Uncoupling protein 2 (UCP2) maps to a region on distal mouse chromosome 7 that has been linked to the phenotypes of obesity and type II diabetes. We recently reported that UCP2 expression is increased by high fat feeding in adipose tissue of the A͞J strain of mice, which is resistant to the development of dietary obesity. More recently, a third UCP (UCP3) was identified, which is expressed largely in skeletal muscle and brown adipose tissue. The UCP2 and UCP3 genes are located adjacent to one another on mouse chromosome 7. Thus, the roles of these UCPs in both metabolic efficiency and the linkage to obesity and diabetes syndromes is unclear. For this reason, we examined the expression of UCP2 and UCP3 in white adipose tissue and interscapular brown adipose tissue and in gastrocnemius͞soleus muscle preparations from the obesity-resistant A͞J and C57BL͞KsJ (KsJ) strains and the obesity-prone C57BL͞6J (B6) mouse strain. In both KsJ and A͞J mice, UCP2 expression in white fat was increased Ϸ2-fold in response to 2 weeks of a high fat diet, but there was no effect of diet on UCP2 levels in B6 mice. In skeletal muscle and in brown fat, neither UCP2 nor UCP3 expression was affected by diet in A͞J, B6, or KsJ mice. However, in brown fat, we observed a 2-3-fold increase in the expression of UCP1 in response to dietary fat challenge, which may be related to diet-induced elevations in plasma leptin levels. Together, these results indicate that the consumption of a high fat diet selectively regulates UCP2 expression in white fat and UCP1 expression in brown fat and that resistance to obesity is correlated with this early, selective induction of UCP1 and UCP2 and is not associated with changes in expression of UCP3.Obesity is a disorder of energy balance in which energy intake is greater than energy expenditure. Methods to control obesity through limiting energy intake have had modest success at best, and it is widely recognized that energy expenditure must be increased in an obese individual if long term weight loss is to be achieved. The recent discovery of several new uncoupling proteins (UCPs) provides new molecular targets for increasing energy expenditure. The UCPs are integral membrane proteins of the mitochondrial inner membrane, where they function as a proton channel or shuttle. These proteins uncouple the process of mitochondrial respiration from oxidative phosphorylation, diminishing the resulting production of ATP and instead yielding dissipative heat. The action of these proteins creates a futile cycle that decreases the metabolic efficiency of the organism. Thus, UCPs are potentially important in disorders of energy balance such as obesity and diabetes (1, 2).

Aim: The aim of this study was to investigate the accuracy of cone-beam computed tomography (CBCT) in assessing maxillary molar furcation involvement (FI). Materials and Methods: Fifteen patients with generalized chronic periodontitis after initial therapy were recruited. CBCT was performed in maxillary molars with probing pocket depths of ≥6 mm and advanced FI, and CBCT images were analysed. Furcation surgery was performed in 20 maxillary molars. Lastly, intrasurgical FI assessments were compared with CBCT-based data. Results: Intra-surgical findings confirmed 82.4% of the CBCT data, with a weighted kappa of 0.917. The agreement between both assessments was the highest in buccal furcation entrances, followed by distopalatal and mesiopalatal furcation entrances. Of the four parameters tested of detailed root anatomy and furcation morphology, the mean length of the root trunk and the width of the furcation entrance revealed by CBCT were consistent with their respective intrasurgical values (p > 0.05). Horizontal bone loss and vertical bone loss were underestimated by CBCT relative to their respective intra-surgical classifications (p ≤ 0.05). Conclusions: Cone-beam computed tomography images demonstrate a high accuracy in assessing the loss of periodontal tissue of the FI and root morphologies in maxillary molars.

Relationship between low-temperature tolerance and vernalization response in t"r,""t "ni.y".

Background The severity of coronavirus disease 2019 (COVID-19) caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is highly heterogeneous. Studies have reported that males and some ethnic groups are at increased risk of death from COVID-19, which implies that individual risk of death might be influenced by host genetic factors. Methods In this project, we consider the mortality as the trait of interest and perform a genome-wide association study (GWAS) of data for 1778 infected cases (445 deaths, 25.03%) distributed by the UK Biobank. Traditional GWAS fails to identify any genome-wide significant genetic variants from this dataset. To enhance the power of GWAS and account for possible multi-loci interactions, we adopt the concept of super variant for the detection of genetic factors. A discovery-validation procedure is used for verifying the potential associations. Results We find 8 super variants that are consistently identified across multiple replications as susceptibility loci for COVID-19 mortality. The identified risk factors on chromosomes 2, 6, 7, 8, 10, 16, and 17 contain genetic variants and genes related to cilia dysfunctions (DNAH7 and CLUAP1), cardiovascular diseases (DES and SPEG), thromboembolic disease (STXBP5), mitochondrial dysfunctions (TOMM7), and innate immune system (WSB1). It is noteworthy that DNAH7 has been reported recently as the most downregulated gene after infecting human bronchial epithelial cells with SARS-CoV-2. Conclusions Eight genetic variants are identified to significantly increase the risk of COVID-19 mortality among the patients with white British ancestry. These findings may provide timely clues and potential directions for better understanding the molecular pathogenesis of COVID-19 and the genetic basis of heterogeneous susceptibility, with potential impact on new therapeutic options.