Objective To investigate the relation between omentin and coronary artery disease.Methods Eighty-eight eases were divided into 2 groups, coronary artery disease group (56 cases, includingacute coronary syndrome 28 cases and stable angina 28 cases), and non-coronary artery disease group (32cases). The plasma omentin levels were assayed by ELISA, and height, weight, blood pressure, totalcholesterol high density lipoprotein cholesterol (HDL-C), low density lipoprotein cholesterol (LDL-C),lriglyeeride (TG), high-sensitivity C-reactive protein were detected. Results The plasma omentin level incoronary artery disease group [(33.4 + 6.4) μg/L] was lower than that in non-coronary artery disease group [(51.8 + 7.7) μg/L](P= 0.034). Logistic analysis showed that the decline of omentin was an independent risk factor of coronary artery disease (P=0.012). Conclusions The decline of omentin is an independent risk factor of coronary artery disease. The plasma omentin may contribute, in part, to the pathogenesis of coronary artery disease.

Objective To investigate the relation between plasma omentin and glycometabolism.Methods Eighty-five cases were divided into 3 groups by glucose tolerance test:diabetes mellitus group (42cases), impaired glucose regulation group (17 cases) and normal glucose regulation group (26 cases). The level of plasma omentin was assayed by ELISA. Results The level of plasma omentin was (53.7 ± 7.7),(40.7 ±9.9) and (30.6 ±5.3) μg/L in diabetes mellitus group, impaired glucose regulation group and normal glucose regulation group. There was significant difference among three groups (P= 0.049) and there was significant difference between diabetes mellitus group and normal glucose regulation group (P= 0.014).The level of plasma omentin in normal glycometabolism was (53.7 ± 7.7) μ g/L , and the level of plasma omentin in abnormal glycometabolism was (33.5 ± 6.0) μ g/L. There was significant difference between them(P = 0.023 ). Logistic analysis showed that the decline of plasma omentin was the independent risk factor ofglycometabolic disturbance (P= 0.027). Conclusion Omentin may play important roles in glycometabolic disturbance.

Objective To investigate the effect of glycated albumin on recurrent cerebral infarction in elderly patients with diabetes mellitus. Methods All of 252 elderly acute cerebral infarction patients with diabetes mellitus were chosen from clinics. They were divided into 2 groups: A group ( glycated albumin <19.0% , 117 patients) and B group ( glycated albumin ≥ 19.0%, 135 patients). The clinical characteristics and the recurrent rate of cerebral infarction were compared between two groups. Results The levels of glycated albumin, fasting blood glucose, total cholesterol, low-density lipoprotein cholesterol and triglycerides in B group were significantly higher than those in A group:(21.00 ± 4.93)%vs. (16.75±1.72)%, (9.84 ± 2.89) mmol/L vs. (5.36 ± 1.00) mmol/L, (5.44 ± 1.30) mmol/L vs. (4.57 ± 1.00) mmol/L, (3.13±0.81) mmol/L vs. (2.58 ± 0.74) mmol/L, (2.34 ± 1.61) mmol/L vs. (1.74 ± 1.47) mmol/L, P<0.01 or<0.05. The recurrent rate of cerebral infarction in B group was significantly higher than that in A group: 53.3%(72/135) vs.36.7%(43/117), χ2 = 6.946, P = 0.008. Logistic regression analysis showed that the increase of glycated albumin was the independent risk factor of recurrent cerebral infarction in elderly patients with diabetes mellitus (P=0.048). Conclusions The recurrent rate of cerebral infarction is increased in elderly diabetes patients with high glycated albumin. The increase of glycated albumin is the independent risk factor of recurrent cerebral infarction.

Objective To compare the levels of thrombomodulin in acute cerebral infarction patients with different blood glucose levels.Methods Four hundred and eighty-nine patients with acute cerebral infarction were selected including 237 patients of non-diabetes (non-diabetes group),117 patients of diabetes and HbA1c ≤7.0％(diabetes controlled well group) and 135 patients of diabetes and HbA1c ＞7.0％ (diabetes controlled badly group).The level of thrombomodulin was assayed by enzyme-linked immunosorbent assay and compared among three groups.Results The level of thrombomodulin was (2.66 ± 1.20) μg/L in non-diabetes group,(2.80 ± 1.43) μg/L in diabetes controlled well group,(3.22 ±1.60) μ g/L in diabetes controlled badly group.There was the increasing of thrombomodulin among non-diabetes group,diabetes controlled well group and diabetes controlled badly group (P =0.030).There was difference between non-diabetes group and diabetes controlled badly group (P =0.008).Conclusion There is the increasing of thrombomodulin in patients with acute cerebral infarction when their blood glucose rising.

Purpose To investigate the distribution of polymorphisms of quinone oxidoreductase 1 (NQO1) C609T gene in breast cancer patients, and to analyze the relationship with breast cancer molecular subtype. Methods Genotyping of C609T rs1800566 lo-cus of NQO1 gene in peripheral blood of 248 cases of female breast cancer were detected using high-throughput TaqMan MGB real-time fluorescence quantitative PCR technology, while the detection of ER, PR, HER-2 and Ki-67 in cancerous tissues were used with immu-nohistochemical staining and FISH gene amplification. Results Among 248 cases of breast cancer patients, CC genotype accounted for 27. 42% (68/248), CT genotype accounted for 49. 60% (123/248), TT genotype accounted for 22. 98% (57/248), which con-sistent with Hardy-Weinberg equilibrium law genetic (P>0. 05). 5 cases of HER-2 (++) who did not undergo FISH testing were re-moved, all the rest were done with FISH detection. Luminal A type accounted for 15. 2% (37/243), Luminal B type accounted for 51. 4% (125/243), HER-2 overexpression type accounted for 19. 8% (48/243), basal cell type accounted for 13. 6% (33/243). Compared with patients carrying the CC genotype, ER and PR positive rates in breast cancer patients carrying CT and TT genotype was significantly higher (P<0. 05), while there was no statistically difference on the expression of HER-2 and Ki-67 proteins in two groups (P>0. 05). There was no statistically difference on distribution of C609T polymorphism of NQO1 gene among different molecular sub-types of breast cancer (P>0. 05). Conclusions Here is no relationship between C609T polymorphism of NQO1 gene and breast cancer molecular subtype, miss rate of NQO1 ( CT+TT) in basal cell carcinoma is lower, and its gene polymorphism may provide the reasonable explanation to the heterogeneity of breast cancer molecular subtype.

Objective:To combine the detection of serum levels of adenosine deaminase (ADA) and T-cell spot test (T-spot.TB),and to explore their significances in diagnosis of pulmonary tuberculosis.Methods:159 patients suspected with pulmonary tuberculosis were selected and divided into pulmonary tuberculosis group and non-tuberculosis group (n=68);80 healthy people were randonly selected as healthy control group.The serum ADA levels and number of T-spot of the subjects in three groups were detected.Ther serum ADA levels and the positive rates of T-spot.TB in various groups and their sensitivities and specifities were compared. Results:The serum ADA level of the patients in pulmonary tuberculosis gruop was (22.10±6.60)U·L-1;those in non-tuberculosis group and healthy control group were (16.90±6.35)and (8.70±5.98)U·L-1;the serum ADA level in pulmonary tuberculosis group was significantly higher than those in non-tuberculosis group and heathy control group (P<0.05).The positive rate of serum ADA level in diagnosis of pulmonary tuberculosis was 56% and the T-spot.TB positive rate in diagnosis of pulmonary tuberculosis was 87.9%. Combined use of parallel test, the detection sensitivity was 91.2%;using the series of joint tests,the specificity was 94.6%.Conclusion:Combined detection of serum level of ADA and T-spot.TB can significantly improve the clinical diagnosis efficacy of pulmonary tuberculosis.

Purpose To investigate the clinical, imaging and pathologic characteristics of dedifferentiated chondrosarcoma.Methods The clinical and pathological data were reviewed in 11 cases of dedifferentiated chondrosarcoma.Results Most of these patients were male (7/11). The mean age was 57.1 years.Most tumors were located in the long bone and pelvis. Imaging showed that bones were extensively destroyed.There was calcification or ossification on focus of infection. The gross specimen showed that cartilage component was located within bone and dedifferentiated sarcoma was found out of the bone.Microscopically, well differentiated chondrosarcoma and poorly differentiated sarcoma components were observed. Six patients died and the average survival time was 14 months.Conclusions Dedifferentiated chondrosarcoma is an unusual subtype of chondrosarcoma with pleomorphic alterations. Further understanding the pathologic features of the tumor is important to increase the accurancy of diagnosis.

Objective To examine the expression of hypoxia inducible factor-1 α (hypoxia-inducible factor 1α,HIF-1α),tumor cell proliferation antigen Ki67 and vascular endothelial growth factor (VEGF) in breast cancer tissues,adjacent tissues and normal breast tissues.Methods Immunohistochemistry HRP method was used to detect the expression of HIF-1α,Ki67 and VEGF in 70 cases of breast cancer tissues and their adjacent tissues and 10 cases of normal breast tissues.Difference of the positive rate was assessed viax2 test,and the correlation between the 3 were analyzed in a disorderly classified manner.Results The positive expression rate of HIF-1α,Ki67 and VEGF in 70 cases of breast cancer tissues was 78.6％ (55/70),88.6％ (62/70) and 65.7％ (46/70) respectively,significantly higher than that in adjacent tissues and normal breast tissues (P ＜ 0.01).The positive expression rate of HIF-1 α,Ki67 and VEGF was closely related with clinical stage,lymph node metastasis and histological grade (P ＜0.05).The expression intensity of HIF-1α was positively correlated with Ki67 and VEGF in breast cancer (P ＜ 0.05).Conclusions Detection of HIF-1 α,Ki67,VEGF may be an important indicator to predict the development,invasion,metastasis and prognosis of breast cancer.Tissue hypoxia may promote the proliferation of breast cancer cell and angiogenesis.A presumption is that HIF-1αmay be a new t()get of breast cancer,thus it deserves further study.

According to its location and function, the oral mucosa can be divided into masticatory mucosa, coated mucosa and special mucosa. Oral masticatory mucosa, including hard palate and gingival mucosa, bears the chewing pressure and friction, and plays an important role in denture restoration. The study on biomechanics of oral masticatory mucosa is helpful to better understand and solve clinical problems related to oral masticatory mucosa. In this review, the progress of biomechanical researches on oral masticatory mucosa was summaried from three aspects: anatomical and physiological analysis, biomechanical characteristics (stress-strain curve, Poisson’s ratio, friction coefficient) and clinical significance, in order to provide further theoretical basis for the researches in oral prosthodontics-related areas.

BACKGROUND:It has been studied that the distribution of bone morphogenetic protein 2 is regular under bone defect situation. OBJECTIVE:To observe the expression of bone morphogenetic protein 2 in rabbit radial defect site with different lengths. METHODS:Forty-eight New Zealand rabbits were divided into two groups randomly, 0.5 cm bone defect and 3.0 cm bone defect were made by wire saw at the middle part of radius bone after anaesthesia. RESULTS AND CONCLUSION:Western blot results showed that in the 0.5 cm bone defect group, the expression of bone morphogenetic protein 2 of the tissues in the bone defect site was increased gradual y at 1, 3, 4 weeks after operation, and the expression in each defect group was increased when compared with that immediately after injury (P<0.05). In the 3.0 cm bone defect group, the expression of bone morphogenetic protein 2 of tissues in bone defect site was increased gradual y and reached to its peak at 3 weeks after the operation (P<0.05), and the peak value in the 3.0 cm bone defect group was significantly higher than that in 0.5 cm bone defect group (P<0.05). The peak value was maintained in high level. The comparison of bone cal us formation showed that the bone cal us formation of 3.0 cm bone defect group was less than that of the 0.5 cm bone defect group at 3 and 4 weeks after operation (P<0.05). The results indicate that expression of the bone morphogenetic protein 2 in 3.0 cm bone defect site is increased significantly, but the expression level cannot make the bone defect heal itself.