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The inherent randomness in economic factors causes complex and irregular behaviour that affects financial system stability and economic growth. Such chaotic behaviour can make it difficult to synchronize financial systems. The chaotic finance system synchronization precision maintains financial stability and economic growth. In this paper, the controller design procedure assumes that the financial system is exposed to unknown bounded exogenous disturbances and model uncertainties. This research proposes a novel direct adaptive control strategy that achieves robust synchronization of two identical four-dimensional finance chaotic (FDFC) systems. The proposed controller establishes a faster, smoother synchronization error vector convergence to zero. The controller design procedure does not eliminate the closed-loop's nonlinear terms and is independent of the financial system parameters. These controller's attributes accomplish the closed-loop robust performance. Further, this controller uses real-time estimates of unknown model uncertainties and bounds to compensate for unknown exogenous disturbances. Computer simulation results and proofs of theoretical analysis based on the Lyapunov stability theory confirm that the proposed control technique compels the error vector trajectories to the origin in a short transient time with less active oscillations for all signals. The paper includes comparative computer simulations for verifying the theoretical findings. [ABSTRACT FROM AUTHOR]

The precise anti-synchronization control of uncertain chaotic systems has always remained an interesting problem. The anti-synchronization control of multiple different orders uncertain chaotic systems increases the complexity and enhances the security of the information signal in secure communications. Hence, it confines the hacking in digital communication systems. This paper proposes a novel adaptive control technique and studies the double combination anti-synchronization of multiple different orders uncertain chaotic systems. The proposed adaptive feedback control technique consists of three fundamental nonlinear components. Each component accomplishes a different objective; (i) stability of the closed-loop, (ii) smooth and fast convergence behaviour of the anti-synchronization error, and (iii) disturbance rejection. The theoretical analysis in (i) to (iii) uses the Lyapunov stability theory. This paper also provides parameters adaptation laws that stabilize the uncertain parameters to some constants. The paper discusses the simulation results of two representative examples of four different orders uncertain chaotic systems. These examples demonstrate anti-synchronization among hyperchaotic Lü, uncertain chaotic Shimizu Morioka, uncertain second-order nonlinear duffing, and uncertain parametrically excited second-order nonlinear pendulum systems. The computer-based simulation results certify the efficiency and performance of the proposed anti-synchronization control approach and compare them with peer works. [ABSTRACT FROM AUTHOR]

The synthesis, characterisation and anion binding studies of 2-(2,4-dinitrophenyl)-3-ethoxy-5-methyl-3,4-dihydro-2H-pyrazol-3-ol (1) have been described. 1, bearing electron withdrawing 2,4-dinitophenyl group in its structure, recognises CN−  selectively in CH3CN/H2O (4:1, v/v) medium with a binding constant of 440 M− 1 and visible colour change from yellow to red, whereas no colour change is observed in the presence of other anions such as F− , Cl− , Br− , I− , , AcO− , PhCOO− . Interestingly, in CH3CN, 1 is responsive not only to CN−  but also to F− , , AcO−  and PhCOO−  with a binding-induced visible colour change from yellow to reddish-brown. The strongest binding ability of 1 is observed with CN−  in CH3CN, the binding constant being 1.34 × 105 M− 1, whereas the binding constants of F−  and oxyanions ( , AcO− , PhCOO− ) are found to be lower by one order or more in magnitude. 1H NMR titrations of 1 are carried out with CN−  and F− , which not only provide the evidence for the hydrogen-bonding interaction between the alcohol –OH of 1 and anions, but also offer some invaluable information about the structure of the sensor–anion complexes. [ABSTRACT FROM PUBLISHER]

The study was undertaken to investigate the effect of zinc (Zn) on glutathione S-transferase (GST) and superoxide dismutases (SOD) activities and on the expressions of cytosolic Cu, Zn-SOD (SOD1), mitochondrial Mn-SOD (SOD2), γ-glutamyl cysteine synthetase (γ-GCS) and heme oxygenase-1 (HO-1) in the nigrostriatal tissue of rats. Additionally, Zn-induced alterations in the neurobehavioral parameters, lipid peroxidation (LPO), striatal dopamine and its metabolites and tyrosine hydroxylase (TH) protein expression were measured to assess their correlations with the oxidative stress. Zn exposure reduced the locomotor activity, rotarod performance, striatal dopamine and its metabolites and TH protein expression. LPO, total SOD, SOD1 and SOD2 activities were increased while GST and catalase were reduced in a dose and time dependent manner. Expressions of SOD1 and HO-1 were increased while no change was observed in SOD2 and γ-GCS expressions. The results obtained suggest that Zn-induced augmentation of total SOD, SOD1, SOD2 and HO-1 was associated with increased oxidative stress and neurodegenerative indexes indicating the involvement of both cytosolic and mitochondrial machinery in Zn-induced oxidative stress leading to dopaminergic neurodegeneration. [ABSTRACT FROM AUTHOR]

Long-term exposure to cypermethrin induces the nigrostriatal dopaminergic neurodegeneration in adult rats and its pre-exposure in the critical periods of brain development enhances the susceptibility during adulthood. Monoamine transporters, xenobiotic metabolizing enzymes and oxidative stress play critical roles in the nigrostriatal dopaminergic neurodegeneration. The study was undertaken to investigate the effects of cypermethrin on DAT, VMAT 2, CYP2E1, GST Ya, GST Yc and GSTA4-4 expressions, CYP2E1 and GST activities and lipid peroxidation in the nigrostriatal system of adult rats with/without post-natal exposure to cypermethrin. Cypermethrin reduced VMAT 2 and increased CYP2E1 expressions without causing significant change in DAT. Although GSTA4-4 mRNA expression and lipid peroxidation were increased, no significant changes were observed in GST Ya and GST Yc expressions and total GST activity. The results obtained demonstrate that long-term exposure to cypermethrin modulates VMAT 2, CYP2E1, GSTA4-4 expressions and lipid peroxidation, which could contribute to the nigrostriatal dopaminergic neurodegeneration. [ABSTRACT FROM AUTHOR]

Oxidative stress is implicated in Parkinson's disease (PD). Metallothioneins (MT), cytochrome P450 IIE1 (CYP2E1) and glutathione S-transferases alpha4-4 (GSTA4-4) are involved in oxidative stress-mediated damage. Altered dopamine transporter (DAT) and vesicular monoamine transporter-2 (VMAT-2) are also documented in PD. The present study was undertaken to investigate the effect of Zn and PQ co-exposure on neurodegeneration in rats. A significant reduction was observed in spontaneous locomotor activity (SLA), striatal dopamine (DA) levels, tyrosine hydroxylase (TH) immunoreactivity, glutathione reductase (GR) and catalase activity along with increased lipid peroxidation (LPO) and glutathione peroxidase (GPx) activity after Zn and/or PQ exposure. Zn and/or PQ exposure increased gene expression of DAT, CYP2E1, GSTA4-4, MT-I and MT-II, but reduced the expression of VMAT-2. Protein expression analysis of TH, VMAT-2 and DAT showed results similar to those obtained with gene expression study. Zn and PQ co-exposure caused a more pronounced effect than that of individual exposure. The results obtained in this study suggest that, similar to PQ, Zn induced neurodegeneration via alterations in oxidative stress and expression of the above-mentioned genes. However, the effect of Zn+PQ was only slightly higher than that of alone, indicating that probably Zn and PQ follow some different molecular events leading to neurodegeneration. [ABSTRACT FROM AUTHOR]

Yb(OTf)3 in an ionic liquid [bmim][BF4] has been described as an efficient catalyst for the thia-Michael addition of thiols to α,β -unsaturated ketones to give β -aryl-β-mercapto ketones in 82-94% yield and the catalyst along with ionic liquid was recycled and reused. [ABSTRACT FROM AUTHOR]

Oxidative stress plays a crucial role in the manifestations of maneb (MB) and paraquat (PQ)-induced toxicity including MB+PQ-induced Parkinson's disease (PD). Polymorphonuclear leukocytes (PMNs) actively participate in the oxidative stress-mediated inflammation and organ toxicity. The present study was undertaken to investigate the MB- and/or PQ-induced alterations in the indices of oxidative stress in rat PMNs. Animals were treated with or without MB and/or PQ in an exposure time dependent manner. In some sets of experiments, the animals were pre-treated with NOS inhibitors NG-nitro-L-arginine methyl ester (L-NAME) and aminoguanidine (AG) along with respective controls. A significant increase in myeloperoxidase (MPO), superoxide dismutase (SOD), nitric oxide, iNOS expression and lipid peroxidation (LPO) was observed in PMNs of MB- and/or PQ-treated animals, while catalase and glutathione S-transferase (GST) activities were attenuated. L-NAME and AG significantly reduced the augmented nitrite content, iNOS expression and MPO activity to control level in MB and PQ exposed animals. Although the augmented LPO was also reduced significantly in L-NAME and AG treated rat PMNs, the level was still higher as compared with controls. Alterations induced in SOD and GST activities were not affected by NOS inhibitors. The results thus suggest that MB and/or PQ induce iNOS-mediated nitric oxide production, which in turn increases MPO activity and lipid peroxidation, thereby oxidative stress. [ABSTRACT FROM AUTHOR]