Associations between smoking, passive smoking, GSTM-1, NAT2, and rectal cancer.
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Cigarette smoking has been identified as a risk factor for colon cancer, however, much less is known about the association between cigarette smoking and rectal cancer. The purpose of this article is to evaluate the associations between rectal cancer and active and passive cigarette smoking and other forms of tobacco use. We also evaluate how genetic variants of GSTM-1 and NAT2 alter these associations. A population-based case-control study of 952 incident rectal cancer cases and 1205 controls was conducted. Detailed tobacco use information was collected as part of an interviewer-administered questionnaire. DNA was extracted from blood to examine genetic variants of GSTM-1 and NAT2. Cigarette smoking was associated with an increased risk of rectal cancer in men [odds ratio (OR)=1.5, 95% confidence interval (CI), 1.1-2.1 for current smokers; OR=1.7, 95% CI, 1.3-2.3 for smoking >20 pack-years of cigarettes relative to never-smokers]. After adjusting for active smoking, exposure to cigarette smoke of others also was associated with increased risk among men (OR=1.5, 95% CI, 1.1-2.0). Neither GSTM-1 genotype nor NAT2-imputed phenotype was independently associated with rectal cancer. However, the risk associated with smoking cigarettes among those who were GSTM-1 null relative to those who never smoked and had the GSTM-1 present genotype was OR=2.0 (95% CI, 1.2-3.3). This interaction was of borderline significance (P=0.08). Men who had the combined GSTM-1 present genotype and who were rapid acetylators had no increased risk from cigarette smoking. There were no significant associations between cigarette smoking and rectal cancer among women. This study shows that men who smoke cigarettes, especially those who smoke >20 pack-years, are at increased risk of rectal cancer. This association may be influenced by GSTM-1 genotype. Furthermore, exposure to cigarette smoke of others may increase risk of rectal cancer among men who do not smoke. (+info)
Predisposition locus for major depression at chromosome 12q22-12q23.2.
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Major depression disorder is a common psychiatric disease with a major economic impact on society. In many cases, no effective treatment is available. The etiology of major depression is complex, but it is clear that the disease is, to a large extent, determined genetically, especially among individuals with a familial history of major depression, presumably through the involvement of multiple predisposition genes in addition to an environmental component. As a first step toward identification of chromosomal loci contributing to genetic predisposition to major depression, we have conducted a genomewide scan by using 628 microsatellite markers on 1,890 individuals from 110 Utah pedigrees with a strong family history of major depression. We identified significant linkage to major depression in males at marker D12S1300 (multipoint heterogeneity LOD score 4.6; P=.00003 after adjustment for multiple testing). With additional markers, the linkage evidence became highly significant, with the multipoint heterogeneity LOD score at marker D12S1706 increasing to 6.1 (P=.0000007 after adjustment for multiple testing). This study confirms the presence of one or more genes involved in psychiatric diseases on the q arm of chromosome 12 and provides strong evidence for the existence of a sex-specific predisposition gene to major depression at 12q22-q23.2. (+info)
Antioxidants, carotenoids, and risk of rectal cancer.
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Numerous properties suggest that antioxidants and carotenoids may be valuable chemopreventive agents. A population-based case-control study of 952 rectal cancer cases and 1,205 controls from Northern California and Utah was conducted between September 1997 and February 2002. Detailed diet history, medical history, and lifestyle factors interviews were conducted. Dietary antioxidants were not associated with rectal cancer risk in men. For women, relative to the highest level of intake, low intake of dietary lycopene (odds ratio (OR) = 1.7, 95% confidence interval (CI): 1.0, 2.8) or vitamin E (OR = 2.2, 95% CI: 1.1, 4.3) was associated with an increased risk of rectal cancer. Alpha-, beta-, and gamma-tocopherol were associated with an approximate twofold increased risk of rectal cancer in women. Associations were stronger for women aged > or = 60 years for vitamin E and tocopherols (alpha-tocopherol OR = 3.6, 95% CI: 1.4, 9.4; gamma-tocopherol OR = 5.3, 95% CI: 2.1, 13.2; delta-tocopherol OR = 1.9, 95% CI: 0.9, 4.0), except for beta-tocopherol, for which risk increased twofold for all women. Associations differed by estrogen status for beta-carotene, lycopene, and vitamin E. These results suggest that vitamin E and lycopene may modestly reduce the risk of rectal cancer in women. (+info)
Detection of pediatric respiratory and gastrointestinal outbreaks from free-text chief complaints.
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We conducted a retrospective study to ascertain the potential of free-text chief complaints collected in pediatric emergency departments to serve as surveillance data for early detection of outbreaks. We determined that automatically coded chief complaint data provide a signal that reflects outbreaks in a population of children less than five years of age. Using the Exponentially Weighted Moving Average (EWMA) detection algorithm, we measured the timeliness, sensitivity, and specificity of free-text chief complaints for predicting outbreaks of pediatric respiratory and gastrointestinal illness. We found that time series of automatically coded free text-chief complaints in pediatric patients correlate well with hospital admissions and precede them by the mean of 10.3 days (95% CI -15.15, 35.5) for respiratory outbreaks and 29 days (95% CI 4.23, 53.7) for gastrointestinal outbreaks. We conclude that free-text chief complaints may play an important role as an early, sensitive and specific indicator of outbreaks of respiratory and gastrointestinal illness in children less than five years of age. (+info)
Plant foods, fiber, and rectal cancer.
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BACKGROUND: Associations between colon and rectal cancer and intakes of vegetables, other plant foods, and fiber have stimulated much debate. OBJECTIVE: We examined the association between rectal cancer and plant food and fiber intakes. DESIGN: Data from 952 incident cases of rectal cancer were compared with data from 1205 population-based controls living in Utah or enrolled in the Kaiser Permanente Medical Care Program in northern California RESULTS: Rectal cancer was inversely associated with intakes of vegetables (odds ratio: 0.72; 95% CI: 0.54, 0.98), fruit (0.73; 0.53, 0.99), and whole-grain products (0.69; 0.51, 0.94), whereas a high intake of refined-grain products was directly associated with an increased risk of rectal cancer (1.42; 1.04, 1.92). Similarly, relative to low fiber intakes, high intakes of dietary fiber reduced the risk of rectal cancer (0.54; 0.37, 0.78). The reduced risk of rectal cancer associated with vegetable (0.48; 0.29, 0.80), fruit (0.63; 0.38, 1.06), and fiber (0.40; 0.22, 0.71) intakes was strongest for persons who received the diagnosis after age 65 y. A threshold effect at approximately 5 servings of vegetables/d was needed to see a reduced risk of rectal cancer. CONCLUSIONS: The results suggest that plant foods may be important in the etiology of rectal cancer in both men and women. Age at diagnosis appears to play an important role in the association. (+info)
Submersion injuries in children younger than 5 years in urban Utah.
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Submersion injuries of children younger than 5 years in 4 urban Utah counties from 1984 through 1988 were studied retrospectively to identify associated risk factors. Infants younger than 1 year had the highest rates of both submersion injuries and deaths. The incidence of bathtub drownings was 2 to 3 times higher than reported national rates. All bathtub drownings occurred while the victim was bathing with a young sibling (10 months to 7 years of age) without adult supervision. All drownings in pools and moving bodies of water (rivers, irrigation ditches) resulted from unintentional falls into the water rather than from swimming and wading activities. Drowning prevention strategies should focus on educating parents about the risk of young children bathing with siblings in the absence of adult supervision and fencing regulations for pools and open bodies of moving water. (+info)
Diazotrophic community structure and function in two successional stages of biological soil crusts from the Colorado Plateau and Chihuahuan Desert.
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The objective of this study was to characterize the community structure and activity of N2-fixing microorganisms in mature and poorly developed biological soil crusts from both the Colorado Plateau and Chihuahuan Desert. Nitrogenase activity was approximately 10 and 2.5 times higher in mature crusts than in poorly developed crusts at the Colorado Plateau site and Chihuahuan Desert site, respectively. Analysis of nifH sequences by clone sequencing and the terminal restriction fragment length polymorphism technique indicated that the crust diazotrophic community was 80 to 90% heterocystous cyanobacteria most closely related to Nostoc spp. and that the composition of N2-fixing species did not vary significantly between the poorly developed and mature crusts at either site. In contrast, the abundance of nifH sequences was approximately 7.5 times greater (per microgram of total DNA) in mature crusts than in poorly developed crusts at a given site as measured by quantitative PCR. 16S rRNA gene clone sequencing and microscopic analysis of the cyanobacterial community within both crust types demonstrated a transition from a Microcoleus vaginatus-dominated, poorly developed crust to mature crusts harboring a greater percentage of Nostoc and Scytonema spp. We hypothesize that ecological factors, such as soil instability and water stress, may constrain the growth of N2-fixing microorganisms at our study sites and that the transition to a mature, nitrogen-producing crust initially requires bioengineering of the surface microenvironment by Microcoleus vaginatus. (+info)
Aspirin, NSAIDs, and colorectal cancer: possible involvement in an insulin-related pathway.
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INTRODUCTION: Aspirin and nonsteroidal anti-inflammatory drugs (NSAIDs) have been shown to reduce risk of colorectal cancer. Although inhibition of cyclooxygenase (COX)-2 is generally thought to be the relevant mechanism, aspirin-like drugs apparently are involved in other pathways and mechanisms. We explore the associations between aspirin/NSAIDs, the insulin-related pathway, and the risk of colorectal cancer. METHODS: Genetic polymorphisms of five genes identified as being involved in an insulin-related pathway were genotyped using data collected in a case-control study of 1346 incident colon cancer cases and 1544 population-based controls and 952 incident rectal cancer cases and 1205 controls. Genotypes assessed were the 3' untranslated region poly(A) and the intron 8 BsmI polymorphisms of the VDR gene, a CA repeat polymorphism of the IGF1 gene, the A/C polymorphism at nucleotide -202 of the IGFBP3, the Gly972Arg polymorphism of the IRS1 gene, and the Gly1057Asp polymorphism of the IRS2 gene. RESULTS: Use of aspirin and NSAIDs was associated with a decreased risk of colorectal cancer, with slightly greater protection from NSAIDs than aspirin for rectal cancer. We observed a significant interaction between IRS1 genotype and aspirin/NSAIDs use and risk of colorectal cancer. Relative to the GR/RR IRS1 genotype, a protective effect from the GG IRS1 genotype was seen in those who did not use NSAIDs; use of NSAIDs was protective for all genotypes. These associations were especially strong for those diagnosed prior to age 65 (P interaction = 0.0006). We also observed a significant interaction between aspirin/NSAIDs use and the VDR gene. Having the SS or BB VDR genotypes reduced risk of colorectal cancer among non-aspirin/NSAID users; however, aspirin/NSAIDs reduced risk for all VDR genotypes. CONCLUSIONS: These data support the protective effect of aspirin and NSAIDs on colorectal cancer risk. In addition, the observed interactions for aspirin/NSAIDs and IRS1 and VDR genotypes suggest that mechanisms other than COX-2 inhibition may be contributing to the protective effect of aspirin and NSAIDs on colorectal cancer risk. (+info)