bluuebunny/crossref_metadata_2025_split huggingface dataset:
Essential Role of the Type III Secretion System Effector NleB in Colonization of Mice by
Citrobacter rodentium
Authors: Kelly Michelle , Hart Emily , Mundy Rosanna , Marchès Olivier , Wiles Siouxsie , Badea Luminita , Luck Shelley , Tauschek Marija , Frankel Gad , Robins-Browne Roy M. , Hartland Elizabeth L. 
Published: March 2006

ABSTRACT

Attaching and effacing (A/E) pathogens are a significant cause of gastrointestinal illness in humans and animals. All A/E pathogens carry a large pathogenicity island, termed the locus for enterocyte effacement (LEE), which encodes a type III secretion system that translocates several effector proteins into host cells. To identify novel virulence determinants in A/E pathogens, we performed a signature-tagged mutagenesis screen in C57BL/6 mice by using the mouse A/E pathogen
Citrobacter rodentium
. Five hundred seventy-six derivatives of
C. rodentium
were tested in pools of 12 mutants. One attenuated mutant carried a transposon insertion in
nleB
, which encodes a putative effector of the LEE-encoded type III secretion system (T3SS).
nleB
is present in a genomic pathogenicity island that also encodes another putative effector, NleE, immediately downstream. Using translational fusions with β-lactamase (TEM-1), we showed that both NleB and NleE were translocated into host cells by the LEE-encoded T3SS of enteropathogenic
Escherichia coli
. In addition, deletion of the gene encoding NleB in
C. rodentium
resulted in reduced colonization of mice in single infections and reduced colonic hyperplasia. In contrast, the deletion of other non-LEE-encoded effector genes in
C. rodentium
,
nleC
,
nleD
, or
nleE
, had no effect on host colonization or disease. These results suggest that
nleB
encodes an important virulence determinant of A/E pathogens.
Topical H2 Antagonist Prevents Periodontitis in a Rabbit Model
Authors: Hasturk H. , Kantarci A. , Ebrahimi N. , Andry C. , Holick M. , Jones V. L. , Van Dyke T. E. 
Published: March 2006

ABSTRACTCimetidine is a powerful H2 receptor antagonist that eliminates histamine's effects on chemotaxis, phagocytosis, and superoxide anion production by phagocytes. The purpose of this study was to analyze the clinical and histopathological changes associated with experimental periodontitis in rabbits in response to topically applied cimetidine. Experimental periodontitis was induced in 21 New Zealand White rabbits usingPorphyromonas gingivalis(109CFU) topically applied three times a week for a 6-week period to previously ligatured teeth. Topical application of cimetidine in a liposome carrier for the prevention of periodontitis was evaluated in four groups of four animals each: 1, 10, and 100 mg/ml and no treatment (positive control). In addition, there was a vehicle group (n= 3) that received liposome preparation (carrier) only, and two animals with ligature application alone served as negative controls. Periodontal disease was quantified by direct visualization and radiographical evaluation of bone loss on defleshed skulls and by histological analyses of sections stained with hematoxylin-eosin and tartrate-resistant acid phosphatase. In the no-treatment (positive control) and liposome (vehicle) groups, direct visualization and radiological measurements revealed statistically significant bone loss compared to the negative control. Application of cimetidine at all concentrations tested inhibited inflammation and bone loss by >90%. Histological findings revealed that ligated sites of the positive control and vehicle groups showed significant reduction in bone level (P< 0.05) compared to the three cimetidine groups, with a marked decrease in inflammation. The findings of this study provide morphological and histological evidence that topically active cimetidine is a potent inhibitor ofP. gingivalis-elicited periodontal inflammation, arresting and/or preventing tissue destruction and influencing cell populations present in the inflammatory cell infiltrate.
Spherules Derived from
Coccidioides posadasii
Promote Human Dendritic Cell Maturation and Activation
Authors: Dionne Sara O. , Podany Abigail B. , Ruiz Yvette W. , Ampel Neil M. , Galgiani John N. , Lake Douglas F. 
Published: March 2006

ABSTRACT

Previous studies have shown that dendritic cells (DC) pulsed with T27K, an antigenic preparation derived from spherules (of
Coccidioides posadasii
), activate peripheral blood mononuclear cells (PBMC) from nonimmune subjects as well as from patients with disseminated coccidioidomycosis. In this study, we have assessed the interaction between human DC and
C. posadasii
spherules in order to better understand the initial response between
Coccidioides
and the human host. Whole autoclaved spherules induced lymphocyte transformation in PBMC obtained from immune but not from nonimmune donors. Immature DC (iDC) bound fluorescein isothiocyanate-labeled spherules in a time- and temperature-dependent manner. This binding was blocked by the addition of mannan, suggesting mannose receptor involvement in the DC-
Coccidioides
interaction. Binding was subsequently associated with ingestion and intracellular processing of spherules. Coculturing of spherules with iDC was associated with the development of mature DC that were morphologically, phenotypically, and functionally similar to those induced by tumor necrosis factor alpha and prostaglandin E
2
. Finally, spherules incubated with iDC induced activation of PBMC from nonimmune donors. These data indicate that human DC are capable of binding, internalizing, and presenting antigens from
Coccidioides
spherules and suggest that DC may play a critical early role in the formation of a cellular immune response in human coccidioidomycosis.
RrgA and RrgB Are Components of a Multisubunit Pilus Encoded by theStreptococcus pneumoniae rlrAPathogenicity Islet
Authors: LeMieux Julianna , Hava David L. , Basset Alan , Camilli Andrew 
Published: March 2006

ABSTRACTTherlrApathogenicity islet inStreptococcus pneumoniaeTIGR4 encodes three surface proteins, RrgA, RrgB, and RrgC, and three sortase enzymes. Using transmission electron microscopy, cell fractionation, cell wall sorting signal domain swapping, and Western blotting, we show that RrgA and RrgB are incorporated into a multisubunit pilus inS. pneumoniae.
Posttranslational Regulation of
Mycobacterium tuberculosis
Extracytoplasmic-Function Sigma Factor σ
L
and Roles in Virulence and in Global Regulation of Gene Expression
Authors: Dainese Elisa , Rodrigue Sébastien , Delogu Giovanni , Provvedi Roberta , Laflamme Liette , Brzezinski Ryszard , Fadda Giovanni , Smith Issar , Gaudreau Luc , Palù Giorgio , Manganelli Riccardo 
Published: March 2006

ABSTRACT

In this report, we demonstrate that SigL is posttranslationally regulated by a specific anti-sigma factor, RslA, and contributes to the expression of at least 28 genes. Several of these genes could mediate important cell envelope-related processes. Importantly, a
sigL
-
rslA
mutant strain was significantly attenuated in a mouse model of infection.
The
Treponema denticola
Surface Protease Dentilisin Degrades Interleukin-1β (IL-1β), IL-6, and Tumor Necrosis Factor Alpha
Authors: Miyamoto Meguru , Ishihara Kazuyuki , Okuda Katsuji 
Published: March 2006

ABSTRACT

Dentilisin is a major surface protease and virulence factor of the bacterium
Treponema denticola
. In this study, we found that
T. denticola
reduced inflammatory cytokines, including interleukin-1β (IL-1β), IL-6, and tumor necrosis factor alpha, in peripheral blood mononuclear cells through degradation by dentilisin.
Distinct Kinetics of Effector CD8+Cytotoxic T Cells after Infection withTrypanosoma cruziin Naïve or Vaccinated Mice
Authors: Tzelepis Fanny , de Alencar Bruna C. G. , Penido Marcus L. O. , Gazzinelli Ricardo T. , Persechini Pedro M. , Rodrigues Mauricio M. 
Published: March 2006

ABSTRACTThe kinetics of effector CD8+-T-cell responses to specificTrypanosoma cruziepitopes was investigated after challenge. Our results suggest that the delayed kinetics differs from that observed in other microbial infections and facilitates the establishment of the disease in naïve mice. In contrast, in vaccinated mice, the swift CD8+-T-cell response helps host survival after challenge.
Modeling Lung Cancer Risk in Case-Control Studies Using a New Dose Metric of Smoking
Authors: Thurston Sally W. , Liu Geoffrey , Miller David P. , Christiani David C. 
Published: March 2006

Abstract
Many approaches have been taken to adjust for smoking in modeling cancer risk. In case-control studies, these metrics are often used arbitrarily rather than being based on the properties of the metric in the context of the study. Depending on the underlying study design, hypotheses, and base population, different metrics may be deemed most appropriate. We present our approach to evaluating different smoking metrics. We examine the properties of a new metric, “logcig-years”, that we initially derived from using a biological model of DNA adduct formation. We compare this metric to three other smoking metrics, namely pack-years, square-root pack-years, and a model in which smoking duration and intensity are separate variables. Our comparisons use generalized additive models and logistic regression to examine the relationship between the logit probability of cancer and each of the metrics, adjusting for other covariates. All models were fit using data from a lung cancer study of 1,275 cases and 1,269 controls that has focused on gene-smoking relationships. There was a very significant, linear relationship between logcig-years and the logit probability of lung cancer in this sample, without any need to adjust for smoking status. These properties together were not shared by the other metrics. In this sample, logcig-years captured more information about smoking that is important in lung cancer risk than the other metrics. In conclusion, we provide a general framework for evaluating different smoking metrics in studies where smoking is a critical variable.
Genetic Variation in the Growth Hormone Synthesis Pathway in Relation to Circulating Insulin-Like Growth Factor-I, Insulin-Like Growth Factor Binding Protein-3, and Breast Cancer Risk: Results from the European Prospective Investigation into Cancer and Nutrition Study
Authors: Canzian Federico , McKay James D. , Cleveland Rebecca J. , Dossus Laure , Biessy Carine , Boillot Catherine , Rinaldi Sabina , Llewellyn Midge , Chajès Véronique , Clavel-Chapelon Françoise , Téhard Bertrand , Chang-Claude Jenny , Linseisen Jakob , Lahmann Petra H. , Pischon Tobias , Trichopoulos Dimitrios , Trichopoulou Antonia , Zilis Dimosthenes , Palli Domenico , Tumino Rosario , Vineis Paolo , Berrino Franco , Bueno-de-Mesquita H. Bas , van Gils Carla H. , Peeters Petra H.M. , Pera Guillem , Barricarte Aurelio , Chirlaque María-Dolores , Quirós J. Ramon , Larrañaga Nerea , Martínez-García Carmen , Allen Naomi E. , Key Timothy J. , Bingham Sheila A. , Khaw Kay-Tee , Slimani Nadia , Norat Teresa , Riboli Elio , Kaaks Rudolf 
Published: March 2006

Abstract
Insulin-like growth factor-I (IGF-I) stimulates cell proliferation and can enhance the development of tumors in different organs. Epidemiologic studies have shown that an elevated level of circulating IGF-I is associated to increased risk of breast cancer as well as other cancers. Genetic variants affecting the release or biological action of growth hormone (GH), the main stimulator of IGF-I production, may predict circulating levels of IGF-I and have an effect on cancer risk. We tested this hypothesis with a large case-control study of 807 breast cancer patients and 1,588 matched control subjects nested within the European Prospective Investigation into Cancer and Nutrition. We genotyped 22 common single nucleotide polymorphisms in 10 genes involved in GH production and action (GHRH, GHRHR, SST, SSTR1-SSTR5, POU1F1, and GH1), and in parallel, we measured serum levels of IGF-I and IGFBP-3, its major binding protein, in samples of cases and controls. SST and SSTR2 polymorphisms showed weak but statistically significant associations with breast cancer risk. SSTR5 polymorphisms were associated with IGF-I levels, whereas one polymorphism in GHRHR and one in POU1F1 were associated with IGFBP-3 levels. Our conclusion is that common genetic variation in the GH synthesis pathway, as measured by single nucleotide polymorphisms selected in the present study, is not a major determinant of IGF-I and IGFBP-3 circulating levels, and it does not play a major role in altering breast cancer risk.
Role of Lipid Peroxidation in the Epidemiology and Prevention of Breast Cancer
Authors: Gago-Dominguez Manuela , Castelao J. Esteban , Pike Malcolm C. , Sevanian Alex , Haile Robert W. 
Published: March 2006

Abstract
We have recently proposed a common mechanistic pathway by which obesity and hypertension lead to increased renal cell cancer risk. Our hypothesis posits lipid peroxidation, which is a principal mechanism in rodent renal carcinogenesis, as an intermediate step that leads to a final common pathway shared by numerous observed risks (including obesity, hypertension, smoking, oophorectomy/hysterectomy, parity, preeclampsia, diabetes, and analgesics) or protective factors (including oral contraceptive use and alcohol) for renal cell cancer [Cancer Causes Control 2002;13:287–93]. During this exercise, we have noticed how certain risk factors for renal cell carcinoma are protective for breast cancer and how certain protective factors for renal cell carcinoma increase risk for breast cancer. Parity and oophorectomy, for example, are positively associated with renal cell carcinoma but are negatively associated with breast cancer. Similarly, obesity and hypertension are positively associated with renal cell carcinoma, but obesity is negatively associated with breast cancer in premenopausal women and hypertension during pregnancy is negatively associated with breast cancer. Furthermore, alcohol intake, negatively associated with renal cell carcinoma, is also positively associated with breast cancer. We propose here the possibility that lipid peroxidation may represent a protective mechanism in breast cancer. Although this runs counter to the conventional view that lipid peroxidation is a process that is harmful and carcinogenic, we present here the chemical and biological rationale, based on epidemiologic and biochemical data, which may deserve further consideration and investigation. (Cancer Epidemiol Biomarkers Prev 2005;14(12):2829–39)
Prostate Cancer Screening Behavior in Men from Seven Ethnic Groups: the Fear Factor
Authors: Consedine Nathan S. , Morgenstern Amy H. , Kudadjie-Gyamfi Elizabeth , Magai Carol , Neugut Alfred I. 
Published: March 2006

AbstractRates of prostate cancer screening are known to vary among the major ethnic groups. However, likely variations in screening behavior among ethnic subpopulations and the likely role of psychological characteristics remain understudied. We examined differences in prostate cancer screening among samples of 44 men from each of seven ethnic groups (N = 308; U.S.-born European Americans, U.S.-born African Americans, men from the English-speaking Caribbean, Haitians, Dominicans, Puerto Ricans, and Eastern Europeans) and the associations among trait fear, emotion regulatory characteristics, and screening. As expected, there were differences in the frequency of both digital rectal exam (DRE) and prostate-specific antigen (PSA) tests among the groups, even when demographic factors and access were controlled. Haitian men reported fewer DRE and PSA tests than either U.S.-born European American or Dominican men, and immigrant Eastern European men reported fewer tests than U.S.-born European Americans; consistent with prior research, U.S.-born African Americans differed from U.S.-born European Americans for DRE but not PSA frequency. Second, the addition of trait fear significantly improved model fit, as did the inclusion of a quadratic, inverted U, trait fear term, even where demographics, access, and ethnicity were controlled. Trait fear did not interact with ethnicity, suggesting its effect may operate equally across groups, and adding patterns of information processing and emotion regulation to the model did not improve model fit. Overall, our data suggest that fear is among the key psychological determinants of male screening behavior and would be usefully considered in models designed to increase male screening frequency. (Cancer Epidemiol Biomarkers Prev 2006;15(2):228–37)
Dietary Patterns and Risk of Prostate Cancer in U.S. Men
Authors: Wu Kana , Hu Frank B. , Willett Walter C. , Giovannucci Edward 
Published: March 2006

Abstract
We prospectively investigated the associations between dietary patterns and risk of prostate cancer in the Health Professionals Follow-up Study. Between 1986 and 2000, 3,002 incident prostate cancer cases were identified in our cohort. Using factor analysis, two major dietary patterns were identified, a prudent and a western dietary pattern. Dietary patterns were not appreciably associated with risk of total prostate cancer. For the highest versus the lowest quintiles, the multivariable relative risk (RR) for the prudent pattern was 0.94 [95% confidence interval (CI), 0.83-1.06], and for the western pattern, the multivariable RR was 1.03 (95% CI, 0.92-1.17). Neither were these associated with risk of advanced prostate cancer [highest versus lowest quintile, prudent pattern (RR, 1.01; 95% CI, 0.68-1.49); western pattern (RR, 1.13; 95% CI, 0.77-1.67)]. Higher western pattern scores were suggestively associated with a greater risk of advanced prostate cancer among older men [highest versus lowest quintile (RR, 1.35; 95% CI, 0.97-1.90)], but not after adding processed meat to the model [highest versus lowest quintile (RR, 1.11; 95% CI, 0.75-1.65)]. We did not find any evidence for a protective association between prudent pattern and risk of prostate cancer. The lack of association between a western dietary pattern as identified by factor analysis in our cohort and prostate cancer risk suggests that dietary risk factors for prostate cancer are likely to differ from those for other conditions, such as cardiovascular disease and type 2 diabetes, that have been associated with a western dietary pattern in this cohort. (Cancer Epidemiol Biomarkers Prev 2006;15(1):167–71)
Associations of Mammographic Density with Dietary Factors in Japanese Women
Authors: Nagata Chisato , Matsubara Tomoko , Fujita Hiroshi , Nagao Yasuko , Shibuya Chiken , Kashiki Yoshitomo , Shimizu Hiroyuki 
Published: March 2006

Abstract
Background: A high percentage of mammographic dense area has been strongly associated with a risk of beast cancer. The present cross-sectional study evaluated the relations of percent density with dietary factors, such as fats, protein, dietary fiber, and soy isoflavones.
Methods: Study subjects were 601 (348 premenopausal and 253 postmenopausal) Japanese women who were recruited from a mammographic screening center. The size of the total breast area and the dense area were measured quantitatively using an automated mammographic mass detection method. Intakes of nutrients were estimated with a validated semiquantitative food-frequency questionnaire.
Results: The crude means of the percent density were 39.2% and 18.9% in premenopausal and postmenopausal women, respectively. There were no significant associations of any dietary factors with the percent density in premenopausal women. In postmenopausal women, percent density was significantly positively associated with intakes of protein, total fat, and saturated fat after controlling for covariates; the increase in the means of percent density were 7.2%, 5.6%, and 9.2% in the highest versus lowest quartile of intakes for protein, total fat, and saturated fat, respectively (P for linear trend were 0.006, 0.04, and 0.01, respectively). Carbohydrate intake was inversely associated with percent density; the mean of percent density was 6.0% lower in the highest versus the lowest quartile of intake (Ptrend = 0.03). The associations of dietary factors with dense area were very similar to those with percent density.
Conclusion: These dietary factors may have implications for the risk of breast cancer in postmenopausal women. (Cancer Epidemiol Biomarkers Prev 2005;14(12):2877–80)
Body Mass Index and Serum 1,1,1-Trichloro-2,2-Bis(p-Chlorophenyl)Ethane in Nulliparous Chinese Women
Authors: Perry Melissa J. , Ouyang Fengxiu , Korrick Susan , Venners Scott A. , Altshul Larisa , Xu Xiping , Wang Xiaobin 
Published: March 2006

Abstract
Background: Basic health indicators, such as body mass index (BMI), have been associated with serum 1,1,1-trichloro-2,2-bis(p-chlorophenyl)ethane/1,1-dichloro-2,2-bis(p-chlorophenyl)ethylene (DDT/DDE) levels; however, both positive and inverse associations of BMI with serum DDT/DDE have been reported. Given the association of BMI with a number of outcomes, it may confound studies of DDT/DDE-associated health effects. We investigated the relationship of BMI with serum DDT/DDE accounting for other determinants of exposure among women with relatively recent environmental exposures to DDT.
Methods: Serum DDT/DDE was analyzed in 466 nonsmoking, nulliparous women recruited from Anhui province in China between 1996 and 1998 as part of a reproductive health study of textile workers. The women in the sample were born between 1963 and 1977, 8 to 21 years before China's 1984 DDT ban. We used multivariate linear regression to investigate associations of BMI, age, and birth year with serum DDT/DDE.
Results: Mean (SD) serum total DDT concentration was 32 ng/g (17.8 ng/g). Birth year showed an inverse relationship with serum DDT independent of age. Despite limited variability in BMI, there was a consistent inverse relationship between BMI and serum DDT. Specifically, each kg/m2 increase in BMI was associated with a −1.34 ng/g (95% confidence interval, −2.12 to −0.56 ng/g) decrease in serum total DDT.
Conclusions: There were high total DDT levels in this sample of nulliparous Chinese women relative to Western populations, birth year was more strongly associated with serum DDT than age, and BMI was inversely related to serum DDT in this study.
A Randomized Trial of an Intervention to Increase Fruit and Vegetable Intake in Curatively Treated Patients with Early-Stage Head and Neck Cancer
Authors: Cartmel Brenda , Bowen Deborah , Ross Douglas , Johnson Elizabeth , Mayne Susan T. 
Published: March 2006

AbstractThe leading cause of death in patients who have had curatively treated early-stage head and neck cancer is a second primary cancer of the upper aerodigestive tract (lung, esophagus, larynx, pharynx, and oral cavity cancers). Low fruit and vegetable intake has been associated with increased risk of primary head and neck cancer and the available data suggest that increasing intake following diagnosis may reduce the risk of a second primary cancer. The goal of this study was to develop and test an easily administered intervention to increase fruit and vegetable intake in these patients following diagnosis and treatment. The 6-month intervention was based on the Stage of Change model. Seventy-five early-stage head and neck cancer patients were randomized to either the intervention group or to the “blinded” control group, with diet change data available on 65 patients. Fruit and vegetable intake, assessed using a food frequency questionnaire, and plasma carotenoid concentrations were measured at baseline and at the end of the study period. The change in self-reported intake of fruit and vegetables (servings per day) over the study period was significantly greater (P = 0.009) in the intervention group (n = 35; +2.1) compared with the control group (n = 30; +0.5). Total plasma carotenoids, a biomarker of fruit and vegetable intake, increased by 70 nmol/L in the intervention group as compared with a reduction of 42 nmol/L in the control group, a relative difference of 12% (nonsignificant). An intervention that can be delivered in a physician's office resulted in a significant increase in intake of fruit and vegetables in early-stage head and neck cancer patients. (Cancer Epidemiol Biomarkers Prev 2005;14(12):2848-54)