Objective To analyze variations of hepatic vein in healthy people with 64-slice spiral CT.Methods Seventy-five healthy subjects underwent multi-slice spiral computed(MSCT)hepatic venography.The anatomy of the junction of the hepatic veins with the inferior vena cava and the intrahepatic drainage territory of the hepatic veins and tributaries were evaluated.The hepatic veins were classified according to three anatomic classification(Nakamura's,Marcos's and Kawasaki's classification)methods respectively.Results There was a common trunk of the middle and left hepatic veins before joining the IVC in 86.7%(65/75)of the cases.In 13.3%(10/75)of the cases,the three main hepatic veins joined the IVC separately.The ratios of Nakamura's classification type A,B,C of hepatic veins were 49.4% (37/75),37.3%(28/75),and 13.3%(10/75)respectively.The ratios of Marcos's classification type A,B,C of hepatic veins were 56.0%(42/75),24.0%(18/75),and 20.0%(15/75)respectively. The ratios of Kawasaki's classification type Ⅰ,Ⅱ of hepatic vein were 40.0%(30/75)and 60.0% (45/75).Conclusion Multi-slice spiral CT hepatic venography can provide visualization of peripheral hepatic venous branches in details.

Objective To investigate the current status of unintentional injuries among rural children aged 0-12 years in Shaanxi.Methods Using a three-stage stratified random sampling method to study the status of unintentional injuries among 4668 children aged 0-12 years old during the period of 2010 in rural areas of Shaanxi province.Results The overall incidence of injure was 27.3％,with boys as 28.7％ and girls as 25.6％ respectively(x2=5.91,P=0.015).Age differences in unintentional injuries rate were also significant(x2=9.91,P=0.007),with children under 0-3 years old having the highest rate of injuries,followed by 7-12 and 4-6 year-olds.Falls took the leading type of accidence among both sexes and all age groups.Poorer the family economic situation was,higher the incidence of unintentional injuries appeared.Conclusion Falls was the leading cause of unintentional injuries among rural children in Shaanxi province,with age 0-3 year group appeared the highest to suffer unintentional injuries.Unintentional injuries were associated with the economic status of the families.

This article studied the chemical constituents from the aerial part of Vitis thunbergii var. taiwaniana. The 60% ethanol extract was eluted with 95% ethanol though HP-20 macroporous adsorption resin column. 12 compounds, including (1) betulinic acid, (2)2, 2, 2'-bis (4-hydroxyphenyl) propane bis (2, 3-epoxypropyl) ether, (3) eriodictyol, (4) trans-ε-viniferin, (5) (+)-cis-ε-viniferin, (6) kobophenol A, (7) ampelopsin A, (8) nepalensinol B, (9) cis-miyabenol C, (10) cis-vitisin B, (11) cis-gnetin H and (12) (+)-hopeaphenol, were separated by using normal phase silica gel, ODS, Sephdadex LH-20 column chromatographies and semi-preparative or preparative HPLC. Compounds 2, 5, 6, 8, 9, 10, 11 were separated from the genus Vitis for the first time and compounds 3, 7, 12 were separated from Vitis thunbergii var. taiwaniana for the first time. At a concentration of 50 μmol · L(-1), compound 6, 7 and 11 showed strong cytotoxicity against MCF-7 cell lines with the inhibition rate of 66.58%, 57.16%, 52.84%, respectively.
Antineoplastic Agents, Phytogenic ; pharmacology ; Humans ; MCF-7 Cells ; Plant Extracts ; analysis ; pharmacology ; Vitis ; chemistry

Objective To observe protective effects on rat serum cardiac enzymes and the antioxidant capacity of selenium and vitamin E.Methods According to body weight and 2 × 2 factorial design,eighty male Wistas rats were randomly divided into four groups:low selenium and low vitamin E group(feed containing 23.42％ of the low selenium yeast,excluding vitamin E),low selenium and adequate vitamin E group (feed containing 23.42％ of the low selenium yeast and vitamin E 160 mg/kg),adequate selenium and low vitamin E group(feed containing 46.84％ of the low selenium yeast and sodium seleni 0.25 mg/L in water,excluding vitamin E),adequate selenium and adequate vitamin E group(feed containing 46.84％ of the low selenium yeast,vitamin E 160 mg/kg and sodium selenite 0.25 mg/L in water),20 rats every group.Rats were feed with synthetic feed,and given intraperitoneal anesthesia after 26 weeks of feeding.Blood was collected to observe the impact of selenium and vitamin E on rat cardiac enzymes and myocardial antioxidant capacity and their interactions.Serum creatine kinase (CK) was measured using the continuous monitoring method,creatine kinase isozymes (CK-MB) and lactate dehydrogenase(LDH ) using the immune suppression method,the whole blood GSH-Px assay using the dithiobis nitrohenzoic acid(DTNB) method,serum superoxide dismutase(SOD) using the xanthine oxidase method,total antioxidant capacity (T-AOC) using the complex colorimetry method,the content of propylene glycol (MDA) using the thiobarbituric acid colorimetric method,and reactive oxygen species(ROS) using the colorimetric method.Results Group differences of serum CK,CK-MB,LDH,whole blood GSH-Px activity,serum T-AOC vitality,MDA and ROS content were statistically significant(F=9.797,17.041,48.399,3.744,224.900,49.384,5.045,all P＜ 0.05).Compared with the two low selenium groups and one adequate selenium group,the vitalities of CK,CK-MB,LDH and the contents of MDA[(1577.75 ± 451.87),(1239.15 ± 344.99),(884.25 ± 133.84)U/L,(5.688 ±1.169) × 103 nmol/L; (1474.21 ± 398.38),(1014.84 ± 215.40),(523.00 ± 98.05)U/L,(4.035 ± 0.487 ) × 103 nmol/L and (1180.10 ± 245.51),(948.75 ± 173.68),(676.70 ± 193.63)U/L,(3.406 ± 0.146) × 103 nmol/L]increased significantly in adequate selenium and adequate vitamin E group[( 1056.80 ± 250.98),(721.70 ±129.98),(404.65 ± 72.49)U/L,(3.010 ± 1.270) × 103 nmol/L,all P ＜ 0.05) ].The activity of GSH-Px was obviously increased in the two adequate selenium groups[ (96.611 ± 8.238) × 103,(103.024 ± 8.217) × 103 U/L,all P ＜ 0.05],compared with the two low selenium groups[ (60.356 ± 8.179) × 103,(63.117 ± 8.281) × 103 U/L].Selenium affected the activities of CK,CK-MB and LDH(F =27.09,31.58,29.66,all P＜ 0.01 ),and vitamin E affected the activities of CK-MB and LDH(F=18.9,11.2.all P＜ 0.01 ),but both selenium and vitamin E had no interactions on the activities of CK,CK-MB and LDH (F=0.02,0.001,2.22,all P＞0.05).Selenium affected the activity of GSH-Px and the content of MDA(F=6.74,95.68,all P＜ 0.05),vitamin E affected the activity of T-AOC,the contents of MDA and ROS(F=6.42,36.73,8.43,all P＜0.05),but selenium and vitamin E had interactions only on the content of MDA(F =13.82,P＜ 0.05).Conclusions Long-term selenium or vitamin E deficiency,can reduce the body's antioxidant capacity,leading to the occurrence of myocardial injury.Selenium and vitamin E can improve the body's oxidation capacity,playing a role in myocardial protection.

BACKGROUNDEndogenous hydrogen sulfide (H(2)S) plays an important role in hypertension. The aim of this study was to investigate the role of erythrocyte and serum H(2)S in patients with untreated essential hypertension.

METHODSWe recruited 62 patients (age 22 - 74 years) with untreated prehypertension or hypertension, and 64 normotensive subjects (age 18 - 64 years). We assessed the 3-mercaptopyruvate sulphurtransferase (MPST) protein expression in erythrocytes and measured the H(2)S production from erythrocytes and serum H(2)S levels, then analyzed the association of erythrocytic or serum H(2)S content and blood pressure or cardiovascular risk factors (e.g., age, body mass index (BMI) and dyslipidemia). A stepwise regression analysis was used to evaluate the possible relationship of erythrocytic H(2)S in hypertension.

RESULTSIn hypertensive patients, erythrocyte H(2)S production ((111.04 ± 29.20) nmol/min per 10(8) erythrocytes) was higher than that in controls ((78.85 ± 19.38) nmol/min per 10(8) erythrocytes), and serum H(2)S was also higher. The erythrocytic H(2)S production was associated with increased systolic blood pressure (sBP), diastolic blood pressure (dBP), age, BMI, level of C-reactive protein (CRP), as well as triglycerides (TG) and high density lipoprotein cholesterol (HDL-C). Serum H(2)S was not associated with age or CRP. Stepwise regression analysis showed that erythrocytic H(2)S production was correlated with sBP, TG, HDL-C, low density lipoprotein cholesterol (LDL-C) and blood urea nitrogen (BUN) and serum H(2)S was correlated with dBP and TG. Results of receiver-operating characteristic curve analysis suggested that erythrocytic H(2)S production was a more sensitive predictor of hypertension development than serum H(2)S.

CONCLUSIONErythrocytic or serum H(2)S production is sensitive predictor of hypertension.

Adolescent ; Adult ; Aged ; Erythrocytes ; metabolism ; Female ; Humans ; Hydrogen Sulfide ; blood ; Hypertension ; blood ; metabolism ; Male ; Middle Aged ; Young Adult

OBJECTIVETo investigate the effect of AMPK agonist 5-aminoimidazole-4-carboxamide ribonucleoside (AICAR) on proliferation, differentiation and apoptosis of U937 cells and explore its possible mechanism.

METHODSU937 cells were cultured with different concentrations of AICAR for 24 h and 48 h. Cell proliferation was evaluated. Cell growth curve was analyzed by CCK-8; cell apoptosis was analyzed by cell morphology, Annexin V/7-AAD double labeling. The differentiation of U937 cells was evaluated by expression of CD11b. The Bcl-xL, Bax, Bim, caspase-3 mRNA expressions of U937 cells were determined by real time PCR.

RESULTSAICAR significantly inhibited the growth of U937 cells in a time-and dose-dependent manner, with a 24 h IC50 value of 1.1 mmol/L and 48 h of 0.9 mmol/L. 1.0 mmol/L AICAR didn't induce differentiation of U937 cells with the increase of CD11b expression for 24 h (P > 0.05). The U937 cells apoptosis was confirmed by cell morphology and Annexin V/7-AAD labeling. AICAR induced apoptosis of U937 cells and the apoptosis rate was (6.81 ± 1.16)% at 1 mmol/L AICAR higher than control group (2.74 ± 0.32)% without AICAR for 24 h treatment (P < 0.05). The real time PCR assay revealed that as compared with control group, the expression of Bim and caspase-3 mRNA were increased, while Bcl-xL and Bax were unchanged on the AICAR treatment.

CONCLUSIONAICAR can effectively inhibit proliferation and induce apoptosis of U937 cells. However, it has no significant effect on differentiation of U937 cells. The mechanism may be related with up-regulating Bim and Caspase-3.

Aminoimidazole Carboxamide ; analogs & derivatives ; pharmacology ; Apoptosis ; drug effects ; Cell Differentiation ; drug effects ; Cell Proliferation ; drug effects ; Humans ; Ribonucleotides ; pharmacology ; U937 Cells

Accidents ; statistics & numerical data ; Causality ; Child ; Child, Preschool ; China ; epidemiology ; Female ; Humans ; Infant ; Infant, Newborn ; Male ; Risk Factors ; Rural Population ; Wounds and Injuries ; epidemiology

OBJECTIVETo investigate the sensitivity of imatinib mesylate (IM) on Sup-B15 Ph⁺ acute lymphoblastic leukemia (ALL) cells knockdown of VE-cadherin (CD144), and to further explore its mechanism.

METHODSCD144 in Sup-B15 leukemia cells was stably knock downed via lentivirus-mediated RNA interference (named as Sup-B15/shVEC). The inhibitory effects of IM on Sup-B15/shVEC and Sup-B15 leukemia cells were measured by CCK-8 test, and the apoptosis of those cells was determined by AnnexinV/7-AAD dyeing using flow cytometry, the percentage of CD34⁺CD38⁻ leukemia cells also by flow cytometry. ALDH1 mRNA levels were detected by real-time RT-PCR, and protein levels of CD144, CD133, Bcr-abl and β-catenin by Western blot.

RESULTSIM treatment presented inhibitory effects on Sup-B15/shVEC and Sup-B15 leukemia cells at multiple concentrations of IM. The IC50 of IM on Sup-B15/shVEC and Sup-B15 leukemia cells were 25.1μmol/L and 18.7μmol/L, respectively (P<0.05). After 48h of 20 μmol/L IM treatment, the percentages of apoptosis cell in Sup-B15/shVEC cells and Sup-B15 cell were (13.52±2.06)% and (3.03±0.72) %, respectively (P<0.05). The percentage of CD34⁺CD38⁻ cells in Sup-B15 cells was significantly higher than in Sup-B15/shVEC cells [(2.39±0.28)% vs (0.96±0.07)%, P<0.05). As compared to Sup-B15 cells, the transcription of ALDH1 in Sup-B15/shVEC was remarkably downregulated, and the CD133 protein level was also downregulated in Sup-B15/shVEC cells. Both cytoplasmic and nucleic β-catenin protein levels (but not for Bcr-abl levels) decreased in Sup-B15/shVEC cells as compare to Sup-B15 cells.

CONCLUSIONKnockdown of CD144 sensitized Sup-B15 Ph+ ALL cells to IM. The possible mechanisms underlying this phenomenon might be via inhibiting β-catenin nucleic translocation and facilitating β-catenin degradation.

Antigens, CD ; genetics ; Benzamides ; pharmacology ; Cadherins ; genetics ; Cell Line, Tumor ; Drug Resistance, Neoplasm ; genetics ; Endothelium, Vascular ; drug effects ; metabolism ; Gene Knockdown Techniques ; Humans ; Imatinib Mesylate ; Piperazines ; pharmacology ; Precursor Cell Lymphoblastic Leukemia-Lymphoma ; genetics ; metabolism ; Pyrimidines ; pharmacology ; RNA Interference ; beta Catenin ; metabolism

OBJECTIVETo investigate the change in the expression of tight junction protein ZO-1 in intestinal epithelial cells (Caco-2 cells) and the protective effect of eicosapentaenoic acid (EPA) after adherent-invasive Escherichia coli (E.coli) LF82 infection.

METHODSThe Caco-2 cell line was used to establish an in vitro model of tight junction of intestinal epithelial cells. Caco-2 cells were divided into EPA treatment groups (0, 25, 50, 100, and 200 μmol/L EPA) and EPA (0, 25, 50, 100, and 200 μmol/L EPA)+E.coli LF82 treatment (0, 6, and 12 hours) groups. A microscope was used to observe the morphological characteristics of the cells. MTT assay was used to determine the cell growth curve. The activity of alkaline phosphatase (ALP) at both sides of the cell membrane was compared to evaluate the Caco-2 cell model. MTT assay and flow cytometry were used to investigate the effects of different concentrations of EPA on the survival rate and apoptosis rate of Caco-2 cells. RT-qPCR was used to measure the mRNA expression of ZO-1 in Caco-2 cells after EPA and/or E.coli LF82 treatment. ELISA was used to measure the change in the level of tumor necrosis factor-α (TNF-α) in culture supernatant.

RESULTSAfter EPA treatment (25 and 50 μmol/L), the proliferation of Caco-2 cells was induced in a dose-dependent manner. The survival rates of the cells were significantly higher than those in the control group (P<0.05). The EPA treatment (100 and 200 μmol/L) groups had a significant inhibitory effect on the proliferation of Caco-2 cells in a dose-dependent manner. The survival rates of the cells were significantly lower than those in the control group (P<0.05). The EPA treatment (100 and 200 μmol/L) groups had a significant increase in cell apoptosis rate compared with the control group (P<0.05). The 6- and 12-hour E.coli LF82 treatment groups had decreasing mRNA expression of ZO-1 in Caco-2 cells over the time of treatment and had significantly lower mRNA expression of ZO-1 than the untreated group (P<0.05). The Caco-2 cells treated with E.coli LF82 and 25 or 50 μmol/L EPA for 6 or 12 hours showed an increase in the mRNA expression of ZO-1 with the increasing concentration of EPA, as well as significantly higher mRNA expression of ZO-1 than the Caco-2 cells treated with E.coli LF82 alone (P<0.05). The Caco-2 cells treated with E.coli LF82 alone for 6 or 12 hours had increasing secretion of TNF-α over the time of treatment and had significantly higher secretion than the untreated Caco-2 cells (P<0.05). The Caco-2 cells treated with E.coli LF82 and 25 or 50 μmol/L EPA for 6 or 12 hours showed a reduction in the secretion of TNF-α with the increasing concentration of EPA and had significantly lower secretion than the Caco-2 cells treated with E.coli LF82 alone (P<0.05).

CONCLUSIONSEPA can effectively prevent the destruction of tight junction of intestinal epithelial cells induced by E.coli LF82 infection and inhibit the secretion of inflammatory factors. Therefore, it has a certain protective effect on intestinal mucosal barrier.

Apoptosis ; drug effects ; Caco-2 Cells ; Eicosapentaenoic Acid ; pharmacology ; Escherichia coli ; pathogenicity ; Humans ; Intestinal Mucosa ; metabolism ; microbiology ; RNA, Messenger ; analysis ; Tight Junctions ; drug effects ; Tumor Necrosis Factor-alpha ; secretion ; Zonula Occludens-1 Protein ; genetics

BACKGROUNDStudy of the relationship between mast cells and atherosclerosis is mostly dependent on pathological observation and cytology experiments. To investigate the effects of mast cells degranulation on plaque and their possible mechanisms we used apolipoprotein E knockout mice which had been placed perivascular common carotid collar with mast cells degranulator compound 48-80.

METHODSForty apolipoprotein E knockout mice were fed a western-type diet and operated on with placement of perivascular right common carotid collar. Four weeks after surgery, the mice were intraperitoneally injected with compound 48-80 (0.5 mg/kg) or D-Hanks every other day for 4 times. The serum lipids and activity of tryptase were measured. Tissue sections were stained with hematoxylin and eosin. Corresponding sections were stained with toluidine blue and immunohistochemically with antibodies against macrophage-specific antigen, alpha-smooth muscle actin, interleukin-1beta and von Willebrand factor. Simultaneously, basic fibroblast growth factor was detected by in situ hybridization and immunofluorescence.

RESULTSNo pathological change was observed in common carotid non-collar placement but atherogenesis in common carotid collar placement of both groups. There was a significant increase in plaque area ((5.85+/-0.75) x 10(4) vs (0.86+/-0.28) x 10(4) microm(2), P<0.05), the degree of lumen stenosis ((81+/-15)% vs (41+/-12)%, P<0.05), the activity of tryptase in serum ((0.57+/-0.13) U/L vs (0.36+/-0.10) U/L, P<0.05), and the percentage of degranulated mast cells ((80.6+/-17.8)% vs (13.5+/-4.1)%, P<0.05). The expressions of macrophage-specific antigen, alpha-smooth muscle actin, interleukin-1beta, basic fibroblast growth factor and the density of neovessel in plaque were more in the compound 48-80 group than in the control group.

CONCLUSIONSPerivascular common carotid collar placement can promote atherosclerotic plaque formation in apolipoprotein E knockout mice. Compound 48-80 increases plaque area and the degree of lumen stenosis by the mechanism that compound 48-80 promotes proliferation of smooth muscle cells and aggregation of macrophages. Compound 48-80 promotes angiogenesis in plaque. The mechanism is potentially that compound 48-80 increases the expressions of basic fibroblast growth factor mRNA and protein in plaque. Compound 48-80 enhances the expression of interleukin-1beta in plaque.

Animals ; Apolipoproteins E ; genetics ; Atherosclerosis ; chemically induced ; genetics ; metabolism ; pathology ; Carotid Arteries ; drug effects ; pathology ; Fluorescent Antibody Technique ; Immunohistochemistry ; In Situ Hybridization ; In Vitro Techniques ; Male ; Mast Cells ; drug effects ; metabolism ; Mice ; Mice, Knockout ; p-Methoxy-N-methylphenethylamine ; pharmacology