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Translational medicine is a new term recently which aims to eliminate the barrier between preclinical and clinical medicine,to efficiendy and effectively translate basic scientific findings into drugs and medical devices that benefits patients.This article discussed the meaning of translational medicine in cultivating postgraduates of neurology.According to the preliminary attempt,it is beneficial for postgraduates to form translational medicine philosophy and be high-quality medical talents.

Apoptosis is a main death pattern in many nervous system disease.Erythropoietin(Epo)has been originally characterized as the principal regulator of erythropoiesis by stimulating the proliferation and differentiation of erythroid precursor cells.In recent years,many experimental studies have shown that both Epo and EpoR(erythropoietin receptor)are functionally expressed in the nervous system and that this cytokine exerts a remarkable neuroprotection against nerve cell apoptosis.This article reviews neuroprotective of Epo against apoptosis and outline the involved molecular mechanisms.

c-Jun N-terminal kinases(JNKs)play an integral role in neuronal death in multiple cell lines following a wide variety of stimuli and in a number of physiological functions which have been recognized as important enzymes in cellular function.JNK has been implicated in several neurodegenerative diseases.Data are emerging to extend the understanding of the JNK signaling and confirm the possibility that targeting JNK signaling may offer an effective therapy for pathological conditions in the near future.Because of the involvement of JNK in neuronal diseases,the inhibition of this enzyme is an attractive therapeutic target.

Alzheimer!s disease (AD) is one of the commonest neurodegenerative diseases affected mainly theelderly. AD is characterized by the formation of neuritic plaque in brain, which is composed mainly of extracellular?amyloid deposion, the A?. A?is deprived from serial hydrolysis of amyloid precursor protein (APP) by twosecretases, the ?and ?-secretase respectively. Alternatively, APP can also be sequential processed by ?-secretaseand ?-secretase, which not only preclude the formation of A?, but also generate a large ectodomain (sAPP?) whohas several neuroprotective properties. Thus the secondary processing pathway has become the focus of ADresearch. Many results have indicated that members of the adamalysin family of proteins, mainly the ADAM 10,ADAM 17 and ADAM 9, fulfill some of the criteria required of ?-secretase. Here the biological characteristics of?-secretase, its activity regulation and its potential function as targets for the treatment of AD were summerized.

Objective To study the neuroprotective effects of adeno viral mediated glial cell line derived neurotrophic factor(GDNF) gene transfer in the treatment of Parkinson's disease. Methods Thirty five SD rats were divided into 3 groups which received perinigral injections of recombinant adenovirus encoding GDNF (Ad GDNF)/ LacZ(Ad LacZ) and PBS, respectively. One week later, intrastriatal injection of 6 hydroxydopamine (6 OHDA) was made to induce progressive degeneration of dopaminergic neurons. The neuroprotective effects of Ad GDNF were evaluated by apomorphine induced rotational behavior, immunohistochemical assay of the tyrosine hydroxylase(TH) positive neurons in the midbrain and measurement of monoamine level in the striatum. RT PCR and ELISA were performed to check the expression of the exogenous GDNF gene in the brain. Results Ad GDNF treated rats showed improved motor functions, better survival of TH positive cells in the lesioned substantia nigra (70% vs 30%) and higher DA levels in the lesioned striatum. The exogenous GDNF gene was efficiently expressed in the midbrain. GDNF protein level in the injection site reached 1 ng/10 mg wet tissue 5 weeks after the adenoviral vector delivery, being 16 20 times of that of the Ad LacZ delivery or PBS treated groups. Conclusions Adeno viral mediated GDNF gene intracerebral transfer significantly protected the dopaminergic neurons of nigrostriatal system from 6 OHDA induced injury and is valuable in the treatment of Parkinson's disease.

Objective To investigate the gene expression pattern of metabotropic glutamate receptor- Ⅰ ( mGluR-Ⅰ ), D-p-hydroxyphenylglycine (DHPG) -induced rat hippocampal slice epileptic seizure model. Methods In vitro rat hippocampal sclice was continously perfused with artificial cerebrospinal fluid containing 50 μmol DHPG, and epileptic seizure model was established (DHPG group, n = 3). cDNA microarray chip was applied to explore the gene expression pattern in DHPG group, the differentially expressed genes were screened in comparison with control group ( n = 3), and functional classification analysis was conducted. Results There were 206 up-regulated genes and 489 down-regulated genes, among which 67 up-regulated genes and 86 down-regulated genes differentially expressed by 1.5 fold, 6 up-regulated genes differentially expressed by more than 2.0 folds, and 25 down-regulated genes differentially expressed by less than 0.5 fold. Functional classification analysis revealed that differentially expressed gene function involved in protein binding (19 genes), molecular function, calcium ion binding and nucleotide binding. Conclusion Epileptic seizure and roles of mGluR-Ⅰ agonist may be related to various genes, which is a complicated process. This experiment provides evidences for further researches.

Objective To detect the plasma macrophage inflammatory protein (MIP) levels in patients with early Parkinson' s disease (PD) and to investigate whether plasma MIP was associated with motor and non-motor symptoms in early PD.Methods Fifty-nine patients with early idiopathic PD (Hoehn-Yahr Staging Scale from 1.0 to 2.5) treated in our hospital from January 28,2013 to September 30,2013 and 54 healthy controls were recruited.Plasma MIP-1α and MIP-1β levels were measured by enzyme-linked immunosorbent assay.Motor function was assessed by Unified Parkinson' s Disease Rating Scale Part Ⅲ and Hoehn-Yahr Staging Scale during “on” period.Total non-motor symptoms were assessed by Non-motor Symptoms Questionnaire.Cognitive dysfunction was assessed by Mini Mental State Examination.Autonotic dysfunction was assessed by Scales for Outcomes in Parkinson' s disease-Autonomic.Depression was assessed by Hamilton Depressive Scale (HAMD).Rapid eye movement (REM) sleep behavior disorder was assessed by REM sleep behavior disorder screening questionnaire (RBDSQ).Correlation between plasma MIP levels and scale scores was analyzed by Spearman rank correlation.Results Plasma MIP-1o and MIP-1β levels were not significantly different between early PD patients and healthy controls.However,plasma MIP-1 α level negatively correlated with depression (HAMD score,r =-0.520,P =0.027) and rapid eye movement sleep behavior disorder (RBDSQ score,r =-0.537,P =0.039).Conclusion MIP-1 α may be correlated with depression and RBD in early PD.

Objective To investigate the toxicity of levodopa and dopamine on PC12 cells and neuroprotection of several anti-Parkinson drugs i.e. amantadine,pergolide and selegiline. Methods The possible cytotoxicity of levodopa and dopamine at different dosage on rat pheochromocytoma PC12 cells and the effects of some anti-Parkinson drugs (amantadine,pergolide and selegiline) on levodopa- or dopamine-induced cytotoxicity were determined by MTT assay and flow cytometry. Results There was a concentration- and time-dependent decrease in cell viability and a concentration-dependent increase in apoptotic cells induced by levodopa and dopamine ( P

Objective To investigate the calcium mechanism involved in the A? 25-35-induced neurotoxicity.Methods PC12 cells viability was detected by using MTT assay. Relative change of intracellular calcium concentration was measured by laser confocal microscope.Results MTT assay showed that the cell viability of the three groups (10 ?mol/L A? 25-35?10 ?mol/L A? 25-35+5 ?mol/L nifedipine?10 ?mol/L A? 25-35+10 ?mol/L nifedipine) was decreased by 34.5%, 25.1% and 11.0%,as compared with the control group. 10 ?mol/L nifedipine could protect PC12 cells from A? 25-35-induced damage. A? 25-35 of different concentration (0.1 ?mol/L, 1 ?mol/L, 10 ?mol/L, 20 ?mol/L and 30 ?mol/L) resulted in the elevation of intracellular calcium (about 6.38%, 6.42%, 62.2%, 69.3% and 107.5%) with a dose-dependent manner. Potassium (5 mmol/L, 15 mmol/L and 30 mmol/L) could increase the intracellular calcium after one minute pretreatment of different concentration A? 25-35. Both above mentioned actions were sensitive to the medium calcium and were antagonized by nifedipine, a L-voltage-gated calcium channel antagonist.Conclusion Soluble A? 25-35 may damage the neuronal calcium homeostasis in early stage and make neurons more vulnerable to physiological or pathological stimuli.