Through the practice of outpatient doctor station cored by the outpatient Electronic Medical Records (EMR),the paper discusses the disadvantages of outpatient paper medical records and the advantages of outpatient EMR,summarizes the key points and difficulties in promoting outpatient EMR,and meanwhile points out to pay attention to the integration with other information system,data standardization,perfection of the management system,integrated consultation system and other issues in the practice process.

Adult ; Aged ; Endoscopy ; Female ; Headache ; etiology ; pathology ; Humans ; Male ; Middle Aged ; Nasal Mucosa ; pathology ; Nose ; abnormalities ; pathology

Animals ; Cytological Techniques ; methods ; Cytophotometry ; instrumentation ; methods ; Humans ; Pharmacology ; methods ; trends ; Systems Biology ; methods ; Toxicology ; methods ; trends

Renin-angiotensin system (RAS) is correlative with many diseases. Angio tensin II (AngII) plays an important role as the final effective approach for RAS. This article reviews the main approach to the action and biosynthesis of AngII: including AngII receptor blocker (ARB), chymase inhibitor and ACE2 which were disscoverd recently.

Autophagy is a crucial biological process in eukaryotes, which is involved in cell growth, survival and energy metabolism. It has been confirmed that autophagy mediates toxicity of anticancer drugs, especially in heart, liver and neuron. It is important to understand the function and mechanism of autophagy in anticancer drugs-induced toxicity. Given that autophagy is a double-edged sword in the maintenance of the function of heart, liver and neuron, the autophagy-mediated toxicity are very complicated in the body. We provide a review on the concept of autophagy and current status about autophagy-mediated toxicity of anticancer drugs. The knowledge is crucial in the basic study of anticancer drugs-induced toxicity, and provides some strategies for the development of alleviating the toxicity of anticancer drugs.

Autophagy is a crucial biological process in eukaryotes, which is involved in cell growth, survival and energy metabolism. It has been confirmed that autophagy mediates toxicity of anticancer drugs, especially in heart, liver and neuron. It is important to understand the function and mechanism of autophagy in anticancer drugs-induced toxicity. Given that autophagy is a double-edged sword in the maintenance of the function of heart, liver and neuron, the autophagy-mediated toxicity are very complicated in the body. We provide a review on the concept of autophagy and current status about autophagy-mediated toxicity of anticancer drugs. The knowledge is crucial in the basic study of anticancer drugs-induced toxicity, and provides some strategies for the development of alleviating the toxicity of anticancer drugs.
Antineoplastic Agents ; pharmacology ; toxicity ; Autophagy ; Humans ; Neoplasms ; drug therapy

Objective To research the brain hemodynamic changes in hyperacute cerebral infarction. Methods Focal cerebral ischemia models were presented in 42 healthy New Zealand rabbits by obstructing the unilateral middle cerebral artery with modified O’Brein method. Dynamic scans with intravenous bolus injection of contrast were performed at 0.5, 1, 2, 3, 4, 6h separately after operation by Siemens Somatom Plus 4 Power spiral CT scanner. Then data were input into Siemens Magic View 50 workstation and processed with perfusion CT/VA 10B system. Six cerebral blood functional perfusion maps were obtained. rCBF, rCBV, rTP, rTS of bilateral symmetric interesting regions were calculated. Results Between 0.5-6 hours after operation, the rCBF and rCBV of ischemic cores and peri-ischemic areas decreased subsequently along with times of ischemia developing. rTP、rTS of cores increased at first, then decreased to 0. rTP, rTS of peri-ischemic areas prolonged at all times. Conclusion The ischemic degree, perfusion state of ischemic tissues in brain can be estimated by hemodynamic parameters, which provide useful information for the diagnosis, therapy and prognosis of hyperacute cerebral infarction.

AIM: To study the effect of sphingosine 1-phosphate (S1P) on the increase in microvessel permeability induced by platelet activating factor (PAF). METHODS: The microvessel permeability was assessed by measuring hydraulic conductivity (Lp). To observe the effect of S1P and PAF on vascular endothelial-cadherin (VE-Cadherin), the microvessels were stained with immunofluorescence and examined by laser confocal microscopy. RESULTS: After giving PAF at concentration of 10 nmol/L, the Lp value of rat mesentery microvessel was significantly increased. However, after pretreatment with S1P, PAF did not give rise to a further significant change. The effect of PAF on microvascular endothelial cells could be seen: the formation of endothelial gap was induced, the microvascular fluorescence intensity significantly increased, a large number of fluorescent microspheres (FMs) distributed in the space among the endothelial cells. However, after pretreated with S1P, no obvious gap opening and the FMs accumulation were observed. Compared to normal control, no significant difference of the microvascular fluorescence intensity was found. CONCLUSION: PAF changes the structure of VE-Cadherin, leading to detachment of adherent junction, formation of intercellular gaps, which contributes to the increase in the permeability. S1P improves the increase in the microvessel permeability caused by PAF, which might be mediated by strengthening adherent junction and inhibiting the formation of endothelial gaps.

AIM: To study the protective effects of taurine-magnesium complex (TMC) on endothelium and hemorheology in rats. METHODS: A model of the endothelial damage was made by means of giving rats an injection of adrenaline and making them swim in ice-cold water, then number of circulating endothelial cells (CEC) in whole blood, plasma ET-1 and NO_2~-/NO_3~- content, NOS activity and rheology were determined, respectively. The protective effects of TMC were also observed. RESULTS: An increase in the number of CEC accompanied by abnormal whole blood viscosity, and endothelium-derived ET-1 were observed in model rats. Both the NO_2~-/NO_3~- content and NOS activity were declined significantly in model rats. TMC reduced the number of CEC, resumed NO_2~-/NO_3~- content and NOS activity, and improved the whole blood viscosity in a dose-dependent manner in model rats. CONCLUSION: Ice-cold water bath with adrenaline causes an acute damage of vascular endothelium and abnormal rheology. TMC protects against the injury of vascular endothelium and improves the hemorheology. [