fMRI showed that MCI patients had significant decreases of ALFF in hippocampal formation, parahippocampal cortex and lateral temporal cortex as compared with health controls (t=2.58, 2.43 and 1.75, all P＜0.01), which were closely relevant to the episodic memory. And they had significant increases in temporal-parietal joint and inferior parietal lobule (t=3.14 and 2.77, both P＜0.01). Conclusions MCI patients show significant decreased active intensity of some DMN nodes that is related to episodic memory in resting state. Increased active intensity in MCI patients would be some type of compensation.
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Objective To set up and verify a new scoring system of clock drawing test(CDT).Methods CDT and other neuropsychological tests were applied to 180 normal individuals.170 subjects with mild cognitive impairment(MCI),and 31 patients with mild Alzheimer's disease(AD).The first step of the 30-score system of CDT was to anchor the 4 points of"12-3-6-9".totaling a score of 4 which was the "30-score system A(Anchoring)part";and the other 13 items reflecting the drawing results and totaling a score of 26 made up the so called"30-score system C(Clockfaee)part".the two together had a total score of 30.Thirty-eight subjects underwent Xe-enhanced computed tomography(Xe-CT)scanning for quantitively measuring regional cerebral blood flow(rCBF)of 26 regions of brain.Results Correlations coefficients of the scores of 14 items with the total score in 30-score system of CDT were in the range of 0.48to 0.71(P＜0.01).30-score system C part was closely correlated with indicators of visuospatial and executive function,while 30-score system A part with memory indicators.The sensitivity and specificity of the 30-score system A part score≤2 for detecting MCl were 70.6%and 73.9%.respectively.The sensitivity the specificity of 30-score system C part score≤17 for mild AD were 75.3%and 75.9%.respectively.In the regression equation of 30-score system A and C part.the combined independent variables were the CBF of left frontal cortex and right white matter,respectively.Conclusion The 30-score system A and C part have difierent meanings:30-score system C part could be used to identify AD while 30-score system A part is helpful for identiring MCI.
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<p><b>OBJECTIVE</b>To examine the effect of angiotensin II (Ang II) on nuclear factor-kappa B (NF-kappaB) activation in human endothelial cell line ECV304 and the molecular mechanism by which Ang II activates NF-kappaB.</p><p><b>METHODS</b>ECV304 cells were transiently cotransfected with an NF-kappaB/luciferase reporter gene and inactive NF-kappaB-inducing kinase (NIK), IkappaB kinase alpha (IKK(alpha)), IkappaB kinase beta (IKK(beta)) mutants or vectors, respectively. The effect on NF-kappaB was detected by using an electrophoretic mobility shift assay (EMSA) and overexpression of the mutants enabled blocking of reporter gene activation induced by Ang II. With immunofluorescence and immuno-electronic microscope techniques, including confocal microscopy and gold particle labeled electronic microscopy, definite cytoplasmic-to-nuclear translocations of NF-kappaB activation were detected using subunits p50 and p65 induced by Ang II.</p><p><b>RESULTS</b>The translocation of p50 in nuclei was highly remarkable 2 hours after Ang II stimulation, and the activity was somewhat reduced 6 hours after stimulation to the 18th hour. Northern blot also showed PDGF-B mRNA increased by stimulation of Ang II for 18 hours.</p><p><b>CONCLUSION</b>Ang II is effective in stimulating NF-kappaB activation through a pathway dependent on NIK, IKK(alpha) and IKK(beta), and induces PDGF-B transcription in the endothelial cell line, ECV304.v</p>