Using Mind Maps to Improve Medical Student Performance in a Pharmacology Course at Kunming Medical University.

OBJECTIVE: To determine whether students using mind maps would improve their performance in a final examination at the end of lecture-based pharmacology course. STUDY DESIGN: Aquasi-experimental study. PLACE AND DURATION OF STUDY: Kunming Medical University, from September 2014 to January 2015. METHODOLOGY: One hundred and twenty-two (122) third year undergraduate medical students, starting a 48-hour lecturebased pharmacology course, volunteered to use mind maps as one of their study strategies (intervention group), while the remaining 100 students in the class continued to use their usual study strategies (control group) over the duration of the course. The performance of both groups in the final course examination was compared. Students in the intervention group also completed a questionnaire on the usefulness of mind maps during the course and in preparation for the final examination. RESULTS: The students' performance of intervention group was superior to performance of the control group in all parts of a multi-modal final examination. For the multiple choice questions and comprehensive scores, average marks of 45.97 ±7.22 and 68.07 ±12.77, respectively were acquired by the control group, and 51.77 ±4.95 (p<0.01) and 80.05 ±7.54 (p<0.01), respectively by the intervention group. The median IQR scores for "filling in the blanks" questions, short answers questions and case analyses, were 6.00 (6.00), 8.00 (3.50), 8.75 (5.88), respectively for the control group, and were all significantly higher at 8.00 (4.00) (p=0.024), 10.00 (2.00) (p<0.001), and 11.00 (3.25) (p=0.002), respectively for the interventiongroup. Questionnaire responses showed that 95.45% thought that mind maps helped them to prepare more efficiently for the final exam; 90.91% believed that mind maps helped them to better understand all of pharmacology. Ninety-one percent also thought that mind maps would help them to better understand other disciplines, and 86.36% students would like the lecturers to utilize mind mapping as an alternative to conventional teaching formats, such as the use of Power Point. CONCLUSION: The addition of mind maps to students' study of pharmacology at Kunming Medical University improved their performance in all aspects of a multi-modal final examination.

ASH1L Suppresses Matrix Metalloproteinase through Mitogen-activated Protein Kinase Signaling Pathway in Pulpitis.

INTRODUCTION: Pulpitis is an inflammation of dental pulp produced by a response to external stimuli. The response entails substantial cellular and molecular activities. Both genetic and epigenetic regulators contribute to the occurrence of pulpitis. However, the epigenetic mechanisms are still poorly understood. In this research, we studied the role of the absent, small, or homeotic-like (ASH1L) gene in the process of pulpitis. METHODS: Human dental pulp cells (HDPCs) were stimulated with proinflammatory cytokine tumor necrosis factor alpha (TNF-α). Gene expression profiling was performed to assess the occurrence of epigenetic regulators. Pulp tissue from rat experimental pulpitis was subjected to immunofluorescence to detect the occurrence of ASH1L and trimethylation of lysine 4 histone 3 (H3K4me3). The presence of ASH1L in HDPCs that had been generated by TNF-α stimulation was analyzed by Western blot procedures and cellular immunofluorescence. Once detected, ASH1L was silenced through the use of specific small interfering RNA. The effects of ASH1L on the occurrence and operation of matrix metalloproteinases (MMPs) were then tested by analysis of quantitative polymerase chain reactions, Western blotting, and zymography. Chromatin immunoprecipitation was performed to detect whether ASH1L and H3K4me3 were present in the promoter regions of MMPs. We then used Western blot procedures to examine the nuclear factor kappa B and the mitogen-activated protein kinase (MAPK) responses to the silencing of ASH1L. We also examined the specific pathway involved in ASH1L regulation of the MMPs. RESULTS: After stimulating HDPCs with TNF-α, ASH1L emerged as 1 of the most strongly induced epigenetic mediators. We found that TNF-α treatment induced the expression of ASH1L through the nuclear factor kappa B and MAPK signal pathways. ASH1L was found in both the nucleus and the cytoplasm. TNF-α treatment was particularly active in inducing the accumulation of ASH1L in cellular cytoplasm. As is also consistent with in vitro results, ASH1L was found in increased quantities in experimental dental pulpitis tissue. ASH1L knockdown markedly up-regulated the occurrence of MMP-1, MMP-2, and MMP-13. It also exercised an impact on the enzymatic activity of MMP-2 in HDPCs that had been stimulated with TNF-α. ASH1L knockdown activated the MAPK signal pathway in TNF-α-triggered HDPCs, the inhibition of which reversed the induction of MMPs. CONCLUSIONS: Our research identifies a mechanism by which ASH1L suppresses the occurrence and operation of MMPs during pulpitis. It does this through the MAPK pathway.

Hepatocyte growth factor attenuates hypoxia/reoxygenation injury in cortical neurons / 基础医学与临床

Objective To investigate the protective effect of hepatocyte growth factor (HGF) on cultured Sprague-Dawley rat cortical neurons injured through hypoxia/reoxygenation.Methods Primary cultured cerebral cortical neurons were isolated from newborn rots.Neurons were pre-incubated with different concentrations (15,30 and 60 μg/L) of HGF.The cell viability was detected by MTT.Apoptosis was measured by Hoechst 33258 staining and flow cytometer.Lactate dehydrogenase (LDH) and caspase-3 activity were determined by colorimetry.Results Compared with normal group,hypoxia/reoxygenation treatment significantly decreased cell viability,increased LDH activity and the percentage of apoptotic cells.Pretreatment of HGF for 12 h could remarkably reverse the decrease of cell viability and the increase of apoptosis rate in neurons induced by hypoxia/reoxygenation treatment.HGF pre-treatment also attenuated the activity of LDH and caspase-3 in a dose-dependent manner.The effects of HGF could be inhibited by a special PI3K/Akt pathway inhibitor,LY294002.Condusion HGF could attenuate rat cortical neuron injury induced by hypoxia/reoxygenation.The neuroprotective effect of HGF may be related to activating PI3K/Akt pathway,and further suppressing the expression of caspase-3.

Ischemic postconditioning increases the change of hippocampus rCBF and VEGF following cerebral Ischemic in tree shrews / 基础医学与临床

Objective To find the effect and potential mechanism of ischemic postconditioning relief rCBF and VEGF expression during focal cerebral thrombosis.Methods The thrombotic focal cerebral ischemia was induced by photochemical reaction in tree shrews.The rCBF and VEGF expression in hippocampus CA1 area were detected,by laser-Doppler(LD) fowmeter and immunohistochemistry.Results rCBF reduces along with temporal lasting in cerebral thrombus,especially in 24 h;VEGF expression enhanced after cerebral ischemic,express of VEGF in 12 h is the most intensification(P0.05),mostly in 12 h(P

Effects of ischemic postconditioning on hippocampus CA1 area rCBF and astrocyte activation after cerebral ischemia in tree shrews / 中国病理生理杂志

AIM:To study the effects of ischemic postconditioning(PC) on regional cerebral blood flow(rCBF) and astrocyte(AS) activation in hippocampus CA1 area and to explore the possible mechanism of ischemic PC affecting glial fibrillary acidic protein(GFAP) expression during focal cerebral thrombosis.METHODS:The thrombotic focal cerebral ischemia was induced by photochemical reaction in tree shrews,and ischemic postconditioning was established by cliped ipsilateral carotid of the animal at 4 h after cerebral ischemia.The rCBF and GFAP expressions in hippocampus CA1 area were detected,respectively,by laser-Doppler(LD) fowmeter and immunohistochemistry.RESULTS:The numbers of GFAP positive cells were increased markedly and GFAP expression enhanced(P