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1.
Soft comput ; 24(23): 18249-18258, 2020.
Article in English | MEDLINE | ID: mdl-32837291

ABSTRACT

The distance vector-hop (DV-hop) is a typical localization algorithm. It estimates sensor nodes location through detecting the hop count between nodes. To enhance the positional precision, the weight is used to estimate position, and the conventional wisdom is that the more hop counts are, the smaller value of weight will be. However, there has been no clear mathematical model among positioning error, hop count, and weight. This paper constructs a mathematical model between the weights and hops and analyzes the convergence of this model. Finally, the genetic algorithm is used to solve this mathematical weighted DV-hop (MW-GADV-hop) positioning model, the simulation results illustrate that the model construction is logical, and the positioning error of the model converges to 1/4R.

2.
Chem Asian J ; 14(16): 2780-2784, 2019 Aug 16.
Article in English | MEDLINE | ID: mdl-31207187

ABSTRACT

The Acinetobacter sp. strain M isolated from a contaminated soil sample in Jiangsu Province of China was found to be able to degrade perfluorooctane sulfonamide (PFOSA) effectively. Fluoride anion (F- ) released from PFOSA degradation was detected by ion chromatography, and showed positive correlation to the growth curve of Acinetobacter sp. strain M. The PFOSA degradation efficiency of strain M was approximately 27 %, as assessed by GC analysis. It was shown that enzymes localized outside of cells of Acinetobacter sp. strain M catalyzed the degradation of PFOSA. This further indicates a possibly new (multi-step/pathway) mechanism for PFOSA degradation. It revealed that the extracellular enzyme of the Acinetobacter strain M preferentially cleaves carbon-carbon and carbon-fluorine bonds instead of destroying the carbon-sulfur bond. The growth condition for Acinetobacter sp. strain M was optimized at 30 °C and pH 7.0 in the presence of 2000 mg L-1 of PFOSA and 0.5 % (v/v) of Tween-20. The optimal PFOSA degradation time was found to be 12 h, with a degradation efficiency of 76 % by extracellular enzymes in strain M as determined by GC analysis. The result may provide potential applications for biodegradition of perfluoro organic compounds, such as derivatives of perfluorooctane (C8).


Subject(s)
Acinetobacter/metabolism , Enzymes/metabolism , Fluorocarbons/metabolism , Sulfonamides/metabolism , Acinetobacter/enzymology , Acinetobacter/growth & development , Gas Chromatography-Mass Spectrometry , Soil Microbiology
3.
Cardiovasc Toxicol ; 16(2): 101-10, 2016 Apr.
Article in English | MEDLINE | ID: mdl-25724325

ABSTRACT

Luteolin-7-O-glucoside (LUTG) was isolated from the plants of Dracocephalum tanguticum Maxim. Previous research has showed that LUTG pretreatment had a significant protective effect against doxorubicin (DOX)-induced cardiotoxicity by reducing intracellular calcium overload and leakage of creatine kinase and lactate dehydrogenase. But the underlying mechanisms have not been completely elucidated. In the present study, we investigated the effects of LUTG on H9c2 cell morphology, viability, apoptosis, reactive oxygen species generation, and the mitochondrial transmembrane potentials. The expression of p-PTEN, p-Akt, p-ERK, p-mTOR, and p-GSK-3ß were detected by Western blotting. Compared with DOX alone treatment group, the morphological injury and apoptosis of the cells in groups treated by DOX plus LUTG were alleviated, cell viability was increased, ROS generation was lowered remarkably, and mitochondrial depolarization was mitigated. In DOX group, the expression of p-PTEN was lower than normal group and the expression of p-Akt and p-ERK was higher than normal group. In the groups treated with LUTG (20 µM), the expression of p-PTEN was upregulated and the expression of p-Akt, p-ERK, p-mTOR, and p-GSK-3ß was downregulated. These results indicated that the protective effects of LUTG against DOX-induced cardiotoxicity may be related to anti-apoptosis through PTEN/Akt and ERK pathway.


Subject(s)
Cardiotonic Agents/pharmacology , Doxorubicin/toxicity , Flavones/pharmacology , Glucosides/pharmacology , MAP Kinase Signaling System/drug effects , PTEN Phosphohydrolase/biosynthesis , Proto-Oncogene Proteins c-akt/biosynthesis , Animals , Antibiotics, Antineoplastic/toxicity , Cell Survival/drug effects , Cell Survival/physiology , Dose-Response Relationship, Drug , MAP Kinase Signaling System/physiology , Myocytes, Cardiac/drug effects , Myocytes, Cardiac/metabolism , Rats
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