Objective To investigate the relationship between metabolic syndrome and colorectal cancer. And to further prevent the risks of colorectal cancer and provide methods and evidences.Methods A literature search was performed through CNKI,Wanfang,PubMed,Ovidsp,Cochrane data within the time limit of November 2005 to November 2015.According to the inclusion and exclusion criteria,the studies were screened and the data were extracted.Then,meta -analysis was performed using Review Manager 5.3.5.Results A total of 14 studies(6 case-control studies and 8 cohort studies)met the inclusion criteria.Meta analysis showed that with metabolic syndrome had a higher risk of colorectal cancer incidence compared with the control group without metabolic syndrome(OR =1.18,95%CI:1.33cv1.22,P <0.05).Stratified analysis showed that metabolic syndrome increased the risk of color-ectal cancer between men and women population.The combined effect of the OR respectively (OR =1.12,95%Cl:1.09 -1.14,P <0.05;OR =1.13,95%Cl:1.05 -1.22,P <0.05),the differences were statistically significant. Meta analysis showed that metabolic syndrome was not associated with an increased risk of colon cancer mortality (OR =1.05,95%CI:0.92 -1.19,P =0.46).Conclusion This meta analysis indicate a positive association between meta-bolic syndrome and colorectol cancer incidence,and the association has no gender differences.The metabolic syndrome does not increase the risk of colon cancer death.More prospective cohort study needed to further confirm it.

Objective To study the treatment of pancreatic injury accompanied with nervous injury. Methods 22 patients were divided into three groups. They were treated with different method and comparable in the duration of hospital stay, the time of nervous function recovery to normal,placement time of catheterization tube, complications and change of sera albumin.Results The duration of hospital stay were significantly shortened in combined therapy group patients than in control group. Combined therapy can promote recover of nervous function, reduce time to conserve catheterization tube. Reduce complications of pancreatic injury with accompanied nervous injury by combined treatment with somatostatin and growth hormone, it also can increase protein synthesis, correct hypoalbuminemia and reduce complication.Conclusions In combination of somatostatin and growth hormone early used to treat pancreatic trauma accompanied with nerves injure has valuable to heal pancreatic injure and recover the nervous function.

AIM: To investigate the effect of paclitaxel on the quantitative growth of rabbit's vascular smooth muscle cells (SMCs) and endothelial cells (ECs) and their relationship in vitro. METHODS: An ex vivo model of endothelium repair was developed in which rabbit's SMCs were inoculated in the upper chamber and rabbit's ECs in the lower chamber of a co-culture system. 3 H-TdR incorporation and cell counting were used to determine the effect of paclitaxel on the quantitative proliferation of rabbit's vascular ECs and SMCs. The migration rate was analyzed to determine the effect of paclitaxel on the migration of rabbit's vascular ECs and SMCs. The IC50 of paclitaxel on ECs and SMCs was calculated. RESULTS: The 3 H-TdR incorporation, cell counting and migration of rabbit's vascular SMCs were inhibited by paclitaxel of 1 nmol·L-1-1 μmol·L-1 in a concentration-dependent manner (n=6, P<0.01). The 3 H-TdR incorporation and cell counting of rabbit's vascular ECs were inhibited by paclitaxel of 10 nmol·L-1-1 μmol·L-1 and migration by paclitaxel of 1 nmol·L-1-1 μmol·L-1 in a concentration-dependent manner (n=6, P<0.01). The 3 H-TdR incorporation assay resulted in the IC50 of 10.09±0.47 nmol·L-1 on SMCs and 19.06±0.35 nmol·L-1 on ECs proliferation. The migration assay resulted in the IC50 of 9.16±0.54 nmol·L-1 on SMCs and 5.37±0.51 nmol·L-1 on ECs migration. Paclitaxel (10 nmol·L-1, 20 min) inhibited SMCs growth of the confluent ECs group during the observed period. However, increased SMCs growth was observed in the proliferative ECs group 10 days after paclitaxel intervention. CONCLUSION: Paclitaxel inhibits not only SMCs but also ECs growth in rabbit's vascular. The delayed SMCs proliferation is closely related with the delayed ECs regeneration induced by paclitaxel.

ABSTRACT:Hypertension,the first risk factor for stroke and coronary heart disease in the Chinese population, seriously endangers people’s health.At present,China has more than 270 million people with hypertension and an annual increase rate of 1 0 million people.Then how to improve prevention and treatment of hypertension has become an urgent need to solve major medical and social problems.In the past,research on hypertension mainly focused on the peripheral area,while recent research has shown that the central regulation plays an important role in the development of hypertension. Hypothalamic paraventricular nucleus (PVN ), which plays a key role in maintaining cardiovascular activity, can directly control the sympathetic preganglionic neurons and regulate peripheral sympathetic nerve activity,thus being closely related to the development of hypertension.Research in recent years shows that the comprehensive effects of proinflammatory cytokines (PIC ),reactive oxygen species (ROS),renin-angiotensin system (RAS),neurotransmitter (NT)and nuclear factorκB (NF-κB)are involved in the pathogenesis of hypertension.However,it is unclear how these neurohormones in PVN are activated,how they interact with each other and what role they play in the regulatory mechanism of hypertension.Therefore,the key focus of this research is to explore the impact of activated neurohormones in PVN on hypertension.This study will provide new content for the study on hypertension.

Objective To investigate the protective effect of n-butanol extract from the roots of Potentilla anserina (NP) on hypoxic hippocampal neurons in neonatal rats.Methods Primary cultured hippocampal neurons were pretreated with different concentration of NP (0.25,0.0625,and 0.0156 mg/mL) before incubation in a low oxygen (0.1％) environment for 4 h.Cell viability was evaluated by Trypan blue staining assay.Lactate dehydrogenase (LDH) released by neurons into the medium was measured.The activity of superoxide dismutase (SOD) in cell cytosol was determined using nitroblue tetrazolium.Morphological changes and mitochondrial function were observed by transmission electron microscopy.Results Hypoxic injury could decrease the cells viability of neuron,enhance LDH release (P ＜ 0.05),decrease SOD activity,and increase mitochondrial injury.Pretreatment with NP significantly increased cell viability,decreased LDH release (P ＜ 0.05),promoted SOD activity (P ＜ 0.05),and remarkably improved cellular ultra-microstructure compared with the model group.Conclusion NP could protect the primary hippocampal neurons from hypoxic injury by attenuating mitochondrial cell death.

The noninvasive measurement of liver stiffness (LS) was evaluated by transient elastography (FibroScan) and the possible influencing factors from the patients' clinical situations including age, gender, liver inflammation represented by alanine transaminase (ALT) and total billirubin (TBIL) level, HBV replication (HBV DNA loads), portal vein pressure (portal vessel diameter, PVD), splenic thickness (SPT) and body mass index (BMI) were analyzed in patients with chronic hepatitis B (CHB). A total of 466 patients including 31 patients with acute-on-chronic liver failure (ACLF), and 435 patients with chronic hepatitis B (CHB) among which 82 patients were diagnosed with liver cirrhosis (LC) by clinical manifestations and liver B-type ultrasonic inspection were enrolled at Tongji Hospital from April to December 2009. LS was measured by a FibroScan device (EchoSens, France). Simultaneously, ALT and TBIL levels, HBV DNA loads, PVD, SPT and BMI in all patients were also tested. Forty-one healthy volunteers served as controls. The values of LS were correlated positively with ages of CHB patients and significantly higher in males than in females. In patients with BMI>28 kg/m(2) (obesity) and abnormal levels of ALT and TBIL, LS values were significantly increased as compared with those having normal levels of ALT and TBIL. The patients with ACLF had the highest LS value. Furthermore, LS values in the patients with LC were significantly higher than those in patients without LC. It is concluded that noninvasive measurement of liver fibrosis by FibroScan provides an alternative method to evaluate liver fibrosis of patients with CHB. In order to properly illustrate the stiffness value taken by transient elastography, patients' gender should be taken into consideration and it is also suggested to avoid possible influencing factors including liver inflammation (high levels of ALT and TBIL) and obesity (high BMI).

Objective To explore the optimum voltage for digital chest radiography in adult. Methods PMMAs of Different thickness (7.2, 9.0, 10. 8 and 12. 6 cm) were used to simulate chest of different depth ( 17. 5, 22. 5, 27.0 and 32. 5 cm). The combinants of contrast-detail Cdrad 2.0 phantom and above PMMAs were exposed with automatic exposure control (AEC) and different tube voltages. The images of these combinants were obtained and the entrance surface dose (ESD) was recorded. The imaging quality factor (IQF) was calculated and the curves were drawn between the ESD,IQF and kV. The PMMAs of different thickness, on which a contrast object ( PMAA of 5 cm diameter and 1.8 cm thickness ) was placed, were exposed with the same condition used for above test. Their images were obtained and SNRs were calculated. Results The ESD, SNR and IQFinv of different chest depth decreased with increase of kV.When tube voltages of 70, 100 and 140 kV were used, for 17. 5 cm chest depth, the ESD was 0. 22, 0. 09 and 0. 06 mGy, the IQF was 43.3, 58. 8 and 72. 0, the SNR was 7.5, 6. 2 and 5.0; for 22. 5 cm chest depth, the ESD was 0.37, 0.12 and 0.06 mGy, the IQF was 56. 0, 61.4 and 65.3, the SNR was 6. 4, 5.2 and 3. 8; for 27. 0 cm chest depth, the ESD was 0. 52, 0. 20 and 0. 09 mGy, the IQF was 54. 2, 64. 3 and 91. 0, the SNR was 6. 0, 4. 8 and 3. 5; for 31.5 cm chest depth, the ESD was 0.53, 0.24 and 0. 10 mGy,the IQF was 53.2, 66. 8 and 95.3, the SNR was 5. 7, 4. 5 and 3. 0. Conclusion To balance ESD, SNR and IQF, proper tube voltage should be chosen for chest radiography according to thickness and constitution of patients.

ObjectiveTo investigate the relationship between aging-induced neointimal formation and Jagged 1 dynamic expression in endothelium after arterial injury in rats. MethodsForty healthy male Sprague-Dawley rats aged 3 months (young adult) and 22 months (old) were selected, and thirty of them were subjected to balloon catheter injury at the thoracic aorta. Morphometry analysis was applied to evaluate neointima/media ratio at 28 days after arterial injury. Immunohistochemistry was used to observe the dynamic expressions of Jaggedl in endothelium and the proliferating cell nuclear antigen (PCNA) in neointima at 7 days, 14 days and 28 days after arterial injury respectively. Cell co-culture system was developed by inoculating endothelial cells(EC) in the upper chamber and smooth musele eells(SMC) in the lower chamber. Fluorescence activated cell sorter (FACS) was used to assay the effect of aging on the expression of Jagged 1 in EC. ＜'3＞H-TdR incorporation and cells counting were used to determine the influence of EC of different ages of rats on platelet derived growth factor (PDGF)-induced proliferation and migration of SMC. ResultsThe neointima/media ratio were obviously higher in old rats than in young rats (0.35±0.02 vs. 0.28±0.01, n=5, P＜0.01). Compared with the young counterparts, old rats showed in immunohistochemistry that the Jaggedl in endothelium displayed a delayed up-regulation and quickly diminished evolvement pattern. The maximal enhancing level of Jaggedl in old rats was much lower than that in young ones. However, the increased extent of PCNA in neointima was significantly higher in old rats than that in young ones. Jagged 1 expression in EC in old rats was significantly lower than that in young one[(46.6±6.3)% vs. (85.4±4.0)%,n=3, P＜0.05]. The SMC co-cultured with EC in old rats exhibited higher proliferation and migration capability than those in young ones after exposure to PDGF of 10ng/ml[2H-TdR incorporation: (26 438±1857) cpm/well vs. (16 698±2076)cpm/well, n=5, P＜0.05. migration:(32±4) cells/field vs. (18±5) cells/field, n=5, P＜0. 05]ConclusionsThe up-regulation of Jaggedl in EC is impaired in aged rats, which is closely related to aging-indueed SMC proliferation and migration. It also suggests that Jagged1 might be involved in the process of aging-exaggerated neointima formation.

Objective To investigate the effects of carboxymethytl pachymaram ( CMP ) on the methylation of SOCS-1 (suppressor of cytokine signaling-1) gene and the in vitro maturation of human mono-cyte-derived dendritic cells (DCs).Methods Human DCs were induced from the peripheral blood mono-cytes in vitro with the treatment of recombined human GM-CSF and interleukin-4 ( IL-4 ) and cultured with different concentrations of CMP (10, 50, and 100 mg/L).The methylation and expression of SOCS-1 gene were analyzed by methylation-specific polymerase chain reaction (MSP) and real-time PCR, respectively. The phenotypic markers of DCs were detected by flow cytometry .Mixed lymphocyte reaction ( MLR) and ELISA were performed to measure the lymphocyte proliferation induced by DCs and IL-12 secretion by DCs . Results CMP promoted the methylation of SOCS-1 gene, but inhibited the expression of SOCS-1 gene in dendritic cells at the concentrations of 50 mg/L and 100 mg/L.The expression of phenotypic markers (CD80, CD83, CD86 and HLA-DR), IL-12 secretion and lymphocyte proliferation induced by DCs were significantly enhanced in a dose dependent manner with the treatment of CMP .Compared with control group , the levels of methylated SOCS-1 gene and IL-12 and the lymphocyte proliferation index were increased upon the stimulation with 50 mg/L and 100 mg/L of CMP (P<0.01), but the expression of SOCS-1 gene was de-creased.The expression of CD80, CD83 and HLA-DR on DCs in the presence of 100 mg/L of CMP were higher than those of control group (P<0.05).Conclusion CMP could induce the methylation of SOCS-1 gene and the maturation of DCs derived from peripheral blood monocytes .

Poly ( aspartic acid-co-leucine) was synthesized, modified via ethylenediamine, conjugated with 1,4,7,10-tetraazacyclododecane-1,4,7,10-tetraacetic acid (DOTA) and finally chelated with gadoliniumⅢ, yielding PL-A2-DOTA-Gd. The T1-relaxivity (15. 3 mmol-1 ·L·s-1 ) of PL-A2-DOTA-Gd was 2. 6 times than that of Gd-DOTA (5. 8 mmol-1·L·s-1) in D2O. The results of magnetic resonance imaging experiments showed significant enhancement in the rat liver after intravenous administration of PL-A2-DOTA-Gd, which persisted longer than Gd-DOTA. The mean percentage enhancements of liver parenchyma were 65. 1%±5. 2%and 21. 3%±4. 9%, for PL-A2-DOTA-Gd and Gd-DOTA, respectively.