As an important component of the social system, physician-patient relationship plays a guiding and fundamental role in creating a harmonious healthcare environment. However, due to certain social, ethical and moral factors, the current physician-patient relationship is not favorable, and various contradictions in physician-patient relationship are becoming barriers in building up a harmonious society. In order to enable medicine return to its "merciful" nature, restitute the respect for patients, the dignity of doctors, find the memorable warmth in the medical service world, hospitals must pay close attention to humanistic care in the management dimension in order to establish a harmonious relationship between doctors and patients.

Objective:To investigate the relation of counselors'and therapists'interpersonal personality on the ethical behavior of dual relationship.Methods:Totally 177 practitioners (21-65 years old) were investigated with 4 interpersonal personality subscales of the Chinese Personality Inventory (CPAI) and the Questionnaire of the attitude of counselors to the ethical behavior of dual relationship.Results:There were no differences of 4 dimension of interpersonal personality on the 6 items of professional relationship between higher and lower groups (Ps ＞ 0.05),but on the other 5 types of dual relations respectively,there were 6 (9％),10 (15％),12 (18％) and 21 items'(32％) score showing statistically difference (Ps ＜ 0.05).Furthermore,more items had score difference on social relationship.Conclusion:It suggests that the counselors'and therapists'interpersonal personality may be related to the ethical behavior in dual relationship.

OBJECTIVE:To promote the drug use in a legal way.METHODS:The legal issues were analyzed,which included standardization of specially administrated drugs,exchange or replacement of prescribed drugs,usage and dosage of prescribed drugs,informed consent of patients,etc.RESULTS&CONCLUSION:There still exist problems in clinical drug use,the relevant laws and regulations should be further standardized and identified.

Objective To evaluate the effects of sevoflurane preconditioning on zonula occludens-1 (ZO-1) during myocardial ischemia-reperfusion (I/R) in rats in vitro.Methods Adult male Wistar rats,weighing 250-300 g,were anesthetized with intraperitoneal pentobarbital 30 mg/kg and heparinized.Their hearts were excised and perfused in a Langendorff apparatus with K-H solution saturated with 95％ O2-5％ CO2 at 37 ℃.Eighteen isolated rat hearts were randomly assigned into 3 groups (n =6 each) using a random number table:control group (group C),group I/R and sevoflurane preconditioning group (group S).At 10 min of equilibration,the hearts were perfused with K-H solution for 110 min in group C,the hearts were perfused with K-H solution for 20 min,and then subjected to 30 min of ischemia followed by 60 min of reperfusion in group I/R,and the hearts were perfused with K-H solution saturated with 3％ sevoflurane for 15 min followed by 5 min washout,and then subjected to 30 min of ischemia followed by 60 min of reperfusion in group S.At the end of equilibration,immediately before ischemia,and at 15 and 60 min of reperfusion (T1,2),HR,left ventricular end-diastolic pressure (LVEDP),left ventricular developed pressure (LVDP),+ dp/dtmax and-dp/dtmax were recorded.The development of arrhythmias was recorded during reperfusion and scored.At 60 min of reperfusion,myocardial specimens were obtained from the apex of heart for determination of the expression of ZO-1 in myocardial tissues (by Western blot) and for observation of distribution of ZO-1 and connexin43 (Cx43) (by immunofluorescence).Results Compared with group C,HR,LVDP,+ dp/dtmax and-dp/dtmax were significantly decreased and LVEDP was increased at 15 and 60 min of reperfusion,scores of arrhythmia was increased,and ZO-1 expression was down-regulated in I/R group.Compared with group I/R,HR,LVDP,+ dp/dtmax and-dp/dtmax were significantly increased and LVEDP was decreased at 15 and 60 min of reperfusion,arrhythmia was decreased,and ZO-1 expression was up-regulated in group S.ZO-1 and Cx43 were co-localized at the intercalated disk.ZO-1 was redistributed in the lateralization of the membrane and co-localized with Cx43 in group I/R.The incidence of ZO-1 lateralization was significantly decreased in group S.Conclusion The mechanism by which sevoflurane preconditioning decreases reperfusion arrhythmia is related to inhibition of down-regulation of expression and redistribution of ZO-1 and inhibition of redistribution of Cx43 in rats.

Objective To evaluate the effects of sevoflurane preconditioning on wnt/glycogen synthase kinase-3 beta (GSK-3β)/β-catenin signaling pathway during myocardial ischemia-reperfusion (I/R) injury in rats in vitro.Methods Ault male Wistar rats,weighing 220-280 g,were heparinized and anesthetized with intraperitoneal 3％ pentobarbital 30 mg/kg.Their hearts were rapidly excised and perfused in a langendorff apparatus with oxygenated (95％ O2-5％ CO2) K-H solution at 37 ℃.After 15 min of equilibration,36 isolated hearts were randomly divided into 3 groups (n=12 each) using a random number table:sham operation group (group S),group I/R and sevoflurane preconditioning group (group SP).After 30 min of equilibration,the hearts were continuously perfused for 150 min in group S.The isolated hearts were subjected to 30 min of ischemia followed by 120 min of reperfusion.In SP group,the hearts were perfused for 15 min with K-H solution containing 2.4％ sevoflurane,followed by 5 min washout before reperfusion.At the end of equilibration and 30 min of reperfusion,HR,left ventricular end-diastolic pressure (LVEDP),left ventricular developed pressure (LVDP) and ± dp/dtmax were recorded.The severity of arrhythmias was assessed during reperfusion.At 60 min of reperfusion,3 hearts in each group were chosen for measurement of expression of wnt3a,phosphor-GSK-3β (p-GSK-3β) and β-catenin (by Western blot).At 120 min of reperfusion,6 hearts in each group were chosen for determination of myocardial infarct size by TTC staining.Results Compared with group S,HR,LVDP,+dp/dtmax and -dp/dtmax were significantly decreased,and LVEDP was increased at 30 min of reperfusion,arrhythmia scores and the percentage of myocardial infarct size were increased,and the expression of wnt3a,p-GSK-3β and β-catenin was down-regulated in I/R group.Compared with group I/R,HR,LVDP,+dp/dtmax and-dp/dtmax were significantly increased,and LVEDP was decreased at 30 min of reperfusion,arrhythmia scores and the percentage of myocardial infarct size were decreased,and the expression of wnt3a,p-GSK-3β and β-catenin was up-regulated in group SP.Conclusion Sevoflurane preconditioning attenuates myocardial I/R injury by activating wnt/GSK-3β/β-catenin signaling pathway in isolated rat hearts.

Objective To study the effect of estrogen on myocardial injury in hypothyroidism rats and to reveal the pathology of occurrence and development of the myocardial injury in hypothyroidism rats.Methods The model of hypothyroidism rats was established by feeding propylthiouracil.The pathology of the female group ( n =40 ) and male group ( n =40 ) was observed dynamicly.The presence of myocardial apoptosis cell was demonstrated by the method of terminal deoxynucleotidyl transferase mediated dTUP nick end labeling (TUNEL).And the immunohistochemistry was used to determine the expression of Caspase-3 and Bcl-2 in the myocardial cells.Results The myocardial cell apoptosis appeared in hypothyroidism rats.With the development of the disease,the apoptosis myocardial cell was increased progressively (Female rats group:the numbers of myocardial cell apoptosis at 3,6,8,10,and 12 weeks were 16.40 ± 2.62,29.50 ± 2.67,34.50 ± 3.34,42.70 ±3.24,and 56.00 ± 2.90 respectively,P ＜ 0.05 ; Male rats group:the numbers of myocardial cell apoptosis at 3,6,8,10,and 12 week were 21.60 ± 2.67,35.50 ± 2.94,41.70 ± 2.96,46.70 ± 3.11,and 60.70 ± 3.31respectively,P ＜ 0.05 ),which indicated that estrogen may be related to myocardial cell apoptosis.Conclusion The myocardial cell apoptosis is related with the myocardial injury in hypothyroidism rats.Myocardial cell apoptosis may result in the myocardial injury.The estrogen participates in regulating apoptosis,but its function gradually weakens with the development of the hypothyroidism.

Objective To evaluate the relationship between calmodulin protein kinase Ⅱ (CaMK Ⅱ) and levosimendan against arrhythmias induced by myocardial ischemia-reperfusion (I/R) in rats in vitro.Methods Thirty male Wistar rats,weighing 250-300 g,were randomly divided into 3 groups (n =10 each) using a random number table:control group (group C),I/R group and levosimendan group (group L).Their hearts were rapidly excised and perfused in a langendorff apparatus with K-H solution saturated with 95％ O2-5％ CO2 at 36.5-37.5 ℃.At 20 min of equilibration,the hearts were perfused with K-H solution for 60 min in group C.The hearts were subjected to 30 min of ischemia followed by 30 min reperfusion with K-H solution in group I/R.The hearts were subjected to 30 min of ischemia followed by 30 min reperfusion with K-H solution containing 300 nmol/L levosimendan in group L.Left ventricle developed pressure (LVDP),left ventricle end-diastolic pressure (LVEDP),+ dP/dt-dP/dtmax and heart rate (HR) were recorded immediately before ischemia and at 15 and 30 min of reperfusion.Arrhythmia was recorded during reperfusion and scored.Specimens were obtained from the apex of heart at 30 min of reperfusion for determination of the intracellular calcium concentration ([Ca2 +] i).Myocardial specimens were obtained from the left ventricle at 30 min of reperfusion to detect CaMK Ⅱ activity.Results Compared with group C,arrhythmia score,[Ca2+]i and CaMK [Ⅱ activity were significantly increased,and LVDP,+ dP/dtmax,-dP/dtmax and HR were decreased,and LVEDP was increased at 15 and 30 min of reperfusion in group I/R.Compared with group I/R,the number of ventricular premature beat,arrhythmia score,[Ca2+] i and CaMK Ⅱ activity were significantly decreased,and LVDP,+ dP/dtmax,-dP/dtmax and HR were increased,and LVEDP was decreased at 15 and 30 min of reperfusion in group L.Conclusion Inhibition of CaMK Ⅱ activity is involved in the mechanism by which levosimendan decreases the development of arrhythmias induced by myocardial I/R in rats.

Objective To explore the clinical significance of peripheral blood smear and bone marrow examination in the etiological diagnosis of panhematopenia.Methods 180 cases of panhematopenia were selected and were given peripheral blood smear and bone marrow examination,and the results were analyzed.Results There were 50 cases of panhematopenia because of non hematopoietic system diseases.Among 50 cases of non-hematopoietic system disease,there were 20 cases of chronic hepatitis,3 cases of cirrhosis,4 cases of lung cancer,10 cases of malignant tumors,3 cases of endocarditis,7 cases of connective tissue-like illness,1 case of gastric cancer,1 case of systemic lupus erythematosus and 1 case of hypersplenism.Due to diseases of the hematopoietic system,there were 130 cases of panbematopenia.Among 130 cases of panhematopenia due to diseases of the hematopoietic system,there were 74 cases of acute leukemia(AL),13 cases of myelodysplastic syndrome(MDS),13 cases of aplastic anemia(AA) and 30 cases of megaloblastic anemia(MA).Conclusion Peripheral blood smear and bone marrow examination is conducive to diagnose the cause of the panhematopenia.Bone marrow examination could improve the accuracy rate of panhematopenia.

0.05), but did inhibit activity of iNOS (P

normal morphology + cervicitis).