A study on load-deflection behavior of two-span continuous concrete beams reinforced with GFRP and steel bars

Continuous concrete beams are commonly used as structural members in the reinforced concrete constructions. The use of fiber reinforced polymer (FRP) bars provide attractive solutions for these structures particularly for gaining corrosion resistance. This paper presents experimental results of eight two-span continuous concrete beams; two of them reinforced with pure glass fiber reinforced polymer (GFRP) bars and six of them reinforced with combinations of GFRP and steel bars. The continuous beams were tested under monotonically applied loading condition. The experimental load-deflection behavior and failure mode of the continuous beams were examined. In addition, the continuous beams were analyzed with a numerical method to predict the load-deflection curves and to compare them with the experimental results. Results show that there is a good agreement between the experimental and the theoretical load-deflection curves of continuous beams reinforced with pure GFRP bars and combinations of GFRP and steel bars. Copyright © 2017 Techno-Press, Ltd.Firat University Scientific Research Projects Management UnitThe presented research study was financially supported by Cukurova University Scientific Research Projects Directorate (Project No. FDK-2015-4924). The experimental work was assisted by Cukurova University laboratory staffs. The authors would like to thank for these contributions

Clinical significance of hepatocyte growth factor, platelet-derived growth factor-AB, and transforming growth factor-alpha in bone marrow and peripheral blood of patients with multiple myeloma

WOS: 000242284300014PubMed ID: 17050506Angiogenesis is a process that plays an important role in the growth and progression of cancer; growing evidence suggests that neovascularization is important in hematologic malignancies. Increased angiogenic potential has been identified in multiple myeloma (MM). In this study, investigators simultaneously measured the levels of hepatocyte growth factor (HGF), platelet-derived growth factor-AB (PDGF-AB), and transforming growth factor-alpha (TGF-alpha) through enzyme-linked immunosorbent assay in the bone marrow (BM) and peripheral blood (PB) of 30 patients with MM and 10 healthy controls. Differences in HGF values in BM sera were significant (P=.001) between patients and controls. In detailed analyses of HGF, PDGF-AB, and TGF-alpha, according to disease stage, a significant correlation was found between disease stage and BM HGF (P=.047), BM TGF-alpha (P=.021), and PB PDGF-AB (P=.006), respectively. When correlations between all other parameters were analyzed, significance was noted between PB TGF-alpha and lactate dehydrogenase (P=.02), PB TGF-alpha and PB HGF (P=.002), BM TGF-alpha and CD38 (P=.046), BM TGF-alpha and BM HGF (P=.000), BM TGF-alpha and BM PDGF-AB (P=.048), BM HGF and PB HGF (P=.044), and BM PDGF-AB and PB PDGF-AB (P=.000). BM HGF levels had a significant effect on overall survival, with disease severity assessed in terms of disease stage (P=.001 8, log-rank test). These data show that in patients with MM, high levels of BM HGF, BM TGF-alpha, and PB PDGF-AB were associated with advanced disease stage; in addition, HGF played a significant role in disease processing and was related to disease severity. These findings have also led to the concept of a symbiotic relationship between the growth of myeloma cells and HGF, TGF-alpha, and PDGF-AB in BM

The role of posterior instrumentation and fusion after anterior radical debridement and fusion in the surgical treatment of spinal tuberculosis: Experience of 127 cases

Long periods of immobilization, progressive kyphosis and graft failure are the major postoperative problems encountered after anterior radical surgical treatment for tuberculosis of the spine. Posterior fusion and instrumentation can be an effective solution for these problems. Effectiveness of posterior fusion and instrumentation was investigated in this study on the basis of the cases with anterior procedure only, and with combined anterior-posterior procedures. One hundred twenty-seven cases of tuberculosis of the spine were surgically treated between 1987 and 1995. All had either I or more of conditions such as spinal cord compression and neurological deficit, vertebral body collapse and kyphosis, or wide paravertebral abscess unresponsive to medical treatment. Of these, 57 had only anterior radical procedure between the years 1987 and 1993. Seventy cases had posterior instrumentation and fusion after the anterior procedure between the years 1991 and 1995. In about two third of the patients (81) autogenous iliac strut graft and in one third of them (40) autogenous fibular strut graft (cases with more than 2 level involvement) was used along with rib grafts after debridement. Twenty-one of the 57 patients who had only anterior procedure demonstrated a postoperative increase of kyphosis of more than 10 degrees. Increased kyphosis was due to graft slippage in 3, resorption in 2 and subsidence in 16 patients. No such increase or graft failure was noted in cases of combined anterior-posterior procedure. The difference in terms of kyphosis was found to be statistically significant (P = 0.047). Anterior radical debridement and strut graft is the golden standard in the surgical treatment of spinal tuberculosis, but it should always be accompanied by posterior instrumentation and fusion to shorten the immobilization period and hospital stay, obtain good and long lasting correction of kyphosis, and prevent further collapse and graft failure

Tissue Doppler imaging and NT-proBNP levels show the early impairment of ventricular function in patients with beta-thalassaemia major

WOS: 000247267600002PubMed ID: 17608095B-thalassaemia major is a chronic haemolytic anaemia, and congestive heart failure (CHF) is the most common cause of death in this disease. N terminal pro B type natriuretic peptide (NT-proBNP) increases with the severity of CHF and predicts the prognosis. The aim of this study was to investigate the relation between left ventricular systolic and diastolic function determined by standard pulsed wave Doppler (PWD), tissue Doppler imaging (TDI) and NT-proBNP in patients with B-thalassaemia major. Thirty-four patients with B-thalassaemia major and 34 healthy individuals were included in the study. Blood samples were taken for NT-proBNP. All patients and controls underwent echocardiographic examination. All cardiac chambers were significantly increased in the patient group. Left and right ventricular (LY, RV) ejection fractions and all diastolic parameters were normal in the patients and controls. Tissue Doppler imaging (TDI) showed a significant decrease in IV and RV S-m velocities in patients compared to the controls. NT-proBNP levels were also significantly higher in the patient group. There was a negative correlation between serum NT-proBNP levels and IV Sm and RV Sm velocities in patients (r = -0.426, P = 0.006 and r = -0.409, P = 0.009, respectively). Linear regression analysis showed that LV S-m and RV S-m were independent predictors for NT-proBNR Our findings suggest that although iron overload in patients with B-thalassaemia major impairs the systolic and diastolic functions of both ventricles, it impairs the systolic function earlier than diastolic function. Tissue Doppler imaging is an easy and reliable method in the early determination of ventricular dysfunction in these patients

p53 but not p16(INK4a) induces growth arrest retinoblastoma-deficient hepatocellular carcinoma cells

Background/Aim: Both p16(INK4a) and p53 proteins are negative regulators of the cell cycle. In human hepatocellular carcinomas (HCC), the loss of function of p53, retinoblastoma (pRb) and p16(INK4a) genes by different mechanisms has been largely documented, but their hepatocellular effects are poorly known. We compared the growth-inhibitory effects of p16(INK4a)and p53 proteins in Hep3B cell line-derived clones. Methods: Cells were transfected with inducible p16(INK4a) and p53 expression vectors, and stable clones were analyzed for transgene expression by Western blotting and immunoperoxidase staining. Effects on cell growth were analyzed by in vitro growth assay, thymidine incorporation and flow cytometry. Biochemical effects of p53 were tested by Northern blotting of p21(Cip1) transcripts and by Western blotting of p21(Cip1) mdm-2, bax, cyclin-dependent kinase 2 and cyclin E proteins. The pRb protein was studied by Western blotting and immnunoprecipitation assays. Results: The induction of p16(INK4a) protein expression did not affect in vitro growth of cells. In contrast, p53 protein in its wild-type conformation provoked a growth arrest accompanied by transactivation of p21(Cip1) gene and accumulation of p21(Cip1), bax and mdm-2 proteins, p53-induced growth arrest was due to a cell cycle arrest at the GI/S transition, probably mediated by p21(Cip1) protein, which inhibits cyclin-dependent kinase 2/cyclin E complexes. Conclusions: The lack of detectable pRb protein and resistance of cells to p16(INK4a) strongly suggest that p53 is able to arrest the growth of HCC cells by a mechanism independent of 'p53-retinoblastoma pathway'. These findings are applicable to HCC with abberrations of both p53 and pRb genes, and may not represent the universal effects of p53 in hepatic cells

p53 but not p16(INK4a) induces growth arrest in retinoblastoma-deficient hepatocellular carcinoma cells

Cataloged from PDF version of article.Background/Aim: Both p16(INK4a) and p53 proteins are negative regulators of the cell cycle. In human hepatocellular carcinomas (HCC), the loss of function of p53, retinoblastoma (pRb) and p16(INK4a) genes by different mechanisms has been largely documented, but their hepatocellular effects are poorly known. We compared the growth-inhibitory effects of p16(INK4a)and p53 proteins in Hep3B cell line-derived clones. Methods: Cells were transfected with inducible p16(INK4a) and p53 expression vectors, and stable clones were analyzed for transgene expression by Western blotting and immunoperoxidase staining. Effects on cell growth were analyzed by in vitro growth assay, thymidine incorporation and flow cytometry. Biochemical effects of p53 were tested by Northern blotting of p21(Cip1) transcripts and by Western blotting of p21(Cip1) mdm-2, bax, cyclin-dependent kinase 2 and cyclin E proteins. The pRb protein was studied by Western blotting and immnunoprecipitation assays. Results: The induction of p16(INK4a) protein expression did not affect in vitro growth of cells. In contrast, p53 protein in its wild-type conformation provoked a growth arrest accompanied by transactivation of p21(Cip1) gene and accumulation of p21(Cip1), bax and mdm-2 proteins, p53-induced growth arrest was due to a cell cycle arrest at the GI/S transition, probably mediated by p21(Cip1) protein, which inhibits cyclin-dependent kinase 2/cyclin E complexes. Conclusions: The lack of detectable pRb protein and resistance of cells to p16(INK4a) strongly suggest that p53 is able to arrest the growth of HCC cells by a mechanism independent of 'p53-retinoblastoma pathway'. These findings are applicable to HCC with abberrations of both p53 and pRb genes, and may not represent the universal effects of p53 in hepatic cells

β-Thalassemia mutations and hemoglobinopathies in Adana, Turkey: results from a single center study

INTRODUCTION: β-Thalassemia and hemoglobinopathies are common genetic disorders in Turkey and in this retrospective study our aim was to determine the frequency of β-thalassemia and hemoglobinopathies in Adana, which is one of the biggest cities located in the southern part of Turkey. MATERIAL AND METHODS: Data from 3000 individuals admitted to Seyhan Hereditary Blood Disorders Center in Adana were evaluated. The blood samples were collected into EDTA-containing tubes and hematological parameters were analyzed using an automatic cell counter. High performance liquid chromatography technique was used to determine the type of hemoglobin. Molecular screening of the β-globin gene was performed with β-Globin StripAssay. RESULTS: Of 3000 cases, 609 were diagnosed as β-thalassemia or hemoglobinopathy. We have found that the rates of occurrence of β-thalassemia and hemoglobinopathies are 13.46% and 6.83% respectively in this area. We have identified 18 different β-thalassemia mutations and three separate abnormal hemoglobins: HbS, HbD Los Angeles, and HbE. In molecular analyses, β-thalassemia gene mutations of IVSI.110 (G > A), codon 8 (–AA), IVSI.1 (G > A), IVSI.6 (T > C), –30 (T > A), IVSII.1 (G > A), codon 39 (C > T), codon 44 (–C), IVSI.5 (G > C), codon 5 (–CT), codon 8/9 (+G), IVSII.745 (C > G), codon 22 (7bp del), –101(C > T), codon 36/37 (–T), IVSI.15 (T > G), codon 6 (–A), –88 (G > A) were detected. CONCLUSIONS: Considering the high incidence of mutations that we have found, β-thalassemia and hemoglobinopathies still seem to be a public health problem in Adana

beta-Thalassemia mutations and hemoglobinopathies in Adana, Turkey: results from a single center study

WOS: 000306150200004PubMed ID: 22851993Introduction: beta-Thalassemia and hemoglobinopathies are common genetic disorders in Turkey and in this retrospective study our aim was to determine the frequency of beta-thalassemia and hemoglobinopathies in Adana, which is one of the biggest cities located in the southern part of Turkey. Material and methods: Data from 3000 individuals admitted to Seyhan Hereditary Blood Disorders Center in Adana were evaluated. The blood samples were collected into EDTA-containing tubes and hematological parameters were analyzed using an automatic cell counter. High performance liquid chromatography technique was used to determine the type, of hemoglobin. Molecular screening of the beta-globin gene was performed with beta-Globin StripAssay. Results: Of 3000 cases, 609 were diagnosed as beta-thalassemia or hemoglobinopathy. We have found that the rates of occurrence of beta-thalassemia and hemoglobinopathies are 13.46% and 6.83% respectively in this area. We have identified 18 different beta-thalassemia mutations and three separate abnormal hemoglobins: HbS, HbD Los Angeles, and HbE. In molecular analyses, beta-thalassemia gene mutations of IVSI.110 (G>A), codon 8 (-AA), IVSI.1 (G>A), IVSI.6 (T>C), -30 (T>A), IVSII.1 (G>A), codon 39 (C>T), codon 44 (-C), IVSI.5 (G>C), codon 5 (-CT), codon 8/9 (+G), IVSII.745 (C>G), codon 22 (7bp del), -101(C>T), codon 36/37 (-T), IVSI.15 (T>G), codon 6 (-A), 88 (G>A) were detected. Conclusions: Considering the high incidence of mutations that we have found, beta-thalassemia and hemoglobinopathies still seem to be a public health problem in Adana