ABSTRACT
Virtual reality (VR) technology is a kind of human-computer interaction technology, which has been widely used in teaching. In the acute mountain sickness rescue teaching practice, we simulated the plateau environment, operation process of prevention and treatment of mountain disease via VR, which were compared with traditional teaching model. Clinical medical undergraduates were selected as the research objects, and the practice effect was compared and analyzed. VR technology makes more rich and diverse teaching methods in acute mountain sickness rescue teaching practice, which has significant advantages in improving the teaching environment and overcoming the shortage of equipment and space. We have optimized the instructional design, realized the teaching mode by combination of virtuality and reality, and improved the teaching quality and test scores.
ABSTRACT
OBJECTIVE To establish an in vitro blood-cerebrospinal fluid barrier (BCB) model to investigate the underlying mechanism of lead-induced BCB injuries.METHODS The in vitro BCB model was established by Z310 cells.Different concentrations of Pb(AC)2 (2.5,5.0 and 10.0 mmol·L-1) were used for 24,48 and 72 h.Transendothelial electrical resistance (TEER) and flux of FITC-dextran were performed to determine the permeability of the in vitro BCB model.Western blotting and immunofluorescence methods were used to observe the expression of tight junction protein ZO-1 and occludin.RESULTS Compared with control group,Pb(AC)2 2.5,5.0 and 10.0 mmol· L-1 exposure for 48 h to Z310 cells had no significant effect on survival rate and density.TEER in different groups was gradually increasing.At the 12th day after Pb(AC)2 exposure,the values of TEER and flux of FITC-dextran in Pb(AC)2 5 and 10 mmol· L-1 groups were significantly decreased (P＜0.05).Western blotting and immunofluorescence images showed that the expression of ZO-1 and occludin were significantly decreased (P＜0.05) after Pb(AC)2 exposure for 48 h.CONCLUSION Lead exposure can cause the breakdown of BCB barriers,and this effect may be mediated by reducing the expression of ZO-1 and occludin proteins.
ABSTRACT
<p><b>OBJECTIVE</b>To study the effect of emodin on the proliferation, cell cycle distribution, apoptosis and expression of hematopoietic growth factors in bone marrow mesenchymal stem cells (BMSCs).</p><p><b>METHODS</b>The proliferation of rat BMSCs exposed to emodin was analyzed using MTT assay, and flow cytometry was used to detect the apoptosis and cell cycle changes of the exposed cells. Real-time quantitative PCR was used to determine the mRNA expression of the hematopoietic growth factors.</p><p><b>RESULTS</b>Exposure to 0.1 and 1 µg/ml emodin for 48 and 72 h significantly enhanced the proliferation of BMSCs (P<0.01). The cells exposed to 0.1 µg/ml emodin showed significantly increased percentage of cells in G2/M phase (P<0.05), and 1 µg/ml emodin exposure caused increased cells in S phase (P<0.01) and decreased cells in G1/G0 phase (P<0.05). Emodin exposure for 48 h resulted in significantly decreased cell apoptosis (P<0.05). BMSCs treated with 0.1 µg/ml emodin showed a significant increase in the expression of thrombopoietin mRNA (P<0.05).</p><p><b>CONCLUSION</b>Emodin can promote the proliferation of BMSCs in vitro possibly by regulating the cell cycle distribution, cell apoptosis and thrombopoietin expression.</p>
Subject(s)
Animals , Rats , Apoptosis , Cell Cycle , Cell Proliferation , Emodin , Pharmacology , Hematopoietic Cell Growth Factors , Metabolism , Mesenchymal Stem Cells , Cell Biology , RNA, MessengerABSTRACT
Objective To study the relationship between the serum homocysteine ( Hcy ) levels in patients with first-episode depression and event related potentials ( ERP ) P300.Methods 117 first-episode depressive patients were selected as the case group,and 110 healthy volunteers were selected as the health control group,the de-termination of serum Hcy levels in the two groups were detected by enzyme linked immunosorbent assay,measured by the Shenzhen Brain Master brain evoked potential system to complete the visual P300.Results The serum Hcy levels of the case group was (14.0 ±9.8)μmol/L,which was higher than (10.5 ±7.5)μmol/L of the health control group (t=-3.087,P <0.05).The N1,N2 incubation period of the case group were (91.4 ±18.6) ms,(235.4 ± 30.5)ms,respectively,which were longer than (88.6 ±13.0)ms,(204.3 ±20.3)ms of the health control group(t=1.305,8.990,all P<0.01);The P3 incubation period of the case group were (359.5 ±30.0)ms,which was longer than (327.2 ±41.8)ms of the health control group(t=6.685,P<0.05).The target P3,non-target P2 amplitude of the case group were (4.1 ±2.0)μV,(4.2 ±1.9)μV,respectively,which were singnificantly lower than (6.8 ± 3.8)μV,(6.6 ±3.6) μV of the health control group( t=-6.694,-6.485,all P<0.01).The P2 incubation period of Hcy case group was (194.4 ±13.6) ms,which was longer than (163.1 ±21.8) ms of the non Hcy case group(t=8.486,P<0.01).The P3 incubation period of Hcy case group was (357.0 ±24.5)ms,which was longer than (337.1 ±45.5)ms of the non Hcy case group(t=2.645,P<0.05).The target P3,non-target P2 amplitude of the Hcy case group were (5.4 ±1.5)μV,(5.2 ±1.2) μV,which were significantly lower than (5.8 ±3.8)μV, (5.4 ±3.2)μV of the Hcy case group(t=-0.745,-0.208,all P<0.01).Conclusion The serum Hcy levels in patients with first-episode depression increased, and P300 latency, amplitude decreased, the cognitive function is related to Hcy metabolism disorder and depression damage.