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Search Results: 1 - 10 of 97520 matches for " Guillermo I Perez-Perez "
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Correction: Early-Life Family Structure and Microbially Induced Cancer Risk
Martin J Blaser,Abraham Nomura,James Lee,Grant N Stemmerman,Guillermo I Perez-Perez
PLOS Medicine , 2007, DOI: 10.1371/journal.pmed.0040100
Abstract:
Early-Life Family Structure and Microbially Induced Cancer Risk
Martin J Blaser ,Abraham Nomura,James Lee,Grant N Stemmerman,Guillermo I Perez-Perez
PLOS Medicine , 2007, DOI: 10.1371/journal.pmed.0040007
Abstract: Background Cancer may follow exposure to an environmental agent after many decades. The bacterium Helicobacter pylori, known to be acquired early in life, increases risk for gastric adenocarcinoma, but other factors are also important. In this study, we considered whether early-life family structure affects the risk of later developing gastric cancer among H. pylori+ men. Methods and Findings We examined a long-term cohort of Japanese-American men followed for 28 y, and performed a nested case-control study among those carrying H. pylori or the subset carrying the most virulent cagA+ H. pylori strains to address whether family structure predicted cancer development. We found that among the men who were H. pylori+ and/or cagA+ (it is possible to be cagA+ and H. pylori? if the H. pylori test is falsely negative), belonging to a large sibship or higher birth order was associated with a significantly increased risk of developing gastric adenocarcinoma late in life. For those with cagA+ strains, the risk of developing gastric cancer was more than twice as high (odds ratio 2.2; 95% confidence interval 1.2–4.0) among those in a sibship of seven or more individuals than in a sibship of between one and three persons. Conclusions These results provide evidence that early-life social environment plays a significant role in risk of microbially induced malignancies expressing five to eight decades later, and these findings lead to new models to explain these interactions.
The effect of H. pylori eradication on meal-associated changes in plasma ghrelin and leptin
Fritz Francois, Jatin Roper, Neal Joseph, Zhiheng Pei, Aditi Chhada, Joshua R Shak, Asalia de Perez, Guillermo I Perez-Perez, Martin J Blaser
BMC Gastroenterology , 2011, DOI: 10.1186/1471-230x-11-37
Abstract: Veterans referred for upper GI endoscopy were evaluated at baseline and ≥8 weeks after endoscopy, and H. pylori status and body weight were ascertained. During the first visit in all subjects, and during subsequent visits in the initially H. pylori-positive subjects and controls, blood was collected after an overnight fast and 1 h after a standard high protein meal, and levels of eight hormones determined.Of 92 enrolled subjects, 38 were H. pylori-negative, 44 H. pylori-positive, and 10 were indeterminate. Among 23 H. pylori-positive subjects who completed evaluation after treatment, 21 were eradicated, and 2 failed eradication. After a median of seven months following eradication, six hormones related to energy homeostasis showed no significant differences, but post-prandial acylated ghrelin levels were nearly six-fold higher than pre-eradication (p = 0.005), and median integrated leptin levels also increased (20%) significantly (p < 0.001). BMI significantly increased (5 ± 2%; p = 0.008) over 18 months in the initially H. pylori-positive individuals, but was not significantly changed in those who were H. pylori-negative or indeterminant at baseline.Circulating meal-associated leptin and ghrelin levels and BMI changed significantly after H. pylori eradication, providing direct evidence that H. pylori colonization is involved in ghrelin and leptin regulation, with consequent effects on body morphometry.The healthful regulation of energy homeostasis in humans, depends on centrally-acting hormones such as ghrelin and leptin [1,2]. Serum ghrelin concentrations increase during fasting, and decrease after eating [3]; ghrelin decreases energy expenditure and promotes weight gain [4]. In contrast, leptin produced primarily by adipocytes, reduces appetite and increases energy utilization [5]. The gastric epithelium expresses both ghrelin and leptin (and their receptors) [6,7]; inflammation can modify their production [8,9].Helicobacter pylori, which colonizes the human stom
Asthma Is Inversely Associated with Helicobacter pylori Status in an Urban Population
Joan Reibman, Michael Marmor, Joshua Filner, Maria-Elena Fernandez-Beros, Linda Rogers, Guillermo I. Perez-Perez, Martin J. Blaser
PLOS ONE , 2008, DOI: 10.1371/journal.pone.0004060
Abstract: Background Microbial exposures have been suggested to confer protection from allergic disorders and reduced exposures to gastrointestinal microbiota have been proposed as an explanation for the increase in asthma prevalence. Since the general prevalence of Helicobacter pylori has been decreasing, we hypothesized that H. pylori serostatus would be inversely related to the presence of asthma. Methods Adults were recruited to participate in the New York University (NYU)/Bellevue Asthma Registry in New York City. Adult asthma cases (N = 318) and controls (N = 208) were identified and serum IgG antibodies to H. pylori whole cell antigens or the immunodominant CagA antigen were measured. Results As expected, the asthma cases and controls differed with respect to atopy and lung function. Seropositivity to H. pylori or CagA antigen was present in 47.1% of the total case and control study population. Asthma was inversely associated with CagA seropositivity (OR = 0.57, 95% CI = 0.36–0.89). Median age of onset of asthma (doctor's diagnosis) was older (21 years) among individuals with CagA+ strains than among H. pylori- individuals (11 years) (p = 0.006). Conclusion These data are consistent with the hypothesis that colonization with CagA+ H. pylori strains is inversely associated with asthma and is associated with an older age of asthma onset in an urban population. The data suggest H. pylori as a marker for protection. Trial Registration ClinicalTrials.gov NCT00212537
Comparative Genome Analysis of Campylobacter fetus Subspecies Revealed Horizontally Acquired Genetic Elements Important for Virulence and Niche Specificity
Sabine Kienesberger, Hanna Sprenger, Stella Wolfgruber, Bettina Halwachs, Gerhard G. Thallinger, Guillermo I. Perez-Perez, Martin J. Blaser, Ellen L. Zechner, Gregor Gorkiewicz
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0085491
Abstract: Campylobacter fetus are important animal and human pathogens and the two major subspecies differ strikingly in pathogenicity. C. fetus subsp. venerealis is highly niche-adapted, mainly infecting the genital tract of cattle. C. fetus subsp. fetus has a wider host-range, colonizing the genital- and intestinal-tract of animals and humans. We report the complete genomic sequence of C. fetus subsp. venerealis 84-112 and comparisons to the genome of C. fetus subsp. fetus 82-40. Functional analysis of genes predicted to be involved in C. fetus virulence was performed. The two subspecies are highly syntenic with 92% sequence identity but C. fetus subsp. venerealis has a larger genome and an extra-chromosomal element. Aside from apparent gene transfer agents and hypothetical proteins, the unique genes in both subspecies comprise two known functional groups: lipopolysaccharide production, and type IV secretion machineries. Analyses of lipopolysaccharide-biosynthesis genes in C. fetus isolates showed linkage to particular pathotypes, and mutational inactivation demonstrated their roles in regulating virulence and host range. The comparative analysis presented here broadens knowledge of the genomic basis of C. fetus pathogenesis and host specificity. It further highlights the importance of surface-exposed structures to C. fetus pathogenicity and demonstrates how evolutionary forces optimize the fitness and host-adaptation of these pathogens.
Assessment of the toll-like receptor 4 Asp299Gly, Thr399Ile and interleukin-8 -251 polymorphisms in the risk for the development of distal gastric cancer
Elvira Garza-Gonzalez, Francisco J Bosques-Padilla, Sandra I Mendoza-Ibarra, Juan P Flores-Gutierrez, Hector J Maldonado-Garza, Guillermo I Perez-Perez
BMC Cancer , 2007, DOI: 10.1186/1471-2407-7-70
Abstract: Our aim was to investigate whether the presence of the TLR4 Asp299Gly, TLR4 Thr399Ile and IL-8-251 A/T polymorphisms had any influence in the development of distal GC in a Mexican population.We studied 337 patients that were divided in two groups: 78 patients with histologically confirmed distal GC and 259 non-cancer controls. The presence of H. pylori in the control population was defined by positive results of at least two of four diagnostic tests: serology, histology, rapid urease test and culture. Human DNA was purified and genotyped for TLR4 Asp299Gly polymorphism by pyrosequencing, for TLR4 Thr399Ile by PCR-RFLP and for IL8-251 by the amplification refractory mutation system (ARMS)-PCR.The non-cancer control group was found to be in Hardy-Weinberg equilibrium at the polymorphic loci studied (chi-square H-W = 0.58 for IL8-251, 0.42 for TLR4 Asp299Gly and 0.17 for TLR4 Thr399Ile). The frequencies of mutated alleles (homozygous plus heterozygous) were compared between cases and controls. We found no significant difference for TLR4- Asp299Gly [the 7.7% of distal GC patients and 7.7 % non-cancer controls (p = 0.82)] and for TLR4 Thr399Ile [the 1.3% of GC patients and the 5% of the control population (p = 0.2)]. In contrast, for IL-8-251 A/T, 80.77% of the GC patients and 66.4% in the control group age and gender matched had at least one copy of mutated allele (OR = 2.12, 95% CI = 1.1–4.2) (p = 0.023).This study showed that the IL8-251*A allele could be related to the development of distal gastric cancer in this Mexican population.Helicobacter pylori almost exclusively colonize the mucous layer of the human stomach and reside in the host for years, decades or maybe lifelong. In approximately 10% of cases, the organism is associated with diverse clinical outcomes, including non-ulcer dyspepsia, peptic ulcer disease, and distal gastric cancer [1].Both host and environmental factors have been associated with this clinical diversity. Host factors are mainly related to t
Serologic host response to Helicobacter pylori and Campylobacter jejuni in socially housed Rhesus macaques (Macaca mulatta)
Sabine Kienesberger, Guillermo I Perez-Perez, Juan L Rivera-Correa, Rafael Tosado-Acevedo, Huilin Li, Andre Dubois, Janis A Gonzalez-Martinez, Maria Dominguez-Bello, Martin J Blaser
Gut Pathogens , 2012, DOI: 10.1186/1757-4749-4-9
Abstract: Two cohorts of monkeys were analyzed. The first cohort consisted of 30 monkeys and was used to establish an enzyme-linked immunosorbent assay (ELISA) for H. pylori antibodies detection. To evaluate colonization of those macaques, stomach biopsies were collected and analyzed for the presence of H. pylori by histology and culture. C. jejuni ELISAs were established using human serum with known C. jejuni antibody status. Next, plasma samples of the 89 macaques (Cohort 2) were assayed for antibodies and then statistically analyzed.An H. pylori IgG ELISA, which was 100% specific and 93% sensitive, was established. In contrast, the IgA ELISA was only 82% specific and 61% sensitive. The CagA IgG assay was 100% sensitive and 61% of the macaques were positive. In cohort 2, 62% macaques were H. pylori sero-positive and 52% were CagA positive. The prevalence of H. pylori IgG and CagA IgG increased with monkey age as described for humans. Of the 89 macaques 52% showed IgG against C. jejuni but in contrast to H. pylori, the sero-prevalence was not associated with increasing age. However, there was a drop in the IgG (but not in IgA) mean values between infant and juvenile macaques, similar to trends described in humans.Rhesus macaques have widespread exposure to H. pylori and C. jejuni, reflecting their social conditions and implying that Rhesus macaques might provide a model to study effects of these two important human mucosal bacteria on a population.Helicobacter pylori are Gram-negative bacteria that colonize the gastric mucosa of humans across the world. However, H. pylori is disappearing from populations in developed countries [1,2]. In developing countries, up to 90% of the adult population carries the organism [3,4]. H. pylori is acquired early in life [5,6] and generally persists unless hosts are treated with antibiotics [1]. Gastric H. pylori colonization increases risk of peptic ulcer disease as well as adenocarcinoma of the distal stomach [7]. In addition to negative e
A blow up condition for a nonautonomous semilinear system
Aroldo Perez-Perez
Electronic Journal of Differential Equations , 2006,
Abstract: We give a sufficient condition for finite time blow up of the nonnegative mild solution to a nonautonomous weakly coupled system with fractal diffusion having a time dependent factor which is continuous and nonnegative.
Helicobacter pylori Seropositivity and Risk of Lung Cancer
Jill Koshiol, Roberto Flores, Tram K. Lam, Philip R. Taylor, Stephanie J. Weinstein, Jarmo Virtamo, Demetrius Albanes, Guillermo Perez-Perez, Neil E. Caporaso, Martin J. Blaser
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0032106
Abstract: Lung cancer is the leading cause of cancer mortality worldwide. Helicobacter pylori (H. pylori) is a risk factor for distal stomach cancer, and a few small studies have suggested that H. pylori may be a potential risk factor for lung cancer. To test this hypothesis, we conducted a study of 350 lung adenocarcinoma cases, 350 squamous cell carcinoma cases, and 700 controls nested within the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study (ATBC) cohort of male Finnish smokers. Controls were one-to-one matched by age and date of baseline serum draw. Using enzyme-linked immunosorbent assays to detect immunoglobulin G antibodies against H. pylori whole-cell and cytotoxin-associated gene (CagA) antigens, we calculated odds ratios (ORs) and 95% confidence intervals (95% CIs) for associations between H. pylori seropositivity and lung cancer risk using conditional logistic regression. H. pylori seropositivity was detected in 79.7% of cases and 78.5% of controls. After adjusting for pack-years and cigarettes smoked per day, H. pylori seropositivity was not associated with either adenocarcinoma (OR: 1.1, 95% CI: 0.75–1.6) or squamous cell carcinoma (OR: 1.1, 95% CI: 0.77–1.7). Results were similar for CagA-negative and CagA-positive H. pylori seropositivity. Despite earlier small studies suggesting that H. pylori may contribute to lung carcinogenesis, H. pylori seropositivity does not appear to be associated with lung cancer.
mRNA levels of TLR4 and TLR5 are independent of H pylori
Elvira Garza-González, Virgilio Bocanegra-García, Francisco Javier Bosques-Padilla, Juan Pablo Flores-Gutiérrez, Francisco Moreno, Guillermo Ignacio Perez-Perez
World Journal of Gastroenterology , 2008,
Abstract: AIM: To determine if the presence H pylori or its virulence affect toll-like receptor 4 (TLR4) and TLR5 mRNA expression levels.METHODS: For the in vivo assays, gastric biopsies were obtained from 40 patients and H pylori status was determined. For the in vitro assays, human gastric adenocarcinoma mucosal cells (AGS) were cultured in the presence or absence of twelve selected H pylori strains. H pylori strains isolated from culture-positive patients and selected strains were genotyped for cagA and vacA. The cDNA was obtained from mRNA extracted from biopsies and from infected AGS cells. TLR4 and TLR5 mRNA levels were examined by real-time PCR.RESULTS: The presence of H pylori did not affect the mRNA levels of TLR4 or TLR5 in gastric biopsies. The mRNA levels of both receptors were not influenced by the vacA status (P > 0.05 for both receptors) and there were no differences in TLR4 or TLR5 mRNA levels among the different clinical presentations/histological findings (P > 0.05). In the in vitro assay, the mRNA levels of TLR4 or TLR5 in AGS cells were not influenced by the vacAs1 status or the clinical condition associated with the strains (P > 0.05 for both TLR4 and TLR5).CONCLUSION: The results of this study show that the mRNA levels of TLR4 and TLR5 in gastric cells, both in vivo and in vitro, are independent of H pylori colonization and suggest that vacA may not be a significant player in the first step of innate immune recognition mediated by TLR4 or TLR5.
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