ABSTRACT
In order to promote the integration between disciplines, the convergence between basic course and clinical teaching, increasing students ability including the active learning and life-long learning ability, finding problem and solving problem ability, teamwork spirit and so on. After nearly 3 years preparation, Hebei Medical University successfully carried out the PBL teaching in Seven-year Clinical Medicine Science. Combining with the teaching activities, formative assessment was carried out, and PBL teaching website was established. The reform has already achieved initial results, got good responds from teachers and students. Through the study, it has been confirmed that the PBL teaching method in Hebei Medical University is effective and worthy to reference.
ABSTRACT
Objective To explore the control effect of proactive monitoring on senile stroke women with Escherichia coli infection caused by indwelling catheter.Methods From October 2011 to September 2012 elderly female stroke patients with indwelling urinary catheter were chosen in the department of neurology and were given proactive monitoring,which included the following:management of antibiotics has been humanized,urinary catheter care used first-cleaning and then disinfection method,pathogen monitoring professionals directly went to the bacteria room for obtaining information.The monitoring results were compared with those last year.Results The urinary Escherichia coli infection in monitoring popu-lations declined sharply,Escherichia coli infection rate reduced from 20.5％ to 3.6％.The urinary infection rate in hospitalized patients reduced from 10.8％ to 5.7％ respectively.The preventive application of an-tibacterial drugs greatly reduced from 70.0％ to 24.7％.The nursing staff all mastered the nursing method of the catheter.Conclusions To give proactive monitoring to senile stroke women with indwelling urinary catheter can control Escherichia coli and other bacteria induced urinary infection due to indwelling catheter significantly,demonstrate a deterrent effect on unreasonable application of antibiotics,which can be recommended to control other indwelling catheter induced urinary hospital infection.
ABSTRACT
Objective To investigate the changes of neuroglobin (Ngb) expression in the CA1 hippocampus after cerebral ischemia and the effect of limb ischemic preconditioning (LIP) on it in young and aged rats. Methods SD rats aged 3 months and 21-23 months with permanently occluding bilateral vertebral arteries were randomly divided into cerebral ischemic group and LIP + cerebral ischemic group, respectively. The expression of Ngb mRNA and protein in the hippocampus were investigated by reverse transcription-polymerase chain reaction (RT-PCR) and Western blot methods. The profile of delayed neuronal death (DND) of pyramidal neurons in the hippocampus CA1 was evaluated by using thionin staining under light microscope by determining the neuronal density (ND) and histological grade (HG). Results Ngb mRNA and protein expressions were 0.16±0.02 and 0.32±0.07, 0.52±0.04 and 0.91±0.06, 0.09±0.01 and 0.22±0.08, 0.21±0.01 and 0.66± 0. 06 in young cerebral ischemia group, LIP + young cerebral ischemia group, aged cerebral ischemia group and LIP + aged cerebral ischemia group, respectively. The expressions of Ngb mRNA and protein after cerebral ischemia for 8 minutes in aged rats were decreased compared with those in the young rats which suffered an identical cerebral ischemia with the aged rats (P<0.05). LIP up-regulated Ngb mRNA and protein expressions in both young and aged rats which suffered cerebral ischemia (P<0.05). However, the up-regulation of Ngb expression in aged rats was significantly less than that in young rats (P<0.05). Neuropathological evaluation showed that ND was 38.8±10.9, 171.5±16.9, 21.2±12.2 and 102.7±15.4 in young cerebral ischemic group, LIP + young cerebral ischemic group, aged cerebral ischemic group and LIP + aged cerebral ischemic group, respectively. It showed that obvious DND of pyramidal neurons was found in young and aged rats after cerebral ischemia. Although LIP effectively protected the pyramidal neurons in the CA1 hippocampus against DND normally induced by ischemic insult, the neuroprotection of LIP for aged rats was less effective than that for young rats. Conclusions The expression of Ngb and the up-regulation effect of LIP on the expression in aged rats are significantly decreased compared to those in young rats when the rats suffer cerebral ischemia. These differences may be one of underlying reasons why the aged rats exhibit severe DND after cerebral ischemia and why the neuroprotective effect of LIP is less in the aged rats than that in the young rats.
ABSTRACT
AIM: To explore the role of NO/ inducible nitric oxide synthase (iNOS) in the metabotromi glutamate receptor 2/3C (mGluR2/3) mediated-brain ischemic tolerance induced by cerebral ischemic preconditioning (CIP), and to observe the influences of α-methyl- (4-tetrazolyl- phenyl) glycine (MTPG), an antagonist of mGluR2/3, on the expression of iNOS during the induction of brain ischemic tolerance. METHODS: Thirty-six Sprague-Dawley rats were subjected to four vessel occluding global brain ischemic model. Thionin staining and immunohistochemistry were used for neuropathological evaluation and assay of iNOS expression in the hippocampal CA1 subregion of the rats. RESULTS: In the sham group, weak expression of iNOS was detected. The expression of iNOS in the CIP and CIP+ischemic insult groups were increased significantly compared with that in the sham group. Administration of MTPG via lateral cerebral ventricle 20 min before CIP blocked the up-regulation of iNOS induced by CIP, but had no influence on the pyramidal neuron survival. However, in the MTPG+CIP+ischemic insult group, the expression of iNOS was extremely intensive compared to that in CIP and MTPG+CIP groups. Importantly, this up-regulation was accompanied with obvious delayed neuronal death. CONCLUSION: NO/iNOS pathway plays an important role in the process of mGluR2/3 mediated-brain ischemic tolerance induced by CIP.
ABSTRACT
AIM:To observe the protective effect of allitridi on hippocampal neuron of rats with cerebral ischemia-reperfusion (I/R) injury and to investigate its effects on P53 expression in hippocampus.METHODS: The global cerebral ischemia-reperfusion models were established by 4-vessel occlusion. Allitridi at doses of 10, 20 or 30 mg/kg was injected through rat’s tail vein, half dose at 30 min before brain ischemia and another half dose at 10 min after reperfusion were injected, respectively. The hippocampus of rat was removed 24 h after reperfusion. Toluidine blue staining was applied to estimate morphologic changes. Flow cytometry was used to evaluate neuronal apoptosis rate of hippocampus. Immunohistochemistry was used to observe the expression of P53 protein.RESULTS: Compared with sham group, survival neuronal density in I/R group was significantly depressed. The rate of neuronal apoptosis and the expression of P53 protein were significantly increased. Allitridi significantly increased the number of survival neurons in hippocampus compared to I/R group. Meanwhile, allitridi remarkably inhibited the rate of neuronal apoptosis and the expression of P53 protein.CONCLUSION: Allitridi has protective role against brain ischemia reperfusion injury. The mechanism may be involved in blocking P53 protein expression in hippocampus of rats with ischemia-reperfusion.