Objective To research the relationship between anaemia and inflammatory in patients with heart failure .Methods 284 cases of patients with heart failure were enrolled and divided into 2 groups (anaemia group and non‐anaemia group) .The serum levels of of brain natriuretic peptide (BNP) ,high‐sensitivity C‐reactive protein (hs‐CRP) ,blood urine nitrogen (BUN) and creati‐nine (Crea) were measured ,and the results were analyzed .Results The levels of BNP ,hs‐CRP and Crea of anaemia group were sig‐nificantly higher than those of non‐anaemic group (P<0 .01) .The results of logistic regression demonstrated that hs‐CRP was in‐dependently associated with anaemia (P=0 .021) .Conclusion The occurrence and development of inflammation are independently associated with anaemia in the patients with heart failure .

Objective The aim of this study was to investigate which inflammatory markers allow an accurate differentiation of septic and gouty arthritis.Methods In 2013 January to 2014 January 33 patients with septic arthritis and 29 patients with gouty arthritis.Detected white blood cells,C-reactive protein and uric acid of inflammatory markers in plasma and tested lac-tate,glucose,uric acid,lactate dehydrogenase and white blood cell count inflammatory markers in the synovial fluid.MedCalc 13.0 software were used for statistical analysis.Results There were no significantly different between serum C-reaction protein and WBC counts with two groups.Synovial lactate showed the greatest diagnostic potential (AUC=0.898,sensitivi-ty=96.9%,specificity=72.4%)followed by serum uric acid (AUC=0.818)and synovial uric acid (AUC=0.808).Con-clusion Lactate in the synovial fluid has excellent diagnostic potential to differ septic arthritis from gouty arthritis.Synovial lactate levers above 1.7 mmol/L almost proofed septic arthritis.

To clarify the source of deviations of drug combination effects evaluated with different drug interaction mathematical models, the cytotoxicity of SAHA and arsenic trioxide and their combinations were observed in a series of human cancer cell lines and a normal cell line. The combined effects were evaluated with three drug interaction models: Loewe Additivity (LA), Bliss Independence (BI) and Chou's Median Effect Model. The evaluations with three different models were further compared with each other. We demonstrated that when dose-response curves were fitted with the same method, similar evaluated results for drug combinations would be derived with different models. The deviations of evaluated effects of drug combinations were attributed to different curve fitting methods used rather than the models themselves. The effects of drug combinations showed discrepancies on different cell lines, and at different combined drug concentrations on same cell line.

Objective To analyze expression of miR-324-5p in plasma of CHD patients by real-time PCR and identification of early diagnosis,for CHD.Methods In 2012 June to 2013 February 76 patients and 13 normal controls who were included in the study had measurement of plasma expression levels of miR-324-5p by real-time PCR.MedCalc 13.0 software were used for statistical analysis and comprehensive evaluation of miR-324-5p in CHD disease for diagnosis.Results Analysis of re-ceiver operating curve (ROC)showed that area under the curve (AUC)was 0.731 and best diagnostic threshold was 0.116 1.The sensitivity was 64.5% and specificity of 84.6%.Conclusion Circulating miR-324-5p as a biomarker for early diagno-sis of CHD has some-extent clinical value,but needs combined with other medical indicators.

Objective To observe the changes of the cells of human hepatocellular carcinoma (HepG2)using RNA for silencing the expression of COMMD7 gene,and investigate related mechanism of COMMD7 gene promoting HepG2 proliferation.Methods COMMD7 gene shRNA was designed and constructed into COMMD7-shRNA plasmid.HepG2 cells were divided into the HepG2 group,control-shRNA group (empty vectors were infected) and COMMD7-shRNA group (positive vectors were infected).Cells shapes were observed by fluorescence microscope after infecting.The expression of COMMD7 and expression and phosphosylation of extracellular regulated protein kinase1/2 (ERK1/2) and MEK1/2 protein were measured by Western blot.The cell vitality was measured by cholecystokinin octapeptide (CCK-8),and the apoptosis of cell was detected by flow cytometry.The measurement data with normal distribution were presented as (x) ± s.The comparisons among groups were evaluated with the one-way ANOVA,and pairwise comparison was analyzed by the LSD-t test.Results The cells were oval or spindle shapes and displayed green fluorescent after infected successfully.The results of Western blot showed that the relative quantitative expression of COMMD7 protein in the HepG2 group,control-shRNA group and COMMD7-shRNA group were 0.90 ±0.18,1.03 ±0.05 and 0.23 ±0.03,respectively,with a significant difference among the 3 groups (F =152.08,P ＜ 0.05),and the expression of COMMD7 protein in the COMMD7-shRNA group was significantly lower than those in the other 2 groups (t =20.74,21.16,P ＜ 0.05).The results of CCK-8 showed that the scores of the HepG2 vitality in the HepG2 group,control-shRNA group and COMMD7-shRNA group were 1.193 ±0.024,1.225 ±0.034 and 1.147 ±0.021,respectively,with a significant difference among the 3 groups (F =6.90,P ＜ 0.05),and the HepG2 vitality in the COMMD7-shRNA group was significantly lower than those in the other 2 groups (t =3.53,3.69,P ＜ 0.05).The results of flow cytometry showed that the apoptosis rate of HepG2 in the HepG2 group,control-shRNA group and COMMD7-shRNA group were 6.1％ ± 0.3％,7.8％ ± 0.5％ and 20.9％ ± 1.4％,showing a significant difference among the 3 groups (F =270.80,P ＜0.05),and the apoptosis rate of HepG2 in the COMMD7-shRNA group was significant higher than those in the other 2 groups (t =21.77,19.36,P ＜0.05).The results of Western blot showed that the relative quantitative expression of phosphorylation (p)-ERK1/2 and p-MEK1/2 in the HepG2 group,control-shRNA group and COMMD7-shRNA group were 0.932 ±0.046,0.945 ±0.017,0.553 ±0.052 and 0.452 ±0.031,0.468±0.027,0.263 ± 0.022,respectively,showing significant differences among the 3 groups (F =93.61,49.16,P ＜ 0.05),and the relative quantitative expression of p-ERK1/2 and p-MEK1/2 in the COMMD7-shRNA group were significantly lower than those in the other 2 groups (t =11.94,12.17,9.33,8.65,P ＜ 0.05).Conclusions COMMD7 gene can promote HepG2 proliferation via activating ERK/mitogen-activated protein kinase (MAPK) signaling pathway,and its mechanism may be promoting the phosphorylation of expression of ERK1/2 and MEK1/2.

Objective To investigate the neuroprotective effect and possible mechanism of Compound Porcine Cerebroside and Ganglio-side Injection (CPCGI) on cerebral ischemia-reperfusion injury in rats. Methods Healthy adult male Sprague-Dawley rats were divided into sham group (n=10), model group (n=10), CPCGI low dosage group (n=10) and high dosage group (n=10), and control group (Ginkgo biloba extract, n=10). All the rats was subjected to middle cerebral artery occlusion (MCAO) for two hours and reperfusion except sham group, and received treatment for fourteen days once reperfusion started. They were tested with modified Neurological Severity Score one, three, seven and fourteen days after MCAO, and adhesive-removal test and beam-walking test fourteen days after MCAO. The expression of Beclin1, PINK1 and Parkin were detected with Western blotting. Results Compared with the model group, the Neurological Severity Score reduced (P<0.05) and the time crossing the beam reduced (P<0.01) in all the medical groups fourteen days after MCAO, and the time removing the adhesive paper reduced in the CPCGI groups (P<0.01). The expression of Beclin1 and Parkin decreased and the PINK1 level increased in the model group (P<0.01), and it was reversed in all the CPCGI groups (P<0.05). Conclusion CPCGI could relieve the cerebral ischemia-re-perfusion injury in rats through the regulation in mitophagy.

Objective To analyze the epidemiology and clinical features of the critical congenital heart diseases in neonates,and to summarize the main points on pre-operative treatments.Methods We retrospectively analyzed all critical congenital heart disease in newborns admitted to CICU from June 2014to June 2015.Depict entity distribution,the main symptoms,and the key points on their treatments,also the indi-cation of intubation and their operation time were summarized.Results In totally 96cases,transposition of the great artery,with and without the intact ventricle septum,was the biggest category and counts for 49%in our group.Severe cyanosis was the main symptom for 62.5% of all cases.Another key symptom was the heart failure(33.3%).Eight-seven cases were intubated during their treatments,in which 41were intubated as soon as they were admitted and 40cases were done in the first 24hours after their admission.One case died before treatment due to interrupted aortic arch.All the rest received operations during their hospital stay. Conclusion Transposition of great artery is the dominating entity in critical congenital heart diseases in new-borns;severe cyanosis is the main symptom.Treatment should be based on each characteristic anatomy and hemodynamics features.Rigorous and dynamic monitoring on the homeostasis and metabolic index determines the indication of intubation and surgery time.

Objective To determine the effect of COMMD7 inhibition on invasion and migration in liver cancer stem cells (LCSCs),and investigate the possible mechanism.Methods After LCSCs were infected by shRNA lentiviral vectors of COMMD7,adhesion assay and Transwell assay were used to detect the invasion and migration,and phalloidin staining was employed to observe the morphological changes.Western blotting was adopted to measure the expression of E-cadherin,N-cadherin and Vimentin.Results COMMD7 knockdown significantly inhibited the invasion and migration of LCSCs.The relative cell quantity of adhesion was 1.00 ± 0.12 and 2.35 ± 0.20 respectively in control cells and infected cells,suggesting there were significantly more adhesive cells in the infected group (P ＜ 0.05).The relative cell quantity per visual field of migration was 1.00 ±0.04 and 0.24±0.03,and that of invasion was 1.00 ±0.05 and 0.24 ±0.04 respectively in the control cells and infected cells,and there were significantly less invasive and migrated cells in the infected group (P ＜0.05).What's more,COMMD7 knockdown also induced some morphological changes of cells corresponding to the weakened abilities of migration and invasion.All the changes above were associated with up-regulation of E-cadherin (P ＜ 0.05) and down-regulation of N-cadherin and Vimentin (P ＜0.05),the molecules related to mesenchymal-epithelial transition (MET).Conclusion COMMD7 knockdown inhibits the invasion and migration in LCSCs,which may be through its regulation on the MET course.

Objective To explore the 3-D anatomical structure of blood vessel around the pancreas and its clinical significance.Methods Fifty objects were scanned by 64-slice CT of GE,the artery,portal vein,spleen vein,superior mesenteric vein and inferior mesenteric vein were 3-D reconstructed by Myrian system,and the scientific data were recorded.Results The artery,portal vein,spleen vein,superior mesenteric vein and inferior mesenteric vein were all reconstructed;the length of portal vein was(44.28±10.23)mm and the length of post-pancreas trunk was(32.13±7.08)mm;the angle between portal vein and spleen vein were classified into three types:the angle of type Ⅰ was<90°,angle of type Ⅱ was=90°,and angle of type Ⅲ was>90 °.30％of the inferior mesenteric vein fed into the spleen vein,56％fell into the superior mesenteric vein and 14％came into the the meeting point of the spleen vein and superior mesenteric vein.Conclusion The 3-D reconstruction of blood vessels around the pancreas can provide the anatomical basis for surgeon and reduce the risk of pancreatic surgery before operation.

Objective To investigate the mechanism of COMMD7,a hepatocellular carcinoma gene,promoting human hepatocellular carcinoma cell line (HePG2 cells)proliferation and migration.Methods The specific siRNA (small interference RNA)was designed for COMMD7 gene,siRNA transfected HepG2 cells was set as Si-HePG2 group,and the PTEN inhibitor treating group (Si +BpV-HePG2),the control group (HePG2),the empty vector group (HePG2 was infected empty vector,N-HePG2 group)were also set up.qRT-PCR was per-formed to evaluate the mRNA expression changes of COMMD7 and PTEN,and Western blot was performed to test the expression changes of COMMD7,PTEN,p-AKT,and AKT.MSP method was performed to detect methylation level.CCK8 was performed to test cell proliferation a-bility.Transwell was performed to detect the invasion of cells.Results The results of qRT-PCR showed that the expression of COMMD7 gene in Si-HePG2 group was lower (0.101 times)than the control group and the N-HePG2 group,and the expression of PTEN gene was higher (2.841 times)than the control group and the N-HePG2 group,and all the results above were of statistically singificant difference (P <0.05). The results of Western blot showed that in Si-HePG2 group,the expression of COMMD7 reduced obviously,the expression of PTEN increased and the expression of p-AKT was significantly inhibited.In Si +Bpv-HePG2 group,the expression of PTEN was significantly inhibited and the expression of p-AKT was increased.The result of MSP showed that compared with the control group and the N-HePG2 group,Si-HePG2 group was more obviously demethylated,which indecated that the expression of COMMD7 gene could induce PTEN demethylation.The results of CCK8 showed that the proliferation in Si-HePG2 group was decreased compared with the control group,N-HePG2 group and Si +BpV-HePG2 group,and the difference was singificant (P <0.05).The results of Transwell showed that the numbers of cell permeating septum in Si-HePG2 group,N-HePG2 group,control group and PTEN group were (17.4 ±2.7),(36.2 ±3.2),(41.6 ±4.5)and (47.6 ±1.8)respec-tively,which were obviously decreased with a significant difference (P <0.05).Conclusion siRNA interference decreased the expression of COMMD7.It can induced the demethylation of PTEN gene in HePG2 and increase the expression of PTEN gene to inhibit PI3K/AKT signaling pathway,thus decreasing the proliferation,migration and invasion ability of HePG2 cells.