1."Design and implementation of ""ECG challenge"" educational game APP"
Chinese Journal of Medical Education Research 2017;16(3):280-284
ECG is a highly practical discipline,not only requires students to have a solid theoretical foundation,but also requires them to have a wealth of clinical practice (graph reading) capacity.This study aims to improve the students' ability of reading ECG,and introduces the game logic and mechanism,to design and implement the educational games APP.The structure of this APP includes learning module,test module,and evaluation and feedback module,which can realize the three functions of independent inquiry,cooperation plus communication,and test challenge.By the development and application of this kind of inquiry medical education game on the mobile terminal,we can provide learners with adaptive,fragmented,and game-based mobile learning environment.
2.AICAR Blocks the Proliferation of Pulmonary Artery Smooth Muscle Cells by Inhibition of Cell Cycle in G0/G1
Journal of Medical Research 2015;44(5):111-113
Objective To establish the PDGF-BB-induced proliferation of rat pulmonary artery smooth muscle cells(PASMCs), and investigate the effects of the AMPK agonist AICAR on the cell cycle of PASMCs, in order to search new drugs for prevention of pulmo-nary vascular remodeling. Methods 20ng/ml PDGF-BB was used to induced the proliferation of PASMCs, and the effect of 0. 5mmol/L AICAR on the proliferation of PASMCs was observed. Western blot was used to detect the total and phosphorylated AMPK. The prolifer-ation of PASMCs was determined by CCK-8. The mRNA expression of cyclinD1, cyclinE and CDK2/4/6 were detected by flow cytometry analysis cell cycle,quantitative real-time PCR. Results Western blot Results indicated AICAR could promote the activation of AMPK. CCK-8 test Results showed that AICAR blocked the proliferation of PASMCs induced by PDGF-BB. Flow cytometry analysis indicated that AICAR arrested the cell cycle in G0/G1 to S phase. RT-PCR Results demonstrated that AICAR inhibited the mRNA expression of cy-clinD1, cyclinE and CDK2/4/6. Conclusion The AMPK agonist AICAR can block the proliferation of PASMCs induced through arrest cell cycle in G0/G1-S phase by regulation the mRNA expression of cyclin D1, cyclinE, CDK2/4/6, and AICAR has a potential applica-tion in preventing pulmonary vascular remodeling.
3.Raloxifene combined with calcium phosphate cement for repair of rabbit mandibular defects
Chinese Journal of Tissue Engineering Research 2014;(25):3993-3997
BACKGROUND:Raloxifene is the third generation of selective estrogen receptor modulators, which can decrease bone loss, increase bone mineral content, and reduce fracture risk. OBJECTIVE: To study the effects of raloxifene combined with self-setting calcium phosphate cement on the repair of rabbit mandibular defects. METHODS:Totaly 36 New Zealand white rabbits were selected to prepare 8 mm×4 mm×3 mm mandibular defect models, and then randomized equaly into experimental group (raloxifene, 7.5 mg/kg per day, combined with self-setting calcium phosphate cement), drug group (raloxifene, 7.5 mg/kg per day), artificial bone group (self-setting calcium phosphate cement). Rabbits were sacrificed 4, 8 and 12 weeks later, respectively, for measurement of bone morphogenetic protein 2 using immunohistochemistry method and transforming growth factor β using a laser scanning confocal microscope. RESULTS AND CONCLUSION:After 4 and 8 weeks, the expression of bone morphogenetic protein 2 was obviously higher in the experimental group than the drug and artificial bone groups; after 12 weeks, bone remodeling was basicaly complete in the experimental group, and the expression of bone morphogenetic protein 2 became lower than that in the other two groups. The expression of transforming growth factor β in the experimental group was gradualy increased and reached the peak at 8 weeks, while in the drug and artificial bone groups, the expression of transforming growth factor β exhibited an increasing trend within 4-12 weeks, which was close to the peak. These findings suggest that raloxifene can promote early expression of bone morphogenetic proteins and early calus formation as wel as accelerate the repair of bone defects with calcium phosphate cement.
4.Expression and clinical value of surviving in mononuclear cells of bone marrow and peripheral blood of children with acute leukemia
Journal of Third Military Medical University 2003;0(22):-
Objective To study the survivin expression in mononuclear cells of both bone marrow and peripheral blood in childhood acute leukemia(AL).Methods Twenty-one children with AL were divided into newly diagnosed group(n=12) and complete remission(CR) group(n=9).The control group was consisted of 15 children without tumor.Mononuclear cells were separated from bone marrow and peripheral blood (PBL) by gradient density centrifugation and RNA was extracted,and RT-PCR was performed to detect survivin mRNA.Results In newly diagnosed AL group,6 out of 12 patients had positive survivin expression in bone marrow(50%) and 4 out of 11 patients in the PBL(36.37%),both of which were higher than the control group(P0.05).In 9 CR patients,all the patients had the negative expression in the PBL,but 1 positive expression in bone marrow(11.11%).The positive expression in CR group was significantly lower than the newly diagnosed AL group.The only one patient with positive survivin expression in CR group had relapse 7 weeks later.In newly diagnosed patients,the average immature leukocytes were(76.43?43.28)?10~(9)/L in the patients with positive survivin expression and(13.85?5.86)?10~(9)/L in those with negative survivin expression(P
5.Surgical indications and postoperative management of Crohn's disease in children
Chinese Journal of Applied Clinical Pediatrics 2016;31(19):1449-1450
Crohn's disease is a transmural and chronic granulomatous inflammation and it can easily complicated with enterostasis,intestinal obstruction,intestinal perforation,fistula,abscess and massive hemorrhage of gastrointestinal tract.Therefore,patients with Crohn's disease often need surgery,but the surgical indications and postoperative management is still full of challenge.Preventing postoperative recurrence and reducing the complications is essential.
6.Anatomic and functional reconstruction of the spinal posterior column after resection of intraspinal neoplasms
Chinese Journal of Orthopaedic Trauma 2016;18(6):535-538
Objective To investigate the operative outcomes of anatomic and functional reconstruction of the spinal posterior column after resection of intraspinal neoplasms.Methods From January 2010 through October 2014,we treated 32 patients with intraspinal neoplasm in the spine.They were 18 men and 14 women,13 to 62 years of age (average,38 years).The neoplasm was detected in the cervical spine in 10 cases,in the thoracic spine in 14 and in the lumbar spine in 8.All cases received expansive open door laminoplasty via the posterior approach for resection of the intraspinal neoplasm,followed by replantation and titanium plate fixation for anatomic and functional reconstruction of the spinal posterior column.The neural functional recovery,spinal motion and sagittal diameter of the spinal canal before and after operation,spinal stability and graft fusion were observed.Results The patients were followed up for 3 to 23 months (average,13 months).All the intraspinal neoplasms were completely resected.The Frankel grading of neural functional recovery was improved differently in all the cases.By the final follow-ups,the spinal motion was normal in all the cases,without any significant limitation.Graft fusion and rigid internal fixation were achieved in all the cases.Short-term follow-ups revealed no signs of spondylolisthesis or spinal instability.At the final follow-ups,the 3-D CT reconstruction showed no significant shortening in the sagittal diameter of the same spinal canal before and after operation (P >0.05).Conclusions For intraspinal neoplasm in the spine,the whole vertebral lamina is opened or removed via the posterior approach to resect the neoplasm,followed by reduction of the vertebral lamina and mini titanium plate fixation to reconstruct the anatomy and function of the original spine.This is an ideal way to treat intraspinal neoplasms in the spine.
7.Trim family and tumor
Qingmei YANG ; Zumin XU ; Chengnong GUAN
Journal of International Oncology 2015;(6):442-444
Studies show that some Trim family proteins are associated with tumorigenesis and cancer progression.Trim members are differently expressed in various cancers including lung cancer,hepatocellular carcinoma,colon cancer,stomach cancer and breast cancer.Trim proteins are found to be involved in tumor progess by modulating the expression of tumor associated genes via several signaling pathways such as p53 and NF-κB pathway.Members of Trim family can be used as oncogenes or anti-oncogenes in the biological processes such as tumor cell proliferation,cell differentiation,cell apoptosis and metastasis.
8.Molecular epidemiological study of GJB2 mutations in the prelingual deafness in northwestern China
Jing GUAN ; Yufen GUO ; Baicheng XU
Medical Journal of Chinese People's Liberation Army 1981;0(04):-
Objective To investigate the molecular epidemiology of GJB2 mutations as a causative effect of prelingual deafness in northwestern China. Methods The medical history of 274 deaf-mute students was collected. Blood samples were obtained from them with informed consent. GJB2 gene sequences of genomic DNAs were amplified by polymerase chain reaction (PCR) with a pair of primers, and bidirectional sequencing of PCR products was performed and analyzed with DNAStar Software. Results A total number of 274 deaf-mute students were diagnosed as non-syndromic hearing impairment, and profound prelingual deafness. Two kinds of polymorphism, seven pathologic mutations and one novel mutation were revealed in the GJB2 screenings of them, and 79G→A and 341A→G were polymorphism with high frequency. Conclusion GJB2 gene mutation is the causative gene in the prelingual deafness with a high incidence of 10.95% in northwestern China. Based on the investigation, it is clear that screening of GJB2 gene mutation should play a significant role in early diagnosis of deaf-mutism in this region.
9.A CLINICAL OBSERVATION OF MARINE GEL IN THE TREAT- MENT OF CONDYLOMA ACUMINATA
Yaolin XU ; Jianping LI ; Meijun GUAN
Chinese Journal of Marine Drugs 1994;0(02):-
ABSTRACT There is few drug made in China for curing Codyloma acuminata(CA.'). We manu factured a kind of gel for curing CA with a relatively new marine drug and a anti-cancer medicine i. e a derivative of cantharidin. The clinical observation on 58 patients with a total effective rate of 96. 5 per cent showed that the prescription is reasonably made up玹he new dosage form has a lasting curative effect in curing CA. It is used easily and has no toxicity,or allergic reaction.
10.Study on platelet-activating factor-induced apoptosis in neurons and NMDA signal pathway
Yun XU ; Lan WANG ; Dening GUAN
Journal of Clinical Neurology 2001;0(05):-
Objective To investigate whether N-methyl-D-aspartate(NMDA) signal pathway is involved in platelet-activating factor(PAF)-induced apoptosis in neurons.Methods Mice cortex neurons were treated by PAF in different dose for 24 hours or pretreated by a PAF receptor antagonist BN52021, an NMDA receptor antagonist MK801 and a nitric oxide synthase(NOS) inhibitor L-NAME for 30 min. Then the neurons were stained by propidium iodide(PI)/calcein AM and the images were taken by a digital camera on a fluorescent microscope. Neuron death ratio(%) was calculated. In the mean time, neuron NOS(nNOS) expression of the cells was detected by Western Blot method, as well as nNOS activity was measured by 3H radioimmunoassay.Results (1)Neuronal death increased after neurons were treated with 0.01, 0.1, 0.3 and 0.6 ?mol/L PAF 24 h. There were signifitantly changed in 0.3 ?mol/L and 0.6?mol/L comparing control. (2)PAF-induced neurotoxicity was prevented not only by BN5021, but also by MK-801 or L-NAME. (3)PAF enhanced nNOS expression and activity in neurons.Conclusion NMDA signal pathway is involved in platelet-activating factor-induced neurotoxicity.