Isocitrate dehydrogenases(IDHs)are considered as key enzymes in the tricarboxylic acid cycle. Recurrent mutations in the IDH1 and IDH2 genes are recently found in several human cancers. Those point mutations specifically affect IDH1 and IDH2 active site arginine residues and confer a neomorphic enzyme function of directly catalyzing α-ketoglutarate(α-KG)to R-2-hydroxyglutarate(R-2-HG). R-2-HG can com-petitively inhibits α-KG-dependent enzymes and may therefore contribute to the occurrence and development of tumor. In addition,Mutation status of IDH1 and IDH2 are closely relative to the progress and prognosis of cer-tain tumor. Thus IDH1 and IDH2 are considered to be promising biomarkers for early diagnosis and prognosis and targeted therapy.

A total of 906 subjects with no history of diabetes who had undergone coronary angiography were included in this study and categorized into four groups according to the level of fasting plasma glucose (FPG):≤5.5 mmoL/L,5.6-6.0 mmol/L,6.1-6.9 mmoL/L,and ≥ 7.0 mmol/L.Significant coronary artery disease (CAD) was defined as ≥ 50％ reduction of lumen diameter at least in one major coronary artery.The severity of coronary atherosclerosis was defined by the Gensini score.The clinical data,laboratory indexes,and coronary angiography results were compared among various groups.The risk factors for the prevalence and severity of angiographic CAD were analyzed.The results showed that the prevalence of angiographic CAD,the number of diseased vessels,and the Gensini score were increasing with increasing FPG levels among four groups (P＜0.05 or P＜0.01).The FPG level was significantly correlated with angiographic CAD (P =0.004) and the Gensini score (P =0.010),suggesting that FPG was an independent risk factor for the prevalence and severity of angiographic CAD.

Objective To observe the effects of low frequency electrical stimulation (LFES) on the proliferation of endogenous brain neural stem cells (NSCs) and on the expression of basic fibroblast growth factor (bFGF)and epidermal growth factor (EGF) in rats with acute cerebral infarction; to explore the therapeutic mechanism of LFES in improving neural function. Methods Fifty-four rats were randomly divided into a LFES group, a placebo stimulation group and a sham-operated group. Each group was further divided into 3rd day, 7th day and 14th day subgroups, with 6 rats in each subgroup. An acute cerebral infarction model was induced in the rats of the LFES and placebo stimulation groups by middle cerebral artery occlusion (MCAO). Three days after the operation, rats in the LFES group began LFES treatment (frequency 30 Hz, pulse width 250 μs, current intensity 3 mA, 10 min/d) ,while the placebo stimulation group was treated identically but without electricity. The rats in the sham-operated group had no special treatment. The expression of nestin positive cells in the subgranular zone of the hippocampus and the subventricular zone was detected by immunohistochemical staining. The expression of bFGF, EGF proteins and mRNA in the ischemic hemisphere was detected by Western blotting and RT-PCR analysis. A screen test was applied to evaluate motor function. Results Nestin-positive cells in the subgranular and subventricular zones of rats in the LFES group increased significantly more than in the placebo stimulation group at the 7th and 14th day. The expression of bFGF, EGF proteins and mRNA in the ischemic hemisphere was up-regulated compared to the placebo stimulation group at the 7th and 14th day. At the 14th day a difference in motor function was observed in rats in the LFES group compared with the placebo stimulation group. Conclusion LFES can promote the proliferation of endogenous brain NSCs and the expression of bFGF and EGF in rats with acute cerebral infarction. It can also improve motor function and enhance neural plasticity in the brain.

BACKGROUND: The existing electrocardiogram(ECG)measurement strongly depends on medical professionals and inefficient high-intensity,or relies on automatic identification method which is not accurately enough.Thus,this is difficult to meet high-speed testing,accurate results and ease application for common people.OBJECTIVE: To develop a new method that was simple and efficient to apply and very easy to learn.METHODS: Algorithms were programmed and test software was developed by delphi7.0.ECG was drawn on screen.The apex,the starting point and the ending point as well as the J-point of each ECG wave were clicked by mouse or stylus.Then the wave parameters and an initial diagnosis could be quickly obtained by test software.RESULTS AND CONCLUSION: The parameters of ECG waveform such as wave height,wave time,PR interval,ST segment,QT segment,PP/RR time,cardiac electrical axis and so on could be accurately measured,and heart rate,heart rhythm and the deflection of cardiac electrical axis could be diagnosed correctly.The method was simple to learn and easy to imply,and it was also efficient,quick and accurate.Thus,it could greatly improve the efficiency of measurement and analysis for specialists,and could meet application requirements of general medicals and ordinary people.

Objective To study the effects of Lxn on CD133 + PANC-1 pancreatic cancer cells.Methods CD133 + PANC-1 cell were isolated by magnetic activated cell sorting (MACS).The properties of the CD133 + PANC-1 cells and Lxn effects on CD133 + PANC-1 cell proliferation in transplanted tumor in nude mice were determined by floating spheres test and tumor xenograft assays.Cell proliferation was assayed by Cell Counting Kit-8 (CCK-8).The Bcl-2,Bax protein and mRNA expression of CD133 + PANC-1 cells treated by Lxn were analyzed by Western blot and Quantitative real-time PCR (qRT-PCR).Results We successfully isolated the CD133 + PANC-1 cells and cultured in serum free medium,CD133 + PANC-1 cells formed sphere,while CD133-PANC-1 cells grew with adherence slowly and then underwent apoptotic process.CD133 + PANC-1 cells showed high tumorigenic in athymic BALB/c mice.Lxn suppressed the growth of transplanted tumor obviously.Compared with control group [(225.52 ± 34.09) mm3],tumor volume decreased significantly (P ＜ 0.05).Significant reduction in cell proliferation was observed in response to Lxn in PANC-1 CD133 + cells by CCK-8 assay with concentration and time dependent manners (P ＜ 0.05).Treated by Lxn,Bcl-2 expression decreased,Bax expression increased.Conclusions Lxn inhibits the proliferation of CD133 + PANC-1 cells probably through a mechanism down-regualting Bcl-2 and up-regulating Bax.

Objective To study changes in synaptic plasticity in the contralesional mirror area of the cortexes of rats with cerebral infarction treated by low-frequency electrical stimulation(LFES)and to explore the therapeutic mechanism of LFES on the molecular level.Methods Forty-eight Sprague-Dawley rats were randomly allocated into a LFES group,a placebo group and a sham-operation group.Following middle cerebral artery occlusion(MCAO),rats in the LFES group were treated with LFES for 7 d(20 min/d),while the ones in placebo group were connected with the same LFES device but without electricity.Rats in the sham-operation group were subjected to a MCAO operation without occlusion and then received no special treatment.Synaptic ultra-structures and the expression levels of glia fibrillary acidic protein(CFAP)and synaptophysin in the contralesional mirror area of the cortexes of the rats in each group were measured with electron-microscopy and Western blotting.Results Compared with the placebo group or the rats before treatment,rats treated with LFES exhibited ultra-structural changes in the form of larger curvature of synaptic interfaces and narrower synaptic clefts.GFAP expression levels did not fluctuate significantly,but the expression of synaptophysin was significantly up-regulated.Conclusion LFES treatment can induce active changes in synaptic plasticity in the contralesional mirror area of the cortex of rats after cerebral infarction.

Objective To study the effects of low-frequency electrical stimulation(LFES)on motor function and the expression of glia fibrillary acidic protein(GFAP)around cerebral infarction sites in rats.Methods Fifty-four male adult Sprague-Dawley rats were randomly divided into a LFES group,a placebo group and a sham operation group(18/group).All groups were randomly divided into 3 treatment groups.A rat model of middle cerebral artery occlusion(MCAO)was established using intraluminal filament occlusion.Treatment was carried out 3 d after the operation.Rats in the LFES treatment groups were stimulated with LFES for 3,7 or 14 days (10 min/d);the placebo groups were treated in the same way without electric stimulation;the sham operation subgroups didn't receive any therapy.Scores on a beam-walking test,a rotating pole test and a screen test were assessed at each time point mentioned above.Expression of GFAP was also assessed using immunohistochemcal techniques.Results The paralysed limbs recovered motor function better in the LFES groups than in the control groups.GFAP-positive cells were more numerous at the margins of the infarction area in the treated groups than in the control groups.Conclusions LFES might increase the expression of GFAP,which might be an important mechanism in improving brain plasticity after cerebral ischemia,aiding the recovery of the central nervous system and rebuilding its functioning.

Objective To explore the differences in morphology and structure of collagen fiber of the hilar bile duct between human and rat. Methods The morphology and structure of vertical and horizontal cross-section of human and rat collagen fiber of the normal and dilated hilar bile duct, and their changes under stress were observed after Masson trichrome staining. Results The morphology and structure of collagen fiber of hilar bile duet in human was similar to that in rat. The collagen fiber mainly distributed in the middle and outer layer of the hilar bile duct. The wave-like collagen fiber bundles were arranged in parallel, consistent with the longitudinal axis direction of the bile duct, and connected by the small branches. Conclusions The morphology and structure of collagen fiber of the hilar bile duct in human is similar to that in rat. The anatomical structure of the collagen fiber is adapted to its function.

ObjectiveTo evaluate the various methods of choledochoplasty in the repair of major bile duct defects in Mirizzi syndrome.MethodsThis is a retrospective study on 3 patient with Mirizzi syndrome with a large bile duct defect.These defects were repaired by using a vascular gastric pedicle patch in our department from July 2008 to November 2011.The authors searched the domestic medical literature on surgical repair for Mirizzi syndrome in the past ten years.The patients were treated by various surgical methods,and they were analyzed according to the Csendes Classification.ResultsThere were no surgical complications in our three patients.There was one patient with a Csendes type Ⅲ,while the remaining 2 patients were with Csendes type Ⅳ.At a median follow- up of 2.5 years,no patient developed signs of chronic cholangitis.In the medical literature,there were 93 patients who were with Csendes type Ⅰ ; and 58 patients were treated by cholecystectomy only,while 35 patients were treated by partial cholecystectomy plus mucosal ablation.Of the 40 patients with type Ⅱ,29 patients were treated by direct fistula repair,9 patients by pedicle gallbladder flap and 2 patients by pedicle round ligament.Of the 20 patients with type Ⅲ,9 patients were treated by pedicle gallbladder flap.1 patient by pedicle round ligament,3 patients by pedicle gastric flap and 7 patients by Rouxen- Y hepaticojejunostomy.For the 5 patients with type Ⅳ,they were treated by Roux-en- Y hepaticojejunostomy.Of these 159 patients,postoperative complications included biliary fistula (n=1 ),upper gastrointestinal bleeding (n=1),and biliary stricture (n=1).All the remaining patients were cured.ConclusionIn patients with Mirizzi Syndrome,the choice of treatment depends on the size of the fistula.For patient with a major tissue defect in the common hepatic duct,a pedicle vascular gastric flap is a good treatment.

Objective To screen and clone the genes related to alopecia areata. Methods Dermal papillae of lesional and non lesional follicles were separated from alopecia areata scalp respectively. Suppression subtractive hybridization was used to investigate the difference of expressed genes in dermal papillae of lesional (tester) and non lesional (driver) follicles, and the differentially expressed genes in dermal papillae of lesional follicles were cloned and sequenced. Results A subtractive library of dermal papillae of lesional follicles from alopecia areata was established. A differentially expressed gene in dermal papillae of lesional follicles was successfully cloned and proved to be an autoantigen gene. Conclusions The subtractive library may contain the differentially genes related to alopecia. The autoantigen gene related to alopecia areata need to be further investigated.