Objective To explore learning burnout psychology and professional identity of nursing students studying at the traditional Chinese medicine college.Methods 200 students were surveyed by learning burnout and professional commitment scale.Results Learning burnout level of nursing students was higher,depression scores were the highest in four dimensions.Professional commitment kept within medium level.The professional identity was low.The inheritance commitment score was the lowest in each dimension analysis.Conclusions Schools and teachers should take corresponding measures to improve professional commitment level,so as to reduce learning burnout level and ensure long-term stable development of nursing profession.

OBJECTIVE To investigate the distribation of the AmpC enzyme in Acinetobacter baumannii isolated from burned patients. METHODS Susceptibility tests were used to detect antibiotic resistance to 20 kinds of antimicrobial drugs in 20 strains of A. baumannii isolated from burned patients, AmpC enzyme genes were detected by PCR and partial positive products were chosen to sequence. RESULTS Drug resistances to ?-lactam antibiotics in 20 strains of A. baumannii isolated from burned patients had exceeded 85% except levofloxacin or cefoperazone/sulbactam. Of ADC genes 95% were positive, but all DHA genes were negative. Through sequence and Blast analysis, partial ADC positive products were identical with that of EF546445. CONCLUSIONS The multidrug resistance of A. baumannii isolated from burned patients to ?-lactam antibiotics is serious. AmpC enzyme mediated by chromosome, ADC, prevails in A. baumannii isolated from burned patients.

OBJECTIVE To investigate the disseminateion of the carbapenemase in Acinetobacter baumannii isolated from burned patients.METHODS Susceptibility tests of 20 strains of A.baumannii isolated from burned patients to 20 kinds of antimicrobial drugs were detected.Subsequently,seven genes encoding carbapenemase,including OXA-23,OXA-24,OXA-51,OXA-58,IMP,VIM and SIM,were detected by PCR and genes of partial positive products were sequenced.RESULTS Drug resistances to ?-lactam antibiotics of 20 strains of A.baumannii isolated from burned patients all exceeded 85% except to levofloxacin or cefoperazone/sulbactam.Nineteen strains(95%) were OXA-23 genes positive and all other genes were negative.Through sequence and Blast analysis,OXA-23 gene products were identical with that of CAB69042.1.CONCLUSIONS The multidrug resistance of A.baumannii isolated from burned patients to ?-lactam antibiotics is critical.Carbapenemase of OXA-23 prevails in A.baumannii isolated from burned patients.

BACKGROUND: Metabotropic glutamate receptor(mGluR) is G-protein coupled membrane receptors, which participate in various physiology or pathology process in brain, but how it induce brain ischemic tolerance(BIT)is unclear.OBJECTIVE: To study roles of mGluR2/3 and mGluR1/5 in the BIT induction.DESIGN: Randomized controlled study based on experimental animals.SETTING: Neurological department of provincial hospital and pathophysiological department of basic institute in a university.MATERIALS: The study was conducted at the Pathophysiological Department, Institute of Basic Medicine, Hebei Medical University from May 2002 to May 2003. Totally 64 healthy male SD rats were selected from the Experimental Animal Center of Hebei Medical University. Glial fibrillary acidic protein (GFAP) antibody, MTPG and(s)-4C3HPG were got from Sigma Company.INTERVENTIONS: 4 vessel occlusion(4VO) brain ischemic models in rats stained with thionine staining and GFAP immunohistochemistry staining. were used. Sixty-four rats, of which bilateral vertebral arteries were occluded permanently by electrocautery, were divided into the following 8groups: sham operation group, cerebral ischemic preconditioning(CIP)group, ischemic insult group; BIT group; MTPG + sham operation group;MTPG+BIT group; MTPG+ischemia group and(s) -4C3HPG+BIT coup. All the rats were killed 7 days after the operation or the final ischemic treatment. Cerebral sections were selected and stained with thionine staining and GFAP immunohistochemistry staining.MAIN OUTCOME MEASURE: The changes of the morphologic hippocampal pyramidal cell and GFAP expression of astrocyte.RESULTS: ① The 8 minutes ischemic insult increased the histological grade(HG) in CA1 area, decreased the pyramidal neuronal density(ND)and increased the expression of GFAP significantly( P ＜ 0.05) . ② The above changes were not observed in the BIT group, indicating that the CIP could protect pyramidal neurons against the 8-minute ischemic insult. ③The protective effects of the CIP were blocked by MTPG or(s)-4C3HPG, as manifested by significant increases in HG and decreases in ND in the groups of MTPG + BIT, MTPG + ischemia and(s)-4C3HPG + BIT( P ＜ 0.05).CONCLUSION: MTPG or (s) -4C3HPG could block the induction of BIT induced by CIP, but mGluR2/3 or mGluR1/5 could participate in the induction of BIT by which protect effect of mGluR is further induced.

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.

Objective To investigate the pattern of the cerebral white matter lesions in patients with mild and moderate Alzheimer's disease(AD)and healthy controls using proton magnetic resonance spectroscopy(~1H-MRS)and diffusion tensor imaging(DTI).Methods Twenty AD patients and Twenty healthy controls were recrnited.All subjects underwent clinical examination,neuropsychological assessment.The quantitative analysis of N-acetylaspartate(NAA),myoinositol(mI),Chotine(Cho)and Creatine(Cr)resonance signals in region of interests(ROIs)located in the paraventricular white matter region bilaterally were measured.Ratios of NAA/Cr,mI/Cr and Cho/Cr were calculated in two groups.In addition,conventional MRI and DTI scanning were received,fractional anisotropy(FA)and mean diffusivity(MD)values of white matter in the same regions were measured respectively.Results No significant difference between two groups were observed in NAA/Cr ratio(P＞0.05).A significantly increased mI/Cr and Cho/Cr were found in AD patients than in controls(P＜0.05).FA and MD values in AD patients were 0.470±0.082 and 0.771±0.099,and in controls were 0.539±0.068 and 0.691±0.064,respectively.FA value decreased significantly in AD patients(P＜0.05),M D value increased significantly in AD patients(P＜0.05).After controlling for age-related,partial correlation analysis revealed a negtive correlation between mI/Cr and FA value in the patients with AD(P＜0.05).No correlation between mI/Cr and MD was found(P＞0.05).Conclusion The results suggest that not only the gray matter is injured,but also the white matter is abnormal in AD patients.Combining ~1H-MRS with DTI alterations could provide the valuable informations about white matter lesions in AD patients.

BACKGROUND: A new method, i.e., heparin slow-release stent implantation combined with myocardium drilling, is discovered for myocardial revasculadzation, which remarkably improves myocardial perfusion. OBJECTIVE: To investigate the effect of heparin slow-release stent implantation combined with myocardium drilling on myocardial regeneration of pigs with acute myocardial infarction.METHODS: Anterior descending coronary of pig was ligated to induce myocardial infarction model, which was randomly divided into control and implantation groups, with 6 pigs for each group. Self-made borer was used in the implantation group to drill two transmural channels (3.5 mm diameter) on epicardium. A heparin slow-release stent was fixed in the transmural channel. Following intravenous injection, BrdU was used to label DNA duplication so as to observe stromal cell-derived factor-1 (SDF-1) mRNA expression, myocardial perfusion, newborn yocardium, and heart function prior to and following implantation. RESULTS AND CONCLUSION: As compared with control group, SDF-1 expression was enhanced in the implantation group at 6 weeks after stent implantation (P < 0.001), perfusion mass defect percentage was significantly decreased (P < 0.001), ejection fraction of left ventricle was increased (P < 0.05), newborn myocardium was increased (P< 0.001), and survival myocardium in the ischemic region was increased (P < 0.001). The results demonstrated that heparin slow-release stent implantation combined with myocardium drilling could repair damaged myocardial cells and improve heart function through increasing SDF-1 expression and myocardial perfusion.

AIM: To explore the role of NO in the induction of brain ischemic tolerance (BIT) by observing changes of NOS activity and NO_2-/NO_3- content following a transient cerebral ischemia. METHODS: The rat 4-vessel occluding brain ischemic model was used. 140 male Wistar rats were divided into sham, cerebral ischemic preconditioning (CIP), ischemic insult and CIP+ischemic insult groups. An occlusion of the 4 vessels for 3 min was normally used as CIP, and a relative long one for 10 min was used as ischemic insult. When CIP was followed by ischemic insult, the interval between them was 3 d. The CA1 region of the hippocampus of rats was dissected out at 0 h, 2 h, 16 h, 24 h, 36 h, 72 h and 7 d after the last time of ischemia to assay its NOS activity and NO_2-/NO_3- content. RESULTS: The NOS activity and NO_2-/NO_3- content began to increase at 16 h, peaked at 24 h and decreased to basal level at 36 h of reperfusion after CIP. The duration of the up-regulation of NOS activity and NO_2-/NO_3- content was much shorter than that of BIT, which usually takes place 1-7 d after CIP. The pattern of upregulation of the NOS activity and NO_2-/NO_3- content was similar to the CIP group, but the maximum (24 h) was much more than that in CIP group (P

OBJECTIVETo evaluate the effect of infiltration resin on masking white spot lesions by assessing the change in the white spot area.

METHODSSeventy-four maxillary anterior teeth with post-orthodontic decalcification teeth were investigated in this study. All teeth were treated with infiltration resin according to manufacturer recommendation. Standardized digital images were taken before, immediately after, and one week after treatment. The results were classified into three groups: com-pletely masked, partially masked and unchanged. The images of partially masked teeth were analyzed using an image analysis software. The size of the white spot lesion (W) and the whole-tooth facial surface (T) were measured, and the W:Tratio (%) was calculated. Statistical evaluation of the lesions was performed using Kruskal-Wallis and Mann-Whitney tests.

RESULTSAmong the 74 teeth, 20 (27%) teeth were classified as completely masked and 54 (73%) teeth were classified as partially masked; no tooth was unchanged. The W:T ratio significantly decreased from 39.28% before treatment to 9.46% after treatment (P < 0.05).

CONCLUSIONResin infiltration is an effective treatment for masking white spot lesion. However, the masking effect depends on the lesion depth and activity.

AIM: To explore whether free radicals participate in cerebral ischemic tolerance and the up-regula-tion of p38 MAPK and ERK signaling pathways in rats induced by limb ischemic preconditioning (LIP). METHODS: A total of 128 Wistar rats with permanent occlusion of bilateral vertebral arteries were randomly divided into sham group (n=16), cerebral ischemia (CI) group (n=16), LIP+CI group (n=16), DMTU (a free radical scavenger)+LIP+CI group (n=64) and DMTU+sham group (n=16). Six rats in each group were used to observe the delayed neuronal death (DND) in hippocampal CA1 region by thionin staining at 7 d after the end of operation. Other 10 rats in each group were used to de-tect the expression of p38 MAPK and ERK in hippocampal CA1 region by immunohistochemistry and Western blot. RE-SULTS: Lethal CI resulted in obvious DND in hippocampal CA1 region. However, LIP reversed the above injurious changes, represented by the decrease in histological grade and the increase in neuronal density compared with CI group (P<0. 01). Moreover, LIP significantly up-regulated the expression of p38 MAPK and ERK in hippocampal CA1 region com-pared with CI group (P<0. 01). Administration of free radical scavenger DMTU via femoral vein before LIP partially re-versed the neuroprotective effect of LIP, and blocked the up-regulation of p38 MAPK and ERK expression in hippocampal CA1 region in rats compared with LIP+CI group (P<0. 01). CONCLUSION: Free radicals are involved in the neuropro-tection and up-regulation of p38 MAPK and ERK expression induced by LIP in rats.