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Objective: This study is aimed to investigate interfacial micro gaps between bases and hard setting calcium hydroxide liner. Materials and Methods: Twelve sound extracted human maxillary premolars were selected and immersed in 0.1% thymol solution. Samples were subjected to Class I cavity preparations with the width of 2.5 mm buccolingually, 3 mm mesiodistally, and 2 mm depth from the dentinoenamel junction (DEJ). The cavities were lined with hard setting calcium hydroxide lining (Dycal®), (Dentsply, USA) and then divided randomly into two groups. The cavities were restored with smart dentin replacement (SDR®), (Dentsply, Germany) and glass ionomer cement Ketac™ N100 (3M ESPE, USA) for Group 1 and 2, respectively, (n = 6 for each group) up to DEJ level. All samples were then packed with composite resin. Samples were cut longitudinally using a hard tissue cutter (Exact, Japan) and sanded with increasing grit sandpaper (#320, #500, #800, and #1200) for 30 s each and subjected for interfacial micro gaps analysis using scanning electron microscopy. Results: There was a significant difference of micro gap formation between two groups of base materials and hard setting calcium hydroxide (Dycal®) (P < 0.05). Conclusions: Lesser micro gap between Dycal® and SDR® compared to Dycal® and Ketac™ N100 suggested SDR® as a better base material to be used with Dycal® for deep caries management.

Objective: The aim of this study was to examine the association between changes in blood oxidative stress level/activity and changes in memory performance among postmenopausal women.Methods: This study involved 39 postmenopausal women who received estrogen-progestin therapy (EPT) for16 weeks. Verbal learning and memory performance were assessed using the Malay Version of Auditory VerbalLearning Test before and after 16 weeks of EPT. Oxidative stress levels/activities before and after 16 weeks of EPTwere determined using commercially available kits. Data were analyzed using paired t test and r. P G 0.05 wasconsidered significant.Results: The activities of glutathione peroxidase and catalase were considerably increased (P G 0.05), but thelevel of 4-hydroxynonenal was notably decreased (P G 0.05), after 16 weeks of EPT. There were positive correla-tions between changes in plasma superoxide dismutase and changes in trial A2 scores (r = 0.36, P G 0.05), andbetween changes in the ratio of blood reduced glutathione to oxidized glutathione and changes in trial A2 scores (r =0.34, P G 0.05).Conclusions: Sixteen weeks of EPT increase blood antioxidant capacity. However, most of the changes inoxidative stress level/activity are not significantly associated with changes in the memory performance of post-menopausal women.KeyWords:Estrogen-progestin therapy YPostmenopauseYOxidativestress YMalayVersion ofAuditoryVerbalLearning Test.

Ageing and stress exposure may lead to memory impairment while oxidative stress is thought to be one of the underlying mechanisms involved. This study aimed to investigate the potential protective effects of Tualang honey supplementation on memory performance in aged rats exposed to noise stress. Tualang honey supplementation was given orally, 200 mg/kg body weight for 28 days. Rats in the stress group were subjected to loud noise, 100 dB(A), 4 hours daily for 14 days. All rats were subjected to novel object recognition test for evaluation of memory performance. It was observed that the rats subjected to noise stress exhibited significantly lower memory performance and higher oxidative stress as evident by elevated malondialdehyde and protein carbonyl levels and reduction of antioxidant enzymes activities compared to the nonstressed rats. Tualang honey supplementation was able to improve memory performance, decrease oxidative stress levels, increase brain-derived neurotrophic factor (BDNF) concentration, decrease acetylcholinesterase activity, and enhance neuronal proliferation in the medial prefrontal cortex (mPFC) and hippocampus. In conclusion, Tualang honey protects against memory decline due to stress exposure and/or ageing via enhancement of mPFC and hippocampal morphology possibly secondary to reduction in brain oxidative stress and/or upregulation of BDNF concentration and cholinergic system.