Trends in esophageal cancer and body mass index by race and gender in the state of Michigan

<p>Abstract</p> <p>Background</p> <p>Adenocarcinoma of the esophagus has been increasing in incidence in the U.S. over the past several decades, particularly among white males. The factors driving the racial disparity in adenocarcinomas rates are not well understood.</p> <p>Methods</p> <p>Here we examine trends in both esophageal cancer incidence and body mass index (BMI) in a geographically defined cohort by gender and race. Age-adjusted esophageal cancer incidence rates from 1985 to 2005 were calculated from data collected by the Michigan state cancer registry. Trends were analyzed along with trends in BMI data obtained from the Behavioral Risk Factor Survey administered by the Centers for Disease Control.</p> <p>Results</p> <p>Overall, age adjusted incidence rates in esophageal carcinoma increased from 4.49 to 4.72 cases/100,000 persons per year in Michigan from 1985 to 2005. Among white males, the rate of adenocarcinomas increased by 0.21 cases/100,000 per year to a maximum of 6.40 cases/100,000 in 1999, after which these rates remained constant. There was a slight but non-significant increase in the rate of adenocarcinomas among African American males, for whom the average incidence rate was 8 times lower than that for white males (0.58 vs 4.72 cases/100,000 person years). While average BMI is rising in Michigan (from 26.68 in 1988 to 30.33 in 2005), average BMI was slightly higher among African Americans on average, and the rates of increase in BMI were not different between African American males and white males.</p> <p>Conclusion</p> <p>The disparity between African American males and white males is not explained by ecological-level trends in BMI. Further research to identify the factors responsible for this disparity, possibly including anatomic fat distribution, are required.</p

Two common nonsynonymous paraoxonase 1 (PON1) gene polymorphisms and brain astrocytoma and meningioma

<p>Abstract</p> <p>Background</p> <p>Human serum paraoxonase 1 (PON1) plays a major role in the metabolism of several organophosphorus compounds. The enzyme is encoded by the polymorphic gene <it>PON1</it>, located on chromosome 7q21.3. Aiming to identify genetic variations related to the risk of developing brain tumors, we investigated the putative association between common nonsynonymous <it>PON1 </it>polymorphisms and the risk of developing astrocytoma and meningioma.</p> <p>Methods</p> <p>Seventy one consecutive patients with brain tumors (43 with astrocytoma grade II/III and 28 with meningioma) with ages ranging 21 to 76 years, and 220 healthy controls subjects were analyzed for the frequency of the nonsynonymous <it>PON1 </it>genotypes L55M rs854560 and Q192R rs662. All participants were adult Caucasian individuals recruited in the central area of Spain.</p> <p>Results</p> <p>The frequencies of the <it>PON1 </it>genotypes and allelic variants of the polymorphisms <it>PON1 </it>L55M and <it>PON1 </it>Q192R did not differ significantly between patients with astrocytoma and meningioma and controls. The minor allele frequencies were as follows: <it>PON1 </it>55L, 0.398, 0.328 and 0.286 for patients with astrocytoma, meningioma and control individuals, respectively; <it>PON1 </it>192R, 0.341, 0.362 and 0.302 for patients with astrocytoma, meningioma and control individuals, respectively. Correction for age, gender, or education, made no difference in odds ratios and the <it>p </it>values remained non-significant. Haplotype association analyses did not identify any significant association with the risk of developing astrocytoma or meningioma.</p> <p>Conclusions</p> <p>Common nonsynonymous <it>PON1 </it>polymorphisms are not related with the risk of developing astrocytoma and meningioma.</p

A review of the human vs. porcine female genital tract and associated immune system in the perspective of using minipigs as a model of human genital Chlamydia infection

International audienceAbstractSexually transmitted diseases constitute major health issues and their prevention and treatment continue to challenge the health care systems worldwide. Animal models are essential for a deeper understanding of the diseases and the development of safe and protective vaccines. Currently a good predictive non-rodent model is needed for the study of genital chlamydia in women. The pig has become an increasingly popular model for human diseases due to its close similarities to humans. The aim of this review is to compare the porcine and human female genital tract and associated immune system in the perspective of genital Chlamydia infection. The comparison of women and sows has shown that despite some gross anatomical differences, the structures and proportion of layers undergoing cyclic alterations are very similar. Reproductive hormonal cycles are closely related, only showing a slight difference in cycle length and source of luteolysing hormone. The epithelium and functional layers of the endometrium show similar cyclic changes. The immune system in pigs is very similar to that of humans, even though pigs have a higher percentage of CD4+/CD8+ double positive T cells. The genital immune system is also very similar in terms of the cyclic fluctuations in the mucosal antibody levels, but differs slightly regarding immune cell infiltration in the genital mucosa - predominantly due to the influx of neutrophils in the porcine endometrium during estrus. The vaginal flora in Göttingen Minipigs is not dominated by lactobacilli as in humans. The vaginal pH is around 7 in Göttingen Minipigs, compared to the more acidic vaginal pH around 3.5–5 in women. This review reveals important similarities between the human and porcine female reproductive tracts and proposes the pig as an advantageous supplementary model of human genital Chlamydia infection