Objective To observe the changes of short-chain acyl-CoA dehydrogenase (SCAD) expression on human umbilical vein endothelial cell (HUVEC) apoptosis and investigate its relationship with apoptosis. Methods The HUVEC was cultured normally for 2-3 days. The apoptotic model of HUVEC was established by tert-butyl hydrogen peroxide (tBHP). The HUVEC was treated by different concentrations of tBHP (0, 10, 20, 30, 40, 50 μmol/L) for 12 hours and different time (0, 3, 6, 9, 12 hours) with 50 μmol/L tBHP to establish the apoptotic model of HUVEC. The cell viability was detected by methyl thiazolyl tetrazolium (MTT), the mRNA expression of SCAD was determined by real-time polymerase chain reaction (PCR), the protein expression of SCAD was achieved by Western Blot. The best concentrate and time were determined to interfere the HUVEC to achieve the apoptotic model of HUVEC. The SCAD gene of HUVEC was knocked down by RNA interference sequence (siRNA274, siRNA414, siRNA679). The mRNA expression of SCAD, the protein expression of SCAD and the activity of SCAD enzyme were detected to achieve the best RNA interference sequence. The HUVEC was intervened by the best RNA interference sequence and tBHP. The cell activity and apoptosis rate, the enzyme activity of SCAD, the mRNA and protein expression of SCAD, the contents of reactive oxygen species (ROS), aderosine triphosphate (ATP) and free fatty acid (FFA) were detected to observe the effect of SCAD on apoptosis of HUVEC. Results ① The cell viability, the mRNA expression and the protein expression of SCAD were decreased gradually in a concentration and time dependent manner with the increase of tBHP concentration and the prolongation of intervention time. The decline was most significant in the group of the 50 μmol/L tBHP to interfere HUVEC for 12 hours. ② The siRNA679 transfection was the most significant in reducing SCAD mRNA and protein expressions among the three interference sequences (siRNA274, siRNA414, siRNA679). ③ Compare with blank control group, the cell viability was significantly decreased in the siRNA679 group (A value: 0.48±0.09 vs. 1.00±0.09, P < 0.01), the apoptotic rate of HUVEC was significantly increased [(29.96±2.09)% vs. (2.90±1.90)%, P < 0.01], the expression of SCAD mRNA and SCAD protein, the activity of SCAD enzyme and the content of ATP were significantly decreased [SCAD mRNA (2-ΔΔCt): 0.50±0.16 vs. 1.34±0.12, SCAD/α-Tubulin: 0.67±0.11 vs. 1.00±0.06, the activity of SCAD enzyme (kU/g): 0.38±0.04 vs. 0.53±0.04, the content of ATP (μmol/g): 0.14±0.02 vs. 0.19±0.01, all P < 0.05], the contents of FFA and ROS were significantly increased [FFA (nmol/g): 0.84±0.07 vs. 0.47±0.04, ROS (average fluorescence intensity): 647.5±23.7 vs. 434.2±46.5, both P < 0.01]. Meanwhile, SCAD siRNA treatment triggered the same apoptosis as HUVEC treated with tBHP. Conclusions Down-regulation of SCAD may play an important role in HUVEC apoptosis. Increase in the expression of SCAD may become an important part in intervening HUVEC apoptosis.

Objective? To?Study?the?changes?of?short-chain?acyl-CoA?dehydrogenase?(SCAD)?in?heart?failure?(HF)?after?myocardial?infarction?(MI),?and?the?effect?of?aerobic?exercise?on?SCAD.? Methods? Healthy?male?Sprague-Dawley?(SD)?rats?were?divided?into?sham?operation?group?(Sham?group),?sham?operation?swimming?group?(Sham+swim?group),?HF?model?group?(LAD?group)?and?HF?swimming?group?(LAD+swim?group)?by?random?number?table?method,?with?9?rats?in?each?group.?The?left?anterior?descending?branch?of?coronary?artery?(LAD)?was?ligated?to?establish?a?rat?model?of?HF?after?MI.?In?Sham?group,?only?one?loose?knot?was?threaded?under?the?left?coronary?artery,?and?the?rest?operations?were?the?same?as?those?in?LAD?group.?Rats?in?Sham+swim?group?and?LAD+swim?group?were?given?swimming?test?for?1?week?after?operation?(from?15?minutes?on?the?1st?day?to?60?minutes?on?the?5th?day).?Then?they?were?given?swimming?endurance?training?(from?the?2nd?week?onwards,?60?minutes?daily,?6?times?weekly,?10?weeks?in?a?row).?Tail?artery?systolic?pressure??(SBP)?was?measured?before?swimming?endurance?training?and?every?2?weeks?until?the?end?of?the?10th?week.?Ten?weeks?after?swimming?training,?echocardiography?was?performed?to?measure?cardiac?output?(CO),?stroke?volume?(SV),?left?ventricular?ejection?fraction?(LVEF),?shortening?fraction?(FS),?left?ventricular?end-systolic?diameter?(LVESD),?left?ventricular?end-diastolic?diameter?(LVEDD),?left?ventricular?end-systolic?volume?(LVESV),?and?left?ventricular?end-diastolic??volume?(LVEDV).?Morphological?changes?of?heart?were?observed?by?Masson?staining.?Apoptosis?of?myocardial?cells?was?detected?by?transferase-mediated?deoxyuridine?triphosphate-biotin?nick?end?labeling?stain?(TUNEL)?and?apoptosis?index?(AI)?was?calculated.?Reverse?transcription-polymerase?chain?reaction?(RT-PCR)?and?Western?Blot?were?used?to?detect?the?mRNA?and?protein?expression?of?myocardial?SCAD?respectively.?In?addition,?the?enzyme?activity?of?SCAD,?the?content?of?adenosine?triphosphate?(ATP)?and?free?fatty?acid?(FFA)?in?serum?and?myocardium?were?detected?according?to?the?kit?instruction?steps.? Results? Compared?with?Sham?group,?Sham+swim?group?showed?SBP?did?not?change?significantly,?with?obvious?eccentric?hypertrophy?and?increased?myocardial?contractility,?and?LAD?group?showed?persistent?hypotension,?obvious?MI,?thinning?of?left?ventricle,?and?decreased?myocardial?systolic/diastolic?function.?Compared?with?LAD?group,?SBP,?systolic/diastolic?function?and?MI?in?LAD+swim?group?were?significantly?improved?[SBP?(mmHg,?1?mmHg?=?0.133?kPa):?119.5±4.4?vs.?113.2±4.5?at?4?weeks,?120.3±4.0?vs.?106.5±3.7?at??6?weeks,?117.4±1.3?vs.?111.0±2.3?at?8?weeks,?126.1±1.6?vs.?119.4±1.9?at?10?weeks;?CO?(mL/min):?59.10±6.31?vs.?33.19±4.76,?SV?(μL):?139.42±17.32?vs.?84.02±14.26,?LVEF:?0.523±0.039?vs.?0.309±0.011,?FS:?(28.17±2.57)%?vs.?(15.93±3.64)%,?LVEDD?(mm):?8.80±0.19?vs.?9.35±0.30,?LVESD?(mm):?5.90±0.77?vs.?7.97±0.60,?LVEDV?(μL):?426.57±20.84?vs.?476.24±25.18,?LVESV?(μL):?209.50±25.18?vs.?318.60±16.10;?AI:?(20.4±1.4)%?vs.?(31.2±4.6)%;?all?P??0.05).? Conclusion? The?expression?of?SCAD?in?HF?was?significantly?down-regulated,?and?the?expression?was?significantly?up-regulated?after?aerobic?exercise?intervention,?indicating?that?swimming?may?improve?the?severity?of?HF?by?up-regulating?the?expression?of?SCAD.

Objective: To observe the vascular and bronchial abnormalities in subsolid nodules on high resolution CT (HRCT), and analyze its correlations with the classification and subtypes of lung adenocarcinoma. Methods: Pathological and radiographic data of 315 surgically resected subsolid nodules (226 were pure ground-glass opacities, and 89 were part solid nodules with tiny solid components ≤ 6 mm) were retrospectively reviewed. The morphologic changes of the blood vessels and bronchia/bronchioles in ground-glass opacity on HRCT were evaluated, and their correlations with histopathology classification were analyzed. Chi-square test was performed for analysis of correlations with categorical variables, whereas the one-way ANOVA analysis was performed for analysis of correlations with continuous variables (e.g., lesion dimension). Results: Forty-eight pre-invasive lesions (PILs), 29 minimally invasive adenocarcinomas (MIAs), and 238 invasive adenocarcinomas (IACs) were analyzed. IACs were divided into 2 groups according to the percentage of lepidic pattern: lepidic predominant (lepidic pattern ≥ 50%, n=145), and non-lepidic predominant (lepidic patten<50%, n=93). The prevalence of vascular and bronchial abnormalities was higher in IACs (59.24% & 18.49% in IACs, 13.79% & 3.45% in MIAs, and 0% & 0% in PILs). The abnormalities of vessels and bronchi in nodules on HRCT were correlated with the PIL/MIA/IAC classifications (χ²=69.797, P<0.001, χ²=14.213, respectively). Moreover the prevalence of valcular and bronchial abnormalities significantly increased from non-lepidic predominant IACs (78.49%, 26.88%) compared to lepidic predominant IACs (46.90%, 13.10%), these morphologic abnormalities correlated with a higher percentage of non-lepidic pattern, which were considered with higher invasiveness, in IACs (P<0.001, χ²=22.139, P=0.012, χ²=6.253, respectively). Conclusion The morphologic changes of blood vessels and bronchia/bronchioles within the subsolid nodules on HRCT help to differentiate IAC from PIL and MIA, also correlate with the proportion of non-lepidic pattern in IACs, even when the solid component undeveloped or very tiny.

AIM:To investigate the effect of short-chain acyl-CoA dehydrogenase ( SCAD) on collagen expres-sion and proliferation of rat cardiac fibroblasts and to explore the relationship between SCAD and cardiac fibrosis . METHODS:The model of proliferation and collagen expression of rat cardiac fibroblasts induced by angiotensin II was es -tablished.After treatment with siRNA-1186, the expression of SCAD at mRNA and protein levels , fatty acids beta oxida-tion rate, ATP, the enzyme activity of SCAD and free fatty acids in the rat cardiac fibroblasts were determined . RESULTS:The mRNA and protein expression of SCAD was decreased in the rat cardiac fibroblasts induced by angiotensin II compared with the control cells , and the expression of collagen I and collagen III was significantly upregulated .Com-pared with negative control group , SCAD expression and activity , fatty acid beta-oxidation rate and ATP significantly de-creased in siRNA-1186 group, but the content of free fatty acids were obviously increased in the rat cardiac fibroblasts , and the expression of collagen I and collagen III was significantly up-regulated.CONCLUSION:The expression and synthesis disorder of collagen may be triggered by down-regulation of SCAD .SCAD may be a promising therapeutic target for myocar-dial fibrosis .

A cold saponification method for determination of 5 lutein stereoisomers in dairy products by high performance liquid chromatography ( HPLC ) was developed. Samples were cold-saponified at room temperature and extracted by n-hexane/petroleum/dichloromethane ( 2: 2: 1 , V/V/V ) . Then 5 lutein stereoisomers were separated on a YMC C30 column with gradient elution using methanol/methyl tert-butyl ether as the mobile phase, and data were acquired by a photodiode array detector at wavelength of 445 nm. The calibration curve was linear in the range of 0 . 127-5 . 082 mg/L with correlation coefficient of 0 . 9999 , and the recoveries were from 96 . 7% to 102 . 2% with the RSDs in the range of 4 . 1%-5 . 4% ( n=6 ) . The limit of detection was 0 . 010 μg/g ( S/N=3 ) , and the limit of quantification was 0 . 030 μg/g ( S/N=10 ) . By presenting results of good accuracy, precision and sensitivity, this method validates its suitability for routine analysis of 5 lutein stereoisomers in dairy products.

AIM:To investigate the expression of poly(ADP-ribose) polymerase-2 (PARP-2) during rat car-diac hypertrophy in vitro and in vivo, and to explore the effects of PARP-2 on the cardiac hypertrophy.METHODS:Ab-dominal aortic coarctation ( AAC) was performed to establish a model of pressure overload-induced cardiac hypertrophy in SD rats.The expression of PARP-2 at mRNA and protein levels in the myocardium was determined by real-time PCR and Western blot.The hypertrophy model of the cardiomyocytes was induced by treating the cells with angiotensinⅡ( AngⅡ) . PARP-2 was knocked down by siRNAs in neonatal rat cardiomyocytes and the cardiomyocyte hypertrophy was evaluated by measuring the mRNA levels of ANF, BNP, and β-MHC and the cellular surface area.RESULTS: The expression of PARP-2 at mRNA and protein levels was both increased in the AAC rats as compared with those in the sham animals.The expression of PARP-2 at mRNA and protein levels was also increased in a time-and concentration-dependent manner in AngⅡ-induced hypertrophy model of the cardiomyocytes.In the neonatal rat cardiomyocytes, knockdown of PARP-2 ex-pression by siRNA attenuated AngⅡ-induced cardiac hypertrophy of the cardiomyocytes, indicating that endogenous PARP-2 played a positive regulatory role in cardiac hypertrophy.CONCLUSION:The mRNA and protein levels of PARP-2 in-crease in the in vitro and in vivo models of cardiac hypertrophy.Knockdown of PARP-2 protects cardiomyocytes from hyper-trophy.

AIM:To investigate the change of short-chain acyl-CoA dehydrogenase (SCAD) expression during cardiomyocyte apoptosis and to explore the relationship between SCAD and cardiomyocyte apoptosis .METHODS: The neonatal rat cardiomyocytes treated by tert-butyl hydroperoxide (tBHP) were used as the model of cardiomyocyte apoptosis . The cell viability , the expression of SCAD at mRNA and protein levels , the activity of SCAD and the content of free fatty acids were determined .RESULTS:The mRNA and protein expression of SCAD decreased in the cardiomyocyte apoptosis model.Compared with negative control group , SCAD expression and activity were both significantly decreased in siRNA-1186 group, but the content of free fatty acids were obviously increased in the cardiomyocytes .Meanwhile, SCAD siRNA treatment triggered the same apoptosis as cardiomyocytes treated with tBHP .CONCLUSION: Down-regulation of SCAD may play an important role in primary cardiomyocyte apoptosis .Increase in the expression of SCAD may become an impor-tant part in intervening cardiomyocyte apoptosis .

[ABSTRACT]AIM:ToinvestigatethedifferenteffectsofERK1/2/PPARα/SCAD(short-chainacyl-CoAdehy-drogenase) signal pathways on the cardiac hypertrophy induced by insulin-like growth factors 1 ( IGF-1) or phenylephrine ( PE) .METHODS:The neonatal rat cardiomyocytes induced by IGF-1 were used as the model of physiological cardiac hypertrophy , and those induced by PE were used as the model of pathological cardiac hypertrophy .The surface area of the cardiomyocytes, the expression of p-ERK1/2, PPARαand SCAD, the activity of SCAD and the content of free fatty acid in the cardiomyocytes were measured .RESULTS:Compared with the control cells , the surface area of the cardiomyocytes in-duced by IGF-1 and PE were both increased .Compared with the controls , the expression of SCAD and PPARα, and the activity of SCAD in the cardiomyocytes induced by IGF-1 were increased , while the expression of p-ERK1/2 was de-creased.However, the cardiomyocytes treated with PE showed decreased expression of SCAD and PPARα, decreased activ-ity of SCAD and increased expression of p-ERK1/2.Meanwhile, the decrease in free fatty acid in IGF-1-induced cardio-myocytes and the increase in PE-induced cardiomyocytes indicated that the fatty acid utilization was increased in the cardio -myocytes induced by IGF-1, but decreased in the cardiomyocytes induced by PE .CONCLUSION: The changes of p-ERK1/2, PPARαand SCAD in the cardiac hypertrophy induced by IGF-1 or PE indicate that the effects of ERK 1/2/PPARα/SCAD signal pathways are different between physiological cardiac hypertrophy and pathological cardiac hypertro -phy , and that SCAD may be a molecular marker of these 2 different cardiac hypertrophies and a potential therapeutic target for pathological cardiac hypertrophy .

AIM: To investigate the effects of fenofibrate on angiotensin Ⅱ ( AngⅡ)-induced cardiomyocyte hypertrophy .METHODS:Primary neonatal cardiomyocytes were pretreated with fenofibrate (10μmol/L) for 1 h followed by stimulation with AngⅡ(100 nmol/L).The mRNA levels of ANF, BNP andβ-MHC were measured by real-time PCR. Western blotting was employed to determine the nuclear translocations of NFATc 4 and p65-NFκB.Co-immunoprecipitation was used to investigate the interaction of NFATc 4 with p65-NFκB in the nucleus of cardiomyocytes .In addition, the DNA binding activity of NFATc4 on the BNP promoter was determined by EMSA .RESULTS:Fenofibrate significantly inhibited AngⅡ-induced cardiomyocyte hypertrophy .Fenofibrate treatment inhibited the nuclear translocations of NFATc 4 and p65-NFκB, as well as the interactions of NFATc 4 with p65-NFκB in the nucleus of cardiomyocytes induced by AngⅡ.Fenofi-brate inhibited the binding activity of NFATc 4 with the BNP promoter , which was strengthened by AngⅡ.CONCLU-SION:Fenofibrate enhances the interaction of NFATc 4 with PPARα, decreases the interaction of NFATc 4 with p65-NFκB in the nucleus of cardiomyocytes , and inhibits the DNA binding activity of NFATc 4 induced by AngⅡ, which may be the important mechanisms of fenofibrate on inhibiting cardiac hypertrophy .

This study was aimed to discover core agent for the treatment of ulcerative colitis and explore the medication rules . A total of 525 ulcerative colitis medical records in the Jiangsu Province Hospital of TCM were selected from 2009 to 2013 . The records were input into the structured information acquisition system of clinical diagnosis and treatment . The complex network analysis was used to analyze core drugs of prescription and drug compatibility after data mining and rule processing . The results showed that the core drugs are Diyu , Huanglian, Muxiang, Baishao, Xianhecao, Danggui, Chaobaizhu, Huangqin, Zicao, Yiyiren, Fuling, Shanyao. It was concluded that data mining can be an objective method in the analysis of core drugs and compatibility in the treatment of ulcerative colitis. It can also be used to guide the clinical prescription medication.