Recent related researches pointed out that a series of adverse reactions may occur when homocysteine (Hcy) level exceeded normal range .More and more studies indicated that Hcy level abnormal elevating was an inde‐pendent risk factor for cardiovascular diseases .This article summarized its related research situation .

CXCR7 is a new receptor of chemokine CXCL12 after CXCR4.The present study shows that CXCL12/CXCR7 biological axis has important influence to the development of a variety of tumors,similar to CXCL12/CXCR4 biological axis.CXCR7 is present in many kinds of tumor tissues and tumor cells widely,and plays an important role in tumor cells growth,proliferation,adhesion and migration.Restraining CXCR7 expression or blocking the CXCR7 signaling pathways may offer new strategies for the treatment of tumors.

ObjectiveTo evaluate the feasibility and clinical significance of emergency bedside ultrasound-guided central venous catheterization performed by emergency department doctors.Methods The clinical data of 216 patients, who underwent central venous catheterization in the Department of Emergency of Shengjing Hospital of China Medical University from January 2009 to June 2014 were retrospectively analyzed. All the patients received femoral vein puncture or internal jugular vein catheterization. The patients were divided into three groups according to the method of catheterization: 72 patients received emergency ultrasound-guided central venous catheterization by emergency doctors independently were assigned as A group, 72 patients underwent catheterization by emergency doctors after being demarcated by ultrasound doctors served as B group, and 72 patients who underwent catheterization method guided by traditional landmark served as C group. Success rate, time spent for catheterization, number of attempts for intubation, and incidence of complications were compared among three groups.Results As compared with that of groups B and C, a higher success rate [98.61% (71/72) vs. 83.33% (60/72), 73.61% (53/72), bothP< 0.01] was found in group A, also with a shorter successful time for insertion of the catheter (minutes: 5.5±2.5 vs. 9.6±3.7, 16.6±7.2, bothP< 0.05), less frequency of the catheter insertion (times: 1.0±0.0 vs. 1.8±0.7, 2.7±2.6, bothP<0.05), and lower incidence of changing puncture site due to insert failure [1.4% (1/72) vs. 8.3% (6/72), 20.8% (15/72), bothP< 0.05], lower incidence of mechanical and infective complication [15.3% (11/72) vs. 41.7% (30/72), 59.7%(43/72), bothP< 0.05], and also lower catheterization related infection risk [13.9% (10/72) vs. 15.3% (11/72), 12.5%(9/72), bothP> 0.05].Conclusion Emergency bedside ultrasound-guided catheterization resulted in higher success rate and less related complication, therefore it can be recommended for widely application in emergency department treatment.

Objective To explore the reporting process of our health risk warning system and its long-term effectiveness.Methods A total of 1 168 individuals who were identified as higher risk populations from July 2011 to June 2012 in our Health Mangement Center were served as the control group,and another 973 adults who were identified as higher risk individuals from July 2012 to May 2013 were assigned to the study group.Diagnosis and treatment were based on our health risk reporting process and follow-up system.Paired t test and paired contingency table x2 test were used for data analysis.Results The rate of follow-up (97％ vs 100％,x2=30.503,P＜0.05),consultation (83.48％ vs 93.63％,x2=52.142,P＜ 0.05),mean treatment time ((3.0±0.5) vs (1.5±0.5) d,t=69.12,P＜0.05) and patient satisfaction (87.84％ vs 96.20％,x2=48.361,P＜0.05) were significantly different between the two groups,although no statistically significant difference of incidence of adverse events was found (0.26％ vs 0.10％,x2 =0.102,P＞0.05).Conclusion Our health risk warning system may reduce the time for physical examination and improve disease diagnosis level and patients' satisfaction.Moreover,our health manatement system and health service quality should further be improved in practice.

Background and purpose:Esophageal cancer is a serious disease threatening human health, and it is very difficult to understand the development mechanism and find the therapeutic methods for esophageal cancer. In recent years, B7-H3, as a new member of B7 immunoregulatory superfamily, overexpressed in multiple tumor types, is considered to be a new tumor marker and potential therapeutic target. This study aimed to detect the expression of B7-H3 in esophageal cancer cell lines TE-1, TE-13, Eca-109 and exploring the effect of B7-H3 siRNA on cell proliferation, migration and invasionin vitro in human esophageal cancer Eca-109 cell line. Methods:The expression of B7-H3 in esophageal cancer cell lines TE-1, TE-13 and Eca-109 were detected by reverse transcription polymerase chain reaction (RT-PCR). B7-H3 siRNA and control siRNA were transfectedin vitro into human esophageal cancer Eca-109 cells using LipofectamineTM 2000. The expressions of B7-H3 mRNA and protein in Eca-109 cells were analyzed by RT-PCR and Western blot. The proliferation, migration and invasion abilities of Eca-109 cells were measured by MTT assay, wound scrape assay and transwell invasion assayin vitro,respectively.Results:All tested cultured esophageal cancer cell lines constitutively expressed B7-H3 mRNA under normal conditions (TE-1 0.382±0.008, TE-13 0.399±0.008, Eca-109 0.428±0.012). After transfection, the expression of B7-H3 mRNA levels decreased in B7-H3 siRNA transfected group, compared with control siRNA transfected group (0.128 5±0.000 2vs 0.532 4±0.000 7,P<0.01) and untransfected group (0.128 5±0.000 2vs 0.540 3±0.001 3,P<0.01), while its protein expression levels were also signiifcantly lower than the control transfection group (0.421 4±0.004 8vs 0.500 6±0.012 9,P<0.05) and untransfected group (0.421 4±0.004 8vs 0.492 1±0.014 8, P<0.05). Compared with control transfected and untransfected cells, Eca-109 cell migration and invasion abilities decreased significantly (P<0.05) by siRNA interference, but no significant difference was observed between their proliferative capacity (P>0.05).Conclusion:All tested esophageal cancer cell lines constitutively express B7-H3 mRNA. B7-H3 siRNA interference inhibits Eca-109 cell migration and invasion abilities. B7-H3 may have a critical role in regulating Eca-109 cell progression.

Intracerebral hemorrhage is a disease with high mortality and morbidity. This article discussed the application of magnetic resonance diffusion tensor imaging for intracerebral hemorrhage clinical research, and its limitations and prospect.

AIM:NLRP3 inflammasome was identified as the cellular machinery responsible for activation of inflammatory processes .The present study investigated whether the activation of NLRP 3 inflammasomes contributes to hyperhomocysteinemia ( HHcy)-induced in-flammation and atherosclerosis .METHODS:ApoE-/-mice were fed regular diet , high fat ( HF) diet or HF plus high methionine (HM) diet for 10 weeks.NLRP3 shRNA or scramble shRNA viral suspension was injected twice at the 2nd and the 6th weeks after HFHM treatment.The whole aortas and aortic root sections were stained with Oil Red O for atherosclerotic lesion .Plasma lipids, ho-mocysteine ( Hcy) , IL-1βand IL-18 levels were measured .We also examined the effect of Hcy on NLRP 3 inflammasomes activation in THP-1 differentiated macrophages in the presence or absence of NLRP 3 siRNA, caspase-1 inhibitor Z-WEHD-FMK, or antioxidant N-acetyl-L-cysteine ( NAC) .RESULTS:HFHM treatment induced HHcy in ApoE-/-mice.Increased plasma levels of IL-1βand IL-18, aggravated macrophage infiltration into atherosclerotic lesion , and accelerated development of atherosclerosis were detected in HHcy mice, which were associated with the activation of NLRP 3 inflammasomes.Silencing the NLRP3 gene significantly suppressed NLRP3 inflammasomes activation , reduced plasma levels of proinflammatory cytokines , attenuated macrophage infiltration , and improved HHcy-induced atherosclerosis .Moreover, we found that Hcy activated NLRP3 inflammasomes and promoted subsequent production of IL-1βand IL-18 in macrophages, which were blocked by NLRP3 gene silencing, Z-WEHD-FMK, or NAC.CONCLUSION:These data suggest that the activation of NLRP 3 inflammasomes contributes to HHcy-induced inflammation and atherosclerosis .Hcy activates NLRP3 inflammasomes in reactive oxygen species dependent pathway in macrophages .

BACKGROUND:Acute exercise is believed to regulate appetite and influence feeding behaviors by controling the synthesis and secretion of gastrointestinal peptide hormones to regulate appetite and feeding behavior influence, but the smal sample size leads to widely different results.
OBJECTIVE:To clarify the effect of acute exercise on peptide YY levels in adults using Meta-analysis method. METHODS:A computer-based search of PubMed, Google Scholar, Sport Discus, Web of Knowledge and CNKI was performed for relevant articles published before January 2014. The literatures eligible were studied by evaluating the publication bias, checking the heterogeneity and analyzing the sensitivity by software of RevMan5.1.
RESULTS AND CONCLUSION:(1) There were a total of 188 participants in the 18 trials reported in 11 articles. The Meta-analysis results revealed a mean effect for acute exercise to increase peptide YY values (standardized mean difference=0.25, 95% confidence interval =0.05-0.46,P=0.01), and therefore, there was a significantly statistical difference in the peptide YY levels between the acute exercise group and control group (P< 0.05). Moreover, results from the sensitivity analysis showed no influences on the findings of Meta-analysis. (2) Five randomized controled trails in the three included articles were related to peptide YY (3-36). There was a maximal heterogeneity among these studies; therefore, a random-effect model was utilized. The result revealed a mean effect for acute exercise to increase peptide YY (3-36) values (standardized mean difference =1.80, 95% confidence interval =0.27-3.32,P=0.02). The findings from this meta-analysis show that acute exercise may influence appetite by increasing levels of peptide YY in adults.

BACKGROUND:Current researches on whether the intramuscular injection of heterogeneous umbilical cord mesenchymal stem cells (UC-MSCs) is safe or not lack theoretical basis. OBJECTIVE:To explore the effects of intramuscular injection of heterogeneous UC-MSCs on expression of myocardial vascular endothelial growth factor (VEGF), cardiac troponin I (cTnI) and serum VEGF, hepatocyte growth factor (HGF), insulin-like growth factor 1 (IGF-1) and granulocyte macrophage colony stimulating factor (GM-CSF) in normal Wistar rats. METHODS:A total of 60 Wistar rats were divided into six groups randomly. Rats in the six groups were respectively administrated with intramuscular injection of PBS, Dulbecco’s modified Eagle’s medium, hUC-MSC supernatant, 0.25×105, 1.0×105, 4.0×105 hUC-MSCs. Rats received a second intramuscular injection 4 weeks after first injection. Eight weeks later, the blood sample and myocardial tissue were taken. The serum concentration of VEGF, HGF, IGF-1 and GM-CSF were measured with enzyme-linked immunosorbent assay kit. The myocardial VEGF and cTnI expression were detected by immunohistochemical technique. RESULTS AND CONCLUSION:There was no significant difference in the serum concentration of the VEGF, HGF, IGF-1 and GM-CSF among the groups before and after injection (P>0.05). In the same group, no statistical significant changes in the serum concentration of the VEGF, HGF, IGF-1 and GM-CSF were found among the rats before and after injection (P>0.05). Eight weeks after injection, weak positive expression of the VEGF in the cytoplasm of cardiocytes in the six groups was observed, and strong positive expression of the cTnI in the cytoplasm of cardiocytes in the six groups was observed. There was no significant difference in the VEGF and cTnI content in the myocardium among the groups (P>0.05). Intramuscular injection of hUC-MSCs or the supernatant of hUC-MSCs had no effects on the serum concentration of the VEGF, HGF, IGF-1, GM-CSF and the myocardial VEGF and cTnI expression in normal Wistar rats.

Aim To explore the relationship between Mre11/Rad50/Nbs1 ( MRN ) complex focus formation and DNA double-strand breaks( DSBs) caused by cinob-ufagin in human hepatocellular carcinoma HepG2 cells. Methods The Na+,K+-ATPaseα1 subunit expression level in liver cancer tissues was detected by immunohis-tochemistry. After HepG2 cells were treated with 5μmol·L-1 cinobufagin for 6, 12 and 24 h, the drug-in-duced DSBs were assessed by single cell gel electro-phroesis ( SCGE ) , the gene transcription and protein levels of Mrel1, Nbs1, Rad50 and p53 were evaluated by Real time-PCR and Western blot. The cell cycle in parallel was analyzed by flow cytometry. Results The Na+, K+-ATPase α1 subunit expression level in liver cancer tissues was significantly increased compared with the tissue adjacent to carcinoma ( P <0. 05 ) . The 5μmol · L-1 cinobufagin could induce the DSBs in a time-dependent manner (P <0. 05), and it could up-regulate the gene expression levels of Mre11, Nbs1, Rad50 and p53 in HepG2 cells ( P<0. 05 ) . The pro-portions of HepG2 cells in S phase were ( 21. 32 ± 4. 21) % in the control group, and (33. 25 ± 5. 72) %, (56. 72 ± 6. 29) % and (67. 32 ± 9. 42) % in HepG2 cells treated with 5 μmol · L-1 cinobufagin for 6, 12 and 24 h, respectively. The proportions of cells in S phase in cinobufagin groups were significantly increased compared with the control group ( P<0. 05 ) . Conclu-sion Cinobufagin could induce the cell cycle arrest in liver cancer HepG2 cells by activation of Mre11/Rad50/Nbs1 Complex.