bluuebunny/crossref_metadata_2025_split huggingface dataset:
Life course determinants of insulin secretion and sensitivity at age 50 years: the Newcastle thousand families study
Authors: Pearce Mark S , Unwin Nigel C , Parker Louise , Alberti K. George M. M. 
Published: June 2005

AbstractBackgroundSuboptimal nutrition during fetal life and infancy is suggested to increase insulin resistance in adulthood. This study investigated the proportion of variance in insulin secretion and resistance accounted for by factors operating at different stages of life using a cohort of all 1142 births in the city of Newcastle, UK in May and June 1947.MethodsDetailed information was collected prospectively during childhood, including birth weight, growth and socio‐economic circumstances. At age 50, 412 study members attended for clinical examination. Fasting and 30‐min plasma insulin and glucose levels were determined and HOMA‐IR and insulin secretion derived.ResultsBirth weight was not a significant predictor of HOMA‐IR after adjustment for percent body‐fat and waist‐hip ratio. Duration of breastfeeding was significantly negatively associated with HOMA‐IR in men. For both genders, fetal life explained directly little variation in either HOMA‐IR or insulin secretion (0.1–5.6%). Compared to early life, adult lifestyle and body composition directly explained larger proportions of the variances for insulin secretion and HOMA‐IR for men (11 and 22% respectively) and women (5.9 and 34%).ConclusionsInsulin secretion is largely unexplained by these data. For insulin resistance, the evidence suggests a limited impact of early life and a larger impact of adult factors. Copyright © 2005 John Wiley & Sons, Ltd.
Simultaneous Determination of Copper and Bismuth by Anodic Stripping Voltammetry Using H‐Point Standard Addition Method with Simultaneous Addition of Analytes
Authors: Shams Esmaeil , Abdollahi Hamid , Hajian Reza 
Published: June 2005

AbstractSimultaneous determination of bismuth and copper by anodic stripping voltammetry using H‐point standard addition method (HPSAM) with simultaneous addition of analytes is described. The effect of various parameters including acid concentration, accumulation time, accumulation potential and concentration ratio of analytes in the standard solution on the sensitivity and accuracy of method were investigated. The results of applying the H‐point standard addition method showed that Cu2+ and Bi3+ could be determined simultaneously with the concentration ratios of Cu2+ to Bi3+ varying from 1 : 15 to 16 : 1 in the mixed sample. The method was successfully applied to the simultaneous determination of copper and bismuth in some synthetic mixtures.
Magnet Incorporated Carbon Electrodes: Methods for Construction and Demonstration of Increased Electrochemical Flux
Authors: Dunwoody Drew C. , Ünlü Murat , Wolf Angela K. H. , Gellett Wayne L. , Leddy Johna 
Published: June 2005

AbstractMagnetic fields at electrodes increase flux through dynamics. Magnetically modified electrodes sustain a permanent magnetic field because magnetic materials are either attached to the electrode surface or incorporated into the electronic conductor of the electrode. Thus far, magnetically modified electrodes have been produced by coating electrode surfaces with composites of Nafion and magnetic microparticles. Glassy carbon and platinum electrodes as well as fuel cell electrodes modified with Nafion and magnetic microparticles exhibit enhanced flux as compared to similar nonmagnetic composites. Here, magnet incorporated carbon electrodes (MICEs) are presented. Two examples are described: magnet incorporated carbon paste electrodes (MICE‐Ps) and magnet incorporated carbon epoxy electrodes (MICE‐Es). Voltammetrically driven fluxes for MICEs are higher than those for the corresponding nonmagnetic controls (carbon paste (CPEs) and carbon epoxy (CEEs) electrodes).
Investigation of two‐dimensional channel flow with a partially compliant wall using finite volume–finite difference approach
Authors: Zhang X. , Ajaykumar R. , Sudharsan N. M. , Kumar K. 
Published: June 2005

AbstractThis paper presents a numerical simulation of steady two‐dimensional channel flow with a partially compliant wall. Navier–Stokes equation is solved using an unstructured finite volume method (FVM). The deformation of the compliant wall is determined by solving a membrane equation using finite difference method (FDM). The membrane equation and Navier–Stokes equation are coupled iteratively to determine the shape of the membrane and the flow field. A spring analogy smoothing technique is applied to the deformed mesh to ensure good mesh quality throughout the computing procedure. Numerical results obtained in the present simulation match well with that in the literature. Copyright © 2005 John Wiley & Sons, Ltd.
Cytogenetic evaluation of a large series of hepatoblastomas: Numerical abnormalities with recurring aberrations involving 1q12–q21
Authors: Tomlinson Gail E. , Douglass Edwin C. , Pollock Brad H. , Finegold Milton J. , Schneider Nancy R. 
Published: June 2005

AbstractHepatoblastoma is a malignant embryonal liver tumor that occurs almost exclusively in infants and very young children. Previous cytogenetic studies of hepatoblastoma have investigated small series or individual cases. This report is on the cytogenetics of a large series of 111 hepatoblastoma specimens, with cytogenetic results consecutively karyotyped over a 12‐year period. Abnormal karyotypes were observed in 55 cases (∼50% of the total). Numerical aberrations were observed in 41 cases (36% of the total), particularly trisomies of chromosomes 2, 8, and 20. Chromosome losses were less common than chromosome gains. Structural abnormalities were observed in 43 cases (39% of the total). Unbalanced translocations resulting in trisomy 1q and involving breakpoints at 1q12–21 were the most common structural abnormality, observed in 20 tumors (18% of total cases); the corresponding translocated chromosome was highly varied. The previously reported t(1;4) was observed in seven cases. Most tumors with translocations involving 1q12–21 also displayed numerical chromosome aberrations, the most common of which were chromosomal trisomies, whereas tumors with other structural rearrangements had fewer numerical abnormalities. Supplementary material for this article can be found on the Genes, Chromosomes, and Cancer website at http://www.interscience.wiley.com/jpages/1045‐2257/suppmat/index.html. © 2005 Wiley‐Liss, Inc.
Identification of steroid derivatives that function as potent antiandrogens
Authors: Miyamoto Hiroshi , Marwah Padma , Marwah Ashok , Yang Zhiming , Chung Chin‐Ying , Altuwaijri Saleh , Chang Chawnshang , Lardy Henry 
Published: June 2005

AbstractWe have hypothesized that some steroid derivatives bind to the androgen receptor (AR) with very low androgenic activity and therefore potentially function as better AR antagonists than clinically used antiandrogens, such as flutamide. Indeed, we previously found such a compound, 3β‐acetoxyandrosta‐1,5‐diene‐17‐one ethylene ketal (ADEK), with some estrogenic activity. Here we report the identification of 2 additional steroid derivatives, 3β‐hydroxyandrosta‐5,16‐diene (HAD) and androsta‐1,4‐diene‐3,17‐dione‐17‐ethylene ketal (OAK), as new potent antiandrogens. Like ADEK, HAD and OAK could interrupt androgen binding to the AR and suppress both dihydrotestosterone‐ and androstenediol‐induced transactivations of wild‐type and mutant ARs in prostate cancer cells. These 2 compounds also inhibited prostate‐specific antigen expression in LNCaP as well as growth of different AR‐positive prostate cancer cell lines stimulated by androgen. Significantly, HAD and OAK had only marginal agonist effects, as compared to hydroxyflutamide. More importantly, in contrast to ADEK, OAK was shown to possess marginal estrogenic activity. These results strengthen our hypothesis and suggest that selective steroid derivatives could be potent antiandrogenic drugs with less unfavorable effects for the treatment of prostate cancer. © 2005 Wiley‐Liss, Inc.
Differential MHC class II component expression in HPV‐positive cervical cancer cells: Implication for immune surveillance
Authors: Zehbe Ingeborg , Höhn Hanni , Pilch Henryk , Neukirch Claudia , Freitag Kirsten , Maeurer Markus J. 
Published: June 2005

AbstractEffective eradication of human papillomavirus (HPV)‐positive tumors may require CD8+ and CD4+ T‐cell‐mediated immune responses. Ectopic expression of MHC class II surface molecules has been described in the context of cervical cancer, but coexpression with other components of the MHC class II antigen presentation pathway has not been addressed. We have evaluated the MHC class II antigen presentation pathway in malignant squamous epithelium of HPV+ cervical cancer lesions by in situ costaining HLA‐DR with CLIP or DMA/DMB. Cervical cancer cells exhibit 3 MHC class II phenotypes: (i) DR+/CLIP+ or DM+; (ii) DR+/CLIP‐ or DM‐; and (iii) DR‐/CLIP+ or DM+. The identical profile has been identified in HPV+ ME180 cells, which serve as a target for HLA‐DR4‐restricted and HPV68, E7‐specific CD4+ T cells. IFN‐γ pretreatment of ME180 cells, associated with differential trafficking of MHC class II molecules, is necessary for effective T‐cell recognition. Although proinflammatory cytokines may facilitate MHC class II‐restricted antigen recognition in tumor cells, different phenotypes of the MHC class II antigen presentation pathway may be associated with evasion from CD4+‐mediated cellular immune responses. © 2005 Wiley‐Liss, Inc.
Alcohol intake in adolescence and mammographic density
Authors: Vachon Celine M. , Sellers Thomas A. , Janney Carol A. , Brandt Kathleen R. , Carlson Erin E. , Pankratz Vernon S. , Wu Fang‐Fang , Therneau Terry M. , Cerhan James R. 
Published: June 2005

AbstractAdolescent exposures may be important in the development of breast cancer later in life. We examined the association of adolescent alcohol consumption and adult mammographic density, a strong risk factor for breast cancer. Women within the Minnesota Breast Cancer Family Cohort with detailed mammogram and risk factor information (n = 1,893) formed our sample. Breast cancer cases were excluded. Adolescent alcohol consumption (before age 18) was solicited through a mailed questionnaire. Percent density (PD) was estimated using the computer‐assisted thresholding program, Cumulus. Statistical analyses were performed using linear mixed effect models. Women who reported ever drinking alcohol before age 18 (n = 390; 21%) had a higher unadjusted PD than women who never drank during adolescence (
$\hat{\mu}$unadj = 26.5% vs. 22.2%), but this difference disappeared with adjustment for risk factors for mammographic density ($\hat{\mu}$adj = 21.0% vs. 21.2%, p = 0.94). Adult PD was not associated with age at initiation, amount of alcohol consumed at one sitting or frequency of alcohol use before age 18. The lack of differences was seen across strata of menopausal status. There was suggestion of higher PD among heavy and more frequent drinkers (24.0%, 95% CI 21.1–26.8%) compared to lighter (21.3%, 95% CI 20.3–22.3%) and never drinkers (21.4%, 95% CI 20.9–21.9%) and also among regular adolescent drinkers who were daily or weekly adult drinkers (25.0%, 95% CI 23.0–27.0%) compared to less regular drinkers in these 2 time periods (23.0–23.4%). However, these associations were not statistically significant (p = 0.27 and p = 0.22, respectively). In summary, there was no evidence that adolescent alcohol use was associated with large and persistent effects on adult PD. © 2005 Wiley‐Liss, Inc.
B7‐1 and B7‐2 act differentially in the induction of a T cell response: Their impact for a HLA‐matched and HLA‐mismatched anti‐tumor immunotherapy
Authors: Kronfeld Kai , Abken Hinrich , Seliger Barbara 
Published: June 2005

AbstractThe efficacy of T cell‐based immunotherapy is primarily due to efficient cellular activation that requires the engagement of 2 separate signals, i.e., via the T cell receptor complex and via co‐stimulatory molecules the prototype of which is CD28. In cellular activation, the CD28 ligands B7‐1 (CD80) and B7‐2 (CD86) are thought to play nearly identical roles in T cell activation. We monitored the T cell response upon co‐culture with HLA Class I‐matched and mismatched renal carcinoma cells, respectively, that express different levels of B7‐1 and B7‐2, respectively. In a HLA Class I‐mismatched co‐culture, T cell proliferation, IFN‐γ and GM‐CSF secretion equally depend on the levels of B7‐1 and B7‐2 on tumor cells. In contrast, in a HLA Class I‐matched situation, B7‐2 is more effective in the induction of IFN‐γ and GM‐CSF secretion than B7‐1, but both B7 molecules induce T cell proliferation equally efficient. B7‐2 is more effective than B7‐1 in inducing TNF‐α and IL‐10 secretion in both HLA Class I‐matched and mismatched situations. The distinct patterns of cytokine induction by B7‐1 and B7‐2 obviously depend on the HLA Class I compatibility. These conclusions have substantial implications for the development of B7‐based vaccines used for immunotherapies. © 2005 Wiley‐Liss, Inc.
Correlation of DNA damage in epidemic dropsy patients to carcinogenic potential of argemone oil and isolated sanguinarine alkaloid in mice
Authors: Das Mukul , Ansari Kausar M. , Dhawan Alok , Shukla Yogeshwer , Khanna Subhash K. 
Published: June 2005

AbstractIn recent times, a higher incidence of gall bladder carcinoma in the Indo‐Gangetic basin has been linked with the consumption of contaminated mustard oil. Consumption of mustard oil contaminated with argemone oil (AO) is well known to cause clinical manifestation referred to as “epidemic dropsy.” Because sanguinarine, an active alkaloid of AO, has been shown to intercalate DNA, a possible correlation of DNA damage in epidemic dropsy patients to tumorigenic potential of AO and isolated sanguinarine alkaloid in mice was investigated in the present study. Single topical application of AO (0.15–0.3 ml) or isolated sanguinarine (4.5–18 μmol) followed by twice‐weekly application of tetradecanoylphorbolmyristate acetate (TPA) for 25 weeks resulted in formation of tumors. Histopathologically these tumors were of squamous cell carcinoma type and similar to those found in the positive control group using dimethylbenzanthracene (DMBA)/TPA. The activities of cutaneous γ‐glutamyl transpeptidase (GGT) and glutathione‐S‐transferase P (GST‐P), marker enzymes of tumorigenesis, were found to exhibit higher expression in AO or isolated sanguinarine/TPA treated groups when compared to control. The higher expression of p53 and p21/WAF1 in skin after single topical application of AO or isolated sanguinarine further confirms the tumorigenic response. Single topical application of AO or isolated sanguinarine alkaloid to mice showed significant DNA damage in terms of Olive tail moment (89–129%), tail length (54%) and tail DNA (153–205%) using Comet assay in skin cells. Further, the extent of DNA damage in blood cells of epidemic dropsy patients in alkaline Comet assay was found to be significantly higher as compared to normal population, indicating the genotoxic response of AO exposure. Although the genotoxic lesions may be repaired to some extent on withdrawal of consumption of AO contaminated mustard oil and the residual genotoxic effects caused by AO may not be expressed as signs of carcinogenesis. Environmental factors or hormonal changes during aging process may lead to stimulate/promote the genetically altered latent cells to form neoplastic lesions and can act as one of the etiological factors responsible for higher incidence of gall bladder carcinoma in the population of Indo‐Gangetic basin. © 2005 Wiley‐Liss, Inc.
Antibody response to a non‐conserved C‐terminal part of human histone deacetylase 3 in colon cancer patients
Authors: Shebzukhov Yuriy V. , Koroleva Ekaterina P. , Khlgatian Svetlana V. , Belousov Pavel V. , Kuz'mina Ksenia E. , Radko Boris V. , Longpre Fanny , Lagarkova Maria A. , Kadachigova Tatiana S. , Gurova Olga V. , Meshcheryakov Andrey A. , Lichinitser Mikhail R. , Knuth Alexander , Jager Elke , Kuprash Dmitry V. , Nedospasov Sergei A. 
Published: June 2005

AbstractAntibodies to cancer antigens can often be detected in the sera of patients, although the mechanism of the underlying humoral immune response is poorly understood. Using immunoscreening of tumor‐derived cDNA expression libraries (SEREX), we identified human histone deacetylase 3 (HDAC3) as serologically defined antigen in colon cancer. Closely related HDAC1 and HDAC2 do not elicit humoral response in colon cancer patients. We show that the C‐terminal region of HDAC3 protein lacking the homology to other Class I HDAC contains at least 3 distinct B‐cell epitopes that are recognized by the serum antibodies. HDAC3 in combination with other SEREX antigens may become a useful molecular biomarker with diagnostic or prognostic value for a subset of colon cancer patients. Supplementary material for this article can be found on the International Journal of Cancer website at http://www.interscience. wiley.com/jpages/0020‐7136/suppmat/index.html. © 2005 Wiley‐Liss, Inc.
Hyperforin, a bio‐active compound of St. John's Wort, is a new inhibitor of angiogenesis targeting several key steps of the process
Authors: Martínez‐Poveda Beatriz , Quesada Ana R. , Medina Miguel Ángel 
Published: June 2005

AbstractHyperforin, a phloroglucinol derivative found in St. John's wort related mainly to its antidepressant effects, has been reported recently to induce apoptosis in tumour cells and to inhibit cancer invasion and metastasis. We show that hyperforin inhibits angiogenesis in vitro in bovine aortic endothelial cells and in vivo in the chorioallantoic membrane assay. In a variety of experimental systems representing the sequential events of the angiogenic process, hyperforin treatment of endothelial cells resulted in strong inhibitory effects. Hyperforin inhibited the growth of endothelial cells in culture. Capillary tube formation on Matrigel was abrogated completely by addition of hypeforin at the low micromolar range. Hyperforin also exhibited a clear inhibitory effect on the invasive capabilities of endothelial cells. Zymographic assays showed that hyperforin treatment produced a complete inhibition of urokinase and a remarkable inhibition of matrix metalloproteinase 2. Our data indicates that hyperforin is a compound that interferes with key events in angiogenesis, confirming the recent and growing evidence about a potential role of this compound in cancer and metastasis inhibition and making it a promising drug for further evaluation in the treatment of angiogenesis‐related pathologies. © 2005 Wiley‐Liss, Inc.
RNASEL germline variants are associated with pancreatic cancer
Authors: Bartsch Detlef K. , Fendrich Volker , Slater Emily P. , Sina‐Frey Mercedes , Rieder Harald , Greenhalf William , Chaloupka Brunhilde , Hahn Stephan A. , Neoptolemos John P. , Kress Ralf 
Published: June 2005

AbstractThe RNASEL (encoding ribonuclease L) gene Glu265X mutation has been implicated in familial prostate cancer, and an association between the RNASEL Arg462Gln variant and sporadic and familial prostate cancer, has also been suggested. Because prostate cancer occurs in some familial pancreatic cancer families, we evaluated the role of the RNASEL gene variants Glu265X and Arg462Gln in the etiology of pancreatic cancer. Exon 2 of the RNASEL gene was directly sequenced in the germline of 36 familial and 75 sporadic pancreatic cancer patients and in 108 controls. The Glu265X mutation was identified in one (2.8%) familial and one (1.3%) sporadic pancreatic cancer case, but not in any of the controls. Arg462Gln variants were identified in 61 (56%) controls and in 55 (73%) sporadic pancreatic cancer cases with 8 (7%) and 12 (16%) homozygotes, respectively (p = 0.009). For homozygous carriers the increased risk for pancreatic cancer was 3.5 (odds ratio [OR] = 3.53, 95% confidence interval [CI] = 1.11–11.46, p = 0.03). The population attributable fraction (PAF) was 38.7% (95% CI = 0.08–0.80). In familial pancreatic cancer no association between Arg462Gln genotypes and pancreatic cancer risk was evident. In sporadic pancreatic cancer there were no significant differences between Arg462Gln genotypes regarding clinical characteristics. In familial pancreatic cancer, however, patients with Arg462Gln variants had more aggressive tumors with more high grade cancers (OR = 15.40, p = 0.009) and more distant metastases (OR = 7.00, p = 0.04) than patients with the wild‐type genotype. Our results suggest that RNASEL variants Glu265X and Arg462Gln may contribute to the tumorigenesis of sporadic and familial pancreatic cancer, which has to be proven in large scale studies. © 2005 Wiley‐Liss, Inc.
Involvement of the immune response in the cure of metastatic murine CT‐26 colon carcinoma by low electric field‐enhanced chemotherapy
Authors: Plotnikov Alexander , Tichler Thomas , Korenstein Rafi , Keisari Yona 
Published: June 2005

AbstractLow electric field cancer treatment‐enhanced chemotherapy (LEFCT‐EC) is a new treatment modality that combines chemotherapeutic agents and low electric field stimulation. LEFCT‐EC was found to destroy malignant mouse tumors and cause massive death of tumor cells. This may enable the immune system cells to efficiently recognize and eliminate tumor cells at the primary tumor site and at metastatic foci. Mice with 15 mm diameter intracutaneous colon carcinomas (CT‐26) were injected with BCNU (35 mg/kg), and 2 min later the tumors were exposed to low electric fields (intensity 40 V/cm, pulse duration 180 μs, frequency 500 Hz) for 12 min (LEFCT‐EC). We found that treatment with LEFCT‐EC achieved complete cure of 93% of the animals. In comparison, electric fields alone (13% cure), chemotherapy alone (0%), surgery (15%) or a combination of surgery and bis‐chloroethyl‐nitrosurea, carmustine (BCNU; 84%) treatments resulted in lower cure rates. After treatment and cure with LEFCT‐EC, 50% of the cured mice developed resistance to a tumor challenge (surgery + BCNU only 15%). Furthermore, splenocytes from cured animals protected naive animals from a tumorigenic dose of tumor cells. Separation of spleen cells into lymphocyte subpopulations indicated a major role for CD4 and CD8 T cells in this protection. FACS analysis revealed restoration of normal splenocyte subpopulation proportions impaired by cytotoxic chemotherapy. Our results suggest that LEFCT‐EC can directly destroy primary tumors and facilitate the destruction of metastatic disease by enforcement of antitumor immune responses. © 2005 Wiley‐Liss, Inc.