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  1. Ahmad AH, Abdul Aziz CB
    Malays J Med Sci, 2014 Dec;21(Spec Issue):46-54.
    PMID: 25941463 MyJurnal
    Pain, while salient, is highly subjective. A sensation perceived as painful by one person may be perceived as uncomfortable, not painful or even pleasant to others. Within the same person, pain may also be modulated according to its threat value and the context in which it is presented. Imaging techniques, such as functional magnetic resonance imaging and positron emission tomography, have identified a distributed network in the brain, the pain-relevant brain regions, that encode the sensory-discriminative aspect of pain, as well as its cognitive and affective/emotional factors. Current knowledge also implicates the prefrontal cortex as the modulatory area for pain, with its subdivisions forming the cortico-cortical pathway, an alternative pain modulatory pathway distinct from the descending modulatory pathway of pain. These findings from neuroimaging in human subjects have paved the way for the molecular mechanisms of pain modulation to be explored in animal studies.
  2. Azman KF, Zakaria R, Abdul Aziz CB, Othman Z
    Oxid Med Cell Longev, 2016;2016:1549158.
    PMID: 27119005 DOI: 10.1155/2016/1549158
    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.
  3. Siran R, Ahmad AH, Abdul Aziz CB, Ismail Z
    J Physiol Biochem, 2014 Dec;70(4):877-89.
    PMID: 25218926 DOI: 10.1007/s13105-014-0356-x
    REM sleep is a crucial component of sleep. Animal studies indicate that rapid eye movement (REM) sleep deprivation elicits changes in gene expression. Down regulatory antagonist modulator (DREAM) is a protein which downregulates other gene transcriptions by binding to the downstream response element site. The aim of this study is to examine the effect of REM sleep deprivation on DREAM expression in ventrobasal thalamic nuclei (VB) of rats. Seventy-two male Sprague-Dawley rats were divided into four major groups consisting of free-moving control rats (FMC) (n = 18), 72-h REM sleep-deprived rats (REMsd) (n = 18), 72-h REM sleep-deprived rats with 72-h sleep recovery (RG) (n = 18), and tank control rats (TC) (n = 18). REM sleep deprivation was elicited using the inverted flower pot technique. DREAM expression was examined in VB by immunohistochemical, Western blot, and quantitative real-time polymerase chain reaction (qRT-PCR) studies. The DREAM-positive neuronal cells (DPN) were decreased bilaterally in the VB of rats deprived of REM sleep as well as after sleep recovery. The nuclear DREAM extractions were increased bilaterally in animals deprived of REM sleep. The DREAM messenger RNA (mRNA) levels were decreased after sleep recovery. The results demonstrated a link between DREAM expression and REM sleep deprivation as well as sleep recovery which may indicate potential involvement of DREAM in REM sleep-induced changes in gene expression, specifically in nociceptive processing.
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