DNA sequences of tobacco chloroplast genes for tRNASer (GGA), tRNAThr (UGU), tRNALeu (UAA), tRNAPhe (GAA): the tRNALeu gene contains a 503 bp intron

Summary The location and nucleotide sequence of tobacco chloroplast genes for tRNA^Ser (GGA), tRNA^Thr (UGU), tRNA^Leu (UAA) and tRNA^Phe (GAA) (trnS-GGA, trnT-UGU, trnL-UAA and trnF-GAA, respectively) have been determined. These genes are located in the 10 kbp BamHI fragment which lies in the middle of the large single-copy region of the chloroplast DNA. The gene order is trnS-trnT-trnL-trnF. The trnS, trnL and trnF are encoded on the same strand while the trnT on the opposite strand. The trnL contains a 503 bp intron like maize and broad bean trnL-UAAs.     

Determination of hydrophobicity of myelinic,synaptosomal, and mitochondrial surfaces in the rat brain

The hydrophobicity of myelinic, synaptosomal and mitochondrial surfaces in the rat brain was measured using the nonionic surfactant, C₁₈H₃₇O(CH₂CH₂O)₁₃H. This method is based on the adsorption of the hydrophobic alkyl group of the surfactant by the hydrophobic sites on the surfaces. Each preparations was mixed with an excess of the surfactant and the surfactant remaining in the supernatants was determined spectrophotometrically by measuring the absorbance of tetrabromophenolphthalein ethylester at 690 nm. The greatest amount was adsorbed by myelin, followed by synaptosomes and mitochondria. The hydrophobicity is shown to be a reflection of the surface lipids. This method showed good reproducibility and was useful for the quantitative determination of hydrophobicity.     

Incidence Rate of Needlestick and Sharps Injuries in 67 Japanese Hospitals: A National Surveillance Study

Background

Determining incidence rates of needlestick and sharps injuries (NSIs) using data from multiple hospitals may help hospitals to compare their in-house data with national averages and thereby institute relevant measures to minimize NSIs. We aimed to determine the incidence rate of NSIs using the nationwide EPINet surveillance system.

Methodology/Principal Findings

Data were analyzed from 5,463 cases collected between April 2009 and March 2011 from 67 Japanese HIV/AIDS referral hospitals that participated in EPINet-Japan. The NSI incidence rate was calculated as the annual number of cases with NSIs per 100 occupied beds, according to the demographic characteristics of the injured person, place, timing, device, and the patients’ infectious status. The NSI incidence rates according to hospital size were analyzed by a non-parametric test of trend. The mean number of cases with NSIs per 100 occupied beds per year was 4.8 (95% confidence interval, 4.1–5.6) for 25 hospitals with 399 or fewer beds, 6.7 (5.9–7.4) for 24 hospitals with 400–799 beds, and 7.6 (6.7–8.5) for 18 hospitals with 800 or more beds (p-trend<0.01). NSIs frequently occurred in health care workers in their 20 s; the NSI incidence rate for this age group was 2.1 (1.6–2.5) for hospitals having 399 or fewer beds, 3.5 (3.0–4.1) for hospitals with 400–799 beds, and 4.5 (3.9–5.0) for hospitals with 800 or more beds (p-trend<0.01).

Conclusions/Significance

The incidence rate of NSIs tended to be higher for larger hospitals and in workers aged less than 40 years; injury occurrence was more likely to occur in places such as patient rooms and operating rooms. Application of the NSI incidence rates by hospital size, as a benchmark, could allow individual hospitals to compare their NSI incidence rates with those of other institutions, which could facilitate the development of adequate control strategies.     

Inhibitory effect of apple pectin and culture condensate of Bifidobacterium longum on colorectal tumors induced by 1,2-dimethylhydrazine in transgenic mice harboring human prototype c-Ha-ras genes.

The number and tumor score of colorectal tumors induced by 1,2-dymethylhydrazine in transgenic (Tg) mice carrying human c-Ha-ras genes were significantly reduced by ingestion of apple pectin (AP) or a culture condensate of Bifidobacterium longum (MB) when compared with a control diet. There was no statistical difference in the incidence of colorectal tumors in Tg mice between the AP or MB diet and the control diet. This study demonstrated that Tg mice are a useful tool for screening inhibition of colorectal tumors by functional foods.     

Involvement of the PA28gamma-dependent pathway in insulin resistance induced by hepatitis C virus core protein

The hepatitis C virus (HCV) core protein is a component of nucleocapsids and a pathogenic factor for hepatitis C. Several epidemiological and experimental studies have suggested that HCV infection is associated with insulin resistance, leading to type 2 diabetes. We have previously reported that HCV core gene-transgenic (PA28gamma(+/+)CoreTg) mice develop marked insulin resistance and that the HCV core protein is degraded in the nucleus through a PA28gamma-dependent pathway. In this study, we examined whether PA28gamma is required for HCV core-induced insulin resistance in vivo. HCV core gene-transgenic mice lacking the PA28gamma gene (PA28gamma(-/-)CoreTg) were prepared by mating of PA28gamma(+/+)CoreTg with PA28gamma-knockout mice. Although there was no significant difference in the glucose tolerance test results among the mice, the insulin sensitivity in PA28gamma(-/-)CoreTg mice was recovered to a normal level in the insulin tolerance test. Tyrosine phosphorylation of insulin receptor substrate 1 (IRS1), production of IRS2, and phosphorylation of Akt were suppressed in the livers of PA28gamma(+/+)CoreTg mice in response to insulin stimulation, whereas they were restored in the livers of PA28gamma(-/-)CoreTg mice. Furthermore, activation of the tumor necrosis factor alpha promoter in human liver cell lines or mice by the HCV core protein was suppressed by the knockdown or knockout of the PA28gamma gene. These results suggest that the HCV core protein suppresses insulin signaling through a PA28gamma-dependent pathway.     

Globular adiponectin protected ob/ob mice from diabetes and ApoE-deficient mice from atherosclerosis

The adipocyte-derived hormone adiponectin has been shown to play important roles in the regulation of energy homeostasis and insulin sensitivity. In this study, we analyzed globular domain adiponectin (gAd) transgenic (Tg) mice crossed with leptin-deficient ob/ob or apoE-deficient mice. Interestingly, despite an unexpected similar body weight, gAd Tg ob/ob mice showed amelioration of insulin resistance and beta-cell degranulation as well as diabetes, indicating that globular adiponectin and leptin appeared to have both distinct and overlapping functions. Amelioration of diabetes and insulin resistance was associated with increased expression of molecules involved in fatty acid oxidation such as acyl-CoA oxidase, and molecules involved in energy dissipation such as uncoupling proteins 2 and 3 and increased fatty acid oxidation in skeletal muscle of gAd Tg ob/ob mice. Moreover, despite similar plasma glucose and lipid levels on an apoE-deficient background, gAd Tg apoE-deficient mice showed amelioration of atherosclerosis, which was associated with decreased expression of class A scavenger receptor and tumor necrosis factor alpha. This is the first demonstration that globular adiponectin can protect against atherosclerosis in vivo. In conclusion, replenishment of globular adiponectin may provide a novel treatment modality for both type 2 diabetes and atherosclerosis.     

Discovery of novel antiviral agents directed against the influenza A virus nucleoprotein using photo-cross-linked chemical arrays

The nucleoprotein (NP) of the influenza virus is expressed in the early stage of infection and plays important roles in numerous steps of viral replication. NP is relatively well conserved compared with viral surface spike proteins. This study experimentally demonstrates that NP is a novel target for the development of new antiviral drugs against the influenza virus. First, artificial analogs of mycalamide A in a chemical array bound specifically with high affinity to NP. Second, the compounds inhibited multiplication of the influenza virus. Furthermore, surface plasmon resonance imaging experiments demonstrated that the binding activity of each compound to NP correlated with its antiviral activity. Finally, it was shown that these compounds bound NP within the N-terminal 110-amino acid region but their binding abilities were dramatically reduced when the N-terminal 13-amino acid tail was deleted, suggesting that the compounds might bind to this region, which mediates the nuclear transport of NP and its binding to viral RNA. These data suggest that compound binding to the N-terminal 13-amino acid tail region may inhibit viral replication by inhibiting the functions of NP. Collectively, these results strongly suggest that chemical arrays are convenient tools for the screening of viral product inhibitors.     

A RANKL-inducible gene Znf216 in osteoclast differentiation

Osteoclasts possess catabolic activity in mineralized tissues and are involved in bone remodeling coordinating with osteoblasts. Although the pathway using receptor and activator of NF-kappa B (RANK) and its ligand, RANKL, is known to be essential for osteoclast differentiation, their precise mechanisms are not fully understood. Using DNA microarray technology, we searched for genes that were up-regulated after RANKL stimulation in the macrophage cell line, RAW264.7 cells. A gene, Znf216, which encodes a zinc-finger protein, was detected among those genes up-regulated after RANKL stimulation. Expression of Znf216 was also induced by other cytokines such as TNFalpha and IL-1beta. Although ectopic expression of full-length ZNF216 abrogated osteoclast differentiation, its truncated forms accelerated it. No significant inhibitory effect on the NF-kappa B pathway was observed, however. These results suggest that ZNF216 is a potent inhibitory factor for osteoclast differentiation and that the mechanism is unlikely due to direct attenuation of the NF-kappa B pathway.