Objective To investigate the incidence and the risk factors of the vascular disease in lower limbs of patients with type 2 diabetes(T2DM).Methods To retrospectively analyze 318 cases with T2DM patients.All the patients were checked on both lower limbs by color ultrasonic Doppler.The differences of ordinary and biochemical indicators between PVD group and non-PVD group were compared.Results There were 67.2％ (205/318) patients who had vascular disease in lower limbs with type 2 diabetes.Age,course of disease,HbAlC,TC,TG,SBP,DBP and BMI in PVD group were significantly higher than those in non-PVD group( P ＜ 0.01 ).Conclusion There was higher incidence of the vascular disease in lower limbs of patients with type 2 diabetes.And the independent risk factors were hypertension,hyperglycemia,hyperlipemia.It could help to prevent the development of lower limb blood vessel pathological changes in DM patients by controlling the levels of blood pressure,lipid and blood sugar strictly.

Objective:To explore the moderating effect of self-differentiation between life events and coping styles. Methods:Totally 584 college freshmen from Beijing and Jiangsu were selected to fill in the Adolescent Self-Rating Life Events Check-list (ASLEC),Differentiation of Self Inventory(DSI)and Simplified Coping Style Ques-tionnaire (SCSQ). Results:Self-differentiation had a moderating effect between life events and coping styles. The predicting effect of life events on negative coping was 0. 03 in the higher self-differentiation group (P>0. 05 ) while in the lower self-differentiation group,it was 0. 27 (P<0. 00 1 ). Conclusion:It suggests that higher self-differ-entiation could relieve the negative effect of life events to coping styles.

Members of the tripartite-motif (TRIM) protein family share a highly conserved domain architecture known as RBCC motif,which is composed of a RING finger domain,one or two B-box domains,a coiled-coil domain as well as diverse types of C-terminal regions.TRIM proteins can not only maintain the normal physiological functions of the body,but also regulate the development of various diseases.In the current review,we focus on recent advances in the structures of TRIM proteins and their functions in the development of viral infection,cancer and neurodegenerative disease.

Objective To investigate the effect of sufentanil on norepinephrine (NE)-induced contraction of thoracic aorta isolated from rats with spontaneous hypertension (SH) .Methods Eight male rats with SH weighing 250-300 g were used in this study. The rats were decapitated and their thoracic aortas were isolated and cut into rings 2-3 mm in length. The aorta rings were suspended for isometric tension recording. The aortic rings obtained from SH rats were divided into 4 groups ( n = 8 each) : control group and 3 sufentanil groups. The contraction of aortic rings in response to NE in the absence (control) and presence of 3 concentrations of sufentanil 7 × 10-11 ,2 × 10-10 and 1 × 10-9 mol/L was recorded. Results The amplitude of NE-induced contraction of thoracic aorta was significantly greater in 3 sufentanil groups than in control group. Sufentanil significantly inhibited the NE-induced aortic contration in proportion to concentration. Conclusion Sufentanil can inhibit NE-induced contraction of thoracic aorta isolated from rats with SH in a concentration-dependent manner.

Twenty patients of traumatic cervical disc herniation in mono-segment were reconstructed after discectomy with a cage filled with autogenous cancellous illict-bone graft.Neither fracture nor dislocation was found by radiograph or magnetic resonance imaging.The average follow-up period was 22 months (range:6 - 36 months) and the average duration of bone graft fusion 4.9 months.No complications of internal fixation occurred.With this new cage,traumatic cervical disc herniation might be safely treated.

BACKGROUND:Spinal cord ischemia-reperfusion injury is a serious secondary injury of the spinal cord. Multifactor could contribute to the mechanism of this injury, and many therapeutic measures emerge, but the therapeutic effect is not ideal.
OBJECTIVE:To investigate the protective effects and mechanism of hydrogen-rich saline on spinal cord ischemia-reperfusion injury in rabbits.
METHODS:ZIVIN method was adopted to prepare the model of spinal cord ischemia-reperfusion injury. The rabbit models were randomly divided into model group, sham operation group, and hydrogen-rich saline group.
RESULTS AND CONCLUSION:Improved Tarlov scores for the evaluation of motor function were significantly increased in hydrogen-rich saline group compared with the model group at 6, 12, 24, 72 hours after reperfusion (P<0.01). The contents of malondialdehyde were significantly lower (P<0.05), while catalase activity was significantly higher (P<0.05) in hydrogen-rich saline group than that in model group at 72 hours after reperfusion. Hematoxylin-eosin staining revealed that, spinal cord anterior-horn motor neurons maintained intact structure in sham operation group;more necrotic spinal cord anterior-horn motor neurons were found in model group, and granular-vacuolar degeneration occurred in the endochylema. In hydrogen-rich saline group, the structure of spinal cord anterior-horn motor neurons was basical y intact, only a smal amount of spinal cord anterior-horn motor neurons appeared vacuolar degeneration. TUNEL staining showed no apoptotic spinal cord anterior-horn motor neurons in sham operation group. Many inflammatory cel s and apoptotic neurons were found in model group. There were few inflammatory cel s and apoptotic neurons in hydrogen-rich saline group. Hydrogen-rich saline can prevent the apoptosis of spinal cord anterior-horn motor neurons in rabbits with spinal cord ischemia-reperfusion injury, and the underlying mechanism is associated with antioxidative effect.

AIM To study effects of desulfated and poly sulfated heparin derivatives on rat mast cell (MC) degranulation. METHODS Different methods were used to prepare different sulfated heparin derivatives: 2 O desulfated heparin (2DeSH),N desulfated reacetylated heparin (NDeSAcH),6 O desulfated heparin (6DeSH),poly sulfated heparin (PSH). Passive MC degranulation induced by ovalbumin in rats to was employed observe the effects of different sulfated derivatives on rats MC degranulation. RESULTS All the sample groups were found of obvious inhibition of MC degranulation( P

Objective To observe the effects of genistein on PCNA expression and cell cycle in fibroblasts derived from human hypertrophic scar in order to explore the mechanism of its inhibition on hypertrophic scar (HS) fibroblast proliferation. Methods The human hypertrophic scar fibroblasts were cultured in vitro. Genistein with various concentrations (25, 50, 100 μmol/L) was co-cultured in the medium for 48 hours. The expression of PCNA was detected with immunocytochemical staining method and the cell cycle was measured with flow cytometry. Results Genistein could significantly decrease PCNA expression in HS fibroblasts, especially when its concentration at 50 μmol/L or 100 μmol/L. The cell percentage of G0～G1 phase decreased with drug′s concentration, and G2～M percentage increased conversely, implying the suspension of mitosis. In 100 μmol/L group, most cells blocked at S phase and a hypodiploid apoptosis peak could be observed ahead of G1 phase. Conclusion Genistein can inhibit the proliferation of human hypertrophic scar by blocking cell division as well as decreasing DNA synthesis.

Objective To detect anti-clinically amyopathic dermatomyositis (CADM)-140 antibody in patients with dermatomyositis (DM) or CADM,and to estimate its clinical correlation.Methods Serum samples were collected from 22 patients with DM,16 patients with CADM,46 patients with other connective tissue diseases complicated by interstitial lung disease(including 8 cases of polymyositis,15 cases of systemic lupus erythematosus,5 cases of systemic sclerosis,6 cases of Sj(o)gren syndrome,6 cases of mixed connective tissue disease,6 cases of idiopathic pulmonary fibrosis),and 5 normal human controls.Enzyme-linked immunosorbent assay (ELISA) was performed with the recombinant melanoma differentiation-associated gene 5(rMDA)as a substrate to measure the anti-CADM-140 antibody in these serum samples.Clinical manifestations were compared between patients with anti-CADM-140 antibody and those without.Results The anti-CADM-140antibody was found in 43.8% (7/16) of patients with CADM and 9.1%(2/22) of patients with DM(P<0.05),but absent in the patients with other connective tissue diseases and in the normal human controls.A significant incroase was observed in anti-CADM-140 antibody-positive patients with DM/CADM in the incidence of cutaneous ulceration and necrosis,interstitial lung disease and rapidly progressive interstitial lung disease (8/9 vs.6.9%,P<0.01;9/9 vs.48.3%,P<0.01;5/9 vs.0,P<0.05),serum lactate dehydrogenase level(328.3±104.2 vs 241.1±100.3 IU/L P<0.05),erythrocyte sedimentation rate(40.8±23.1 vs.22.5±16.8 mm/1 h,P<0.05),high resolution computed tomography score(122.9±54.8 vs.70.0±59.8,P<0.05)compared with anti-CADM-140 antibody-negative patients with DM/CADM.The ereatine kinase level was significantly lower(156.3±260.8 vs.1806.2±3737.1 IU/L P<0.05)in anti-CADM-140 antibody-positive patients with DM/CADM than in anti-CADM-140 antibody-negative patients with DM/CADM,while no significant difference was noted in the positivity rate of antinuclear antibodies or incidence of malignancies between the antibody-positive and-negative patients with DM/CADM.Conclusions Anti-CADM.140 antibody not only is useful for the diagnosis of interstitial lung disease in patients with DM/CADM,but also may serve as a serum marker for rapidly progressive interstitial lung disease.Monitoring of serum anti-CADM-140 antibody might help to predict the progression of interstitial lung disease in patients with DM/CADM.

Insulin resistance (IR) is a complex metabolic disorder related to several diseases including type 2 diabetes (T2DM), hypertension and dyslipidemia. These diseases are all independent risk factors for cardiovascular disease. Lipid metabolism disorder has toxic effects on cells and may cause or aggravate IR in performance of elevated plasma levels of triglyceride (TG) and free fatty acids (FFA), the last one is an independent risk factor for IR. It has been clear that FFA may induce IR by endoplasmic reticulum (ER) stress, oxidative stress, apoptosis and inflammation, although the specific mechanisms remained unknown. The present paper summarizes the related molecules involved in the pathogenic process of IR and its mechanism, might provide a theoretical basis for the molecular mechanism of IR caused by FFA, and therapeutic reference for clinical treatment of IR and prevention of T2DM.