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The considerable similarity in the growth paths of the Chinese and Indian economies since their respective reforms has changed after the 2008 crisis. This article tries to understand the trajectories of different parameters of economic growth in the two countries, and how these changed after the crisis. Growth has declined in both the economies, more consistently in China, compared to India. The share of exports in GDP has also declined in both economies. The dependence of the Chinese economy on exports has decreased; however, its dependence on investment has increased. Investment's share in GDP in China has increased, whereas it has decreased in India. The structure of the manufacturing sector in China has undergone changes, which is not the case for India. The increase in the share of services and decline in the share of manufacturing in China implies that the production structure is becoming less unbalanced. JEL classification: E58, E62, F32, F41 [ABSTRACT FROM AUTHOR]

In recent days, the hike in obesity‐mediated epidemics across the globe and the prevalence of obesity‐induced cardiovascular disease has become one of the chief grounds for morbidity and mortality. This epidemic‐driven detrimental events in the cardiac tissues start with the altered distribution and metabolism pattern of high‐density lipoprotein and low‐density lipoprotein (LDL) leading to cholesterol (oxidized LDL) deposition on the arterial wall and atherosclerotic plaque generation, followed by vascular spasms and infarction. Subsequently, obesity‐triggered metabolic malfunctions induce free radical generation which may further trigger pro‐inflammatory signaling and nuclear factor kappa‐light‐chain‐enhancer of activated B cells transcriptional factor, thus inducing interferon‐gamma, tumor necrosis factor‐alpha, and inducible nitric oxide synthase. This terrifying cardiomyopathy can be further aggravated in type 2 diabetes mellitus, thereby making obese diabetic patients prone toward the development of myocardial infarction (MI) or stroke in comparison to their nondiabetic counterparts. The accelerated oxidative stress and pro‐inflammatory response induced cardiomyocyte hypertrophy, followed by apoptosis in obese diabetic individuals, causing progression of athero‐thrombotic vascular disease. Being an efficient antioxidative and anti‐inflammatory indolamine, melatonin effectively inhibits lipid peroxidation, pro‐inflammatory reactions, thereby resolving free radical‐induced myocardial damages along with maintaining antioxidant reservoir to preserve cardiovascular integrity. Prolonged melatonin treatment maintains balanced body weight and serum total cholesterol concentration by inhibiting cholesterol synthesis and promoting cholesterol catabolism. Additionally, melatonin promotes macrophage polarization toward the anti‐inflammatory state, providing a proper shield during the recovery period. Therefore, the protective role of melatonin in maintaining the lipid metabolism homeostasis and blocking the atherosclerotic plaque rupture could be targeted as the possible therapeutic strategy for the management of obesity‐induced acute MI. This review aimed at orchestrating the efficacy of melatonin in ameliorating irrevocable oxidative cardiovascular damage induced by the obesity–diabetes correlation. [ABSTRACT FROM AUTHOR]

C−H bond activation has surfaced as a transformative toolbox for the efficient assembly of biologically important molecules. However, despite of major advances in palladium, rhodium and silver catalysis, yet palladium(II)‐ catalyzed, iodobenzene diacetate (PIDA) mediated C−H bond activation in azole skeleton has deluged with interesting wining outcome. Concentrating on that we herein report on the involvement of 4‐functionalized 1,4‐dihydropyridines (R‐DHPs) as the representative surrogates of benzoyl, pivalyl and ethoxycarbonyl groups and in presence of PIDA it releases appropriate functional radical (following single electron transfer oxidation of R‐DHPs under thermal condition)to become the part of ortho‐ functionalized azoles via Pd(II) catalysis. In case of cyanation reaction, malononitrile has served the key source of nitrile functionality by undergoing oxidative C−CN bond cleavage in presence of PIDA and with the help of Pd(II) catalyst it offers ortho‐cyanated azoles. Additionally, the selective formation of C‐3 benzoyl and ester functionalized indazole derivatives in absence of Pd(II)‐catalyst and the unprecedented formation of homo‐coupling products between two identical 2H‐indazoles are also notable outcome of present strategic access. Overall this protocol operates under mild condition, tolerates a wide range of structural moieties and gives versatile azole derivatives in high efficiency. The antioxidant properties of the synthesized 2‐thiophenyl benzoyl selenazole and isoselenazole are further evaluated using a chemically defined method. The Copper‐ascorbate (Cu−As) was utilized as an oxidative stress generator. Out of screened azoles, the 2‐benzoyl isoselenazole compound (3 i) displays magnificent antioxidant property as compared to the 2‐thiophenyl benzoyl selenazole (3 g). [ABSTRACT FROM AUTHOR]

An efficient and fascinating protocol has been devised for the preparation of fused furan moieties involving a Rh(II) catalyzed one-pot C-H activation/concomitant tandem annulation process, employing an enolic compound and β-keto sulfoxonium ylide as the reacting conjugates. The developed technique demands only Rh 2 (TFA) 4 as the catalyst to proceed forward and is devoid of additional metallic or nonmetallic additives. The skeletal transformation of naphthoquinone fused furan to highly decorated naphthoquinone fused indolizines is a promising synthetic application.