Two Interesting Avian Records from Kutch, Gujarat State

Volume: 99Start Page: 115End Page: 11

Occurrence, status and breeding of Podiceps cristatus (Linn.) and Fulica atra Linn

Volume: 88Start Page: 439End Page: 44

Stranded Whales on the Gujarat Coast

Volume: 98Start Page: 272End Page: 27

Recovery of a Ringed Demoiselle Crane Grus Virgo in Kutch

Volume: 100Start Page: 624End Page: 62

Distribution of the slenderbilled gull (Larus genei Breme) in the Gulf of Kachchh, Gujarat

Volume: 85Start Page: 420End Page: 42

On the Status of Hypocolius Ampelinus Bonaparte in the Indian Subcontinent

Volume: 99Start Page: 306End Page: 30

Sturnus Malabaricus Blythii in Gujarat State

Volume: 99Start Page: 531End Page: 53

Heightened efficacy of nitric oxide-based therapies in type II diabetes mellitus and metabolic syndrome

Type II diabetes mellitus (DM) and metabolic syndrome are associated with accelerated restenosis following vascular interventions due to neointimal hyperplasia. The efficacy of nitric oxide (NO)-based therapies is unknown in these environments. Therefore, the aim of this study is to examine the efficacy of NO in preventing neointimal hyperplasia in animal models of type II DM and metabolic syndrome and examine possible mechanisms for differences in outcomes. Aortic vascular smooth muscle cells (VSMC) were harvested from rodent models of type II DM (Zucker diabetic fatty), metabolic syndrome (obese Zucker), and their genetic control (lean Zucker). Interestingly, NO inhibited proliferation and induced G0/G1 cell cycle arrest to the greatest extent in VSMC from rodent models of metabolic syndrome and type II DM compared with controls. This heightened efficacy was associated with increased expression of cyclin-dependent kinase inhibitor p21, but not p27. Using the rat carotid artery injury model to assess the efficacy of NO in vivo, we found that the NO donor PROLI/NO inhibited neointimal hyperplasia to the greatest extent in type II DM rodents, followed by metabolic syndrome, then controls. Increased neointimal hyperplasia correlated with increased reactive oxygen species (ROS) production, as demonstrated by dihydroethidium staining, and NO inhibited this increase most in metabolic syndrome and DM. In conclusion, NO was surprisingly a more effective inhibitor of neointimal hyperplasia following arterial injury in type II DM and metabolic syndrome vs. control. This heightened efficacy may be secondary to greater inhibition of VSMC proliferation through cell cycle arrest and regulation of ROS expression, in addition to other possible unidentified mechanisms that deserve further exploration