Pain has been considered as a concept of sensation that we feel as a reaction to the stimulus of our surrounding, putting us in harm’s way and acting as a form of defense mechanism that our body has permanently installed into its system. However, pain leads to a huge chunk of finances within the healthcare system with continuous rehabilitation of patients with adverse pain sensations, which might reduce not only their quality of life but also their productivity at work setting back the pace of our economy. It may not look like a huge deal but factor in pain as an issue for majority of us, it becomes an economical burden. Although pain has been researched into and understood by numerous researches, from its definition, mechanism of action to its inhibition in hopes of finding an absolute solution for victims of pain, the pathways of pain sensation, neurotransmitters involved in producing such a sensation are not comprehensively reviewed. Therefore, this review article aims to put in place a thorough understanding of major pain conditions that we experience—nociceptive, inflammatory and physiologically dysfunction, such as neuropathic pain and its modulation and feedback systems. Moreover, the complete mechanism of conduction is compiled within this article, elucidating understandings from various researches and breakthroughs.

Oxidative stress and apoptosis can disrupt the bone formation activity of osteoblasts which can lead to osteoporosis. This study was conducted to investigate the effects ofγ-tocotrienol on lipid peroxidation, antioxidant enzymes activities, and apoptosis of osteoblast exposed to hydrogen peroxide (H₂O₂). Osteoblasts were treated with 1, 10, and 100 μM ofγ-tocotrienol for 24 hours before being exposed to 490 μM (IC₅₀) H₂O₂for 2 hours. Results showed thatγ-tocotrienol prevented the malondialdehyde (MDA) elevation induced by H₂O₂in a dose-dependent manner. As for the antioxidant enzymes assays, all doses ofγ-tocotrienol were able to prevent the reduction in SOD and CAT activities, but only the dose of 1 μM of GTT was able to prevent the reduction in GPx. As for the apoptosis assays,γ-tocotrienol was able to reduce apoptosis at the dose of 1 and 10 μM. However, the dose of 100 μM ofγ-tocotrienol induced an even higher apoptosis than H₂O₂. In conclusion, low doses ofγ-tocotrienol offered protection for osteoblasts against H₂O₂toxicity, but itself caused toxicity at the high doses.

Breast cancer is the malignant tumour that developed from cells of the breast and is the first leading cause of cancer death among women worldwide. Surgery, radiotherapy, and chemotherapy are the available treatments for breast cancer, but these were reported to have side effects. Newcastle disease virus (NDV) known asAvian paramyxovirustype-1 (APMV1) belongs to the genusAvulavirusin a family Paramyxoviridae. NDV is shown to be a promising anticancer agent, killing tumour cells while sparing normal cells unharmed. In this study, the oncolytic and cytotoxic activities of NDV AF2240 strain were evaluated on MDA-MB-231, human mammary carcinoma cell line, using MTT assay, and its inhibitory effects were further studied using proliferation and migration assays. Morphological and apoptotic-inducing effects of NDV on MD-MB-231 cells were observed using phase contrast and fluorescence microscopes. Detection of DNA fragmentation was done following terminal deoxyribonucleotide transferase-mediated Br-dUTP nick end labeling staining (TUNEL) assay, which confirmed that the mode of death was through apoptosis and was quantified by flow cytometry. Furthermore, analysis of cellular DNA content demonstrated that the virus caused an increase in the sub-G1 phase (apoptotic peak) of the cell cycle. It appears that NDV AF2240 strain is a potent anticancer agent that induced apoptosis in time-dependent manner.

Introduction: Poor sleep quality among university students seems to be an important issue to be concerned. It can give great impact on students especially on their academic performance. However, studies regarding sleep quality on medical students in Malaysia are limited. Objective: The objective of this study was to determine the sleep quality of pre-clinical medical students in Universiti Putra Malaysia (UPM) and Universiti Malaya (UM). Methods: This was a cross-sectional study. Self-administered questionnaire was used to collect data from the pre-clinical medical students of UPM and UM. Sleep quality of the students was measured by Pittsburgh Sleep Quality Index (PSQI) questionnaire. All the data were analysed by using SPSS version 21. Results: The study revealed that 63.9% of the respondents had poor sleep quality (PSQI score: more than 5). The prevalence of poor sleepers in UM (67%) was slightly higher than UPM (60.9%). However, the comparison of PSQI score showed no significant difference between UPM and UM respondents (p = 0.082). The average sleep duration per night among respondents was 5 hours 39 minutes (± 1.21 hrs). Only 6.1% of students practiced recommended sleep value per night (>7 hrs). Significant association was found between caffeine intake with sleep quality. Besides, our study showed no association between sleep quality with gender and year of study. Conclusion: Majority of the pre-clinical students in UPM and UM had poor sleep quality and short sleep duration. Only a small number of students practiced recommended sleep value per night.

The nectar produced by bees in nature is known as honey and has been consumed for its nutritional and medicinal properties. There is growing evidence that honey and its compounds have anti-inflammatory, antioxidant and anti-microbial properties that are relevant to the maintenance of health and the prevention of illnesses, including cardiocerebrovascular disease. Cerebral small vessel disease (CSVD) is one of the major risk factors for diseases such as stroke, dementia, Alzheimer’s disease, and Parkinson’s disease. CSVD is prevalent with aging and the presence of vascular risk factors. Its most common deleterious effect on the brain parenchyma is a neurological problem, causing a spectrum of subtle clinical manifestations such as neurocognitive dysfunction, emotional or behavioral disturbances, and gait dysfunction. Moreover, the pathological mechanisms and preventive strategies for CSVD remain elusive, which is reflected in the continued lack of effective therapeutic and preventive therapies. Given the growing literature on honey and its compounds as a superfood-based preventive measure, this narrative review highlights the neuroprotective potentials of honey and its compounds in relation to the current understanding of CSVD pathomechanism.

Osteoporosis is a bone disorder caused by an imbalance in the bone remodelling process, specifically between osteoblastogenesis and osteoclastogenesis, and is associated with increased oxidative stress. This study aims to investigate the antioxidant activity of oil palm leaf extracts (OPLEs) and their effects on osteoclastogenesis in murine macrophages (RAW 264.7), comparing the results with those of vitamin C (VC). Methanol extract of oil palm leaves (MEOPL) demonstrated the highest total phenolic content (TPC) at 284.26 mg GAE/g dry weight. The antioxidant activity, assessed via DPPH scavenging and FRAP assays, showed that MEOPL had a DPPH inhibition rate of 89.41% and a FRAP value of 105.67%. In cytotoxicity assays, MEOPL-treated cells exhibited significantly higher viability compared to VC-treated cells, with viability percentages exceeding 60% at concentrations up to 0.625 mg/mL. MEOPL also significantly reduced osteoclastogenesis, as indicated by a dose-dependent decrease in TRAP-positive multinucleated cells and a notable reduction in RANKL gene expression. These findings suggest that MEOPL possesses superior anti-osteoclastogenic properties compared to VC and holds promise as a potential therapeutic agent for the prevention and treatment of osteoporosis. However, as this study utilised an in vitro model, the direct translation of these results to clinical scenarios is limited, and further in vivo studies are necessary to confirm the clinical relevance of MEOPL.