Production, Location, and Binding of Violacein in Janthinobacterium

Violacein is a purple pigment typically produced by species of Chromobacterium and Janthinobacterium. A soil isolate, identified as Janthinobacterium, was studied. Maximal pigmentation occurred at 250C under aerobic conditions in the Keeble and Cross medium. Intracellular pigment was shown to be located in the cell membrane. Comparision of pigment production and growth curves indicated that violacein is synthesized in the cell and released into the environment possibly as a result of cell lysis. Extracellular pigment is water soluble, makes up 60% of the total pigment and shows a blue shift when compared to solvent extracted pigment. Results from purification indicated that the pigment is non-covalently bound to a small protein and aggregated into a larger molecule

Dichlorido[(1R,2R)-N-(pyridin-2-yl­methyl)cyclo­hexane-1,2-diamine-κ3 N,N′,N′′]mercury(II)

In the title compound, [HgCl2(C12H19N3)], the HgII ion is coordinated by three N atoms of the (1R,2R)-N-(pyridin-2-ylmeth­yl)cyclo­hexane-1,2-diamine ligand and by a Cl atom in the basal plane, and by a second Cl atom in the apical position, within a distorted square-pyramidal geometry. The coordination of the enanti­opure ligand to the metal atom renders the central N atom chiral with an S configuration, so the complex is enanti­omerically pure and corresponds to the S,R,R diastereoisomer. Mol­ecules are linked via weak N—H⋯Cl hydrogen bonds into a one-dimensional hydrogen-bonding supramolecular chain along the crystallographic b axis

Developing Blue Ocean Strategy of Sustainable Product Design and Development for Business Opportunities of BOP Groups in Taiwan

This study expands the definition of the poor group and attempts to delve into and make known the phenomenon of poverty in Taiwan and aims to explore the goals and possibilities of the BOP consumer market. Through a questionnaire survey and expert interviews, this research adopts the concept of sustainability to discuss the lifestyle and consumption characteristics of the BOP group and establishes a design strategic norm of the sustainable products. The findings show that the BOP group in Taiwan is new poverty or working poor and high quality and common prices are the main requirements; these should be introduced into the development model of sustainable design

Structural insights into the gating of DNA passage by the topoisomerase II DNA-gate.

Type IIA topoisomerases (Top2s) manipulate the handedness of DNA crossovers by introducing a transient and protein-linked double-strand break in one DNA duplex, termed the DNA-gate, whose opening allows another DNA segment to be transported through to change the DNA topology. Despite the central importance of this gate-opening event to Top2 function, the DNA-gate in all reported structures of Top2-DNA complexes is in the closed state. Here we present the crystal structure of a human Top2 DNA-gate in an open conformation, which not only reveals structural characteristics of its DNA-conducting path, but also uncovers unexpected yet functionally significant conformational changes associated with gate-opening. This structure further implicates Top2's preference for a left-handed DNA braid and allows the construction of a model representing the initial entry of another DNA duplex into the DNA-gate. Steered molecular dynamics calculations suggests the Top2-catalyzed DNA passage may be achieved by a rocker-switch-type movement of the DNA-gate

Proteomic analysis of rhein-induced cyt: ER stress mediates cell death in breast cancer cells

Rhein is a natural product purified from herbal plants such as Rheum palmatum, which has been shown to have anti-angiogenesis and anti-tumor metastasis properties. However, the biological effects of rhein on the behavior of breast cancers are not completely elucidated. To evaluate whether rhein might be useful in the treatment of breast cancer and its cytotoxic mechanism, we analyzed the impact of rhein treatment on differential protein expression as well as redox regulation in a non-invasive breast cancer cell line, MCF-7, and an invasive breast cancer cell line, MDA-MB-231, using lysine- and cysteine-labeling two-dimensional difference gel electrophoresis (2D-DIGE) combined with MALDI-TOF/TOF mass spectrometry. This proteomic study revealed that 73 proteins were significantly changed in protein expression; while 9 proteins were significantly altered in thiol reactivity in both MCF-7 and MDA-MB-231 cells. The results also demonstrated that rhein-induced cytotoxicity in breast cancer cells mostly involves dysregulation of cytoskeleton regulation, protein folding, the glycolysis pathway and transcription control. A further study also indicated that rhein promotes misfolding of cellular proteins as well as unbalancing of the cellular redox status leading to ER-stress. Our work shows that the current proteomic strategy offers a high-through-put platform to study the molecular mechanisms of rhein-induced cytotoxicity in breast cancer cells. The identified differentially expressed proteins might be further evaluated as potential targets in breast cancer therapy

Neuroprotective effect of paeonol against isofluraneinduced neuroapoptosis and cognitive dysfunction

Purpose: To investigate whether paeonol affords neuroprotection against isoflurane-induced neurotoxicity.Methods: Separate groups of neonatal rat pups were administered paeonol (20, 40 or 80 mg/kg) from post-natal day 3 (P3) to post-natal day 15. On post-natal day 7, the pups were exposed to 6 h of isoflurane (0.75 %) anesthesia. TUNEL assay was performed to assess neuroapoptosis. Cleaved caspase-3 expressions were evaluated by immunohistochemistry and western blotting analysis. The expressions of apoptotic pathway proteins and mitogen activated protein kinases (MAPKs) were assessed by western blotting. The general behaviour of the rats was determined by open field test and elevated maze test. Y-maze test and Morris water maze tests were performed to evaluate working memory and cognition.Results: Isoflurane exposure caused (p < 0.05) severe neuronal apoptosis in the hippocampal region and enhanced caspase-3 expressions. Paeonol supplementation remarkably (p < 0.05) reduced neuronal apoptosis and modulated expressions of apoptotic proteins. The raised expressions of NF-κB, TNF-α, IL-6 and IL-1β and significantly (p < 0.05) enhanced JNK/p38 signalling cascades were inhibited by paeonol. The expression levels of ERK were not significantly (p < 0.05) changed, but there was significant improvement in the general behaviour and working memory of the rats.Conclusion: Paeonol significantly improves cognitive impairments and offers neuroprotection against isoflurane-induced apoptosis via modulating JNK/ERK/p38 MAPK and NF-κB signaling pathways.Keywords: Apoptosis, Isoflurane, Neurodegeneration, Paeonol, Cognitive impairment, Signaling pathway

Crystal structure of an FIV/HIV chimeric protease complexed with the broad-based inhibitor, TL-3

We have obtained the 1.7 Å crystal structure of FIV protease (PR) in which 12 critical residues around the active site have been substituted with the structurally equivalent residues of HIV PR (12X FIV PR). The chimeric PR was crystallized in complex with the broad-based inhibitor TL-3, which inhibits wild type FIV and HIV PRs, as well as 12X FIV PR and several drug-resistant HIV mutants [1-4]. Biochemical analyses have demonstrated that TL-3 inhibits these PRs in the order HIV PR > 12X FIV PR > FIV PR, with K(i )values of 1.5 nM, 10 nM, and 41 nM, respectively [2-4]. Comparison of the crystal structures of the TL-3 complexes of 12X FIV and wild-typeFIV PR revealed theformation of additinal van der Waals interactions between the enzyme inhibitor in the mutant PR. The 12X FIV PR retained the hydrogen bonding interactions between residues in the flap regions and active site involving the enzyme and the TL-3 inhibitor in comparison to both FIV PR and HIV PR. However, the flap regions of the 12X FIV PR more closely resemble those of HIV PR, having gained several stabilizing intra-flap interactions not present in wild type FIV PR. These findings offer a structural explanation for the observed inhibitor/substrate binding properties of the chimeric PR