Fear is a vital survival mechanism across species, triggering responses to threats and aiding in navigating dangerous environments. In humans, it plays a key role in risk assessment and decision-making, contributing to adaptive behaviour and survival. Emotional well-being and inform strategies can be enhanced for managing fear-related disorders by understanding fear's neural processing through fear-evoked stimuli. This study aimed to compare the effects of social (human mutilation) and non-social (wild animals) fear-evoked stimuli on the human brain using the event-related potential (ERP) technique. Thirty-eight participants of mixed gender and ethnicity underwent ERP assessments while being exposed to images of mutilation and wild animals alongside neutral geometric images. Brain activity was measured using a 128 HydroCel Geodesic Sensor Net, focusing on the N200 component, indicative of emotional processing. The analysis revealed that social fear-evoked stimuli (human mutilation images) elicited greater electrophysiological responses in most brain areas than non-social stimuli (wild animal images). This finding suggests that stimuli related to social fears have a greater impact on the brain than non-social fears, likely due to humans' inherent empathy for one another. The gender factor may interfere with this emotional fear processing. It highlights the critical role of social context in fear response. It suggests that understanding these dynamics can guide more effective treatments for anxiety and phobias, opening avenues for further exploration into how psychological interventions influence fear reactions.

The clinical-related input and processing of intestinal afferents to the spinal cord is not well known. This study aims to develop an electrophysiological experimental animal model to study spinal cord afferents from the colon during clinical-related conditions such as hyperexcitability or ischemia. Spinal cord evoked potentials (SCEP) were elicited by colonic stimulation in ten male adult Sprague-Dawley rats anesthetized with thiobarbital, 60 mg kg-1 i.p. After laminectomy (T11 to L5), a tungsten electrode (500 μm; <50Ω) was placed in the spinal dorsum to record SCEP induced by bipolar electrical stimulation of colon mucosa (basal 30 V; 1 ms) at low (0.2 Hz; 10 min) or high (5 Hz; 5 min) frequency. In 3 experiments, after the basal recording, a respiratory arrest was induced by D-tubocurarine to evaluate the ischemia effects. The SCEPs were stable and reliable (n=310), displaying a N1 wave (delay: 3.9±0.1 ms; amplitude 7.78±0.39 μV) and P1 wave (delay 9.96±0.14 ms; amplitude 2.97±0.21 μV). Colonic high-frequency stimulation induced an amplitude increase in both +11% (N1) and +23.7% (P1) (p<0.001). The ischemia induced a linear decay of both wave amplitudes more intense for the P1 wave. sensitive. These results denote the intense colonic input to the lumbar dorsal spinal cord, the presence of spinal sensory potentiation mechanisms induced by colonic high frequency stimulation, and the high oxygen dependency of the neuronal networks involved in the N1 and P1 wave generation. This experimental model could contribute to the study of visceral pain and inflammation, allowing the electrophysiological evaluation of experimental treatment response in experimental colon disease models.

Ruxolitinib is a Janus kinase (JAK) inhibitor that inhibits the JAK/STAT signalling pathway by targeting JAK1 and JAK2, which are crucial for regulating astrogliogenesis. This study assessed the effect of ruxolitinib (5 and 30 mg/kg/day) on developing mouse brains by administering it to pregnant mice from E7.5 to E20.5. No adverse effects were observed in the treated mice. The brains of P1.5 pups were collected, and RNA was extracted to assess markers of neurogenesis and astrogliogenesis through RT-qPCR. The results revealed a significant decrease in Gfap expression (p<0.0001) in both ruxolitinib-treated groups compared to the control, indicating a suppression of astrogliogenesis. Additionally, S100β expression (p<0.05) was significantly reduced in the 30 mg/kg ruxolitinib-treated group. In contrast, the expression of neuronal markers vGLuT1 (p<0.01) and vGLuT2 (p<0.01) increased significantly in the 30 mg/kg treated group, suggesting enhanced neuronal differentiation. Furthermore, 5 and 30 mg/kg ruxolitinib-treated groups showed a significant increase in GAT1 expression (p<0.01) compared to the control group. A marked decrease in Nestin expression was also observed in the 5 mg/kg (p<0.001) and 30 mg/kg (p<0.0001) treated groups. These findings demonstrate that transplacental administration of ruxolitinib modulates key markers involved in neuronal differentiation and gliogenesis in the developing mouse brain, suggesting its potential use in correcting imbalances in early brain development.

Aphasia commonly leads to word retrieval issues, particularly with nouns and verbs. Traditional assessments often focus on single-word. This study uses qualitative and quantitative methods to assess word class deficits in Kannada-speaking Individuals with Aphasia (IWA) compared to Neurotypical Individuals (NTI) in single-word production and discourse production. Twenty IWAs (aged 20-50) and twenty age/gender-matched NTIs were recruited. Confrontation naming evaluated single-word production, while structured picture description (picnic scene) assessed discourse. Both tasks included a fixed set of nouns and verbs for comparison. The results were that IWAs performed poorer than NTIs in both tasks. Statistically significant noun and verb usage differences were observed between IWAs and NTIs in the picture description task (p<0.05). However, word class differences in the IWA group were insignificant across tasks. NTIs showed significant differences only in the picture description task. This study underscores word class deficits in aphasia, particularly at the discourse level. Discourse analysis is crucial for understanding language characteristics in aphasia and should be integrated into routine assessments.

Traumatic brain injury (TBI) poses a significant risk to neurological function, primarily attributable to oxidative stress. Our hypothesis suggests that honey, renowned for its high phenol and flavonoid content, exerts neuroprotective effects by mitigating oxidative stress. This study aims to assess honey's potential as an innovative therapeutic agent in a TBI rat model, primarily focusing on its impact on behaviour, lipid peroxidation, and antioxidant enzyme activity. A total of twenty adult male Wistar rats were randomly divided into four groups: Group A (control), Group B (honey-treated), Group C (TBI-induced), and Group D (honey-treated TBI). We conducted comprehensive assessments using the Rotarod and Elevated Plus Maze tests to evaluate behaviour. Additionally, biochemical evaluations included quantifying lipid peroxidation levels and conducting a detailed analysis of antioxidant enzyme status, specifically emphasising the activity of glutathione (GSH) and catalase (CAT). Our findings indicated that the TBI model rats displayed impaired motor coordination, heightened anxiety-like behaviour, and elevated lipid peroxidation levels. Intriguingly, the honey treatment effectively reversed these behavioural deficits while concurrently reducing lipid peroxidation. Notably, honey treatment significantly augmented the activity of antioxidant enzymes (CAT and GSH); there was a significant increase in CAT activity compared to GSH activity in the treated TBI model. This study supports our hypothesis, demonstrating that honey is a potent neuroprotective agent that counteracts TBI-induced oxidative stress. Our investigation elucidates honey's capacity to alleviate neurobehavioral impairments and mitigate oxidative damage within a TBI model. These results underscore honey's significance as an innovative and promising therapeutic approach in TBI management, emphasizing its potential to enhance neurological outcomes and improve the overall well-being of individuals affected by TBI.

This research investigates the impact that different aspects of advertising have on the attention that a consumer pays to a certain advertisement. To investigate the correlations between the components of advertising and the attention arousal of consumers, six different aspects were tested. After collecting data from mothers, a heat map analysis was performed. The findings suggest that both the text and the visual components of the advertisements influenced the viewers' levels of attention. This research provides two possible hooks that might spike a consumer's attention and arousal in an advertisement. It is the image of a mother and kids together with the quote. The research presents how mother’s attention can be triggered by organic foods, which can help food advertisers to understand better the role of marketing cues in influencing consumers' purchase decisions.

Dyslexia is a learning disability that is neurobiological in origin. Besides, it typically results from a phonological awareness deficit, leading to difficulties with word identification, spelling, and decoding. Dyslexia could lead to secondary consequences such as reading comprehension problems, reduced reading experience, anxiety, and low self-esteem. Recent research has provided strong evidence that congenital brain abnormalities, such as the impaired magnocellular system, play a crucial role in dyslexia. Nonetheless, since 2011, the Ministry of Education Malaysia (MOE), via its Special Education Division, has defined learning disability as pertaining to individuals with similar or higher intellectual functioning in relation to typical students of similar age yet experiencing profound difficulty in spelling, reading, and writing. This definition fails to capture the current findings on dyslexia, and the shortcoming is evident in the question design of the Instrumen Senarai Semak Disleksia (ISD), the dyslexia checklist instrument currently used by MOE for screening students at risk of dyslexia at the entry level of primary schools. The inaccuracy in the definition adopted by MOE may further hinder an accurate understanding of dyslexia among Malaysians. In light of this, this paper aims to explain dyslexia and discuss the associated theories. This paper will review dyslexia screening methods in Malaysia and other countries as well as explain the importance of decoding skills and Rapid Automatised Naming (RAN) using the model of Simple View of Reading (SVR), advocating for increased emphasis on decoding skills and Rapid Automatised Naming in the ISD as a conclusion.

The aim of this minireview is to explore the relationship between auditory (AP) and phonological processing and to probe potential ‘cascade effects’ on literacy development. The overall purpose of this study is to specify auditory deficits in language and literacy outcomes to inform intervention. Important underpinnings of language and literacy development and characteristics of AP, phonological processing, and phonological awareness in children with literacy disorders in light of auditory processing skills. Children with language and literacy impairments experience difficulties processing temporal and/or spectral changes in acoustic stimuli resulting from atypical neural synchronization. On a behavioural level, studies have revealed a relationship between temporal processing skills (e.g., rise time discrimination, frequency modulation sensitivity) and literacy development. While research remains inconclusive on intervention efficacy centred on auditory processing, this review serves as the stepping stone for investigating intervention methods focused specifically on temporal processing. Frameworks associated with literacy deficits and interventions may benefit from auditory modality-specific assessment and interventions.

Patients with movement disorders are in a pre-frail state due to the physical limitation or reduction in tolerance to physical stress. The study was conducted in the Department of Neurology of a tertiary care teaching hospital in Northern-east Rajasthan with 50 patients. Inclusion criteria: patients with parkinsonian features aged >18 years; and willing to give consent regarding participation in the study. Exclusion criteria: patients with age <18 years; not willing to participate in the study; and exclusion of alternative diagnosis. Frailty and pre-frailty states were assessed using the Fried’s criteria. Modified Frailty Index (MFI) was used to classify it as mild, moderate, and severe. Unified Parkinson's Disease Rating Scale (UPDRS), Multisystem Atrophy Rating Scale (MSARS), and Progressive Supranuclear Palsy Rating Scale (PSPRS) were used for respective disorders. The data was compiled using an MS Excel sheet, and SPSS 20 was used for statistical analysis. Thirty-nine patients fulfilled the criteria for “frailty-phenotype”; only 9 were “pre-frail”, and 2 were non-frail. On the MFI, patients with atypical parkinsonism had severe frailty with a mean index score of 0.54, where the mean scores were higher in the progressive supranuclear palsy (PSP) group (0.57) than in the multisystem atrophy (MSA) group (0.5). Patients with idiopathic Parkinson’s disease (IPD) had mild to moderate frailty with a mean score of 0.29 (Range 0.17-0.51). With a higher UPDRS score, the frailty index score in IPD patients was also higher, as was PSPRS in patients with PSP and UMSARS in patients with MSA. The mean MMSE score was also lower in the group with a higher frailty index. The levodopa dose requirement was higher in the frail group than in the non-frail or prefrail group (125mg/day vs. 625mg/day; p<0.05). Frailty is part and parcel of neurodegenerative movement disorders, including movement disorders, and adds to the burden of disease.