Search

Domestic winter indoor temperatures in the USA, UK and other developed countries appear to be following an upwards trend. This review examines evidence of a causal link between thermal exposures and increases in obesity prevalence, focusing on acute and longer-term biological effects of time spent in thermal comfort compared with mild cold. Reduced exposure to seasonal cold may have a dual effect on energy expenditure, both minimizing the need for physiological thermogenesis and reducing thermogenic capacity. Experimental studies show a graded association between acute mild cold and human energy expenditure over the range of temperatures relevant to indoor heating trends. Meanwhile, recent studies of the role of brown adipose tissue (BAT) in human thermogenesis suggest that increased time spent in conditions of thermal comfort can lead to a loss of BAT and reduced thermogenic capacity. Pathways linking cold exposure and adiposity have not been directly tested in humans. Research in naturalistic and experimental settings is needed to establish effects of changes in thermal exposures on weight, which may raise possibilities for novel public health strategies to address obesity. [ABSTRACT FROM AUTHOR]

Cryptococcus neoformans frequently causes fungal meningitis in immunocompromised patients, whereas the related species C. gattii is restricted to tropicalandsubtropical regions,whereit usually infectsimmunocompetentindividuals. Anoutbreak of C. gattii infection thatbeganin1999onVancouverIsland has resulted inendemicC. gattii infectionand causednumeroushumanandveterinary infections;theoutbreak'srangehasspreadtomainlandBritishColumbia.The outbreak-related isolates have been molecular type VGIIa, the major genotype, or VGIIb, the minor genotype. Since 2006,humanand veterinary cases of C. gattii infection have emerged in Washington and Oregon. Multilocus sequence typing demonstrates the spread of C. gattii VGIIa and VGIIb from Vancouver Island to the Pacific Northwest. Clinical strains recovered in Oregon represent a unique VGIIc genotype. [ABSTRACT FROM AUTHOR]

The article offers information on the ability of brown adipose tissue (BAT) to protect against cold and against triglyceride-rich lipoproteins- (TRLs) related conditions in the U.S. It states that TRLs contribute to obesity and vascular disease. Moreover, increasing BAT activity through cold exposure improves TRL clearance, which suggests that BAT activation can be a possible therapeutic approach to humans.

The article discusses a U.S. study which identified progenitor cells present in white fat and skeletal tissues of mice that can be induced to differentiate into brown fat cells. A protein called BMP-7, a known key factor for the development of brown fat cells, was found to induce mouse cells marked with a protein called Sca1 to display characteristics of brown fat cells. The study by Yu-Hua Tseng and colleagues appeared in the 2011 issue of the "Proceedings of the National Academy of Sciences."

The article discusses the discovery of the origin of brown fat which is an energy-using tissue closely related to muscle. Topics include the difference between white fat, which is used to store energy, and brown fat, which burns fat molecules that is used to generate body heat. Also discussed is research by U.S. scientists investigating the role of the gene PRDM16 and how silencing it switched the fat cell's identity to something similar to muscles.