Status of the Lake Baikal Experiment

We review the present status of the Baikal Underwater Neutrino Experiment and report on neutrino events recorded with the detector stages NT-36 and NT-96.Comment: 5 pages, 4 PostScript figures, uses here.sty and mine.sty, submitted to the Proc. of 5th Int. Workshop on Topics in Astroparticle and Underground Physics (LNGS INFN, Assergi, September 7-11, 1997

The Baikal Deep Underwater Neutrino Experiment: Results, Status, Future

We review the present status of the Baikal Underwater Neutrino Experiment and present results obtained with the various stages of the stepwise increasing detector: NT-36 (1993-95), NT-72 (1995-96) and NT-96 (1996-97). Results cover atmospheric muons, first clear neutrino events, search for neutrinos from WIMP annihilation in the center of the Earth, search for magnetic monopoles, and -- far from astroparticle physics -- limnology.Comment: Talk given at the Int. School on Nuclear Physics, Erice, Sept.199

Genome-wide association study of pancreatic fat: The multiethnic cohort adiposity phenotype study

Several studies have found associations between higher pancreatic fat content and adverse health outcomes, such as diabetes and the metabolic syndrome, but investigations into the genetic contributions to pancreatic fat are limited. This genome-wide association study, comprised of 804 participants with MRI-assessed pancreatic fat measurements, was conducted in the ethnically diverse Multiethnic Cohort-Adiposity Phenotype Study (MEC-APS). Two genetic variants reaching genome-wide significance, rs73449607 on chromosome 13q21.2 (Beta = -0.67, P = 4.50x10-8) and rs7996760 on chromosome 6q14 (Beta = -0.90, P = 4.91x10-8) were associated with percent pancreatic fat on the log scale. Rs73449607 was most common in the African American population (13%) and rs79967607 was most common in the European American population (6%). Rs73449607 was also associated with lower risk of type 2 diabetes (OR = 0.95, 95% CI = 0.89-1.00, P = 0.047) in the Population Architecture Genomics and Epidemiology (PAGE) Study and the DIAbetes Genetics Replication and Meta-analysis (DIAGRAM), which included substantial numbers of non-European ancestry participants (53,102 cases and 193,679 controls). Rs73449607 is located in an intergenic region between GSX1 and PLUTO, and rs79967607 is in intron 1 of EPM2A. PLUTO, a lncRNA, regulates transcription of an adjacent gene, PDX1, that controls beta-cell function in the mature pancreas, and EPM2A encodes the protein laforin, which plays a critical role in regulating glycogen production. If validated, these variants may suggest a genetic component for pancreatic fat and a common etiologic link between pancreatic fat and type 2 diabetes

Supplementary Material for: Genetic and Lifestyle Causal Beliefs about Obesity and Associated Diseases among Ethnically Diverse Patients: A Structured Interview Study

<b><i>Background:</i></b> New genetic associations with obesity are rapidly being discovered. People's causal beliefs about obesity may influence their obesity-related behaviors. Little is known about genetic compared to lifestyle causal beliefs regarding obesity, and obesity-related diseases, among minority populations. This study examined genetic and lifestyle causal beliefs about obesity and 3 obesity-related diseases among a low-income, ethnically diverse patient sample. <b><i>Methods:</i></b> Structured interviews were conducted with patients attending an inner-city hospital outpatient clinic. Participants (n = 205) were asked how much they agreed that genetics influence the risk of obesity, type 2 diabetes, heart disease, and cancer. Similar questions were asked regarding lifestyle causal beliefs (overeating, eating certain types of food, chemicals in food, not exercising, smoking). In this study, 48% of participants were non-Hispanic Black, 29% Hispanic and 10% non-Hispanic White. <b><i>Results:</i></b> Over two-thirds (69%) of participants believed genetics cause obesity ‘some' or ‘a lot', compared to 82% for type 2 diabetes, 79% for heart disease and 75% for cancer. Participants who held genetic causal beliefs about obesity held more lifestyle causal beliefs in total than those who did not hold genetic causal beliefs about obesity (4.0 vs. 3.7 lifestyle causal beliefs, respectively, possible range 0-5, p = 0.025). There were few associations between causal beliefs and sociodemographic characteristics. <b><i>Conclusions:</i></b> Higher beliefs in genetic causation of obesity and related diseases are not automatically associated with decreased lifestyle beliefs. Future research efforts are needed to determine whether public health messages aimed at reducing obesity and its consequences in racially and ethnically diverse urban communities may benefit from incorporating an acknowledgement of the role of genetics in these conditions