From both doctors and patients′different perspectives , this paper analyses the causes of conflict of doctor-patient communication , and from the subjective and the objective , the history and reality , individual and social aspects of light on the restricting factors for good doctor -patient communication , and puts forward strengthe-ning the consciousness of active , rule execution , achieving full coverage , explore ways to standard mode , rich di-verse ways and other countermeasures .

AIM To examine the effects of the APP17-mer peptide against A? 25-35 -induced apoptosis and gain some insight into the neuroprotective mechanism of the APP17-mer peptide. METHODS Protective effects of APP17-mer peptide against A? 25-35 -induced apoptosis in SH-SY5Y cell was proved by cell morphology, LM-PCR DNA ladder assay and FCM assay. The antiapoptotic mechanism of APP17-mer peptide was investigated using the MTT assay to measure mitochondrial energy redox state, using the fluorescent probe DCF-DA?Rhodamine 123 to measure relative levels of cellular peroxides and mitochondrial membrane potential and using Western blot for AIF and NF-?B to detect the expression of AIF and NF-?B. RESULTS Damage of cell morphology was ameliorated by pretreating with APP17-mer peptide. The apoptotic rate of the SH-SY5Y cells exposed to A? 25-35 in the presence of APP17-mer peptide decreased from 63.75% to 28.25%. Exposure of SH-SY5Y to A? 25-35 for 48 h resulted in an increase in DCF-DA fluorescence,a decrease in Rhodamine 123 fluorescence and MTT reduction, the results were weakened by pre-incubating with APP17-mer peptide for 30 minutes. Treatment of cells with APP17-mer peptide resulted in a significant attenuation in the expression of AIF and a strong increase in the expression of NF-?B. CONCLUSION APP17-mer is protective against cell apoptosis induced by A? 25-35 by provoking and sustaining upregulation of a key antiapoptotic transcription factor NF-?B, by suppressing oxyradical production and by preserving mitochondrial function and inhibiting the release of apoptotic protein from mitochondria.

BACKGROUND: Learning and memory disorder exist in diabetic rats,which can be improved by APP 17-mer peptide. However, it is unclear whether learning and memory disorder in diabetes mellitus is caused by influencing neuronal mitochondrial transmembrane potentials and apoptosis in hippocampus or not and what is the related action mechanism of APP17-mer peptide.OBJECTIVE: To observe the effects of APP17-mer peptide on neuronal mitochondrial transmembrane potentials (△ψm) and apoptosis in hippocampal area of diabetic rats.DESIGN: A completely randomized, grouping and controlled trial.SETTING: Beijing Research Laboratory for Brain Aging, Beijing Xuanwu Hospital, Capital University of Medical Sciences; the Department of Endocrine, the First Central Hospital of Baoding.MATERIALS: The data measurement of the experiment was carried out in the Instrument Testing Center, the General Hospital of Chinese PLA between May 2002 and August 2002. The modeling and intervention of the experiment was carried out in the Animal Laboratory of Xuanwu Hospital, Capital University of Medical Sciences. Eighteen male Wistar rats were enrolled and randomized into control group, model group and APP17-mer peptide group with 6 rats in each group.METHODS: ① Diabetic models in the model and APP17-mer peptide groups were established by intraperitoneal injection of 60 mg/kg streptozotocin (pH=4.4) in fasted rats(fasting for 12 hours). Three days later, modeling was successful if blood sugar level in caudal vein was more than 15 mmol/L. Rats in the control group were not subjected to modeling.Then, the rats in the APP17-mer peptide group were subjected to the subcutaneous injection of APP17-mer peptide (3.4 μg for each rat once) three times a week and totally for ten weeks, whereas rats in the other groups were given saline of the same volume. ② After ten weeks, rats were anesthetized and decapitated to take out brain tissues, and then hippocampal tissues were isolated in ice bath for preparation of single cell suspension.JC-1 labeled mitochondrial transmembrane potentials and cell apoptosis in hippocampal area were measured by means of flow cytometry. ③ One-way analysis of variance was adopted in the comparison among groups.RESULTS: Eighteen rats were involved in the results analysis. ①Neuronal mitochondrial transmembrane potential was lower in the model group as compared with the control group [(551.91±53.36) vs (809.88±82.41) △ψm,P＜0.01] while it was higher in the APP17-mer peptide group as compared with the model group [(705.99±89.92) vs (551.91±53.36) △ψm, P ＜ 0.05].There was no difference between the APP17-mer peptide group and control group (P=0.146). ②) Apoptotic percentage of single cell in hippocampus was significantly higher in the model group than in the control and APP17-mer peptide groups [(5.32±1.37)%, (1.03±0.55)%, (2.80±0.92)%, P＜0.01, 0.05].CONCLUSION: Neuronal mitochondrial transmembrane potential and cell apoptosis in hippocampus may be involved in the occurrence and development of diabetes mellitus, and APP17-mer peptide plays an improved role in the process.

AIM:To observe the influence of beta-amyloid precursor protein (APP17) on the study ability, memory and the expression of neurotrophin-3 (NT-3), nerve growth factor(NGF)in the hippocampus neuron of the model mice. METHODS: Mice brain aging model were produced with D-galactose(D-gal), the model mice were given hypodermic injection of APP17 peptide. APP17 peptide is the 319-335 peptide sequence of beta-amyloid precursor protein. Eight weeks later, the animals were observed by water labyrinth test and immunohistochemistry assay. RESULT:(1) The whole time needed and total times of wrong response for the D-gal group mice to complete the whole course of the water labyrinth test is significantly higher than the normal control group. (2) The expression of NT-3, NGF in the hippocampus neurons of the mice in APP17 peptide group is significantly higher than that of the normal control group and D-gal mice group, P

AIM: To observe the expression of apoptosis-related proteins in hippocampal neurons of (ovariectomized) (OVX) rats and explore the neuroprotective mechanism of the App17-mer peptide. METHODS: Female Wistar rats were randomly divided into three groups. Bilaterally ovariectomized rats with injection of App 17P peptide (3.5 ?g in 0.1 mL/per rat, three times a week) formed the experimental group (17P+ OVX group). Anti-AIF, Bcl-2 and Bax antibodies were applied in the immunohistochemistry experiment. TUNEL was employed to detect apoptosis. RESULTS: The number of apoptotic neurons was clearly higher in hippocampal and cortex in OVX group than that in OVX+17P group. Immunohistochemistry demonstrated the increased expression of AIF, Bax in hippocampal neurons of OVX group. OVX group showed a significantly reduced expression of Bcl-2 in hippocampal neurons. Hippocampal tissue from OVX group showed the increased expression of AIF, Bax, and showed diminished expression of Bcl-2, treating with App17-mer peptide normalized the expression of these proteins. CONCLUSIONS: The expression of apoptosis-related proteins were abnormal in the OVX rats, App17-mer peptide normalized these changes. Estrogen deficiency induced neuronal apoptosis, and App17-mer peptide diminished apoptosis.

Objective Through the observation on the distribution of hyperphosphorylated Tau,to investigate the connection between hyperphosphorylated Tau and learning, memory tasks. Furthermore, the treatment of App17 on brain tissues of diabetic mice. Methods Diabetic model mouse was produced in the use of streptozotion and App17 peptide as a curative was injected subcutaneously. Four weeks later, removed the brains. Immunohistochemical stainning was done with AT\|8, Tau\|1, again with Tau\|1 antibody after dephosphorylation. Results In the brains of diabetic mice positive AT\|8 reacting neurons were widely distribution in retrosplenial granular cortex, hippocampas, thalamus et al, the cytoplasm was darkly stained, while in normal mice and App17 peptide\|treated diabetic mice positive cells were localized in retrosplenial granular cortex, however, in hippocampas and RSG area, the cytoplasm were poorly stained. Conclusion Hyperphosphorylated Tau is widely expressed in brains of diabetic mice. App17 peptide can improve the hyperphosphorylated Tau in brains of diabetic mice, therefore, it may improve learning ability and memory.\;

Objective To investigate the effect of a peptide,APP17,on regulating the expression of insulin receptor substrate\|1(IRS\|1) and insulin\|like growth factor (IGF\|1R) in neurons of the hippocampus from diabetic mouse. Methods Diabetic mouse models were established by injection of streptozotion.In experimental group,these models were injected with APP17 peptide subcutaneously and their brain sections were taken after 4 weeks of survival. The immunohistochemical stainning of these sections were then performed with IRS\|1 and IGF\|1R antibody.With regard to control groups,the mouse models were only injected saline and gone through the same procedure of immunohistochemistry together with normal mice. Results IRS\|1 and IGF\|1R positive neurons were widely distributed in the hippocampus of the diabetic mice,and the cytoplasm was darkly stained.In the contrast,positive cells in the hippocampus were lightly stained in those normal mice and the APP17 peptide\|treated diabetic mice. Conclusion The expression of IRS\|1 and IGF\|1R could increase in the hippocampus of dabetic mice.The APP17 can regulate the distribution of IRS\|1 and IGF\|1R in the brain of diabetic mice and return them to normal situation.

Objective To investigate the effect of the peptide APP17 on regulating the expression of Bcl\|2,Bax,cAMP response element binding Protein(CREB),Ser\|Thr kinase B/protein kinase B(Akt/PKB),apoptosis inducing factor(AIF) in neurons of the hippocampus from the D\|gal mouse. Methods D\|gal mouse models were established by injection of D\|gal.In experimental group,these models were injected with APP17 petide subcutaneously and their brain sections were taken after 3 months of survival.The immunohistochemical staining of these sections was then performed with Bcl\|2,Bax,CREB,Akt,AIF antibody. Results Bax,AIF positive neurons were widely distributed in the hippocampus of the D\|gal mice,and the cytoplasm was darkly stained.In contrast,positive cells in the hippocampus were poorly stained in those normal mice and the APP17 peptide\|treated D\|gal mice.But Bcl\|2,CREB,AKt positive neurons were widely distributed in the hippocampus of those normal mice and the APP17 peptide\|treated D\|gal mice,and the cytoplasm was darkly stained.In contrast,positive cells in the hippocampaus were poorly stained in the D\|gal mice.Conclusion\ The expression of Bax and AIF could be increased in the hippocampus of D\|gal mice.But the expression of Bcl\|2,CREB,AKt decreased in the hippocampus of D\|gal mice.The APP17 can regulate the distribution of Bcl\|2,Bax,CREB,Akt,AIF in the brain of D\|gal mice and return them to normal situation.\;[

Objective:To analyze a novel epitope of Homo sapiens synapse associated protein and synthesize polyclonal antibody.Methods:FRG4 full-length sequence was obtained by PCR from human fetal liver library;by bioinformatics to detect the second structure of amino acids encoded by FRG4 and its epitope and motifs;by solid-phase peptide synthesis method to synthesize FRG4 peptides,then peptides were immunized to rabbits;by immunohistory to detect the expression of FRG4 in HepG_2 cells.Results:Select 13-peptides PKLVKEEVFWRNY by bioinformatics to synthesize rabbit anti-human FRG4 polyclonal antibody.Antibody purity was 82.79% and antibody dilution was 1∶16 000 detected by ELISA.The antibody had a good reaction and speciality in Western blot,it was mainly expressed in cytoplasm of HepG_2 cells.Conclusion:A novel Homo sapiens synapse associated protein(FRG4) antibody was synthesized successfully.

at model is an ideal MS model for clinical MRI study.