bluuebunny/crossref_metadata_2025_split huggingface dataset:
Modes and Modulations of Antibiotic Resistance Gene Expression
Authors: Depardieu Florence , Podglajen Isabelle , Leclercq Roland , Collatz Ekkehard , Courvalin Patrice 
Published: January 2007

SUMMARYSince antibiotic resistance usually affords a gain of function, there is an associated biological cost resulting in a loss of fitness of the bacterial host. Considering that antibiotic resistance is most often only transiently advantageous to bacteria, an efficient and elegant way for them to escape the lethal action of drugs is the alteration of resistance gene expression. It appears that expression of bacterial resistance to antibiotics is frequently regulated, which indicates that modulation of gene expression probably reflects a good compromise between energy saving and adjustment to a rapidly evolving environment. Modulation of gene expression can occur at the transcriptional or translational level following mutations or the movement of mobile genetic elements and may involve induction by the antibiotic. In the latter case, the antibiotic can have a triple activity: as an antibacterial agent, as an inducer of resistance to itself, and as an inducer of the dissemination of resistance determinants. We will review certain mechanisms, all reversible, that bacteria have elaborated to achieve antibiotic resistance by the fine-tuning of the expression of genetic information.
Current Therapeutics, Their Problems, and Sulfur-Containing-Amino-Acid Metabolism as a Novel Target against Infections by “Amitochondriate” Protozoan Parasites
Authors: Ali Vahab , Nozaki Tomoyoshi 
Published: January 2007

SUMMARYThe “amitochondriate” protozoan parasites of humansEntamoeba histolytica,Giardia intestinalis, andTrichomonas vaginalisshare many biochemical features, e.g., energy and amino acid metabolism, a spectrum of drugs for their treatment, and the occurrence of drug resistance. These parasites possess metabolic pathways that are divergent from those of their mammalian hosts and are often considered to be good targets for drug development. Sulfur-containing-amino-acid metabolism represents one such divergent metabolic pathway, namely, the cysteine biosynthetic pathway and methionine γ-lyase-mediated catabolism of sulfur-containing amino acids, which are present inT. vaginalisandE. histolyticabut absent inG. intestinalis. These pathways are potentially exploitable for development of drugs against amoebiasis and trichomoniasis. For instance,l-trifluoromethionine, which is catalyzed by methionine γ-lyase and produces a toxic product, is effective againstT. vaginalisandE. histolyticaparasites in vitro and in vivo and may represent a good lead compound. In this review, we summarize the biology of these microaerophilic parasites, their clinical manifestation and epidemiology of disease, chemotherapeutics, the modes of action of representative drugs, and problems related to these drugs, including drug resistance. We further discuss our approach to exploit unique sulfur-containing-amino-acid metabolism, focusing on development of drugs againstE. histolytica.
Global Dissemination of
Vibrio parahaemolyticus
Serotype O3:K6 and Its Serovariants
Authors: Nair G. Balakrish , Ramamurthy Thandavarayan , Bhattacharya Sujit K. , Dutta Basabjit , Takeda Yoshifumi , Sack David A. 
Published: January 2007

SUMMARY

Vibrio parahaemolyticus
is recognized as a cause of food-borne gastroenteritis, particularly in the Far East, where raw seafood consumption is high. An unusual increase in admissions of
V. parahaemolyticus
cases was observed at the Infectious Diseases Hospital in Calcutta, a city in the northeastern part of India, beginning February 1996. Analysis of the strains revealed that a unique serotype, O3:K6, not previously isolated during the surveillance in Calcutta accounted for 50 to 80% of the infections in the following months. After this report, O3:K6 isolates identical to those isolated in Calcutta were reported from food-borne outbreaks and from sporadic cases in Bangladesh, Chile, France, Japan, Korea, Laos, Mozambique, Peru, Russia, Spain, Taiwan, Thailand, and the United States. Other serotypes, such as O4:K68, O1:K25, and O1:KUT (untypeable), that had molecular characteristics identical to that of the O3:K6 serotype were subsequently documented. These serotypes appeared to have diverged from the O3:K6 serotype by alteration of the O:K antigens and were defined as “serovariants” of the O3:K6 isolate. O3:K6 and its serovariants have now spread into Asia, America, Africa, and Europe. This review traces the genesis, virulence features, molecular characteristics, serotype variants, environmental occurrence, and global spread of this unique clone of
V. parahaemolyticus
.
Histoplasmosis: a Clinical and Laboratory Update
Authors: Kauffman Carol A. 
Published: January 2007

SUMMARY

Infection with
Histoplasma capsulatum
occurs commonly in areas in the Midwestern United States and Central America, but symptomatic disease requiring medical care is manifest in very few patients. The extent of disease depends on the number of conidia inhaled and the function of the host's cellular immune system. Pulmonary infection is the primary manifestation of histoplasmosis, varying from mild pneumonitis to severe acute respiratory distress syndrome. In those with emphysema, a chronic progressive form of histoplasmosis can ensue. Dissemination of
H. capsulatum
within macrophages is common and becomes symptomatic primarily in patients with defects in cellular immunity. The spectrum of disseminated infection includes acute, severe, life-threatening sepsis and chronic, slowly progressive infection. Diagnostic accuracy has improved greatly with the use of an assay for
Histoplasma
antigen in the urine; serology remains useful for certain forms of histoplasmosis, and culture is the ultimate confirming diagnostic test. Classically, histoplasmosis has been treated with long courses of amphotericin B. Today, amphotericin B is rarely used except for severe infection and then only for a few weeks, followed by azole therapy. Itraconazole is the azole of choice following initial amphotericin B treatment and for primary treatment of mild to moderate histoplasmosis.
Detection of Aminophenylnorharman, a Possible Endogenous Mutagenic and Carcinogenic Compound, in Human Urine Samples
Authors: Nishigaki Rena , Totsuka Yukari , Kataoka Hiroyuki , Ushiyama Hirohumi , Goto Sumio , Akasu Takayuki , Watanabe Tetsushi , Sugimura Takashi , Wakabayashi Keiji 
Published: January 2007

Abstract
Mutagenic/carcinogenic 9-(4′-aminophenyl)-9H-pyrido[3,4-b]indole [aminophenylnorharman (APNH)] is formed from norharman and aniline in the presence of cytochrome P450 3A4/1A2. Because both precursors are widely distributed in the environment, human exposure is unavoidable. To clarify APNH formation in the human body, amounts of the compound in 24-h human urine collected from smokers and nonsmokers, eating a normal diet, were analyzed by liquid chromatography/electrospray ionization tandem mass spectrometry. In addition, norharman and aniline were also analyzed by high-performance liquid chromatography and gas chromatography, respectively. APNH could be detected in all urine samples at levels 49 to 449 pg for smokers and 21 to 594 pg for nonsmokers per 24-h urine, respectively. The amounts of norharman and aniline were 46 to 185 ng and 0.70 to 8.10 μg for smokers and 52 to 447 ng and 0.49 to 5.72 μg for nonsmokers, respectively, per 24-h urine (none of the levels differing significantly between smokers and nonsmokers). To exclude exogenous exposure to norharman and aniline, we analyzed the levels of APNH, norharman, and aniline in urine samples collected from inpatients receiving parenteral alimentation. Similar to the healthy volunteers, all urine samples contained 12 to 338 pg of APNH, 6 to 75 ng of norharman, and 0.33 to 1.86 μg of aniline per 24-h urine. These results suggest that APNH should be considered as a novel endogenous mutagen/carcinogen; thus, it is very important to determine the biological significance of this carcinogen for human cancer development. (Cancer Epidemiol Biomarkers Prev 2007;16(1):151–6)
Common Melanocytic Nevi in 7-Year-Old Schoolchildren Residing at Different Latitudes in Sweden
Authors: Rodvall Ylva , Wahlgren Carl-Fredrik , Ullén Henrik , Wiklund Kerstin 
Published: January 2007

Abstract
Background: Current epidemiologic research shows consistently that increased number of acquired common melanocytic nevi (CMN) is an important risk factor for cutaneous malignant melanoma. The purpose of this study was to investigate the number of CMN in relation to tanning habits and complexion among 7-year-old children residing at different latitudes in Sweden.
Methods: Two municipalities were chosen at latitude 65°N to 68°N in the north of Sweden and two at latitude 57°N in the south. Children born in 1994 and registered in the municipalities were to be included (N = 1,676). A questionnaire was sent to their parents asking about the child's tanning habits. A body examination of CMN of size ≥2 mm was done by the same trained nurse in 1,380 (82.3%) of the children.
Results: CMN was significantly less prevalent among children living in the north with a prevalence of 5.6 [95% confidence interval (95% CI), 4.8-6.5] inland and 6.2 (95% CI, 5.3-7.2) coastal compared with the south with a prevalence of 9.5 (95% CI, 8.2-11.0) inland and 10.4 (95% CI, 8.9-12.0) coastal. In addition, blond hair, blue/gray/green eyes, holidays at seaside resorts abroad, more frequent sunburns, and parents fancying tanning were significant predictors of higher prevalence of CMN.
Conclusions: These findings support previous evidence that the development of CMN is related to the level of sun exposure in childhood expressed as latitude of residence, holidays at seaside resort abroad, and number of sunburns. To reduce the incidence of cutaneous malignant melanoma, a change in attitude and behavior must start with young children and their parents. (Cancer Epidemiol Biomarkers Prev 2007;16(1):122–7)
Role of GSTM3 Polymorphism in the Risk of Developing Esophageal Cancer
Authors: Jain Meenu , Kumar Shaleen , Lal Punita , Tiwari Anu , Ghoshal Uday C. , Mittal Balraj 
Published: January 2007

Abstract
GSTM3 is involved in detoxification of carcinogens and may be important in modulating cancer susceptibility. GSTM3 genotype frequencies were determined in peripheral blood DNA of 149 esophageal cancer patients and 200 nonmalignant controls using the PCR followed by PAGE. Patients who were heterozygous carriers of GSTM3 AB genotype had an enhanced risk for developing esophageal cancer [odds ratio (OR), 2.1; 95% confidence interval (95% CI), 1.1-3.7; P = 0.01]. In males, the risk due to GSTM3 AB genotype increased further (OR, 3.4; 95% CI, 1.7-6.8; P = 0.000). Interaction of GSTM3 AB + BB and GSTM1 null genotypes marginally modulated risk (OR, 2.3; 95% CI, 1.1-3.7; P = 0.01). Association with histology (adenocarcinoma: OR, 3.4; 95% CI, 1.1-10.9; P = 0.03) and tumor site (middle third location: OR, 2.2; 95% CI, 1.1-4.4; P = 0.01; lower third location: OR, 2.6; 95% CI, 1.2-5.6; P = 0.01) was also documented. Our results suggest that GSTM3 polymorphism may influence esophageal cancer susceptibility, in particular modulating the risk for adenocarcinoma histology and tumors of the mid and lower third region. (Cancer Epidemiol Biomarkers Prev 2007;16(1):178–81)
Polymorphisms of Catechol-O-Methyltransferase in Men with Renal Cell Cancer
Authors: Tanaka Yuichiro , Hirata Hiroshi , Chen Zhong , Kikuno Nobuyuki , Kawamoto Ken , Majid Shahana , Tokizane Takashi , Urakami Shinji , Shiina Hiroaki , Nakajima Koichi , Dhir Rajiv , Dahiya Rajvir 
Published: January 2007

Abstract
The estrogen metabolite, 4-hydroxy-estrogen, has been shown to play a role in malignant transformation of male kidneys. To counteract the effects of this catechol-estrogen, the catechol-O-methyltransferase (COMT) enzyme is capable of neutralizing the genotoxic effects of this compound. A polymorphic variant of COMT has been shown to have a reduced enzyme activity, and thus, we hypothesize that single nucleotide polymorphisms of the COMT gene can be a risk factor for renal cell cancer (RCC). To determine this hypothesis, a study of a Japanese male population was used and the genetic distributions of COMT polymorphisms at codons 62 (C→T), 72 (G→T), and 158 (G→A) were analyzed in 157 normal healthy subjects and 123 sporadic RCC (clear cell type) samples by using a sequence-specific PCR technique. These experiments show that the variant genotype (P = 0.025) and allele (P = 0.011) at codon 62 is a risk factor for RCC. The odds ratio and 95% confidence interval for cancer were 3.16 and 1.29 to 7.73, respectively, for the T/T genotype as compared with wild-type. No associations for renal cancer were found at either codons 72 or 158 in this Japanese male population. However, codons 62 and 158 were observed to be in linkage disequilibrium, and haplotype analysis shows the combined forms of T-A, T-G, and C-A to be associated with RCC as compared with C-G (P &lt; 0.001). When evaluating the risk of COMT polymorphisms with grade of cancer, no associations were observed for any of the genotypes. This study is the first to report COMT polymorphism to be associated with RCC. These results are important in understanding the role of COMT polymorphisms in the pathogenesis of RCC. (Cancer Epidemiol Biomarkers Prev 2007;16(1):92–7)
Genetic Admixture among Hispanics and Candidate Gene Polymorphisms: Potential for Confounding in a Breast Cancer Study?
Authors: Sweeney Carol , Wolff Roger K. , Byers Tim , Baumgartner Kathy B. , Giuliano Anna R. , Herrick Jennifer S. , Murtaugh Maureen A. , Samowitz Wade S. , Slattery Martha L. 
Published: January 2007

Abstract
Hispanics in the U.S. Southwest have genetic ancestry from Europeans and from American Indians, two groups with markedly different breast cancer incidence rates. Genetic admixture may therefore bias estimates of associations between candidate cancer susceptibility genes and breast cancer in Hispanics. We estimated genetic admixture using 15 ancestry-informative markers for 1,239 Hispanics and 2,505 non-Hispanic Whites in a breast cancer case-control study in the Southwest, the Four Corners Study. Confounding risk ratios (CRR) were calculated to quantify potential bias due to admixture. Genetic admixture was strongly related to self-reported race and ethnic background (P &lt; 0.0001). Among Hispanic controls, admixture was significantly associated with allele frequency for 5 of 11 candidate gene single nucleotide polymorphisms (SNP) examined. Hispanics in the highest versus the lowest quintile of American Indian admixture had higher mean body mass index at age 30 years (25.4 versus 23.6 kg/m2; P = 0.003), shorter mean height (1.56 versus 1.58 m; P = 0.01), higher prevalence of diabetes (14.8% versus 7.2%; P = 0.04), and a larger proportion with less than a high school education (38.5% versus 23.2%; P = 0.001). Admixture was not associated with breast cancer risk among Hispanics (P = 0.65). CRRs for potential bias to candidate SNP-breast cancer risk ratios ranged from 0.99 to 1.01. Thus, although genetic admixture in Hispanics was associated with exposures, confounding by admixture was negligible due to the null association between admixture and breast cancer. CRRs from simulated scenarios indicated that appreciable confounding by admixture would occur only when within-group candidate SNP allele frequency differences are much larger than any that we observed. (Cancer Epidemiol Biomarkers Prev 2007;16(1):142–50)
High-Order Interactions among Genetic Variants in DNA Base Excision Repair Pathway Genes and Smoking in Bladder Cancer Susceptibility
Authors: Huang Maosheng , Dinney Colin P. , Lin Xin , Lin Jie , Grossman H. Barton , Wu Xifeng 
Published: January 2007

AbstractCancer is a common multifactor human disease resulting from complex interactions between many genetic and environmental factors. In this study, we used a multifaceted analytic approach to explore the relationship between eight single nucleotide polymorphisms in base excision repair (BER) pathway genes, smoking, and bladder cancer susceptibility in a hospital-based case-control study. Overall, we did not find an association between any single BER gene single nucleotide polymorphism and bladder cancer risk. However, in stratified analysis, the OGG1 S326C variant genotypes in ever smokers (odds ratio, 0.74; 95% confidence interval, 0.56-0.99) and ADP-ribosyltransferase (ADPRT) V762A variant genotypes in never smokers (odds ratio, 0.58; 95% confidence interval, 0.37-0.91) conferred a significantly reduced risk. Using logistic regression, we observed that there was a two-way interaction between ADPRT V762A and smoking status. We next used classification and regression tree analysis to explore high-order gene-gene and gene-environment interactions. We found that smoking is the most important influential factor for bladder cancer risk. Consistent with the above findings, we found that the ADPRT V762A was only significantly involved in bladder cancer risk in never smokers and the OGG1 S326C was only significantly involved in ever smokers. We also observed gene-gene interactions among OGG1 S326C, XRCC1 R194W, and MUTYH H335Q in ever smokers. Using multifactor dimensionality reduction approach, the four-factor model, including smoking status, OGG1 S326C (rs1052133), APEX1 D148E (rs3136820), and ADPRT762 (rs1136410), had the best ability to predict bladder cancer risk with the highest cross-validation consistency (100%) and the lowest prediction error (37.02%; P &lt; 0.001). These results support the hypothesis that genetic variants in BER genes contribute to bladder cancer risk through gene-gene and gene-environmental interactions. (Cancer Epidemiol Biomarkers Prev 2007;16(1):84–91)
Mammographic Breast Density as a General Marker of Breast Cancer Risk
Authors: Vachon Celine M. , Brandt Kathleen R. , Ghosh Karthik , Scott Christopher G. , Maloney Shaun D. , Carston Michael J. , Pankratz V. Shane , Sellers Thomas A. 
Published: January 2007

Abstract
Mammographic breast density is a strong risk factor for breast cancer but whether breast density is a general marker of susceptibility or is specific to the location of the eventual cancer is unknown. A study of 372 incident breast cancer cases and 713 matched controls was conducted within the Mayo Clinic mammography screening practice. Mammograms on average 7 years before breast cancer were digitized, and quantitative measures of percentage density and dense area from each side and view were estimated. A regional density estimate accounting for overall percentage density was calculated from both mammogram views. Location of breast cancer and potential confounders were abstracted from medical records. Conditional logistic regression was used to estimate associations, and C-statistics were used to evaluate the strength of risk prediction. There were increasing trends in breast cancer risk with increasing quartiles of percentage density and dense area, irrespective of the side of the breast with cancer (Ptrends &lt; 0.001). Percentage density from the ipsilateral side [craniocaudal (CC): odds ratios (ORs), 1.0 (ref), 1.7, 3.1, and 3.1; mediolateral oblique (MLO): ORs, 1.0 (ref), 1.5, 2.2, and 2.8] and the contralateral side [CC: ORs, 1.0 (ref), 1.8, 2.2, and 3.7; MLO: ORs, 1.0 (ref), 1.6, 1.9, and 2.5] similarly predicted case-control status (C-statistics, 0.64-65). Accounting for overall percentage density, density in the region where the cancer subsequently developed was not a significant risk factor [CC: 1.0 (ref), 1.3, 1.0, and 1.2; MLO: 1.0 (ref), 1.1, 1.0, and 1.1 for increasing quartiles]. Results did not change when examining mammograms 3 years on average before the cancer. Overall mammographic density seems to represent a general marker of breast cancer risk that is not specific to breast side or location of the eventual cancer. (Cancer Epidemiol Biomarkers Prev 2007;16(1):43–9)
Endogenous Androgens and Risk of Epithelial Ovarian Cancer: Results from the European Prospective Investigation into Cancer and Nutrition (EPIC)
Authors: Rinaldi Sabina , Dossus Laure , Lukanova Annekatrin , Peeters Petra H.M. , Allen Naomi E. , Key Timothy , Bingham Sheila , Khaw Kay-Tee , Trichopoulos Dimitrios , Trichopoulou Antonia , Oikonomou Eleni , Pera Guillem , Larrañaga Nerea , Martinez-Garcia Carmen , Ardanaz Eva , Quirós J. Ramón , Tormo María-José , Tjønneland Anne , Olsen Anja , Overvad Kim , Chang-Claude Jenny , Linseisen Jakob , Schulz Mandy , Boeing Heiner , van Gils Carla H. , Bueno-de-Mesquita Bas H. , Pala Valeria , Palli Domenico , Panico Salvatore , Tumino Rosario , Vineis Paolo , Clavel-Chapelon Françoise , Mesrine Sylvie , Boutron-Ruault Marie-Christine , Lundin Eva , Ågren Åsa , Berglund Göran , Manjer Jonas , Kumle Merethe , Lund Eiliv , Slimani Nadia , Saracci Rodolfo , Riboli Elio , Kaaks Rudolf 
Published: January 2007

Abstract
Few epidemiologic studies have examined the hypothesis that circulating androgens are involved in the development of ovarian cancer. We investigated the association between prediagnostic serum levels of androgens and sex hormone–binding globulin (SHBG) and ovarian cancer risk in a case-control study nested within the European Prospective Investigation into Cancer and Nutrition cohort. One hundred and ninety-two ovarian cancer cases and 346 matched controls not using exogenous hormones at baseline blood donation were eligible for the study. Serum levels of testosterone, androstenedione, dehydroepiandrosterone sulfate, and SHBG were measured by direct immunoassays. Free testosterone (fT) was calculated according to mass action laws. Multivariate conditional logistic regression was used to estimate odds ratios adjusted for possible confounders. Overall, there was no association between serum concentrations of androgens or SHBG and ovarian cancer risk. In postmenopausal women, fT concentrations were inversely related to risk [highest versus lowest tertile odds ratio 0.45 (0.24-0.86); Ptrend = 0.01]. Among women diagnosed before the age of 55 years, there was a negative association with SHBG and a positive association with fT and ovarian cancer risk, although these associations were not statistically significant. The present study suggests that circulating androgens and SHBG levels are not strongly associated with ovarian cancer risk, although levels of fT may be associated with an increased risk among women diagnosed at relatively young age. The heterogeneity of results on the associations of fT with ovarian cancer risk in postmenopausal women deserves further investigation. (Cancer Epidemiol Biomarkers Prev 2007;16(1):23–9)