TASK DEFINITION: Given a passage classify if the passage has a definite objective/aim/goal or not. Output '1' if the passage has a defininte objective/aim/goal and output '0' if the passage does not have a definite objective/aim/goal.
PROBLEM: Methionine sulfoxide reduction is an important protein repair pathway that protects against oxidative stress, controls protein function and has a role in regulation of aging. There are two enzymes that reduce stereospecifically oxidized methionine residues: MsrA (methionine-S-sulfoxide reductase) and MsrB (methionine-R-sulfoxide reductase). In many organisms, these enzymes are targeted to various cellular compartments. In mammals, a single MsrA gene is known, however, its product is present in cytosol, nucleus, and mitochondria. In contrast, three mammalian MsrB genes have been identified whose products are located in different cellular compartments.', 'In the present study, we identified and characterized alternatively spliced forms of mammalian MsrA. In addition to the previously known variant containing an N-terminal mitochondrial signal peptide and distributed between mitochondria and cytosol, a second mouse and human form was detected in silico. This form, MsrA(S), was generated using an alternative first exon. MsrA(S) was enzymatically active and was present in cytosol and nucleus in transfected cells, but occurred below detection limits in tested mouse tissues. The third alternative form lacked the active site and could not be functional. In addition, we found that mitochondrial and cytosolic forms of both MsrA and MsrB in Drosophila could be generated by alternative first exon splicing.

SOLUTION: 0

PROBLEM: Information about malaria risk factors at high altitudes is scanty. Understanding the risk factors that determine the risk of malaria transmission at high altitude villages is important to facilitate implementing sustainable malaria control and prevention programs.', 'An unmatched case control study was conducted among patients seeking treatment at health centers in high altitude areas. Either microscopy or rapid diagnostic tests were used to confirm the presence of plasmodium species. A generalized linear model was used to identify the predictors of malaria transmission in high altitude villages.', 'Males (AOR\u200a=\u200a3.11, 95%CI: 2.28, 4.23), and those who traveled away from the home in the previous month (AOR\u200a=\u200a2.01, 95% CI: 1.56, 2.58) were strongly associated with presence of malaria in high altitude villages. Other significant factors, including agriculture in occupation (AOR\u200a=\u200a1.41, 95% CI: 1.05, 1.93), plants used for fencing (AOR\u200a=\u200a1.70, 95% CI: 1.18, 2.52) and forests near the house (AOR\u200a=\u200a1.60, 95% CI: 1.15, 2.47), were found predictors for malaria in high altitude villages.

SOLUTION: 0

PROBLEM: Nuclear factor of activated T-cells 5 (NFAT5) has recently been described to control the phenotype of vascular smooth muscle cells (VSMCs). Although an increase in wall stress or stretch (eg, elicited by hypertension) is a prototypic determinant of VSMC activation, the impact of this biomechanical force on the activity of NFAT5 is unknown. This study intended to reveal the function of NFAT5 and to explore potential signal transduction pathways leading to its activation in stretch-stimulated VSMCs.', 'Human arterial VSMCs were exposed to biomechanical stretch and subjected to immunofluorescence and protein-biochemical analyses. Stretch promoted the translocation of NFAT5 to the nucleus within 24 hours. While the protein abundance of NFAT5 was regulated through activation of c-Jun N-terminal kinase under these conditions, its translocation required prior activation of palmitoyltransferases. DNA microarray and ChiP analyses identified the matrix molecule tenascin-C as a prominent transcriptional target of NFAT5 under these conditions that stimulates migration of VSMCs. Analyses of isolated mouse femoral arteries exposed to hypertensive perfusion conditions verified that NFAT5 translocation to the nucleus is followed by an increase in tenascin-C abundance in the vessel wall.

SOLUTION:
0