Expression of the tobacco mosaic virus movement protein alters starch accumulation inNicotiana benthamiana

Nicotiana benthamiana plants were transformed with the movement protein (MP) gene of tobacco mosaic virus (TMV), usingAgrobacterium-mediated transformation. Plants regenerated from the transformed cells accumulated 30-kDa MP and complemented the activity of TMV MP when infected with chimeric TMVs containing defective MR These transgenic plants displayed stunting, pale-green leaves, and starch accumulations, indicating that TMV MP altered the carbon partitioning for leaves involved in TMV cell-to-cell movement.     

Harmonious Compatibility Dominates Influence of Side‐Chain Engineering on Morphology and Performance of Ternary Solar Cells

A growing number of recent studies have demonstrated the substantial impact of the alkyl side chains on the device performance of organic semiconductors. However, detailed investigation of the effect of side‐chain engineering on the blend morphology and performance of ternary organic solar cells (OSCs) has not yet been undertaken. In this study, the performance of ternary OSCs is investigated in a given poly(4,8‐bis(5‐(2‐ethylhexyl)thiophen‐2‐yl)benzo[1,2‐b;4,5‐b′]dithiophene‐2,6‐diyl‐alt‐(4‐(2‐ethylhexyl)‐3‐fluorothieno[3,4‐b]thiophene‐)‐2‐carboxylate‐2‐6‐diyl)):[6,6]‐phenyl‐C₇₁‐butyric acid methyl ester (PTB7‐Th:PC₇₁BM) host set by introducing various small molecule donors (SMDs) with different terminal side‐chain lengths. As expected, the performance of binary OSCs with SMDs depends greatly on the side‐chain length. In contrast, it is observed that all SMD‐based ternary OSCs exhibit almost identical and high power‐conversion efficiencies of 12.0–12.2%. This minor performance variation is attributed to good molecular compatibility between the two donor components, as evidenced by in‐depth electrical and morphological investigations. These results highlight that the alloy‐like structure formed due to the high compatibility of the donor molecules has a more significant effect on the overall performance than the side‐chain length, offering a new guideline for pairing donor components for achieving high‐performance ternary OSCs.     

The Signaling Mechanism of Contraction Induced by ATP and UTP in Feline Esophageal Smooth Muscle Cells

P2 receptors are membrane-bound receptors for extracellular nucleotides such as ATP and UTP. P2 receptors have been classified as ligand-gated ion channels or P2X receptors and G protein-coupled P2Y receptors. Recently, purinergic signaling has begun to attract attention as a potential therapeutic target for a variety of diseases especially associated with gastroenterology. This study determined the ATP and UTP-induced receptor signaling mechanism in feline esophageal contraction. Contraction of dispersed feline esophageal smooth muscle cells was measured by scanning micrometry. Phosphorylation of MLC₂₀ was determined by western blot analysis. ATP and UTP elicited maximum esophageal contraction at 30 s and 10 μM concentration. Contraction of dispersed cells treated with 10 μM ATP was inhibited by nifedipine. However, contraction induced by 0.1 μM ATP, 0.1 μM UTP and 10 μM UTP was decreased by {"type":"entrez-nucleotide","attrs":{"text":"U73122","term_id":"4098075","term_text":"U73122"}}U73122, chelerythrine, ML-9, PTX and GDPβS. Contraction induced by 0.1 μM ATP and UTP was inhibited by Gαi₃ or Gαq antibodies and by PLCβ₁ or PLCβ₃ antibodies. Phosphorylated MLC₂₀ was increased by ATP and UTP treatment. In conclusion, esophageal contraction induced by ATP and UTP was preferentially mediated by P2Y receptors coupled to Gαi₃ and G q proteins, which activate PLCβ₁ and PLCβ₃. Subsequently, increased intracellular Ca²⁺ and activated PKC triggered stimulation of MLC kinase and inhibition of MLC phosphatase. Finally, increased pMLC₂₀ generated esophageal contraction.     

WebCell: a web-based environment for kinetic modeling and dynamic simulation of cellular networks

SUMMARY: WebCell is a web-based environment for managing quantitative and qualitative information on cellular networks and for interactively exploring their steady-state and dynamic behaviors in response to systemic perturbations. It is designed as a user-friendly web interface, allowing users to efficiently construct, visualize, analyze and store reaction network models, thereby facilitating kinetic modeling and in silico simulation of biological systems of interest. A collected model library is also available to provide comprehensive implications for cellular dynamics of the published models.     

Application of oncoproteomics to aberrant signalling networks in changing the treatment paradigm in acute lymphoblastic leukaemia

Oncoproteomics is an important innovation in the early diagnosis, management and development of personalized treatment of acute lymphoblastic leukaemia (ALL). As inherent factors are not completely known – e.g. age or family history, radiation exposure, benzene chemical exposure, certain viral exposures such as infection with the human T‐cell lymphoma/leukaemia virus‐1, as well as some inherited syndromes may raise the risk of ALL – each ALL patient may modify the susceptibility of therapy. Indeed, we consider these unknown inherent factors could be explained via coupling cytogenetics plus proteomics, especially when proteins are the ones which play function within cells. Innovative proteomics to ALL therapy may help to understand the mechanism of drug resistance and toxicities, which in turn will provide some leads to improve ALL management. Most important of these are shotgun proteomic strategies to unravel ALL aberrant signalling networks. Some shotgun proteomic innovations and bioinformatic tools for ALL therapies will be discussed. As network proteins are distinctive characteristics for ALL patients, unrevealed by cytogenetics, those network proteins are currently an important source of novel therapeutic targets that emerge from shotgun proteomics. Indeed, ALL evolution can be studied for each individual patient via oncoproteomics.     

Synthesis and antimicrobial activity of 7 alpha-amino-23,24-bisnor-5 alpha-cholan-22-ol derivatives

A series of 7 alpha-aminobisnorsteroids were synthesized and their in vitro antimicrobial activity was evaluated regarding Gram-positive and Gram-negative bacteria. The stereoselective reductive amination of 7-ketosteroid 3 with NH(4)OAc, in the presence of NaBH(3)CN, afforded a high yield of 7 alpha-aminosteroid 4. The 3,7-diaminobisnorsteroids were obtained by the reductive amination of 4 with NH(4)OT(f), Boc-spermidine, and Boc-spermine. 3 alpha,7 alpha-Diaminobisnorsterol dihydrochloride 15 showed the highest antimicrobial activity against Streptococcus pyogenes 308 A with a MIC value of 1.6 microg/mL. Hemolytic activities of the compounds 13-20 were determined. Compound 13 showed MHC value at 100 microg/mL.     

Nuclear translocation and DNAse I-like enzymatic activity of Acinetobacter baumannii outer membrane protein A

Acinetobacter baumannii outer membrane protein A (AbOmpA) is a potential virulence factor that induces host cell death. Based on previous findings that AbOmpA translocated into the nuclei of host cells, the cell-death mechanism of AbOmpA through the nuclear targeting was investigated. Acinetobacter baumannii secreted AbOmpA in in vitro culture. The recombinant AbOmpA (rAbOmpA) was internalized by the host cells. The intracellular rAbOmpA was degraded into several forms of subfragments in the cytosol and then two subfragments of rAbOmpA translocated into the nuclei. The rAbOmpA exhibited the divalent cation-dependent endonuclease activity. In an in vivo assay with microinjection of rAbOmpA into the nucleus of fertilized Xenopus laevis eggs, rAbOmpA degraded chromosomal DNA with the characteristic DNA ladders and induced degeneration of the embryos. These results suggest that AbOmpA translocates into the nuclei of host cells and degrades chromosomal DNA by DNAse I-like enzymatic activity, which is a new pathogenic strategy of A. baumannii.     

Arginase Inhibition Ameliorates Hepatic Metabolic Abnormalities in Obese Mice

Objectives

We examined whether arginase inhibition influences hepatic metabolic pathways and whole body adiposity in diet-induced obesity.

Methods and Results

After obesity induction by a high fat diet (HFD), mice were fed either the HFD or the HFD with an arginase inhibitor, N^ω-hydroxy-nor-L-arginine (nor-NOHA). Nor-NOHA significantly prevented HFD-induced increases in body, liver, and visceral fat tissue weight, and ameliorated abnormal lipid profiles. Furthermore, nor-NOHA treatment reduced lipid accumulation in oleic acid-induced hepatic steatosis in vitro. Arginase inhibition increased hepatic nitric oxide (NO) in HFD-fed mice and HepG2 cells, and reversed the elevated mRNA expression of hepatic genes in lipid metabolism. Expression of phosphorylated 5′ AMPK-activated protein kinase α was increased by arginase inhibition in the mouse livers and HepG2 cells.

Conclusions

Arginase inhibition ameliorated obesity-induced hepatic lipid abnormalities and whole body adiposity, possibly as a result of increased hepatic NO production and subsequent activation of metabolic pathways involved in hepatic triglyceride metabolism and mitochondrial function.