Enantiopure bis[{(R or S)-N-1-(Ar)ethyl-2-oxo-1-naphthaldiminato-κ(2)N,O}]nickel(ii) complexes {Ar = C6H5 ( or ), p-OMeC6H4 ( or ), and p-BrC6H4 ( or )} are synthesized from the reactions between (R or S)-N-1-(Ar)ethyl-2-oxo-1-naphthaldimine and nickel(ii) acetate. Circular-dichroism spectra and their density-functional theoretical simulation reveal the expected mirror image relationship between the enantiomeric pairs / and / in solution. CD spectra are dominated by the metal-centered Λ- or Δ-chirality of non-planar four-coordinated nickel, this latter being in turn dictated by the ligand chirality. Single crystal structure determination for and shows that there are two symmetry-independent molecules (A and B) in each asymmetric unit that give a Z' = 2 structure. Two asymmetric and chiral bidentate N^O-chelate Schiff base ligands coordinate to the nickel atom in a distorted square planar N2O2-coordination sphere. The conformational difference between the symmetry-independent molecules arises from the "up-or-down" folding of the naphthaldiminato ligand with respect to the coordination plane, which creates right- (P) or left-handed (M) helical conformations. Overall, the combination of ligand chirality, chirality at the metal and ligand folding gives rise to discrete metal helicates of preferred helicity in a selective way. Cyclic voltammograms (CV) show an oxidation wave at ca. 1.30 V for the [Ni(L)2]/[Ni(L)2](+) couple, and a reduction wave at ca. -0.35 V for the [Ni(L)2]/[Ni(L)2](-) couple in acetonitrile.

Enantiopure dinuclear μ‐aqua‐tetrakis[(R or S)‐N‐1‐(Ar)ethylsalicylaldiminato]di‐Λ‐ or ‐Δ‐nickel(II) [Ar = C6H5 (R‐1/S‐1), p‐MeOC6H4 (R‐2/S‐2), p‐ClC6H4 (R‐3/S‐3), p‐BrC6H4 (R‐4)] complexes have been synthesized from the reaction between (R or S)‐N‐1‐(Ar)ethylsalicylaldimine and nickel(II) acetate. Their CD spectra demonstrate chirality transfer from the ligands to the metal ions and a mirror‐image relationship for the enantiomeric pair R‐3/S‐3 in thf. DSC analyses show that the complexes exhibit an irreversible dissociation to the mononuclear species, which in turn undergo decomposition. The 1H NMR spectra reveal the presence of four salicylaldiminates, one aqua ligand, and two molecules of methanol in each dinuclear complex. They also confirm the existence of a dinuclear‐bridged aqua bis‐octahedral NiII complex in solution. The IR spectra in CH2Cl2 show a very strong band at around 2306 cm–1 due to the νO–H of the bridged aqua ligand. The X‐ray structures of R‐2, S‐2, R‐3, and S‐3 confirm the formation of dinuclear compounds comprising two nickel ions, four salicylaldiminates, and one aqua ligand with two molecules of methanol (or water in S‐2). Each nickel ion is surrounded by two N,O‐chelating salicylaldiminates, a bridging salicyl‐O atom from the neighboring nickel ion, and a bridging aqua ligand in a distorted octahedral polyhedron. Analyses of the absolute structures reveal a diastereomeric induction of the R or S ligand giving a Λ or Δ configuration at the nickel atoms in R‐2/3 or S‐2/3 that is independent of the ligand substituents.

Cigarette smoking is an important risk factor for diabetes, cardiovascular disease and non-alcoholic fatty liver disease. The health risk associated with smoking can be aggravated by obesity. Smoking might also trigger cardiomyocyte (CM) apoptosis. Given that CM apoptosis has been implicated as a potential mechanism in the development of cardiomyopathy and heart failure, we characterize the key signaling pathways in nicotine plus high-fat diet (HFD)-induced CM apoptosis. Adult C57BL6 male mice were fed a normal diet (ND) or HFD and received twice-daily intraperitoneal (IP) injections of nicotine (0.75 mg/kg body weight [BW]) or saline for 16 weeks. An additional group of nicotine-treated mice on HFD received twice-daily IP injections of mecamylamine (1 mg/kg BW), a non-selective nicotinic acetylcholine receptor antagonist, for 16 weeks. Nicotine when combined with HFD led to a massive increase in CM apoptosis that was fully prevented by mecamylamine treatment. Induction of CM apoptosis was associated with increased oxidative stress and activation of caspase-2-mediated intrinsic pathway signaling coupled with inactivation of AMP-activated protein kinase (AMPK). Furthermore, nicotine treatment significantly (P < 0.05) attenuated the HFD-induced decrease in fibroblast growth factor 21 (FGF21) and silent information regulator 1 (SIRT1). We conclude that nicotine, when combined with HFD, triggers CM apoptosis through the generation of oxidative stress and inactivation of AMPK together with the activation of caspase-2-mediated intrinsic apoptotic signaling independently of FGF21 and SIRT1.

α7-Nicotinic acetylcholine receptor (α7nAChR) agonists confer protection against a wide variety of cytotoxic insults and suppress oxidative stress and apoptosis in various cell systems, including hepatocytes. We recently demonstrated that nicotine, when combined with a high-fat diet (HFD), triggers oxidative stress, activates hepatocyte apoptosis, and exacerbates HFD-induced hepatic steatosis in male mice. This study evaluates whether PNU-282987 (PNU), a specific α7nAChR agonist, is effective in preventing nicotine plus HFD-induced hepatic steatosis. Adult C57BL6 male mice were fed a normal chow diet or HFD with 60% of calories derived from fat and received twice-daily intraperitoneal injections of 0.75 mg/kg body weight (BW) of nicotine, PNU (0.26 mg/kg BW), PNU plus nicotine, or saline for 10 weeks. PNU treatment was effective in attenuating nicotine plus HFD-induced increase in hepatic triglyceride levels, hepatocyte apoptosis, and hepatic steatosis. The preventive effects of PNU on nicotine plus HFD-induced hepatic steatosis were mediated by suppression of oxidative stress and activation of adenosine 5'-monophosphate-activated protein kinase (AMPK) together with inhibition of its downstream target sterol regulatory element binding protein 1c (SREBP1c), fatty acid synthase (FAS), and acetyl-coenzyme A-carboxylase (ACC). We conclude that the α7nAChR agonist PNU protects against nicotine plus HFD-induced hepatic steatosis in obese mice. PNU appears to work at various steps of signaling pathways involving suppression of oxidative stress, activation of AMPK, and inhibition of SREBP1c, FAS, and ACC. α7nAChR agonists may be an effective therapeutic strategy for ameliorating fatty liver disease, especially in obese smokers.

Alzheimer's disease is a severe neuron disease that damages brain cells which leads to permanent loss of memory also called dementia. Many people die due to this disease every year because this is not curable but early detection of this disease can help restrain the spread. Alzheimer's is most common in elderly people in the age bracket of 65 and above. An automated system is required for early detection of disease that can detect and classify the disease into multiple Alzheimer classes. Deep learning and machine learning techniques are used to solve many medical problems like this. The proposed system Alzheimer Disease detection utilizes transfer learning on Multi-class classification using brain Medical resonance imagining (MRI) working to classify the images in four stages, Mild demented (MD), Moderate demented (MOD), Non-demented (ND), Very mild demented (VMD). Simulation results have shown that the proposed system model gives 91.70% accuracy. It also observed that the proposed system gives more accurate results as compared to previous approaches.

An estimated 8 million people die each year from tobacco smoking, with an increasing frequency recently being observed in Southeast Asian countries, which is a preventable risk factor for mortality. NAFLD, fibrosis, advancement of hepatocellular carcinoma, and prognosis for those with severe liver disease are all negatively influenced. NAFLD and cigarette usage seem to be a direct link. Oxidative stress and oncogenic signals have been implicated in cancer development in animal models and human clinical trials. The elevated risk of cardiovascular disease and malignancies in those with steatohepatitis and those who have had liver transplants is exacerbated by smoking. We found that smoking cessation may increase treatment response and fibrosis regression rates, decrease hepatocellular carcinoma incidence, and improve liver transplant outcomes. In the last segment, we'll look at electronic cigarettes, a hot subject in public health right now, as well as additional repercussions of smoking.

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