University at Buffalo

About: University at Buffalo is a education organization based out in Buffalo, New York, United States. It is known for research contribution in the topics: Population & Poison control. The organization has 33773 authors who have published 63840 publications receiving 2278954 citations. The organization is also known as: UB & State University of New York at Buffalo.

Phytosterols as Anticancer Dietary Components: Evidence and Mechanism of Action

Abstract: Phytosterols (PS) or plant sterols are structurally similar to cholesterol. The most common PS are beta-sitosterol, campesterol and stigmasterol. Epidemiologic and experimental studies suggest that dietary PS may offer protection from the most common cancers in Western societies, such as colon, breast and prostate cancer. This review summarizes the findings of these studies and the possible mechanisms by which PS offer this protection. These include the effect of PS on membrane structure and function of tumor and host tissue, signal transduction pathways that regulate tumor growth and apoptosis, immune function of the host and cholesterol metabolism by the host. In addition, suggestions for future studies to fill the gaps in our knowledge have been given.

Genome-wide association study identifies variants in the ABO locus associated with susceptibility to pancreatic cancer

Abstract: We conducted a two-stage genome-wide association study of pancreatic cancer, a cancer with one of the lowest survival rates worldwide. We genotyped 558,542 SNPs in 1,896 individuals with pancreatic cancer and 1,939 controls drawn from 12 prospective cohorts plus one hospital-based case-control study. We conducted a combined analysis of these groups plus an additional 2,457 affected individuals and 2,654 controls from eight case-control studies, adjusting for study, sex, ancestry and five principal components. We identified an association between a locus on 9q34 and pancreatic cancer marked by the SNP rs505922 (combined P = 5.37 x 10(-8); multiplicative per-allele odds ratio 1.20; 95% confidence interval 1.12-1.28). This SNP maps to the first intron of the ABO blood group gene. Our results are consistent with earlier epidemiologic evidence suggesting that people with blood group O may have a lower risk of pancreatic cancer than those with groups A or B.

Effects of long-term selenium supplementation on the incidence of type 2 diabetes: a randomized trial.

Abstract: Background Findings from animal models suggest that selenium supplementation improves glucose metabolism. Objective To examine the effect of long-term selenium supplementation on the incidence of type 2 diabetes. Design Secondary analysis of a randomized, double-blind, placebo-controlled trial. Setting Areas of low selenium consumption of the eastern United States. Patients 1202 persons seen in dermatology clinics who did not have type 2 diabetes at baseline. Intervention Oral administration of selenium, 200 microg/d, or placebo. Measurements Incidence of type 2 diabetes. Results During an average follow-up of 7.7 years (SD, 2.7), type 2 diabetes developed in 58 selenium recipients and 39 placebo recipients (incidence, 12.6 cases per 1000 person-years vs. 8.4 cases per 1000 person-years, respectively; hazard ratio, 1.55 [95% CI, 1.03 to 2.33]). The lack of benefit of selenium supplementation on the incidence of type 2 diabetes persisted in analyses stratified by age, sex, body mass index, and smoking status. An exposure-response gradient was found across tertiles of baseline plasma selenium level, with a statistically significantly increased risk for type 2 diabetes in the highest tertile of baseline plasma selenium level (hazard ratio, 2.70 [CI, 1.30 to 5.61]). Limitations Diabetes was a secondary outcome in the parent trial. Diagnoses of diabetes were self-reported but were validated in most participants. The sample was mostly older and white. Conclusions Selenium supplementation does not seem to prevent type 2 diabetes, and it may increase risk for the disease. Click here for related information on selenium.

Bacterial Infection in Chronic Obstructive Pulmonary Disease in 2000: a State-of-the-Art Review

Abstract: It is estimated that in 1995, 16.4 million people in the United States suffered from chronic obstructive pulmonary disease (COPD) (226). COPD is also the fourth most common cause of death in the United States (14). Both the prevalence of and mortality from this disease have been increasing worldwide (118, 226, 330). COPD is defined physiologically by the presence of irreversible or partially reversible airway obstruction in patients with chronic bronchitis and/or emphysema (14). Chronic bronchitis is defined clinically by the presence of cough with sputum production for most days of at least 3 months a year for 2 consecutive years (200). Other causes of chronic cough need to be excluded. Emphysema is defined pathologically as permanent dilation of the airspaces distal to the terminal bronchioles, accompanied by destruction of the alveolar septa in the absence of fibrosis (292). More than 80% of COPD cases encountered in the Western world are related to tobacco smoke exposure. Occupational exposures and alpha-1 antitrypsin deficiency are uncommon precedents for the development of COPD (177, 234). Several potential contributions of bacterial infection to the etiology, pathogenesis, and clinical course of COPD can be identified (219). However, the precise role of bacterial infection in COPD has been a source of controversy for several decades (175, 296, 307). Opinion regarding the contribution of bacteria to the pathogenesis of COPD has ranged from the idea that it has a preeminent role (along with mucus hypersecretion) as embodied in the British hypothesis in the 1950s and 1960s, to the idea that it is a mere epiphenomenon in the 1970s and 1980s (200, 296, 307). In the last decade, new research techniques have become available, and traditionally noninfectious diseases such as peptic ulcer have been shown to be of infectious origin (240). This has renewed interest in the area of bacteria and COPD, and these new research methodologies should lead to a precise delineation of the contribution of bacterial infection to this disease. Five potential pathways by which bacteria could contribute to the course and pathogenesis of COPD can be identified. (i) Childhood lower respiratory tract infection impairs lung growth, reflected in smaller lung volumes in adulthood. (ii) Bacteria cause a substantial proportion of acute exacerbations of chronic bronchitis which cause considerable morbidity and mortality. (iii) Chronic colonization of the lower respiratory tract by bacterial pathogens amplifies the chronic inflammatory response present in COPD and leads to progressive airway obstruction (vicious circle hypothesis). (iv) Bacterial pathogens invade and persist in respiratory tissues, alter the host response to cigarette smoke, or induce a chronic inflammatory response and thus contribute to the pathogenesis of COPD. (v) Bacterial antigens in the lower airway induce hypersensitivity that enhances airway hyperreactivity and induces eosinophilic inflammation. Evidence supporting these roles will be discussed in this review, with an emphasis on information gained from newer research techniques in the last decade. The second part of this review will discuss each of the major pathogens, with emphasis on recent developments related specifically to infections in COPD.