Anhedonia is the loss of pleasure or lack of reaction to pleasurable stimuli, which is a promising phenotype of depression. In order to explore the potential biological mechanism, the recent ad?vances were summarized from researches focused on depression with anhedonia from neuroanatomy,inflamma?tion and immunology,and molecular genetics. The structural and functional brain imaging showed that the ac?tivity in reward?related brain regions of the depressive disorder with an anhedonia was changed during re?ward?related tasks.In addition,some other genetic studies based on the related neurotransmitter,such as do?pamine, together with the findings from the researches on immunological inflammation, may shed light on finding the potential targets for novel antidepressants,besides the 5?HT.

Aplastic anemia (AA) is a Tlymphocyte-mediated autoimmune disease. The research on AA was focused on three areas, which were the pathogenesis of immune dysfunction, hematopoietic stem cell damage and abnormal hematopoietic microenvironment. In recent years, more attentions have been paid on abnormal immune mechanisms in the blood. There are complex intracellular cytokine and signal transduction pathway of pathogenesis in AA. And T-bet/IFN-γ signaling pathway plays an important role in development and progression of AA. This article aimed to review T-bet/IFN-γ signaling pathways in AA.

Objective To study the expression of tansforming growth factor(TGF)-?1 and mRNA in the renal tubules of Streptozotocin(STZ)-induced diabetic nephropathy rats.Methods SD rats were randomly divided into two groups: normal control and diabetic nephropathy.Diabetes was induced by intraperitoneal injection of STZ.And the diabetic rats were randomly divided into four groups: model group,irbesartan treatment group,Haikunshenxi low and high dose group.Twenty-four-hour urine volume and urinary protein excretion were examined at week 4,8,and 12 respectively.All the rats were sacrificed at week 12,and body weight,kidney weight,and serum excretion,serum creatinine,blood urea nitrogen were examined.The expression of TGF-?1and mRNA in rat renal tissue were detected respectively by immunohistochemistry and in situ hybridization.The graphic analysis system and SPSS 11.5 statistics software were used to treat the results.Results The expression of TGF-?1and mRNA in the Haikunshenxi group was depressed greatly(P

【Objective】 To explore the significance of electrocard iogram monitoring during the effective application of radiofrequency energy to s low atrioventricular (AV) nodal pathway ablation. 【Methods】 Slow AV nodal pathway ablation was performed in 58 patients with slownfast AV nodal ree-trant tachyca rdi a (AVNRT). The changes of electrocardiogram were monitored during the effective application of low radiofrequency RF energy (15～25 W). A faster rate of junctio nal ectopy (>150 min-1), ventriculoatrial (VA) block in association with j unctional ectopy, and l ong P-R interval during sinus beat were considered as harbingers of atrioventri cular (AV) block. RF energy deliveries were discontinued as soon as the harbinge rs of AV block occurred. Otherwise, RF energy continued until junctional ectopie s were decreased or vanished. If junctionnal ectopies were not decreased, RF ene rgy continued lasted for 90～120 s. 【Results】 Slow AV nodal pathway ablation w as successful in all patients who had junctional ectopy during the effective del ivery of RF energy. The effective ablation time was (128±26) s. 54 patients exp erienced one time successful ablation, and 4 patients experienced two times abla tion. Unsustained AV block occurred in 6 patinets after RF energy deliveries whi ch were immediately terminated because of VA block in association with junctiona l ectopy in 4 patinets and long P-R interval during sinus beats in 2 patients. No patients developed permanent AV block. Recurrent AVNRT requiring second ablat ion occurred in 2 of 58 successfully ablated slow pathway during (18±16) months of follow-up. 【Conclusion】 RF energy deliveries could be instructed b y intracardiac electrocardiogram monitoring during AVNRT ablation, which could e nhance the successful rate of slow pathway ablation, reduce recurrence and avoide permanent AV block.

AIM:To investigate the protective effect of N-acetylcysteine (NAC) on H9c2 cells from injuries induced by methylglyoxal (MG) and the potential mechanism.METHODS:H9c2 cells were divided into control group, MG treatment group, NAC +MG treatment group, SP600125 pretreatment +MG group, NAC group and SP600125 group.The viability of the H9c2 cells was measured by CCK-8 assay.The protein levels of p-JNK and t-JNK were tested by Western blot .The changes of intracellular reactive oxygen species ( ROS) were evaluated by 2′, 7′-dichlorofluorescein di-acetate (DCFH-DA) staining.Mitochondrial membrane potential (MMP) was measured by rhodamine 123 (Rh123) stai-ning.The morphological changes in apoptotic cardiomyocytes were detected by Hoechst 33258 staining.RESULTS: Du-ring 100~800 μmol/L concentration range , MG caused significantly reduced viability of the H 9c2 cells in a dose-depend-ent manner.NAC had a protective effect on H9c2 cells against the injuries induced by MG during 500~1 500μmol/L con-centration range through raising cell viability , inhibiting cellular oxidative stress and improving MMP ( P <0.01 ) . SP600125,an inhibitor of JNK, showed the protective effect similar to NAC on H9c2 cells against MG-induced injuries, in-cluding attenuating oxidative stress , improving MMP and suppressing apoptosis .CONCLUSION: N-acetylcysteine offers obvious protective effect on H9c2 cells against the injuries induced by methylglyoxal .The underlying mechanisms may be associated with decreasing the production of ROS , ameliorating MMP , inhibiting the activation of JNK and suppressing ap-optosis.

This study was aimed to investigate the effect of Bu-Shen Y i-Sui Sheng-Xue (BSYSSX) method on pro-liferation and differentiation mechanisms of hematopoietic progenitor cells. The rat models were established by 60Co-γrays and cyclophosphamide. Compound Chinese medicine was gavaged to rats of the normal control group, model group, stanozolol group, Yi-Sui Sheng-Xue (YSSX) group, Wen-Shen Sheng-Xue(WSSX) group and Zi-Shen Sheng-Xue (ZSSX) group. Then, serum of rat was prepared. Rat bone marrow cells were incubated with AA rats serum ac-counted for 20% and the number of hematopoietic progenitor cells colony-forming units (CFU) were counted. The level of GATA-1 and PU.1 mRNA in colony cells were detected with RT-PCR. The results showed that compared with the normal control group, the number of bone marrow cells, CFU-E, BFU-E, CFU-GM, as well as the expres-sion of GATA-1 and PU.1 mRNA in the model group decreased significantly (P< 0.01). Compared with the model group, the number of bone marrow cells, CFU-E, BFU-E, CFU-GM of each treatment group were significantly in-creased (P< 0.01). CFU-E and BFU-E of the ZSSX group were better than the YSSX group (P < 0.01). CFU-GM of the ZSSX group was better than the YSSX group and the WSSX group. The expression of GATA-1 and PU.1 mR-NA in each treatment group were significantly higher than the model group (P< 0.01). The expression of GATA-1 mRNA in the ZSSX group was better than the YSSZ group and WSSX group (P< 0.05). The expression of PU.1 mR-NA in the ZSSX group was higher than the YSSX group and WSSX group. It was concluded that BSYSSX method may increase the expression of GATA-1 and PU.1 mRNA in order to promote the proliferation and differentiation of bone marrow hematopoietic progenitor cells. The ZSSX method was better than the YSSX method and WSSX method.

BACKGROUND:Studies have shown that pulsed electromagnetism has a good effect in promoting peripheral nerve regeneration after cerebral infarction and spinal cord injury, and improving memory function in patients with neurological disorders. OBJECTIVE: To investigate the impact of pulsed magnetic field on brain function and endogenous neural stem cell factor in the brain tissue of rats with brain injury. METHODS: Totally 320 adult male Sprague-Dawley rats were randomly divided into model group, pulsed magnetic field 0.1 mT group, pulsed magnetic field 0.3 mT group and pulsed magnetic field 0.5 mT group (n=80 per group). After brain injury models were established using lateral hydraulic strike method, rats in the latter three groups were exposed to pulsed magnetic fields 0.1, 0.3, 0.5 mT, respectively. After electromagnetic radiation 1, 3, 7, 14 days, the motor function of rats was evaluated by beam-walking test and water maze test. Rats were intraperitoneally injected 5-deoxy-uridine (BrdU) at 1 day prior to different radiation time points, and BrdU and nestin expressions in the cerebral cortex were measured by immunohistochemical method. RESULTS AND CONCLUSION: (1) The time of water maze test and the beam-walking test at 1, 3 and 7 days after irradiation was ranked as follows: pulse magnetic field 0.5 mT < pulse magnetic field 0.3 mT < pulse magnetic field 0.1 mT < model group, and there were significant differences between groups (P < 0.05). (2) The expressions of BrdU and nestin at 1, 3 and 7 days after irradiation were highest in the pulse magnetic field 0.5 mT group, successively followed by pulse magnetic field 0.3 mT group, pulse magnetic field 0.1 mT group and model group (P < 0.05). In summary, the pulse magnetic field exhibits remarkable protective effects on the brain function of rats with craniocerebral injury in an intensity-dependent manner. The possible mechanism is related to the activation of neural stem cells and the proliferation of neural stem cells in the brain tissue of rats with craniocerebral injury.

AIM:To evaluate complement activation in patients with all forms of acute coronary syndromes(ACS)and to examine the relationship between the degree of complement activation and myocardial injury.METHODS:The subjects were divided into 2 groups:110 ACS patients(group ACS)and 18 healthy persons(group control).One hundred and ten patients with ACS were divided into 3 sub-group:51 patients with ST-segment elevated myocardial infarction(STEMI),28 patients with non-ST-segment elevated myocardial infarction(NSTEMI)and 31 patients with unstable angina(UA).Complement 3(C3),complement 4(C4),troponin T(TnT)as well as creatine kinase MB(CK-MB)were evaluated.RESULTS:Plasma C3 and C4 peak levels were significantly higher in patients with STEMI [(1 525?302)mg/L and(423?123)mg/L] and NSTEMI [(1 516?289)mg/L and(396?68)mg/L] than those in patients with UA [(1 275?172)mg/L and(356?91)mg/L] and the control subjects [(1 072?196)mg/L and(182?73)mg/L](P

Objective To evaluate the value of the TIMI risk index in predicting 30-day and one-yosr mortality and incidence of heart failure in patients with ST-elevation myocardial infarction (STEMI).Method Data of 229 patients with STEM1 from August 1999 to March 2006 in the First Affiliated Hospital,Sun Yat-sen University,were retrospeclively collected,analyzed and scored with TIMI risk index.When categorized into quintiles(≤12.5,12.5～17.5,17.5～22.5,22.5～30,>30) and modeled as a continuous variable,difference of prediction of 30day and one-year mortality and 30-day incidence of heart failure of patients were compared respectively.Results When categorized into quintilos and modeled as a continuous variable,30-day and one-year mortality and 30-day incidence of heart failure were increasing with increasing score of risk index (P<0.05).The area under the recewer operating characteristic curve were 0.65,0.68,0.67 and 0.70,0.72,0.70,respectively.Conclusions The TIM1 risk index can be used as a simple,rapid and practical tool to risk-stratify patients with STEMI.

Diabetic kidney disease (DKD) is a serious long-term complication and major death cause of patients who have suffered from diabetes mellitus (DM),which is a serious threat to the health of human being.Professor Zhao Zongjiang first came up with the of DKD "consumptive kidney disease" scientific theory,and led the scientific research team for DKD research.Our team had achieved some results,which were mainly focused on the animal experiments and cell culture experiment.And the research fields covered pharmacodynamics,oxidative stress levels and signal transduction pathways.Focusing on the reduction of extracellular matrix in the glomerular mesangial area and tubulointerstitial deposition,inhibition of podocyte injury,inhibition of podocyte apoptosis,inhibition and reversal of podocyte transdifferentiation,inhibition of renal tubular epithelial cell transdifferentiation and other scientific issues,this paper systematically explored the biological mechanism of DKD "consumptive kidney disease" scientific theory.This paper explained how "consumptive kidney disease" scientific theory was proposed and summarized related research results of our research team and developed traditional Chinese medicine (TCM) theory by supplying the TCM "consumptive organ disease" theory.