Search

The compound 3-chlorobenzoate (3-CBA) is a hazardous industrial waste product that can harm human health and the environment. This study investigates the physiological and genetic potential for 3-chlorobenzoate (3-CBA) degradation. Six 3-CBA Gram-negative degraders with different degradation properties belonging to the genera Caballeronia, Paraburkholderia and Cupriavidus were isolated from the soil. The representative strains Caballeronia 19CS4-2 and Paraburkholderia 19CS9-1 showed higher maximum specific growth rates (µmax, h−1) than Cupriavidus 19C6 and degraded 5 mM 3-CBA within 20–28 h. Two degradation products, chloro-cis,cis-muconate and maleylacetate, were detected in all isolates using high-performance liquid chromatography and mass spectrometry. Genomic analyses revealed the presence of cbe and tfd gene clusters in strains 19CS4-2 and 19CS9-1, indicating that they probably metabolized the 3-CBA via the chlorocatechol ortho-cleavage pathway. Strain 19C6 possessed cbe genes, but not tfd genes, suggesting it might have a different chlorocatechol degradation pathway. Putative genes for the metabolism of 3-hydroxybenzoate via gentisate were found only in 19C6, which utilized the compound as a sole carbon source. 19C6 exhibited distinct characteristics from strains 19CS4-2 and 19CS9-1. The results confirm that bacteria can degrade 3-CBA and improve our understanding of how they contribute to environmental 3-CBA biodegradation.

Cupriavidus necator NH9, a 3-chlorobenzoate (3-CB)-degrading bacterium, was isolated from soil in Japan. In this study, the complete genome sequence of NH9 was obtained via PacBio long-read sequencing to better understand the genetic components contributing to the strain's ability to degrade aromatic compounds, including 3-CB. The genome of NH9 comprised two circular chromosomes (4.3 and 3.4 Mb) and two circular plasmids (427 and 77 kb) containing 7,290 coding sequences, 15 rRNA and 68 tRNA genes. Kyoto Encyclopedia of Genes and Genomes pathway analysis of the protein-coding sequences in NH9 revealed a capacity to completely degrade benzoate, 2-, 3-, or 4-hydroxybenzoate, 2,3-, 2,5-, or 3,4-dihydroxybenzoate, benzoylformate, and benzonitrile. To validate the identification of NH9, phylogenetic analyses (16S rRNA sequence-based tree and multilocus sequence analysis) and whole-genome sequence analyses (average nucleotide identity, percentage of conserved proteins, and tetra-nucleotide analyses) were performed, confirming that NH9 is a C. necator strain. Over the course of our investigation, we noticed inconsistencies in the classification of several strains that were supposed to belong to the two closely-related genera Cupriavidus and Ralstonia. As a result of whole-genome sequence analysis of 46 Cupriavidus strains and 104 Ralstonia strains, we propose that the taxonomic classification of 41 of the 150 strains should be changed. Our results provide a clear delineation of the two genera based on genome sequences, thus allowing taxonomic identification of strains belonging to these two genera.

JTT-130 was developed as an intestine-specific MTP inhibitor designed to rapidly catabolize after absorption to avoid causing hepatotoxicity due to hepatic MTP inhibition. In previous reports, we have demonstrated that JTT-130 suppresses dietary lipid absorption in the small intestine without inducing hepatic steatosis. Thus, in this report, JTT-130 was administered to hyperlipidemic animals fed a Western diet to investigate the effect of intestinal MTP inhibition on lipid metabolism and progression of atherosclerosis. JTT-130 potently lowered plasma non-high density lipoprotein-cholesterol, and elevated plasma high density lipoprotein-cholesterol (HDL-C), indicating improvement in atherogenic index in hamsters. HDL fractions obtained after two weeks treatment with JTT-130 significantly increased the efflux of cholesterol from macrophages, as an index parameter of HDL function. Furthermore, long-term treatment with JTT-130 also improved the plasma lipid profile without inducing hepatic steatosis in rabbits, resulting in the suppression of atherosclerosis formation in aortas. From these results, JTT-130 ameliorates lipid metabolism accompanied with the enhancement of the anti-atherosclerotic function of HDL, and attenuates the progression of atherosclerosis in hyperlipidemic animals. These findings indicate that intestinal MTP inhibition may be atherogenic in vivo and that JTT-130 may be a useful compound for the treatment of dyslipidemia and a potential anti-atherogenic drug.

The mechanism by which cholesteryl ester transfer protein (CETP) activity affects HDL metabolism was investigated using agents that selectively target CETP (dalcetrapib, torcetrapib, anacetrapib). In contrast with torcetrapib and anacetrapib, dalcetrapib requires cysteine 13 to decrease CETP activity, measured as transfer of cholesteryl ester (CE) from HDL to LDL, and does not affect transfer of CE from HDL3 to HDL2. Only dalcetrapib induced a conformational change in CETP, when added to human plasma in vitro, also observed in vivo and correlated with CETP activity. CETP-induced pre-β-HDL formation in vitro in human plasma was unchanged by dalcetrapib ≤3 µM and increased at 10 µM. A dose-dependent inhibition of pre-β-HDL formation by torcetrapib and anacetrapib (0.1 to 10 µM) suggested that dalcetrapib modulates CETP activity. In hamsters injected with [3H]cholesterol-labeled autologous macrophages, and given dalcetrapib (100 mg twice daily), torcetrapib [30 mg once daily (QD)], or anacetrapib (30 mg QD), only dalcetrapib significantly increased fecal elimination of both [3H]neutral sterols and [3H]bile acids, whereas all compounds increased plasma HDL-[3H]cholesterol. These data suggest that modulation of CETP activity by dalcetrapib does not inhibit CETP-induced pre-β-HDL formation, which may be required to increase reverse cholesterol transport.

Recently, many people have used Smartphones. The feature of Smartphones is that they are equipped with a mobile operating system (OS) for the control of sensors and modules. In this situation, we can connect external human interaction devices with the Smartphone. Our objective is to know how the external human interaction device affects to the OS. In this paper, we implement the programs for connecting the Wii Remote to the Android. Furthermore, we evaluate the performance of our programs and benchmark the Android while running our programs. We intend to shift our environment to the virtualized environment.

By measuring the i-v characteristics of Y3N@[C80]6- anionic solid at various temperatures and electric field strengths, four conducting phases with i∞v , i∞v2 with low resistance, i∞v4 and i∞v2 with high resistance were observed. First, at temperatures below 100K and field strengths below 30 Vcm-1, the current passing through the sample was a linear function of the d.c. bias voltage due to free moving charges. Second, at the same field strengths, the trapped carrier was thermally activated with activation energies of 13.6meV for temperature range of 100-250 K and 88.7meV for 250-450 K. In this conducting phase, the carrier transport was governed by space charge limited conduction mechanism. Third, when the electric field increased from 30 to 120 Vcm-1, the i became a quartic function of the v because the carrier mobility is a quadratic function of the field strength. A conducting phase with high resistance was observed at temperatures below 100K. The trapped carrier was thermally activated with activation energies of 146.5meV for temperature range of 100-250K and 288.5meV for 250-450K. Finally, in the electric field strengths of 120-2000 Vcm-1, a high resistance phase appeared in the anionic solid at temperatures below 100K. The current was a quadratic function of the d.c. bias voltage, and the carrier mobility was independent of the field strength [ABSTRACT FROM AUTHOR]

The article discusses a study by Kimiko Yamamoto-Tamura and colleagues which isolated a putative porin gene of the Burkholderia sp. NK8 named ompNK8 which suggests permeability for its metabolite. Topics discussed include the bacterial strains, plasmids, and culture conditions in the study, the construction of pOmpNK8 encoding plasmid, and identification of the gene in chemotaxis toward B-ketoadipate.

The article presents research study on isolation and structural determination of 16-membered macrolide named makinolide B from MK-19 strain of Streptomyces bacteria. The topics discussed include cultivation of the bacterial strain, high-resolution electrospray ionization-mass spectrometry of the isolated compound and Nuclear Magnetic Resonance (NMR) chemical shifts and the magnitude of the coupling constants of the macrolide compound.

Spontaneously Diabetic Torii (SDT) rats are a well-known animal model of non-obese type 2 diabetes mellitus. Although this animal model has been studied extensively over the last decade, the incidence rates of Leydig cell hyperplasia and tumors in this model have not been reported. In this study, pathophysiological analyses of the testes were performed on male SDT rats, to understand the effect of insulin treatment on the development of Leydig cell hyperplasia and tumors and the expression of integrins and extracellular matrix proteins. Testicular Leydig cell hyperplasia and tumors were observed in SDT rats at 64 weeks of age but were rarely identified in Sprague-Dawley (SD) rats of the same age. Insulin treatment decreased plasma glucose and HbA1c levels, and interestingly, decreased the number of hyperplastic Leydig cell foci and Leydig cell tumors in treated animals. A similar reduction in the expression of Ki67 in these Leydig cell foci was also observed. In addition, insulin treatment decreased the expression of integrin a5, integrin ß1, integrin avß3, fibronectin, and vitronectin in hyperplastic Leydig cell foci. These results suggest that insulin might decrease the incidence of Leydig cell hyperplasia by reducing Leydig cell proliferation and the expression of integrins and extracellular matrix proteins through the reduction of serum glucose concentrations in these animals. [ABSTRACT FROM AUTHOR]

Investigates the chlorobenzoate dioxygenase genes responsible for substrate specificity of NK8 for chlorobenzoates. Similarity of protein sequences between chlorobenzoate 1,2-dioxygenase and benzoate dioxygenase; Effect of cbeA gene disruption on benzoate and monobenzoate; Implications of NK8 growth absence for 2CB recognition.