Background: Cypermethrin, a widely used type II pyrethroid insecticide, has been increasingly implicated in neurotoxicity through the activation of neuroinflammatory and apoptotic pathways, particularly involving nuclear factor-kappa B (NF-κB) and caspase-3. Nigella sativa possesses several bioactive phytochemicals with established antioxidant and neuroprotective properties, yet their target-specific interactions in cypermethrin-induced neurotoxicity remain poorly understood. Objective: This study investigated the molecular interactions of selected Nigella sativa phytochemicals with NF-κB and caspase-3 to identify potential neuroprotective candidates against cypermethrin-induced neuroinflammation and apoptosis. Methods: An in silico molecular docking approach was employed using PyRx. Thymoquinone, thymol, carvacrol, and p-cymene were docked against human caspase-3 (PDB: 1GFW) and NF-κB p65 (PDB: 1VKX), with cypermethrin included as the reference toxicant. Drug-likeness and ADMET properties were evaluated using Swiss ADME. Results: Cypermethrin exhibited the strongest binding affinities to caspase-3 (-6.2 kcal/mol) and NF-κB (-7.7 kcal/mol), supporting its direct interaction with proteins implicated in neuronal injury. Among the phytochemicals, carvacrol demonstrated the highest affinity for NF-κB (-6.3 kcal/mol), while p-cymene showed the strongest interaction with caspase-3 (-4.8 kcal/mol). All phytochemicals demonstrated favourable pharmacokinetic properties, including blood-brain barrier permeability and zero Lipinski violations, except p-cymene, which showed one violation.

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Background: Di-butyl phthalate (DBP) is a widely used plasticizer and environmental endocrine disruptor known to induce oxidative stress and neurodevelopmental toxicity. The developing brain, particularly regions involved in motor coordination and behaviour, is highly vulnerable to prenatal toxicant exposure. Natural antioxidants such as Nigella sativa oil (NSO) have shown promise in mitigating chemically induced neural damage. Aim: This study investigated the neurobehavioral, biochemical, and histological effects of prenatal DBP exposure and evaluated the protective potential of Nigella sativa oil in Wistar rat offspring. Materials and Methods: Twenty pregnant Wistar rats were randomly assigned to four groups: control, NSO (1 mL/kg b.w.), DBP (500 mg/kg b.w.), and DBP + NSO. Treatments were administered orally from gestational day 4 to 21. Offspring were assessed for neurobehavioral performance using the open field test on postnatal day 35. Cerebellar tissues were analysed for oxidative stress markers including malondialdehyde (MDA), catalase (CAT), and glutathione peroxidase (GPx), and processed for histological evaluation using hematoxylin and eosin and cresyl fast violet staining.

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Background: The kidneys play a critical role in removing waste products and excess water from the blood, as well as maintaining chemical balance. Damage to the kidneys can pose serious health risks. Cannabis sativa (CS) is one of the commonly abused substances and has been associated with various adverse health effects. Objective: This study investigated the ameliorative effects of Vitamin C (Vit C) on CS-induced nephrotoxicity in male and female rats. Method: Different doses of CS (2, 4, and 6 mg/kg) and Vit C (4 mg/kg) were administered orally, both individually and in combination, for a period of three weeks. Kidney function parameters, including urea, creatinine, induced protein, albumin, sodium (Na), and potassium (K), were measured using standard methods. Results: CS administration significantly increased urea and creatinine levels in the high dose groups (4 and 6 mg/kg) compared with the control and low dose (2 mg/kg) groups in both sexes. Conversely, induced protein, albumin, Na, and K levels were significantly decreased in the high dose groups. However, these adverse effects were significantly ameliorated at the 4 mg/kg CS dose when co-administered with Vit C.

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Introduction: Alzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized by cognitive impairment, neuronal degeneration, oxidative stress, and neuroinflammation. Aim: To investigate the effects of Tetrapleura tetraptera extract (TTE) on the prefrontal cortex following aluminum chloride (AlCl₃)-induced Alzheimer’s-like disease in adult male Wistar rats. Methodology: Fifty (50) adult male Wistar rats were randomly assigned into five groups (n = 10). Group I (control) received 2 mL/kg body weight (bw) distilled water. Group II received 200 mg/kg bw AlCl₃, while Groups III and IV received 200 mg/kg bw AlCl₃ plus 250 and 500 mg/kg bw TTE, respectively. Group V received 10 mg/kg bw Donepezil. All treatments were administered orally for 42 days. Following treatment, rats were sacrificed, and the prefrontal cortex was harvested for histological, biochemical, and protein analyses. Results: TT significantly improved behavioural alterations in the elevated plus maze and Morris water maze tests (P<0.05), while reducing tissue amyloid-beta (AB), Glia Fibrillary Acidic protein (GFAP) and phosphorylated tau (p-tau) levels (P<0.05). TT significantly decreased malondialdehyde (MDA) and increased Catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GPx) levels (P<0.05). Neuronal and cortical restoration was observed in TT-treated groups compared with the AlCl₃ group, with greater effects at the high dose. Donepezil similarly restored antioxidant enzyme activities, reduced protein deposits, and improved neuronal and cyto-architectural organization, comparable to high-dose TT.

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This article comprises the following Items: Item 1. Biomedical Engineering (BE, ME & PhD) Programs Biomedical Engineering is the application of engineering disciplines' formulations (of theories and designs) to biology, physiology and medicine, to improve medical monitoring, diagnosis, and therapy. Item 2. Quantitative Physiology Program, jointly with College of Medicine Quantitative Physiology Program can help to develop more precise medical diagnostics. This program involves formulation of Human Physiology courses from physics and engineering perspectives. It comprises two parts: Part I. Fundamental Physiological Processes: Physics and Engineering Modelling, and Part II. Physiological Systems Functions: Physics and Engineering Modelling. Item 3. Precision Quantitative Medicine Program, jointly with College of Medicine The Precision Quantitative Medicine Program is based on my Biomedical Engineering developments in (i) Physiology, Medicine, Orthopaedics and Surgery, (ii) Sports Biomechanics and Medicine, and (iii) Mind-Body Medicine in Psychiatry. This Program can be offered as an MD-PhD (Biomedical Engineering) Program, jointly between the Biomedical Engineering Department and the College of Medicine. Item 4. MD-PhD (Biomedical Engineering) Program, jointly with College of Medicine This Program is intended for medical students interested in combining medical practice with competency in biomedical engineering, to implement BME technologies in clinical research and applications in clinical care in hospitals. The program emphasizes computational medicine and computational surgery. Item 5. Hospital and Healthcare Management (MBA and MD-MBA) Program, jointly with College of Business and College of Medicine The Hospital and Healthcare (HOHM) Program is designed to provide the relevant multidisciplinary knowledgebase in business administration, clinical and hospital engineering, economic and financial management, related to cost-effective operation of hospitals and healthcare delivery (as represented by the three pillars of HOHM depicted below), to healthcare and hospital administrators. Together, these developments constitute a novel model of Biomedical Engineering, contributing to Quantitative Physiology, Precision Quantitative Medicine, and Quality Healthcare Delivery.

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Background: Expressed emotion (EE) refers to the emotional climate within a family, encompassing critical comments, hostility, and emotional over-involvement, as well as warmth and positive remarks. First identified in 1958 through relapse patterns among psychiatric patients discharged to different living arrangements, EE was formalised as a measurable construct with Michael Rutter in 1966. Objective: To revisit the construct of EE and examine its relevance to the course, relapse risk, and management of psychiatric disorders. Methods: This narrative review draws on existing literature on EE across psychiatric conditions, with particular focus on schizophrenia, and examines proposed mechanisms, caregiver burden, and intervention strategies. Discussion: EE has been studied most extensively in schizophrenia, but growing evidence links it to outcomes in depression, bipolar disorder, eating disorders, alcohol use disorder, and dementia. The stress-vulnerability model offers a mechanistic explanation, describing how EE interacts with biological vulnerability and life events to influence relapse. The review also considers the paradox of positive over-involvement, the burden EE places on caregivers amid deinstitutionalisation, and the modifiability of EE through psychoeducation, family therapy, and counselling, supported by validated instruments such as the Level of Expressed Emotion Scale and the Family Attitude Scale.

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Paroxysmal episodes similar to epileptic seizures are called psychogenic non-epileptic seizures (PNES) however, they do not have a corresponding epileptiform correlate on video electroencephalography (vEEG) which is unarguably the current diagnostic gold standard. PNES are well known to be characterized by psychological distress regarding somatic expression but the biological somatization of PNES remains incompletely defined. This narrative review probes evidences on anthropometric (body mass index and waist circumference), structural/volumetric ("microscopic"), and neuroimaging correlates of somatization in PNES. PubMed, Google Scholar, ScienceDirect and ResearchGate were used to generate literature using series of key terms "psychogenic non-epileptic seizures", "somatization", "anthropometric markers", "microscopic markers" and "neuroimaging markers". Various evidences show that patients with PNES carry more than psychological dysfunction but a disproportionately high burden of obesity similar to epileptic cases. Also, volumetric imaging revealed reduced volume of amygdala, hippocampus and altered uncinate fasciculus microstructure. Although, some findings across structural and functional neuroimaging studies are inconsistent but they converge on the limbic-prefrontal emotion-regulation networks dysfunction rather than a single discrete lesion. vEEG therefore remains indispensable, while anthropometric and neuroimaging findings offer adjunctive, biologically informative but not diagnostic, insight into the somatization construct that underlies PNES.

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Diseases causing neurodegeneration, including Alzheimer's disease and Parkinson's disease, encompass several pathological processes such as progressive neuronal damage and increased neuronal loss. Currently, there are limited available therapeutic options capable of halting progression of the disease. The Gut microbiota has emerged as a significant pathway in modulating neuroinflammation, oxidative stress, protein aggregation, neurotransmitter disruption and mitochondrial dysfunction. Simultaneously, natural products including isoflavones, flavonoids, curcumin, alkaloids and turmeric, alongside gut metabolites, have demonstrated great neuroprotective effects through antioxidative and anti-inflammatory mechanisms. This review examines the synergistic interactions between gut microbiota and bioactive compounds in modulating pathways associated with neurodegeneration. Synergy between gut metabolites and bioactives collectively enhances intestinal barrier integrity, regulates immune responses, reduces oxidative damage, and preserves mitochondrial function and influences neurotransmitter synthesis and neuronal signaling. Integrating the gut microbiota with bioactive supplementation of provides a multifaceted intervention for neurodegenerative diseases.

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Neonatal seizures remain a leading cause of acute neurological morbidity in the newborn period, yet a substantial proportion of cases have no identified structural, infective, or metabolic cause. Air pollution, particularly fine particulate matter of 2.5 micrometers or less in diameter (PM2.5), has recently been implicated as a modifiable environmental contributor to seizure risk across the lifespan, with proposed mechanisms centered on oxidative stress, disrupted iron handling, and regulated cell death. Two convergent bodies of evidence are reviewed here: first, epidemiological and mechanistic work linking PM2.5 exposure to seizure exacerbation through impaired nuclear factor erythroid 2-related factor 2 (Nrf2) signalling; and second, the emerging role of ferroptosis, an iron-dependent form of lipid peroxidation-driven cell death, as a downstream effector of this impairment in hippocampal neurons. Because the foetal and neonatal antioxidant system is developmentally immature and iron handling in the perinatal brain is already in flux, this axis may confer disproportionate vulnerability during gestation and the immediate postnatal period, a population in which direct mechanistic data are still lacking. This review synthesises the current evidence, outlines a plausible developmental extension of the Nrf2-ferroptosis hypothesis to neonatal epileptogenesis, and proposes a research agenda to close the gap between adult mechanistic data and perinatal clinical relevance.

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Dissociative and conversion disorders are frequently complicated by skepticism from families and caregivers, which can impede treatment engagement. Conventional psychoeducation often fails by inadvertently suggesting volitional control or fabrication. This paper describes a simple, narrative-based psychoeducational tool, the “Bear Fable” used in outpatient psychiatric practice to reframe such symptoms as involuntary, survival-oriented responses. By combining metaphor, humour, and non-confrontational reframing, this approach reduces defensiveness, validates patient experience, and facilitates therapeutic alliance. Its low resource, culturally adaptable nature makes it particularly suitable for primary care and resource limited settings. Preliminary clinical observations suggest improved family acceptance and earlier disclosure of psychosocial stressors. Formal evaluation is warranted.

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