Neuroscience
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The aim of this study was to investigate the otoprotective effects of Quercetin (Que) against both noise-induced hearing loss (NIHL) and the ototoxicity of silver nanoparticles (SNPs) in rats. Forty-two male Wistar rats were divided into seven groups (n = 6): control, SNPs, Que (100 mg/kg) plus SNPs (100 mg/kg), noise (104 dB), Que plus noise, noise plus SNPs, and noise plus Que plus SNPs. In the weight change results, there was no significant difference between the groups exposed to noise plus SNPs and SNPs compared to the control group. ⋯ Que also decreased the levels of TACT, MDA, IL-6, TNF-α, and NOX3 in the groups exposed to noise and SNPs and increased the SOD level and expression of myosin heavy chain VII (MYH7) and β-tubulin III (TUBB3) proteins. Furthermore, Que decreased structural changes in the animals' cochlea. Our findings indicate that pretreatment with Que efficiently counteracted the adverse effects of noise and SNPs on inner hair cell, outer hair cell, and nerve cells, which are responsible for high-frequency perception.
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Randomized Controlled Trial
Can brain activities of guided metaphorical restructuring predict therapeutic changes?
The present study examined whether brain activities of metaphorical restructuring could predict improvements in emotion and general self-efficacy (GSES). Sixty-two anxious graduates were randomly assigned to either the metaphor group (n = 31) or the literal group (n = 31). After completing the pretest (T1), the participants were first presented with micro-counseling dialogues (MCD) to guide metaphorical or literal restructuring, and their functional brain activities were simultaneously recorded. ⋯ One important limitation is that the results should be interpreted with caution when generalizing to clinical anxiety samples due to the participants were graduate students with anxiety symptoms rather than clinical sample. These results indicated that metaphor restructuring produced greater symptom improvements, and activation in the hippocampus and IFG could predict these symptom improvements. This suggests that the activation of the two regions during the restructuring intervention may be a neural marker for symptom improvements.
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Fear-potentiated startle (FPS) has been widely used to study fear processing in humans and rodents. Human studies showed higher startle amplitudes and exaggerated fear reactivity to unpredictable vs. predictable threats in individuals suffering from post-traumatic stress disorder (PTSD). Although human FPS studies use both sexes, a surprisingly limited number of rodent FPS studies use females. ⋯ However, in the classic FPS, Sprague-Dawley females show reduced proportion between cued fear and cue-elicited vigilant state than males. Lastly, a prominent sex difference is uncovered following unpredictable fear-conditioning (cue and shock un-paired), with Wistar, but not Sprague-Dawley, females showing significantly higher startle overall during the FPS recall, regardless of trial type, and higher contextual fear than males. This striking sex difference in processing unpredictable threats in rodent FPS might help to understand the mechanisms underlying higher incidence of PTSD in women.
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Collective self-esteem (CSE) is an important personality variable, defined as self-worth derived from membership in social groups. A study explored the neural basis of CSE using a task-based functional magnetic resonance imaging (fMRI) paradigm; however, task-independent neural basis of CSE remains to be explored, and whether the CSE neural basis of resting-state fMRI is consistent with that of task-based fMRI is unclear. ⋯ Our findings revealed CSE neural basis in the whole-brain RSFC network, and established the concordance between leverage centrality and the activation pattern (evoked during collective self-worth task) of the identified regions in terms of representing CSE.
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Diabetes Mellitus (DM) and Alzheimer's disease (AD) have been two of the most common chronic diseases affecting people worldwide. Type 2 DM (T2DM) is a metabolic disease depicted by insulin resistance, dyslipidemia, and chronic hyperglycemia while AD is a neurodegenerative disease marked by Amyloid β (Aβ) accumulation, neurofibrillary tangles aggregation, and tau phosphorylation. Various clinical, epidemiological, and lipidomics studies have linked those diseases claiming shared pathological pathways raising the assumption that diabetic patients are at an increased risk of developing AD later in their lives. ⋯ Lipidomics, an analysis of lipid structure, formation, and interactions, evidently exhibits these lipid changes and their direct and indirect effect on Aβ synthesis, insulin resistance, oxidative stress, and neuroinflammation. In this review, we have discussed the pathophysiology of T2DM and AD, the interconnecting pathological pathways they share, and the lipidomics where different lipids such as cholesterol, phospholipids, sphingolipids, and sulfolipids contribute to the underlying features of both diseases. Understanding their role can be beneficial for diagnostic purposes or introducing new drugs to counter AD.