bluuebunny/crossref_metadata_2025_split huggingface dataset:
Corticosterone impairs the mRNA expression and activity of 3β- and 17β-hydroxysteroid dehydrogenases in adult rat Leydig cells
Authors: Badrinarayanan R. , Rengarajan S. , Nithya P. , Balasubramanian K. 
Published: December 2006

Clinical and experimental studies, including our own observations, have shown the adverse effects of excess glucocorticoids on testicular steroid hormone production. The present study was designed to gain insight into the molecular mechanisms by which excess corticosterone impairs Leydig cell steroidogenesis. To achieve this, adult rats were administered with corticosterone-21-acetate (2 mg/100 g body weight) twice daily for 15 days. After the treatment period, rats were killed by decapitation. The testes were removed, decapsulated aseptically and used for the isolation of Leydig cells. Purified Leydig cells were used for assessing the activity of 3β- and 17β-hydroxysteroid dehydrogenases (HSDs) and total RNA isolation. For in vitro studies, purified Leydig cells (7.5 × 106cells) of control rats were plated in culture flasks and exposed to different concentrations (50, 100, 200, 400, and 800 nmol/L) of corticosterone for 24 h. At the end of incubation, total RNA was isolated from cultured Leydig cells, and the mRNA of 3β- and 17β-HSDs was quantified by RT–PCR. A significant reduction in the activities and levels of 3β-HSD type-I and 17β-HSD type-III mRNAs in Leydig cells were observed. In vitro studies demonstrated a dose-dependent significant impairment in both the activity and mRNA expression of these enzymes. These results suggest that corticosterone might have a direct effect on the transcription of the genes of 3β- and 17β-HSD. It is inferred from the present in vivo and in vitro studies that one of the molecular mechanisms by which excess corticosterone decreases the steroidogenic potency of Leydig cells is by suppressing the mRNA expression of 3β-HSD type-I and 17β-HSD type-III enzymes.
Aminonaphthoquinone induces oxidative stress inStaphylococcus aureus
Authors: Medina L.F.C. , Hertz P.F. , Stefani V. , Henriques J.A.P. , Zanotto-Filho A. , Brandelli A. 
Published: December 2006

The biological activity of 5-amino-8-hydroxy-1,4-naphthoquinone (ANQ) on Staphylococcus aureus was investigated in comparison with the unsubstituted 1,4-naphthoquinone (NQ). Complete inhibition of microbial growth was observed with ANQ and NQ at 50 and 10 µg/mL, respectively. The antibacterial effect of naphthoquinones decreased in the presence of sodium ascorbate, but the superoxide scavenger 4,5-dihydroxy-1,3-benzene-disulfonic acid (Tiron) was able to protect S. aureus only from the harmful effect of ANQ. Naphthoquinones blocked oxygen uptake and induced cyanide-insensitive oxygen consumption. When combining rotenone or salicylhydroxamic acid with ANQ or NQ, a slight decrease in respiratory activity was observed. Assays in the presence of naphthoquinones induced an increase of lipid peroxidation in S. aureus, as determined by thiobarbituric acid reactive substances. These results showed that 1,4-naphthoquinones effectively act as electron acceptors and induce an increase in reactive oxygen species that are toxic to S. aureus cells.
The functional response of U937 macrophage-like cells is modulated by extracellular matrix proteins and mechanical strain
Authors: Matheson Loren A. , Maksym Geoffrey N. , Santerre J. Paul , Labow Rosalind S. 
Published: December 2006

Extracellular matrix proteins (ECMs) play a significant role in the transfer of mechanical strain to monocyte-derived macrophages (MDMs) affecting morphological changes in a foreign body reaction. This study investigated how the functional responses of U937 macrophage-like cells differed when subjected to 2 dynamic strain types (nonuniform biaxial or uniform uniaxial strain) while cultured on siloxane membranes coated with either collagen type I or RGD peptide repeats (ProNectin®). Biaxial strain caused an increase in intracellular esterase and acid phosphatase (AP) activities, as well as monocyte-specific esterase (MSE) protein levels in cells that were seeded on either uncoated surfaces (shown previously) or collagen, but not ProNectin®. Released AP activity, but not released esterase activity, was increased on all surfaces. Biaxial strain increased IL-6, but not IL-8 on all surfaces. When cells were subjected to uniaxial strain, intracellular esterase increased on coated surfaces only, whereas intracellular AP activity was unaffected. Both esterase and AP released activities increased on all surfaces. Uniaxial strain increased the release of IL-6 on all surfaces, but IL-8 on coated surfaces only. This study demonstrated for the first time that ECM proteins could specifically modulate cellular responses to different types of strain. Using this approach with an in vitro cell system may help to unravel the complex function of MDMs in the foreign-body reaction.
Body Mass Index, Abnormal Glucose Metabolism, and Mortality from Hematopoietic Cancer
Authors: Chiu Brian C-H. , Gapstur Susan M. , Greenland Philip , Wang Renwei , Dyer Alan 
Published: December 2006

AbstractBackground: High body mass index (BMI) and diabetes have been linked to risk of non-Hodgkin's lymphoma (NHL), but results are inconsistent and most studies use self-reported information. No study has evaluated the association of NHL with postload plasma glucose (PLG) levels, which are positively associated with BMI. We analyzed data from a cohort study to investigate associations of interviewer-measured BMI and PLG with risk of NHL mortality and to explore associations with leukemia and multiple myeloma.Methods: Employees of 84 Chicago-area organizations, with an average age of 40 years at baseline, were screened from 1967 to 1973. Height and weight were measured by study nurses. A 50-g oral glucose load was administered to nondiabetic participants. Of the at-risk cohort of 35,420 men and women, 129 died of NHL, 151 died of leukemia, and 66 died of multiple myeloma during an average of 31 years of follow-up. Hazard Ratios (HR) and 95% confidence intervals (95% CI) were derived from Cox proportional hazards regression models.Results: Among men, there were positive dose-response relations of BMI with mortality from NHL (HR, 2.57; 95% CI, 1.24-5.34 for the highest versus lowest quartile; Ptrend = 0.01) and leukemia (HR, 1.98; 1.07-3.69; Ptrend = 0.02). PLG also was positively related to NHL mortality (HR, 2.86; 95% CI, 1.35-6.06 for the highest versus lowest category; Ptrend = 0.004). For women, a higher BMI was positively associated with leukemia mortality (HR, 2.47; 95% CI, 0.96-6.36; Ptrend = 0.02) and the highest level of PLG was associated with risk of mortality from multiple myeloma (HR, 3.06; 95% CI, 1.05-8.93). The risk estimates for BMI and PLG remained unchanged after adjustment for each factor.Conclusions: High BMI and/or abnormal PLG is associated with higher risk of mortality from NHL and possibly leukemia and from myeloma in women. These findings might have public health significance because BMI and glucose levels are amenable to modification. (Cancer Epidemiol Biomarkers Prev 2006;15(12):2348–54)
Infant Acute Leukemia and Maternal Exposures during Pregnancy
Authors: Pombo-de-Oliveira Maria S. , Koifman Sergio ,   Brazilian Collaborative Study Group of Infant Acute Leukemia
Published: December 2006

AbstractInfant acute leukemia (IAL) has a unique profile characterized by the high incidence of translocations involving the MLL gene located at the 11q23 region. To test the potential role of intrauterine and perinatal factors linked to the risk of IAL development, a hospital-based case-control study was conducted in different cities of Brazil. A total of 202 children (ages 0-21 months) with newly diagnosed IAL was enrolled (1999-2005), and 440 age-matched controls were selected from the same hospitals wherein IAL cases were treated. A statistically significant association between maternal use of hormones during pregnancy and IAL was observed [odds ratio (OR), 8.76; 95% confidence interval (95% CI), 2.85-26.93] in a multivariable analysis. The association of certain exposures during pregnancy (hormones, dipyrone, metronidazole, and misoprostol) and MLL gene rearrangements was tested using a case-case approach. Despite the lack of statistical significance, the magnitude of the OR for maternal exposure to dipyrone (OR, 1.45; 95% CI, 0.75-2.86), metronidazole (OR, 1.72; 95% CI, 0.64-4.58), quinolones (OR, 2.25; 95% CI, 0.70-25.70), and hormones (OR, 1.88; 95% CI, 0.50-7.01) may suggest the occurrence of interactions between such maternal exposures during pregnancy and MLL rearrangements, yielding into IAL development. The strong and statistically significant association between IAL and estrogen exposure during pregnancy observed in this study deserves further investigation to investigate its role in intrauterine leukemogenesis. (Cancer Epidemiol Biomarkers Prev 2006;15(12):2336–41)
Polymorphisms in Metabolic Genes Related to Tobacco Smoke and the Risk of Gastric Cancer in the European Prospective Investigation into Cancer and Nutrition
Authors: Agudo Antonio , Sala Núria , Pera Guillem , Capellá Gabriel , Berenguer Antonio , García Nadia , Palli Domenico , Boeing Heiner , Del Giudice Giuseppe , Saieva Calogero , Carneiro Fatima , Berrino Franco , Sacerdote Carlotta , Tumino Rosario , Panico Salvatore , Berglund Göran , Simán Henrik , Stenling Roger , Hallmans Göran , Martínez Carmen , Bilbao Roberto , Barricarte Aurelio , Navarro Carmen , Quirós José R. , Allen Naomi , Key Tim , Bingham Sheila , Khaw Kay-Tee , Linseisen Jakob , Nagel Gabriele , Overvad Kim , Tjonneland Anne , Olsen Anja , Bueno-de-Mesquita H. Bas , Boshuizen Hendriek C. , Peeters Petra H. , Numans Mattijs E. , Clavel-Chapelon Françoise , Boutron-Ruault Marie-Christine , Trichopoulou Antonia , Lund Eiliv , Offerhaus Johan , Jenab Mazda , Ferrari Pietro , Norat Teresa , Riboli Elio , González Carlos A. 
Published: December 2006

Abstract
Metabolizing enzymes, which often display genetic polymorphisms, are involved in the activation of compounds present in tobacco smoke that may be relevant to gastric carcinogenesis. We report the results of a study looking at the association between risk of gastric adenocarcinoma and polymorphisms in genes CYP1A1, CYP1A2, EPHX1, and GSTT1. A nested case-control study was carried out within the European Prospective Investigation into Cancer and Nutrition, developed in 10 European countries. The study includes 243 newly diagnosed cases of histologically confirmed gastric adenocarcinoma and 946 controls matched by center, age, sex, and date of blood collection. Genotypes were determined in nuclear DNA from WBCs. We found an increased risk of gastric cancer for homozygotes for C (histidine) variant in Y113H of EPHX1 (odds ratio, 1.91; 95% confidence interval, 1.19-3.07) compared with subjects with TC/TT. There was also a significant increased risk for smokers carrying at least one variant allele A in Ex7+129C&gt;A (m4) of CYP1A1 and never smokers with null GSTT1 and allele A in the locus −3859G&gt;A of CYP1A2. Most of these genes are involved in the activation and detoxification of polycyclic aromatic hydrocarbons, suggesting a potential role of these compounds in gastric carcinogenesis. (Cancer Epidemiol Biomarkers Prev 2006;15(12):2427–34)
Risk of Multiple Myeloma following Medication Use and Medical Conditions: A Case-Control Study in Connecticut Women
Authors: Landgren Ola , Zhang Yawei , Zahm Sheila Hoar , Inskip Peter , Zheng Tongzhang , Baris Dalsu 
Published: December 2006

Abstract
Background: Certain commonly used drugs and medical conditions characterized by chronic immune dysfunction and/or antigen stimulation have been suggested to affect important pathways in multiple myeloma tumor cell growth and survival. We conducted a population-based case-control study to investigate the role of medical history in the etiology of multiple myeloma among Connecticut women.
Methods: A total of 179 incident multiple myeloma cases (21-84 years, diagnosed 1996-2002) and 691 population-based controls was included in this study. Information on medical conditions, medications, and medical radiation was obtained by in-person interviews. We calculated odds ratios (OR) as measures of relative risks using logistic regression models.
Results: A reduced multiple myeloma risk was found among women who had used antilipid statin therapy [OR, 0.4; 95% confidence interval (95% CI), 0.2-0.8] or estrogen replacement therapy (OR, 0.6; 95% CI, 0.4-0.99) or who had a medical history of allergy (OR, 0.4; 95% CI, 0.3-0.7), scarlet fever (OR, 0.5; 95% CI, 0.2-0.9), or bursitis (OR, 0.4; 95% CI, 0.2-0.7). An increased risk of multiple myeloma was found among women who used prednisone (OR, 5.1; 95% CI, 1.8-14.4), insulin (OR, 3.1; 95% CI, 1.1-9.0), or gout medication (OR, 6.7; 95% CI, 1.2-38.0).
Conclusions: If our results are confirmed, mechanistic studies examining how prior use of insulin, prednisone, and, perhaps, gout medication might promote increased occurrence of multiple myeloma and how antilipid statins, estrogen replacement therapy, and certain medical conditions might protect against multiple myeloma may provide insights to the as yet unknown etiology of multiple myeloma. (Cancer Epidemiol Biomarkers Prev 2006;15(12):2342–7)
Accuracy of Multiplexed Illumina Platform-Based Single-Nucleotide Polymorphism Genotyping Compared between Genomic and Whole Genome Amplified DNA Collected from Multiple Sources
Authors: Paynter Randi A. , Skibola Danica R. , Skibola Christine F. , Buffler Patricia A. , Wiemels Joseph L. , Smith Martyn T. 
Published: December 2006

Abstract
Association studies designed to identify the genetic determinants underlying complex disease increasingly require sustainable high-quality DNA resources for large-scale single-nucleotide polymorphism (SNP) genotyping. Recent studies have shown that genomic DNA (gDNA) suitable for SNP genotyping can be obtained from buccal cells and from dried blood spots on Guthrie cards. Further, successful SNP genotyping has been done using the reaction product of multiple displacement amplification of gDNA. We evaluated genotype consistency on the Illumina genotyping platform for 717 to 1,744 SNP loci between replicate samples of gDNA and whole genome amplified DNA (wgaDNA) from a variety of sources. Nine healthy adults provided peripheral blood via venipuncture and buccal cells by mouth rinse. DNA was also obtained from urothelial cells in urine samples from five of the nine subjects. gDNA was extracted from all samples, wgaDNA was generated from each gDNA, and all samples were genotyped. To assess SNP genotyping accuracy of DNA obtained from dried blood spots, gDNA was extracted, amplified, and genotyped from peripheral blood samples and paired Guthrie card samples were obtained from eight childhood leukemia patients. Call rates and replicate concordances for all sample types, regardless of amplification, were &gt;97%, with most sample types having call rates and replicate concordances &gt;99%. Using the gDNA from blood samples as the reference for concordances calculated for all other sample types, we observed concordances &gt;98% regardless of sample type or amplification. We conclude that highly multiplexed Illumina genotyping may be done on gDNA and wgaDNA obtained from whole blood, buccal samples, dried blood spots on Guthrie cards, and possibly even urine samples, with minimal misclassification. (Cancer Epidemiol Biomarkers Prev 2006;15(12):2533–6)
Comprehensive Analysis of 22XPCPolymorphisms and Bladder Cancer Risk
Authors: Sak Sei Chung , Barrett Jennifer H. , Paul Alan B. , Bishop D. Timothy , Kiltie Anne E. 
Published: December 2006

AbstractTwo major risk factors for bladder cancer are smoking and occupational exposure to chemicals. The XPC protein is crucial in the recognition and initiation of the nucleotide excision repair pathway which repairs the DNA adducts formed by carcinogens found in cigarette smoke and chemicals. Polymorphisms in the XPC gene have been shown to influence an individual's DNA repair capacity, and hence, increase that individual's susceptibility to cancer. We undertook a case-control study of 547 bladder cancer cases and 579 cancer-free controls to investigate the association between 22 XPC polymorphisms and bladder cancer susceptibility, and investigated gene-environment interactions. We showed that the nonsynonymous polymorphism Ala499Val was in strong linkage disequilibrium with two polymorphisms in the 3′-untranslated region (Ex15-184 and Ex15-177) with Lewontin's D′ ≥ 0.99 and r2 ≥ 0.82. Individuals homozygous for the minor allele of Ala499Val, Ex15-184, or Ex15-177 had an increased risk of bladder cancer compared with those homozygous for the common allele [adjusted odds ratio (95% confidence interval), 1.65 (1.05-2.59), 1.82 (1.12-2.97), and 1.82 (1.12-2.96), respectively]. The associations were somewhat stronger for smokers and those occupationally exposed to chemicals, although tests for gene-environment interactions were not significant. (Cancer Epidemiol Biomarkers Prev 2006;15(12):2537–41)
Hypoxia-Inducible Factor 1 as a Possible Target for Cancer Chemoprevention
Authors: López-Lázaro Miguel 
Published: December 2006

AbstractDespite the intense cancer research carried out in the last 30 years, cancer therapy has not managed to decrease cancer mortality. We need new strategies to control a disease that kills over six million people worldwide every year. It is accepted that cancer chemoprevention (the use of chemicals to prevent, stop, or reverse the process of carcinogenesis) is an essential approach to controlling cancer; yet, the clinical usefulness of this strategy is very limited. Successful implementation of cancer chemoprevention depends on a mechanistic understanding of the carcinogenesis process. Our knowledge about this process is still limited and may therefore be preventing cancer chemoprevention from becoming a widely used anticancer tool. This report discusses recent evidence that suggests that the activation of the hypoxia-inducible factor 1 (HIF-1) is a key event in carcinogenesis and may therefore represent a key target for cancer chemoprevention. Based on an understanding of the mechanisms responsible for HIF-1 activation, possible general strategies for targeting HIF-1 are proposed. Successful implementation of these strategies might turn the great promise of cancer chemoprevention into a fundamental tool for reducing the burden of this disease. (Cancer Epidemiol Biomarkers Prev 2006;15(12):2332–5)
Vitamin D Receptor Genotypes/Haplotypes and Prostate Cancer Risk
Authors: Cicek Mine S. , Liu Xin , Schumacher Fredrick R. , Casey Graham , Witte John S. 
Published: December 2006

Abstract
The vitamin D receptor (VDR) gene has been associated with prostate cancer, although previous results are somewhat equivocal. To further study this, we did a family-based case-control study (N = 918) of the association between prostate cancer and six common VDR variants: Cdx2, FokI, BsmI, ApaI, TaqI, and the poly-A microsatellite. Looking at each variant alone, only FokI and ApaI were associated with disease. The FokI FF genotype was inversely associated with prostate cancer among men with less advanced disease (i.e., Gleason score &lt;7 and tumor stage &lt;T2c), where the odds ratio OR was 0.56 [95% confidence interval (95% CI), 0.31-1.01; P = 0.05]. ApaI, carrying one or two copies of the A allele, exhibited a weak inverse association with disease (OR, 0.64; 95% CI, 0.39-1.03; P = 0.06); this association was strengthened in Caucasian men with more advanced disease (OR, 0.44; 95% CI, 0.21-0.93; P = 0.03). We observed inverse associations between disease and the four-locus FBAt haplotype (OR, 0.48; 95% CI, 0.30-0.76; P = 0.002) and the fbaT haplotype (OR, 0.60; 95% CI, 0.38-0.95; P = 0.03; i.e., in comparison with the FbaT haplotype). These were stronger among men with more advanced disease: for FBAt, the OR was 0.31 (95% CI, 0.16-0.61; P = 0.0008); for fbaT, the OR was 0.32 (95% CI, 0.16-0.64; P = 0.001). These observations support a role for VDR variants in prostate cancer risk but suggest that any potential causal variant(s) may reside on the haplotypes reported here. This would help explain the somewhat equivocal results for VDR genotype-level associations with prostate cancer. (Cancer Epidemiol Biomarkers Prev 2006;15(12):2549–52)
Association of Genetic Variants of O6-Methylguanine-DNA Methyltransferase with Risk of Lung Cancer in Non-Hispanic Whites
Authors: Wang Luo , Liu Hongji , Zhang Zhengdong , Spitz Margaret R. , Wei Qingyi 
Published: December 2006

Abstract
O 6-methylguanine, a methylated damage lesion in DNA, correlates with spontaneous G:C → A:T transition mutations and leads to activation of oncogene K-ras or dysfunction of the tumor suppressor gene p53. O6-methylguanine-DNA methyltransferase (MGMT) is critical for repairing damage to the O6-position of guanine. Therefore, we tested our hypothesis that genetic variants of MGMT are associated with increased lung cancer risk in a Caucasian population of 1,121 lung cancer patients and 1,163 matched cancer-free controls. We genotyped four potentially functional single nucleotide polymorphisms (SNPs) of MGMT: exon 3 codon 84C → T (L84F), exon 5 codon 143A → G (I143V), and two promoter SNPs 135G → T and 485C → A. The allele frequency distributions of the SNPs of codon 84C → T and the promoter 135G → T in the cases were borderline different from that in the controls. After defining the minor allele (T for codon 84C → T and G for codon 143A → G) as the variant allele, we categorized the MGMT genotypes as either 0 variants (84CC-143AA) or 1-4 variants. Compared with 0 variants, those with 1-4 variants showed a statistically significantly increased risk of lung cancer (P = 0.040). Further stratification analysis showed that this increased risk was more pronounced in women, current smokers, and non–small cell lung cancer. We did not find any association between the MGMT promoter SNPs and lung cancer risk. Our findings suggest that non-synonymous SNPs in MGMT are associated with modestly increased risk of lung cancer in Caucasians and need to be further investigated. (Cancer Epidemiol Biomarkers Prev 2006;15(12):2364–9)