Objective To investigate the clinical value of homocysteine (Hcy) ,cystatin C (Cys C) and high‐sensitivity C‐reactive protein (hs‐CRP) in atherosclerosis (AS) .Methods Totally 100 cases of newly diagnosed patients of AS were choosed as the ob‐servation group ,36 cases condition improved markedly of AS after treatment as the treatment group ,and 120 cases of normal medi‐cal groups as the control group ,the Hcy ,Cys C and hs‐CRP in all subjects were detected respectively .Results Hcy ,Cys C and hs‐CRP levels of observation group were significantly higher than those of normal groups ,and the difference was statistically signifi‐cant (P< 0 .05) .While the Cys C and hs‐CRP levels of treatment group were significantly lower than the those of observation group ,the difference was also statistically significant (P< 0 .05) .Conclusion The detection of Serum Hcy ,Cys C and hs‐CRP might be help to the diagnosis ,treatment evaluation and prognosis of AS .

Objective To observe the expression level of inhibitor of differentiation 2 (Id‐2) and matrix metalloproteinases‐9 (MMP‐9) in rectal cancer ,analysis the correlation of the expression level of them ,to study the relationship between the expression level of them and the clinical pathology indicators of rectal cancer .Methods Rectal cancer tissues and normal tissue adjacent to rec‐tal cancer were obtained from the rectal cancer resection of 56 patients with rectal cancer ,using immunohistochemical method to ob‐serve the expression level of Id‐2 and MMP‐9 in normal tissue adjacent to rectal cancer and rectal cancer and Spearman correlation test to detect the correlation between the expression level of Id‐2 and MMP‐9 ;then we analyzed the relationships between the ex‐pression level of Id‐2 and MMP‐9 and the index of rectal cancer clinical pathology .Results The positive expression rate of Id‐2 in the in rectal cancer tissues is more higher than that of normal tissue of adjacent to rectal cancer (73 .21% vs .48 .21% ,P<0 .05) . The positive expression rate of MMP‐9 in the in rectal cancer tissues is higher than that of normal tissue of adjacent to rectal cancer (71 .43% vs .44 .64% ,P<0 .05) .Spearman correlation test showed that there is the positive correlation between the expression level of Id‐2 and MMP‐9 (r=0 .393 ,P=0 .003) .The expression levels of Id‐2 and MMP‐9 in rectal cancer were correlated with the degree of tumor differentiation ,TNM stage and lymph node metastasis (P<0 .05) ,but had no differences between the elements of age and sex (P>0 .05) .Conclusion There is a close relationship between the expression levels of Id‐2 and MMP‐9 in rectal cancer and the occurrence and development of rectal cancer .Rectal cancer with the higher Id‐2 expression level may be the ways to achieve tumor invasion and metastasis through MMP‐9 as a facilitator .

Objective To explore the repair of the open compound wounds in lower extremities caused by multiple factors. Methotis Transplantation of cutaneous.musculo-cutaneous or greater omentum flaps were applied to 155 patients of open compound lower extremity wounds. Results The wound healing rate following first operation was 50% and that following two operations was 14.8%.While the wounds were healed in 7.7% of patients after three operations. Conclusion Transplantations of cutaneous,musculo-cutaneous or greater omentum flaps ale effective to repair and reconstruct the open compound lower extremity wounds.

Background and Objectives: Myocardial ischemia-reperfusion injury (MIRI) refers to the damage of cardiac function caused by restoration of blood flow perfusion in ischemic myocardium. However, long non-coding RNA prostate androgen regulated transcript 1 (PART1)’s role in MIRI remain unclear. Methods: Immunofluorescence detected LC3 expression. Intermolecular relationships were verified by dual luciferase reporter assay. 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, flow cytometry and transferase-mediated dUTP nick-end labeling (TUNEL) assays analyzed cell viability and apoptosis. The release of lactate dehydrogenase was tested via enzyme-linked immunosorbent assay (ELISA). Left anterior descending coronary artery surgery induced a MIRI mouse model. Infarct area was detected by 2,3,5-triphenyltetrazolium chloride staining. Hematoxylin and eosin staining examined myocardial injury. ELISA evaluated myocardial marker (creatine kinase MB) level. Results: PART1 was decreased in hypoxia/reoxygenation (H/R) induced AC16 cells and MIRI mice. PART1 upregulation attenuated the increased levels of Bax, beclin-1 and the ratio of LC3II/I, and enhanced the decrease of Bcl-2 and p62 expression in H/R-treated cells.PART1 upregulation alleviated H/R-triggered autophagy and apoptosis via miR-302a-3p. Mechanically, PART1 targeted miR-302a-3p to upregulate transcription factor activating enhancer-binding protein 2C (TFAP2C). TFAP2C silencing reversed the protected effects of miR-302a-3p inhibitor on H/R treated AC16 cells. We further established TFAP2C combined to dual-specificity phosphatase 5 (DUSP5) promoter and activated DUSP5. TFAP2C upregulation suppressed H/R-stimulated autophagy and apoptosis through upregulating DUSP5.Overexpressed PART1 reduced myocardial infarction area and attenuated MIRI in mice. Conclusion PART1 improved the autophagy and apoptosis in H/R-exposed AC16 cells through miR-302a-3p/TFAP2C/DUSP5 axis, which might provide novel targets for MIRI treatment.

Background and Objectives: Myocardial ischemia-reperfusion injury (MIRI) refers to the damage of cardiac function caused by restoration of blood flow perfusion in ischemic myocardium. However, long non-coding RNA prostate androgen regulated transcript 1 (PART1)’s role in MIRI remain unclear. Methods: Immunofluorescence detected LC3 expression. Intermolecular relationships were verified by dual luciferase reporter assay. 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, flow cytometry and transferase-mediated dUTP nick-end labeling (TUNEL) assays analyzed cell viability and apoptosis. The release of lactate dehydrogenase was tested via enzyme-linked immunosorbent assay (ELISA). Left anterior descending coronary artery surgery induced a MIRI mouse model. Infarct area was detected by 2,3,5-triphenyltetrazolium chloride staining. Hematoxylin and eosin staining examined myocardial injury. ELISA evaluated myocardial marker (creatine kinase MB) level. Results: PART1 was decreased in hypoxia/reoxygenation (H/R) induced AC16 cells and MIRI mice. PART1 upregulation attenuated the increased levels of Bax, beclin-1 and the ratio of LC3II/I, and enhanced the decrease of Bcl-2 and p62 expression in H/R-treated cells.PART1 upregulation alleviated H/R-triggered autophagy and apoptosis via miR-302a-3p. Mechanically, PART1 targeted miR-302a-3p to upregulate transcription factor activating enhancer-binding protein 2C (TFAP2C). TFAP2C silencing reversed the protected effects of miR-302a-3p inhibitor on H/R treated AC16 cells. We further established TFAP2C combined to dual-specificity phosphatase 5 (DUSP5) promoter and activated DUSP5. TFAP2C upregulation suppressed H/R-stimulated autophagy and apoptosis through upregulating DUSP5.Overexpressed PART1 reduced myocardial infarction area and attenuated MIRI in mice. Conclusion PART1 improved the autophagy and apoptosis in H/R-exposed AC16 cells through miR-302a-3p/TFAP2C/DUSP5 axis, which might provide novel targets for MIRI treatment.

Background and Objectives: Myocardial ischemia-reperfusion injury (MIRI) refers to the damage of cardiac function caused by restoration of blood flow perfusion in ischemic myocardium. However, long non-coding RNA prostate androgen regulated transcript 1 (PART1)’s role in MIRI remain unclear. Methods: Immunofluorescence detected LC3 expression. Intermolecular relationships were verified by dual luciferase reporter assay. 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, flow cytometry and transferase-mediated dUTP nick-end labeling (TUNEL) assays analyzed cell viability and apoptosis. The release of lactate dehydrogenase was tested via enzyme-linked immunosorbent assay (ELISA). Left anterior descending coronary artery surgery induced a MIRI mouse model. Infarct area was detected by 2,3,5-triphenyltetrazolium chloride staining. Hematoxylin and eosin staining examined myocardial injury. ELISA evaluated myocardial marker (creatine kinase MB) level. Results: PART1 was decreased in hypoxia/reoxygenation (H/R) induced AC16 cells and MIRI mice. PART1 upregulation attenuated the increased levels of Bax, beclin-1 and the ratio of LC3II/I, and enhanced the decrease of Bcl-2 and p62 expression in H/R-treated cells.PART1 upregulation alleviated H/R-triggered autophagy and apoptosis via miR-302a-3p. Mechanically, PART1 targeted miR-302a-3p to upregulate transcription factor activating enhancer-binding protein 2C (TFAP2C). TFAP2C silencing reversed the protected effects of miR-302a-3p inhibitor on H/R treated AC16 cells. We further established TFAP2C combined to dual-specificity phosphatase 5 (DUSP5) promoter and activated DUSP5. TFAP2C upregulation suppressed H/R-stimulated autophagy and apoptosis through upregulating DUSP5.Overexpressed PART1 reduced myocardial infarction area and attenuated MIRI in mice. Conclusion PART1 improved the autophagy and apoptosis in H/R-exposed AC16 cells through miR-302a-3p/TFAP2C/DUSP5 axis, which might provide novel targets for MIRI treatment.