Detailed dimethylacetal and fatty acid composition of rumen content from lambs fed lucerne or concentrate supplemented with soybean oil

Articles in International JournalsLipid metabolism in the rumen is responsible for the complex fatty acid profile of rumen outflow compared with the dietary fatty acid composition, contributing to the lipid profile of ruminant products. A method for the detailed dimethylacetal and fatty acid analysis of rumen contents was developed and applied to rumen content collected from lambs fed lucerne or concentrate based diets supplemented with soybean oil. The methodological approach developed consisted on a basic/ acid direct transesterification followed by thin-layer chromatography to isolate fatty acid methyl esters from dimethylacetal, oxo- fatty acid and fatty acid dimethylesters. The dimethylacetal composition was quite similar to the fatty acid composition, presenting even-, odd- and branched-chain structures. Total and individual odd- and branched-chain dimethylacetals were mostly affected by basal diet. The presence of 18:1 dimethylacetals indicates that biohydrogenation intermediates might be incorporated in structural microbial lipids. Moreover, medium-chain fatty acid dimethylesters were identified for the first time in the rumen content despite their concentration being relatively low. The fatty acids containing 18 carbon-chain lengths comprise the majority of the fatty acids present in the rumen content, most of them being biohydrogenation intermediates of 18:2n26 and 18:3n23. Additionally, three oxo- fatty acids were identified in rumen samples, and 16-O-18:0 might be produced during biohydrogenation of the 18:3n23

Retinoblastoma Loss Modulates DNA Damage Response Favoring Tumor Progression

Senescence is one of the main barriers against tumor progression. Oncogenic signals in primary cells result in oncogene-induced senescence (OIS), crucial for protection against cancer development. It has been described in premalignant lesions that OIS requires DNA damage response (DDR) activation, safeguard of the integrity of the genome. Here we demonstrate how the cellular mechanisms involved in oncogenic transformation in a model of glioma uncouple OIS and DDR. We use this tumor type as a paradigm of oncogenic transformation. In human gliomas most of the genetic alterations that have been previously identified result in abnormal activation of cell growth signaling pathways and deregulation of cell cycle, features recapitulated in our model by oncogenic Ras expression and retinoblastoma (Rb) inactivation respectively. In this scenario, the absence of pRb confers a proliferative advantage and activates DDR to a greater extent in a DNA lesion-independent fashion than cells that express only HRasV12. Moreover, Rb loss inactivates the stress kinase DDR-associated p38MAPK by specific Wip1-dependent dephosphorylation. Thus, Rb loss acts as a switch mediating the transition between premalignant lesions and cancer through DDR modulation. These findings may have important implications for the understanding the biology of gliomas and anticipate a new target, Wip1 phosphatase, for novel therapeutic strategies

Distribution of the Mosquito Communities (Diptera: Culicidae) in Oviposition Traps Introduced into the Atlantic Forest in the State of Rio de Janeiro, Brazil

The Atlantic Rainforest of South America is one of the major biodiversity hotspots of the world and serves as a place of residence for a wide variety of Culicidae species. Mosquito studies in the natural environment are of considerable importance because of their role in transmitting pathogens to both humans and other vertebrates. Community diversity can have significant effects on the risk of their disease transmission. The objective of this study was to understand the distribution of mosquito communities using oviposition traps in a region of the Atlantic Forest. Sampling was carried out in Bom Retiro Private Natural Reserve (RPPNBR), located in Casimiro de Abreu, Rio de Janeiro, using oviposition traps, which were set in the forest environment, from October 2015 to December 2016. The canonical correspondence analysis was used to assess the influence of the climatic variables (precipitation, maximum dew point, and direction) throughout the seasons on the population density of the mosquito species. The results showed that population density was directly influenced by climatic variables, which acted as a limiting factor for the mosquito species studied. The climatic variables that were significantly correlated with the density of the mosquito species were precipitation, maximum dew point, and direction. Haemagogus janthinomys was positively correlated with the three climatic variables, whereas Haemagogus leucocelaenus was positively correlated with precipitation and maximum dew point, and negatively correlated with direction.2030-01-0

The Pattern of Natural Selection in Somatic Cancer Mutations of Human mtDNA

Tumors frequently contain somatic mutations in the mitochondrial DNA (mtDNA). Whether these mutations have a causal function or are merely an effect is still unclear. As tumor formation is a type of somatic evolution, we examine the cancer mutation pattern for consistency with random forces or selection. We also compare the tumor mutation pattern to that observed in the population to gain insight on the mutation process in cancer. Among germline mtDNAs, all genes show strong deficiency in missense changes, reflecting negative selection during human history. In somatic cancer sequences, mtDNA genes show relaxed negative selection relative to germline, or mutation consistent with neutrality. NADH dehydrogenase subunit 3, cytochrome c oxidase subunit 3 and NADH dehydrogenase subunit 4 L in particular show cancer missense mutation rates 9-18 times that of germline. Bootstrap analysis shows cytochrome B to have cancer changes in positions of unusually high conservation, suggesting that tumors select for mutations in residues of high functionality. Strong negative selection was detected in mitochondrially encoded cytochrome c oxidase 1 (MTCO1), suggesting that tumor cells are dependent upon MTCO1 function. Common population polymorphisms were also frequently reported among somatic tumor mutations. The implication of these \u27somatic polymorphisms\u27 in tumor growth is discussed