Chemical pathways for poly-anionic isomerisation in the metastable anions of tetra-deprotonated naphthalene: an intra-molecular inter-ring proton-transfer.

A surprising chemical pathway involving an intra-molecular proton-transfer between the two different aromatic rings of naphthalene is revealed while exploring the isomerisation in the metastable tetra-anionic species of tetra-deprotonated naphthalene. The pathways are explored through quantum-mechanical computations employing a global reaction route mapping (GRRM) strategy. Notably, several other pathways traced exhibit interesting aspects of poly-anionic isomerisation in the multiply-charged metastable molecular anions, which can provide valuable insights into the mechanisms of ring closure and expansion leading to species like azulenes, cyclodecapentaene, and phenylvinylacetylene. The metastable poly-anionic species along the pathways were also analysed using a nuclear charge stabilisation procedure while employing conventional density functional theory (DFT) with the B3LYP exchange-correlation functional as well as long-range and dispersion corrected DFT/ωB97XD and DFT-D3 methods. Interestingly, the charge stabilisation method using the DFT/B3LYP was found to be more reliable than the dispersion corrected methods.

Molecular anions of polydeprotonated naphthalenes: An investigation on the metastability and deprotonation energies using nuclear-charge stabilization method.

The dianions and trianions of doubly- and triply-deprotonated naphthalenes are investigated using density functional theory (DFT) computations employing hybrid, long-range, and dispersion corrected exchange-correlation functionals. The investigated polyanionic species are found to be metastable with negative electron affinity and are further treated using a nuclear-charge stabilization method. The tunneling lifetimes of these anionic species were estimated to be a few femtoseconds. Notably, the deprotonated energies (DPEs) of naphthalene leading to the formation of triply deprotonated trianions are observed to be affected by the metastability of the dianions and trianions. For the deprotonation of doubly deprotonated dianions, the DPE calculated using the improved methodology based on the stabilization method is found to be nearly 100 kcal/mol more than that computed using the conventional procedure. Though the various DFT approximations employed are in a good agreement for predicting the lifetimes of the metastable species but in the prediction of electron-affinities and deprotonation energies, the dispersion-corrected DFT-D3 significantly disagrees with the long-range corrected DFT methods employing cam-B3LYP and ωB97XD exchange-correlation functionals.

Role of Oxidative Stress and Genetic Polymorphism of Matrix Metalloproteinase-2 and Tissue Inhibitor of Metalloproteinase-2 in COPD.

Chronic obstructive pulmonary disease (COPD), a complaint described by progressive and inadequately reversible limitation in lungs with systemic inflammation, is largely current in India. There's no remedy available so far it is, thus, imperative to understand the underpinning pathogenesis of the complainant. A set of proteases known as Matrix metalloproteinase (MMPs) are especially involved in the process of alveolar destruction and mucus hypersecretion. There are responsible factors in an inheritable position to control COPD like MMPs and TIMPs (Tissue Inhibitor of Metalloproteinases). MMPs degrade extracellular matrix and lead to the pathogenesis of COPD [1]. TIMPs proteins that help to inhibit the Matrix metalloproteinases. [2]. This review summarizes the implicit part of crucial MMP-2 and TIMP-2 in COPD disease. Though the concept seems promising, limited knowledge about the exact functions of a particular MMP in COPD and the complications of MMP in substrate affinity makes this a grueling task. MMP2 and TIMP2 both are directly or indirectly regulated by oxidative stress and epigenetic mechanism which regulates their expressions. COPD is a seditious response to factors like dust, smoke, etc., and triggers extra-pulmonary goods which cause inflammation. [3]. This review explains the relationship between MMP2 and TIMP2 in COPD patients with oxidative stress, its impact on COPD pathogenesis, and gene expression of TIMP2 and MMP2 with their downstream effects. This also gives some insights into therapeutic interventions for targeting these enzymes. MMP2 and TIMP2 both play a role in the development of COPD and they need to be studied with the utmost focus.