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Objective To investigate the diagnostic value of combined detection of serum gastrin-releasing peptide precursor (ProGRP),neuron specific enolization enzyme(NSE)and carcinoembryonicantigen(CEA)in small cell lung cancer(SCLC). Methods 471 patients with lung tumor from department of respiratory medicine and thoracic surgery and 162 healthy people from medical examination center were studied.Serum levels of ProGRP,NSE and CEA were detected by using electrochemi-cal luminescence method.ROC curves were drawn and the area under the curve (AUC)was calculated.Results The levels of ProGRP and NSE were significantly higher in patients with SCLC than those in NSCLC,lung benign disease group and normal control group (P <0.01).The levels of CEA were significantly higher in SCLC than those in patients with lung be-nign disease group and normal control group (P <0.05).The AUC of ProGRP,NSE and CEA in the diagnosis of SCLC were 0.933,0.777 and 0.554,respectively.The sensitivity of ProGRP,NSE and CEA in the diagnosis of SCLC were 82.6%,60.4%,41.6% and the specificity were 95.2%,83.3% and 71.7% respectively.The sensitivity of combined detec-tion of ProGRP,NSE and CEA was 91.3% and the specificity was 65.3%.Conclusion The serum ProGRP detection has a higher diagnostic value for SCLC.The combined detection of ProGRP,NSE and CEA is useful in the early diagnosis of SCLC.
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Genotypes of estrogen receptor gene (ER) α and β in 110 patients with non-alcoholic fatty liver disease (NAFLD) and 100 control subjects were examined by polymerase chain reaction-based restriction fragment length polymorphism.The haplotype analysis was conducted by SHEsis on-line computing platform.The results showed that there were no differences in the genotype frequencies and allele frequencies of ERα at Xba Ⅰ and Pvu Ⅱ enzyme cutting sites between two groups (P > 0.05).There existed significant differences in the genotype frequencies and allele frequencies of ERβ at Rsa Ⅰ and Alu Ⅰ enzyme cutting sites between these two groups (P < 0.05 or P <0.01).The risk of NAFLD in postmenopausal women with R or a allele was 1.833 (95% CI1.209-2.779,P<0.05)or 1.782 (95% CI 1.037-3.061,P<0.05) fold of that with allele r or A.The frequency of r-A haplotype in ERβ was significantly lower in NAFLD group than that in control group (OR =0.529,95% CI 0.348-0.805).Logistic regression analysis showed the relationship of fasting blood glucose,triglyceride,body mass index,diastolic pressure,Alu Ⅰ genotype with NAFLD (all P<0.01).The risk of NAFLD in postmenopausal women with Aa/aa genotype was 1.345 (95% CI 1.028-2.505,P<0.05) folds of that with AA genotype.
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To investigate the relationship of body mass index and non-alcoholic fatty liver disease (NAFLD) in patients with type 2 diabetes mellitus. Three hundred and eleven patients with type 2 diabetes mellitus diagnosed according WHO 1999 consensus criteria and 366 healthy subjects were enrolled in the study. Medical history was acquired and physical examination was conducted, and blood sugar, liver and kidney functions, lipid profile and abdominal ultrasonography color were examined. Sixty seven out of 366 healthy subjects were confirmed to have non-alcoholic fatty liver disease (NAFLD) ,including 51 mild case ( 13.9% ) ,15 moderate cases(4. 1% ) and 1 severe case(0. 3% ) ; while in 311 diabetic patients NAFLD was detected in 144 cases, including 85 mild cases (27.3%) ,53 moderate cases( 17.3% )and 19 severe cases( 1.9% ). The prevalence rate of NAFLD was higher in diabetic patients than control group in BMI < 23.0 kg/m2 group, 23.0 -24. 9 kg/m2 group and 25.0 -29. 9 kg/m2 group(P <0. 01 ) ; however, there was no difference between two groups when BMi ≥30 kg/m2 (P >0. 05 ). The prevalence of NAFLD increased with BMI whether in control group or in diabetic group, especially when BMI > 25 kg/m2. In addition to the prevalence of NAFLD, metabolic syndrome increased with BMI in diabetic patients. These findings indicate that type 2 diabetic patients have a high prevalence of NAFLD, especially in obese patients.
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Human osteoblast was treated with recombinant human connective tissue growth factor (rCTGF). This experiment showed that rCTGF increased membrane type-1 matrix metalloproteinase and matrix metalloproteinase-2 protein expression in a dose- and time-depentent manner in human osteoblasts. rCTGF induced activation of p38 MAPK in human osteoblasts. p38 MAPK inhibitor SB23058 abrogated the effect of rCTGF on the expressions of membrane type-1 matrix metalloproteinase and matrix metalloproteinase-2 in human osteoblasts.
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Objective To evaluate the relationship between hyperuricemia and nonalcoholic fatty liver disease(NAFLD) by observing the prevalence of NAFLD among healthy individuals with different levels of serum uric acid.Methods The data of 5 230 persons from medical centers for health examination were analyzed,such as height,weight,blood pressure,blood lipids,blood sugar, hepatitis-related markers, and abdominal color Doppler ultrasound examination were conducted in the fasting state.The diagnosis of NAFLD was made according to the diagnostic criteria adopted by China Institute of Liver Disease and Alcoholic Liver Disease Group.Results The incidences of overweight or obesity, hypertension,hyperlipidemia, and metabolic syndrome were raised with serum uric acid greater than 333 μmol/L in male and>233 μmol/L in female subjects(P<0.05 or P<0.01). Excluding the metabolic syndrome in male subjects, the incidence of NAFLD was increased with serum uric acid,>333 μmol/L in males or >233 μmol/L in females(P<0.05 or P<0.01). In further studies with subjects without any metabolic syndrome, the detection rate of NAFLD was higher in males than in females at the same serum uric acid level(P<0.01). Logistic regression analysis showed that sex, body mass index, blood glucose, and triglyceride, low-density lipoprotein cholesterol, uric acid grading were risk factors of NAFLD(OR 1.344, 2.500, 1.292, 1.279, 1.244, 1.256 respectively).Conclusion A high serum uric acid level is associated with an increased risk of NAFLD.
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Objective To investigate the effects of recombinant human connective tissue growth factor (rCTGF) on the expression of osteoprotegerin (OPG) and RANKL ( receptor activator of NF-κB ligand ) in human osteoblasts, as well as the mechanisms involved. Methods Human osteoblasts were treated with rCTGF. The expressions of OPG and RANKL were assessed by Western blotting. The expressions of focal adhesion kinase ( FAK), mitogen-activated protein kinase (MAPK) were also observed. Results rCTGF inhibited RANKL protein expression in a dose-and time-depentent manner in human osteoblasts, while the expression of OPG kept unchanged. rCTGF induced activation of p38MAPK and dephosphorylation of FAK in human osteoblasts, but had no effect on ERK and JNK phosphorylation. p38MAPK inhibitor SB23058 abrogated the inhibitory effect of rCTGF on RANKL in human osteoblasts. Conclusion rCTGF inhibits the expression of RANKL in human osteoblasts via activation of p38MAPK and dephosphorylation of FAK.
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Objective To investigate the effects of recombinant human connective tissue growth factor (rCTGF) on the proliferation, differentiation and apoptosis in human osteoblasts. Methods Human osteoblasts were treated with rCTGF, cell proliferation was measured by [3 H] -thymidine ([3 H] -TdR) incorporation method,the activity of alkaline phosphatase (ALP) was determined using α-nitrophenyl phosphate as a substrate, the expression of type Ⅰ collagen was determined by Western blotting, osteocalcin in conditioned media was measured by radioimmune assay, and cell apoptosis was assayed by flow cytometry. Results rCTGF promoted proliferation and differentiation of human osteoblasts in a dose-depentent manner, rCTGF increased ALP activity, osteocalcin and type I collagen secretion in a dose-depentent manner, rCTGF inhibited human osteoblastic apoptosis induced by serum deprivation. Conclusion rCTGF can promote osteoblastic proliferation, and differentiation and protect osteoblast against apoptosis, suggesting that CTGF plays an essential role in bone metabolism.