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To increase the light collection efficiency of a liquid argon (LAr) detector, we optimized the evaporation technique of tetraphenyl butadiene (TPB) on the detector surface and tested the operability of a silicon photomultiplier at LAr temperature. TPB converts LAr scintillations (vacuum ultraviolet light) to visible light, which can be detected using high-sensitivity photosensors. Because the light collection efficiency depends on the deposition mass of TPB on the inner surface of the detector, we constructed a well-controlled TPB evaporator to ensure reproducibility and measured the TPB deposition mass using a quartz crystal microbalance sensor. After optimizing the deposition mass of TPB (30  |$\rm \mu g/cm^2$| on the photosensor window and 42  |$\rm \mu g/cm^2$| on the detector wall), the observed light yield was 12.8 ± 0.3 p.e./keVee using photomultiplier tubes with a quantum efficiency of approximately 30% for TPB-converted light. We also tested the low-temperature tolerance of the silicon photomultiplier, which has a high photon detection efficiency, in a LAr environment. It detected the LAr scintillations converted by TPB with a photon detection efficiency exceeding 50%. [ABSTRACT FROM AUTHOR]

Background: Little is known about the influence of serum level of soluble triggering receptor expressed on myeloid cells 2 (sTREM2), which is a soluble type of an innate immune receptor expressed on the microglia, on the association of the daily sleep duration with the risk of dementia. Methods: A total of 1230 Japanese community‐residents aged 60 and older without dementia were followed prospectively for 10 years (2002–2012). Serum sTREM2 levels were divided into two groups using the median value (334.8 pg/ml). Self‐reported daily sleep duration was grouped into three categories of <5.0, 5.0–7.9, and ≥8.0 h. A Cox proportional hazards model was used to estimate the hazard ratios (HRs) and their 95% confidence intervals (CIs) of daily sleep duration on the risk of dementia according to serum sTREM2 levels. Results: During the follow‐up, 262 subjects developed dementia. In subjects with low serum sTREM2 levels, subjects with ≥8.0 h of daily sleep had a significantly greater risk of dementia (multivariable‐adjusted HR 2.05 [95% CI 1.32–3.19]) than those with 5.0–7.9 h of daily sleep, but those with <5.0 h did not. In contrast, the risk of dementia increased significantly in subjects with both <5.0 (1.95 [1.03–3.68]) and ≥8.0 h of daily sleep (1.48 [1.06–2.07]) in the subjects with high serum sTREM2 levels. Conclusions: The influence of daily sleep duration on risk of dementia differed according to serum sTREM2 levels in the older Japanese population. Short daily sleep may be associated with greater risk of dementia only in subjects with a high serum sTREM2 level. [ABSTRACT FROM AUTHOR]

A large-scale association study is performed to identify mitochondrial haplogroups that might confer resistance against or susceptibility to type 2-diabetes mellitus (T2DM) in Asians. Multivariate logistic-regression analysis has indicated that the mitochondrial haplogroup N9a is associated with resistance against T2DM with an odds ratio of 0.55.

The genome of a radiation-resistant bacterium, Deinococcus radiodurans, contains one uvsE gene and two uvrA genes, uvrA1 and uvrA2. Using a series of mutants lacking these genes, we determined the biological significance of these components to UV resistance. The UV damage endonuclease (UvsE)-dependent excision repair (UVER) pathway and UvrA1-dependent pathway show some redundancy in their function to counteract the lethal effects of UV. Loss of these pathways does not cause increased sensitivity to UV mutagenesis, suggesting either that these pathways play no function in inducing mutations or that there are mechanisms to prevent mutation other than these excision repair pathways. UVER efficiently removes both cyclobutane pyrimidine dimers (CPDs) and pyrimidine (6-4) pyrimidone photoproducts (6-4PPs) from genomic DNA. In contrast, the UvrA1 pathway does not significantly contribute to the repair of CPDs but eliminates 6-4PPs. Inactivation of uvrA2 does not result in a deleterious effect on survival, mutagenesis, or the repair kinetics of CPDs and 6-4PPs, indicating a minor role in resistance to UV. Loss of uvsE, uvrA1, and uvrA2 reduces but does not completely abolish the ability to eliminate CPDs and 6-4PPs from genomic DNA. The result indicates the existence of a system that removes UV damage yet to be identified.

During the first hour after a sublethal dose of ionizing radiation, 72 genes were upregulated threefold or higher in D. radiodurans R1. Thirty-three of these loci were also among a set of 73 genes expressed in RI cultures recovering from desiccation. The five transcripts most highly induced in response to each stress are the same and encode proteins of unknown function. The genes (ddrA, ddrB, ddrC, ddrD, and pprA) corresponding to these transcripts were deleted, both alone and in all possible two-way combinations. Characterization of the mutant strains defines three epistasis groups that reflect different cellular responses to ionizing radiation-induced damage. The ddrA and ddrB gene products have complementary activities and inactivating both loci generates a strain that is more sensitive to ionizing radiation than strains in which either single gene has been deleted. These proteins appear to mediate efficient RecA-independent processes connected to ionizing radiation resistance. The pprA gene product is not necessary for homologous recombination during natural transformation, but nevertheless may participate in a RecA-dependent process during recovery from radiation damage. These characterizations clearly demonstrate that novel mechanisms significantly contribute to the ionizing radiation resistance in D. radiodurans.

Most organisms form Cys-tRN[A.sup.Cys], an essential component for protein synthesis, through the action of cysteinyl-tRNA synthetase (CysRS). However, the genomes of Methanocaldococcus jannaschii, Methanothermobacter thermautotrophicus, and Methanopyrus kandleri do not contain a recognizable cysS gene encoding CysRS. It was reported that M.jannaschii prolyl-tRNA synthetase (C. Stathopoulos, T. Li, R. Longman, U. C. Vothknecht, H. D. Becker, M. Ibha, and D. Soll, Science 287:479-482, 2000; R. S. Lipman, K. R. Sowers, and Y. M. Hou, Biochemistry 39:7792-7798, 2000) or the M. jannaschii MJ1477 protein (C. Fabrega, M. A. Farrow, B. Mukhopadhyay, V. de Crecy-Lagard, A. R. Ortiz, and P. Schimmel, Nature 411:110-114, 2001) provides the 'missing' CysRS activity for in vivo Cys-tRN[A.sup.Cys] formation. These conclusions were supported by complementation of temperature-sensitive Escherichia coli cysS(Ts) strain UQ818 with archaeal proS genes (encoding prolyl-tRNA synthetase) or with the Deinococeus radiodurans DR0705 gene, the ortholog of the MJ1477 gene. Here we show that E. coli UQ818 harbors a mutation (V27E) in CysRS; the largest differences compared to the wild-type enzyme are a fourfold increase in the Km for cysteine and a ninefold reduction in the [k.sub.cat] for ATP. While transformants of E. coli UQ818 with archaeal and bacterial cysS genes grew at a nonpermissive temperature, growth was also supported by elevated intracellular cysteine levels, e.g., by transformation with an E. coli cysE allele (encoding serine acetyltransferase) or by the addition of cysteine to the culture medium. An E. coli cysS deletion strain permitted a stringent complementation test; growth could be supported only by archaeal or bacterial cysS genes and not by archaeal proS genes or the D. radiodurans DR0705 gene. Construction of a D. radiodurans DR0705 deletion strain showed this gene to be dispensable. However, attempts to delete D. radiodurans cysS failed, suggesting that this is an essential Deinococcus gene. These results imply that it is not established that proS or MJ1477 gene products catalyze Cys-tRN[A.sup.cys] synthesis in M. jannaschii. Thus, the mechanism of Cys-tRN[A.sup.Cys] formation in M. jannaschii still remains to be discovered.

In everyday medical settings in Japan, physicians occasionally tell an elderly patient that their symptoms are "due to old age," and there is some concern that patient care might be negatively impacted as a result. That said, as this phrase can have multiple connotations and meanings, there are certain instances in which the use of this phrase may not necessarily be indicative of ageism, or prejudice against the elderly. One of the goals in medical care is to address pain and suffering that develops with age in elderly individuals, and whether or not aging is a disease is inconsequential. However, assuming that an individualized and thorough examination has been performed, there are some conditions that can be attributed only to age. Accordingly, physicians must acknowledge the merits and drawbacks of using the phrase "due to old age," and exercise caution when using it. Both physicians and their elderly patients must share a common awareness of the incomplete and limited nature of modern medicine and its scope, and physicians must help their elderly patients accept and live with the aging phenomenon. [ABSTRACT FROM AUTHOR]

People with a mutation in the genes for connexin 37, plasminogen-activator inhibitor type 1, or stromelysin-1 have a greater than normal risk of having a heart attack. This was the conclusion of researchers who analyzed 112 different mutations in 71 genes in a study of 2,819 heart attack patients and 2,242 healthy volunteers.