A substantial amount data is available on restorative materials used in pediatric dentistry; however, there exists substantial evidence from systematic reviews and randomized clinical trials and clinicians need to examine and understand the available literature evidence carefully to aid them in clinical decision making.

Uric acid, a potent antioxidant for humans, birds, reptiles, and some primate species, is the end-product of purine degradation that is formed in the xanthine/hypoxanthine reactions catalyzed by xanthine oxidase. Associated with the evolutionary loss of urate oxidase (the enzyme that oxidizes uric acid resulting in the formation of allantoin) and resulting increase in concentrations of uric acid is a prolonged life span. Uric acid is known to scavenge peroxynitrite and other free radicals that can cause an imbalance of oxidants leading to oxidative stress. Uric acid also has a role in protecting DNA from single-strand breaks caused by free radicals in the body leading to a protective effect in neurodegenerative diseases. The brain is particularly vulnerable to oxidative stress as it is considered an 'expensive tissue' with a particularly high metabolic rate and comparatively increased utilization of oxygen. Brain tissue is also high in unsaturated lipids, which makes it more susceptible to free radical damage. Oxidative stress is thus linked to the pathogenesis of neurodegenerative diseases and also ischemic brain injury. In this review, we summarize the function of uric acid in alleviating oxidative damage and providing protection to neural cells during injury and disease.

Background and purpose: Aminoguanidine (AG), an inhibitor of advanced glycation endproducts, has been identified as a prominent agent that prevents the fructose-induced arterial stiffening in male Wistar rats. Our aims were to examine whether AG produced benefits on the left ventricular (LV)-arterial coupling in fructose-fed (FF) animals in terms of the ventricular and arterial chamber properties. Experimental approach: Rats given 10% fructose in drinking water (FF) were daily treated with AG (50 mg Á kg À1 , i.p.) for 2 weeks and compared with the untreated FF group. In anaesthetised rats, LV pressure and ascending aortic flow signals were recorded to calculate LV end-systolic elastance (E es , an indicator of myocardial contractility) and effective arterial volume elastance (E a ). The optimal afterload (Q load ) determined by the ratio of E a to E es was used to measure the coupling efficiency between the left ventricle and its vasculature. Key results: There was a significant interaction between fructose and AG in their effects on E a . Fructose loading significantly elevated E a and AG prevented the fructose-derived deterioration in arterial chamber elastance. Both fructose and AG affected E es and Q load , and there was an interaction between fructose and AG for these two variables. Both E es and Q load exhibited a decline with fructose feeding but showed a significant rise after AG treatment in the FF rats. Conclusions and Implications: AG prevented not only the contractile dysfunction of the heart caused by fructose loading, but also the fructose-induced deterioration in matching left ventricular function to the arterial system. Keywords: aminoguanidine; effective arterial volume elastance; fructose loading; end-systolic elastance; ventricular-arterial coupling Abbreviations: AG, aminoguanidine; AGEs, advanced glycation endproducts; BW, body weight; CO, cardiac output; E a , effective arterial volume elastance; E es , left ventricular end-systolic elastance; HR, basal heart rate; LVW, left ventricular weight; P es , end-systolic pressure of the left ventricle; P isomax , peak isovolumic pressure of the left ventricle; Q load , optimal afterload; SV, stroke volume; V ed , end-diastolic volume of the left ventricle; V eed , effective end-diastolic volume of the left ventricle; V 0 , the zero-pressure volume

The cardiac autonomic dysfunction in the absence of any significant changes in vascular dynamics, 4 but not 8 weeks after induction of type 2 diabetes, suggests that the diabetic autonomic neuropathy may precede arterial stiffening and cardiac hypertrophy in the STZ- and NA-treated rats.