Objective: To implement dynamic intelligent management system for patients in mental hospital based on RFID technique so as to achieve safe management for patients and contribute to grasp the patient's status in real time. Methods: The hardware of the designed dynamic intelligent management system was consisted of patient's wristbands (electronic tags), locator, reader and the server. The architecture, hardware and function modules of the system were procedural designed. Results: The new design has changed the traditional supervised situation for psychopath which need many manpower and material resources, and reduced the burden of paramedical staff, and decreased the pressure of management for psychopath and enhanced the management level of modernization in hospital. Conclusion: The dynamic intelligent management system based on RFID technique can enhance the management level of hospital, and accelerate the construction of informatization for hospital and improve the image of hospital.

AIM: To detect the changes of inducible nitric oxide synthase (iNOS) expression in kidney following ischemia-reperfusion(I-R)of hindlimbs and to elucidate their significance. METHODS: I-R was established using the occlusion of the femoral arteries for 4 h and re-opening for 2-24 h in rats. The expression of iNOS mRNA,and iNOS protein and the nitrotyrosine (NT),a marker of peroxynitrite (ONOO -),in renal tissue were detected with reverse transcription-polymerase chain reaction (RT-PCR) and immunohistochemical technique,respectively. The superoxide dismutase (SOD) activity and malondialdehyde (MDA) contents in renal tissue were spectraphotometrically measured. The observation of pathologic changes of renal tissue was made following the inhibition of iNOS by aminoguanidine (AG). RESULTS: Compared with control group,the relative expression level of iNOS mRNA significantly increased in I-R group. There were more iNOS and more NT positive product in the epithelial cells of renal proximal convoluted tubules and thick segments of Henle′ loops in I-R group than control group. The contents of MDA markedly increased,while the activity of SOD significantly decreased in I-R group,compared to those in the control groups. The pathologic changes of kidney became milder in I-R group following the inhibition of iNOS by AG. CONCLUSION: The expression of iNOS mRNA and protein in renal tissue were significantly upregulated,excess induction of NO contributed to the kidney injury during the I-R of hindlimbs.

AIM: To detect the changes of heme oxygenase-1 (HO-1) expression in kidney following ischemia-reperfusion of hindlimbs and to elucidate their significance. METHODS: Health SD rats were randomly divided into normal (N), sham (S), 4h ischemia without reperfusion (I), 4 h ischemia-2, 6, 12, 18 or 24 h reperfusion (I-R) groups and I-R18h+zinc protoporphyrin (ZnPP) group. I-R was established using the occlusion for 4 h and re-opening for 2-24 h of the femoral arteries. In I-R 18 h+ZnPP group, ZnPP (5 ?mol?kg~(-1) body weight) was intravenously injected 6 h and 12 h after reperfusion, respectively. The expression of HO-1 mRNA in kidney was detected with reverse transcription-polymerase chain reaction (RT-PCR). The expression and location of HO-1 protein were detected with immunohistochemical technique. The observation of pathologic changes of kidney was made following the inhibition of HO-1 by ZnPP. RESULTS: The relative expression level of HO-1 mRNA significantly increased in I-R group, compared to those in the control groups, It was maximal in I-R 18 h group, and thereafter expression level of HO-1 mRNA decreased, however significant expression was still detected in I-R 24 h group (P

AIM: To observe the changes in nitric oxide(NO) and peroxynitrite anion (ONOO - ) in the injuried lung following the ischemia-reperfusion of hind limbs and evaluate the contribution of NO and ONOO - to tissue injury. METHODS: A model of hind limbs ischemia was made by clamping infrarenal aorta with a microvascular clip and lung injury occurring after reperfusion. Lung tissue was obtained from the animals received sham operation(group 1),4 hours ischemia without reperfusion(group2), 1 hour reperfusion following 4 hours ischemia (group3) and 4 hours reperfusion following 4 hours ischemia (group4) . The contents of MDA, NO - 2/NO - 3 and the activities of SOD in the lung were examined. Immunohistochemical technique was used to determine the immunoreactivity to iNOS and nitrotyrosine(NT)-a specific "footprint" of peroxynitrite. RESULTS: Compared with group1 and group2,the contents of MDA and NO - 2/NO - 3 increased significantly (P

AIM: To investigate the pathologic changes in the brain and its underlying mechansims during ischemia-reperfusion of rat hindlimbs.METHODS: SD rats were divided into the normal(N), sham(S), 4 h ischemia without reperfusion(I), and 4 h ischemia-2, 6,12,18 or 24 h reperfusion (I-R) groups at random. Ischemia and ischemia-reperfusion were established with the occlusion or/and re-opening of the terminal of abdominal aorta, respectively. The pathologic changes in the brain tissue were morphologically observed. The expression of inducible nitric oxide synthase ( iNOS ) mRNA, and iNOS protein and the nitrotyrosine, a marker of peroxynitrite (ONOO -),in the brain tissue were detected with RT-PCR and immunohistochemical technique, respectively. The brain superoxide dismutase (SOD) activity and malondialdehyde (MDA) contents were spectraphotometrically measured.RESULTS: Hydropic degeneration and severe injury to neurons were only showed in I-R group. Expressions of iNOS mRNA and protein were demonstrated in I-R, I and S groups, which were maximal in I-R 6 h group. iNOS positive neurons and microglias were more spread in I-R 6 h group than those in S and I groups. NT positive neurons were localized in the cerebral cortex and hippcampus of I-R 6 h group. The contents of MDA markedly increased, while the activity of SOD significantly decreased in I-R 6 h group compared to the N, S and I groups. There were no significant changes in MDA and SOD in N, S and I groups.CONCLUSION: Severe ischemia-reperfusion of rat hindlimbs could induce brain injury, and its mechanisms might be related to enhanced expression of iNOS -NO-ONOO - in the brain.

AIM: To observe the changes in heme oxygenase-1(HO-1) expression in the lung after ischmia-reperfusion of hind limbs in rats.METHODS: Hind limbs ischemia was made by clamping infrarenal aorta with a microvascular clip and lung injury was made by following reperfusion. Lung tissue was obtained from the animals subjected to sham operation, 4 h ischemia without reperfusion and 4 h, 8 h, 16 h, 24 h, 48 h reperfusion following 4 h ischemia. The levels of HO-1 mRNA and protein were measured at different times by Northern blot and Western blot. Immunohistochemistry technique was used to determine the cell types responsible for limb ischemic reperfusion induced HO-1 expression. RESULTS: After ischemia-reperfusion of limbs, HO-1 mRNA increased by 4 h, reached a peak at 16 h, and returned toward baseline at 24-48 h. This time course correlated with increased HO-1 protein. Immunohistochemical studies showed HO-1expressed in a variety of cell types, including the airway epithelium, alveolar macrophages and vascular smooth muscular cells. There were no positive signals in sham group and ischemia group both in mRNA levels and protein levels. CONCLUSION: The expression of HO-1 in the lung is not induced by limb ischemia or sham operation, but induced by limb reperfusion after ischemia in rats.

AIM: To detect the changes of heme oxygenase-1(HO-1) expression in brain following ischemia-reperfusion of hindlimbs in rats and to elucidate their significance. METHODS: Ischemia-reperfusion was established using the occlusion for 4 h and re-opening for 2-24 h of the femoral arteries. The expression of HO-1 mRNA in brain was detected with reverse transcription-polymerase chain reaction (RT-PCR). The expression and location of HO-1 protein were detected with immunohistochemical technique. The observation of pathologic changes of brain was made following the inhibition of HO-1 by zinc protoporphyrin (ZnPP). RESULTS: The relative expression level of HO-1 mRNA significantly increased in I-R group, compared to those in control group. It was maximal in I-R 12 h group, and thereafter expression level of HO-1 mRNA decreased, however significant expression was still detected in I-R 24 h group (P

AIM:To investigate the pathologic changes in the brain and its underlying mechansims during ischemia-reperfusion of rat hindlimbs.METHODS:SD rats were divided into the normal(N), sham(S), 4 h ischemia without reperfusion(I), and 4 h ischemia-2, 6,12,18 or 24 h reperfusion (I-R) groups at random. Ischemia and ischemia-reperfusion were established with the occlusion or/and re-opening of the terminal of abdominal aorta, respectively. The pathologic changes in the brain tissue were morphologically observed. The expression of inducible nitric oxide synthase (iNOS) mRNA, and iNOS protein and the nitrotyrosine, a marker of peroxynitrite (ONOO-)，in the brain tissue were detected with RT-PCR and immunohistochemical technique, respectively. The brain superoxide dismutase (SOD) activity and malondialdehyde (MDA) contents were spectraphotometrically measured.RESULTS:Hydropic degeneration and severe injury to neurons were only showed in I-R group. Expressions of iNOS mRNA and protein were demonstrated in I-R, I and S groups, which were maximal in I-R 6 h group. iNOS positive neurons and microglias were more spread in I-R 6 h group than those in S and I groups. NT positive neurons were localized in the cerebral cortex and hippcampus of I-R 6 h group. The contents of MDA markedly increased, while the activity of SOD significantly decreased in I-R 6 h group compared to the N, S and I groups. There were no significant changes in MDA and SOD in N, S and I groups.CONCLUSION:Severe ischemia-reperfusion of rat hindlimbs could induce brain injury, and its mechanisms might be related to enhanced expression of iNOS-NO-ONOO- in the brain.

AIM:To observe the changes in heme oxygenase-1(HO-1) expression in the lung after ischmia-reperfusion of hind limbs in rats.METHODS:Hind limbs ischemia was made by clamping infrarenal aorta with a microvascular clip and lung injury was made by following reperfusion. Lung tissue was obtained from the animals subjected to sham operation, 4 h ischemia without reperfusion and 4 h, 8 h, 16 h, 24 h, 48 h reperfusion following 4 h ischemia. The levels of HO-1 mRNA and protein were measured at different times by Northern blot and Western blot. Immunohistochemistry technique was used to determine the cell types responsible for limb ischemic reperfusion induced HO-1 expression. RESULTS:After ischemia-reperfusion of limbs, HO-1 mRNA increased by 4 h, reached a peak at 16 h, and returned toward baseline at 24-48 h. This time course correlated with increased HO-1 protein. Immunohistochemical studies showed HO-1expressed in a variety of cell types, including the airway epithelium, alveolar macrophages and vascular smooth muscular cells. There were no positive signals in sham group and ischemia group both in mRNA levels and protein levels. CONCLUSION:The expression of HO-1 in the lung is not induced by limb ischemia or sham operation, but induced by limb reperfusion after ischemia in rats.

OBJECTIVETo prepare flexible proanthocyanidins nanoliposomes, and explore the in vitro release behavior of proanthocyanidins flexible nanoliposomes and general nanoliposomes.

METHODFlexible proanthoeyanidins nanoliposomes were prepared proanthocyanidins using a film dispersion method, characterized by transmission electron microscope, and the in vitro release action was studied in different dissolution mediums using dynamic dialyse method with the content of total phenol as index.

RESULTThe in vitro release of both proanthocyanidins flexible nanoliposomes and general nanoliposomes were in accordance with Weibull distribution.

CONCLUSIONProanthocyanidins flexible nanoliposomes without pressure had similar in vitro release behavior with general nanoliposomes.

Drug Delivery Systems ; methods ; Liposomes ; chemistry ; ultrastructure ; Nanospheres ; chemistry ; ultrastructure ; Particle Size ; Proanthocyanidins ; chemistry