A mitochondrial protein fraction catalyzing transport of the K+ analog T1+.

A protein fraction has been obtained from detergent-solubilized mitochondrial membranes by its affinity for quinine, an inhibitor of K+ transport. A peptide derived from the predominant 53 kDa protein in this fraction is found to be identical in sequence to a portion of aldehyde dehydrogenase. Antigenically unrelated bands at 97, 77, 57, and 31 kDa are also seen on polyacrylamide gels. Observations utilizing a fluorescent probe entrapped in the lumen of membrane vesicles indicate that the reconstituted protein fraction imparts permeability to the K+ analog Tl+. These and other findings suggest that the affinity purified fraction includes a cation transport catalyst.     

Study of uranium level in groundwater of Balod district of Chhattisgarh state,India and assessment of health risk

Uranium contamination in groundwater at Balod district of Chhattisgarh state was measured by laser fluorimetric technique. Most of the samples were found under safe limit for uranium contamination as recommended by WHO and USEPA (<30 µg l^?1) except Deur Tarai village (78.93 µg l^?1).The excess lifetime carcinogenic risk and chemical risk due to ingestion of groundwater were calculated using USEPA recommendations.     

Characterisation of wheat germplasm for slow rust resistance against Puccinia striiformis

Thirty-seven wheat germplasm were screened under artificial epiphytotic conditions against stripe rust of wheat at University Research Farm, Chatha, during Rabi, 2013–2014 and 2014–2015. On the basis of final rust severity (FRS), AURPC (Area Under Rust Progress Curve) and CI (Coefficient of Infection), 8 genotypes ((DWR 16, HD2281, VL616, K65, UP2121, HD2329, HD2307 and Lal Bahadur) exhibited partial resistance against the disease. PCR profiles revealed co-dominant pattern with distinct fragment of 150 bp in 14 germplasm, showing the presence of Yr18 gene and 229 bp band in 16 germplasm exhibited absence of Yr18.     

Modular Upgradability in Consumer Electronics: Economic and Environmental Implications

Modularly upgradable product designs have been advocated to offer environmental and economic advantages; however, they are not commonly used in the consumer electronics industry. In this article, we investigate the economic and environmental benefits and challenges of modular upgradability for consumer electronics. From an economic point of view, we posit that the limited adoption of modular upgradability in consumer electronics is owing to various demand‐, technology‐, and competition‐related issues. From an environmental point of view, we posit that modularly upgradable product designs may not necessarily lead to superior environmental outcomes. To reach meaningful conclusions regarding the environmental benefits of modular upgradability, one needs to understand how product architecture affects demand, production, and consumption patterns, which arise from endogenous consumer and manufacturer choices. It is also important to take into account that modular upgradability may have potentially differentiated effects in the production, consumption, and postuse phases of the lifecycle.     

Production of atypical measles in rhesus macaques: evidence for disease mediated by immune complex formation and eosinophils in the presence of fusion-inhibiting antibody.

The severe disease atypical measles occurred when individuals immunized with a poorly protective inactivated vaccine contracted measles, and was postulated to be due to a lack of fusion-inhibiting antibodies. Here, rhesus macaques immunized with formalin-inactivated measles vaccine developed transient neutralizing and fusion-inhibiting antibodies, but no cytotoxic T-cell response. Subsequent infection with measles virus caused an atypical rash and pneumonitis, accompanied by immune complex deposition and an increase in eosinophils. Fusion-inhibiting antibody appeared earlier in these monkeys than in non-immunized monkeys. These data indicate that atypical measles results from previous priming for a nonprotective type 2 CD4 T-cell response rather than from lack of functional antibody against the fusion protein.