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Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the causative agent of coronavirus disease 2019 (COVID-19), could affect brain structure and function. SARS-CoV-2 can enter the brain through different routes, including the olfactory, trigeminal, and vagus nerves, and through blood and immunocytes. SARS-CoV-2 may also enter the brain from the peripheral blood through a disrupted blood-brain barrier (BBB). The neurovascular unit in the brain, composed of neurons, astrocytes, endothelial cells, and pericytes, protects brain parenchyma by regulating the entry of substances from the blood. The endothelial cells, pericytes, and astrocytes highly express angiotensin converting enzyme 2 (ACE2), indicating that the BBB can be disturbed by SARS-CoV-2 and lead to derangements of tight junction and adherens junction proteins. This leads to increased BBB permeability, leakage of blood components, and movement of immune cells into the brain parenchyma. SARS-CoV-2 may also cross microvascular endothelial cells through an ACE2 receptor-associated pathway. The exact mechanism of BBB dysregulation in COVID-19/neuro-COVID is not clearly known, nor is the development of long COVID. Various blood biomarkers could indicate disease severity and neurologic complications in COVID-19 and help objectively diagnose those developing long COVID. This review highlights the importance of neurovascular and BBB disruption, as well as some potentially useful biomarkers in COVID-19, and long COVID/neuro-COVID., Competing Interests: Declaration of Conflicting InterestsThe authors declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: T.C.T. is the scientific director of Algonot, LLC, which develops liposomal flavonoid dietary supplements. The remaining authors declare no conflicts of interest.

Neuroinflammatory and neurodegenerative disorders including Alzheimer's disease (AD), Parkinson's disease (PD), traumatic brain injury (TBI) and Amyotrophic lateral sclerosis (ALS) are chronic major health disorders. The exact mechanism of the neuroimmune dysfunctions of these disease pathogeneses is currently not clearly understood. These disorders show dysregulated neuroimmune and inflammatory responses, including activation of neurons, glial cells, and neurovascular unit damage associated with excessive release of proinflammatory cytokines, chemokines, neurotoxic mediators, and infiltration of peripheral immune cells into the brain, as well as entry of inflammatory mediators through damaged neurovascular endothelial cells, blood-brain barrier and tight junction proteins. Activation of glial cells and immune cells leads to the release of many inflammatory and neurotoxic molecules that cause neuroinflammation and neurodegeneration. Gulf War Illness (GWI) and myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) are chronic disorders that are also associated with neuroimmune dysfunctions. Currently, there are no effective disease-modifying therapeutic options available for these diseases. Human induced pluripotent stem cell (iPSC)-derived neurons, astrocytes, microglia, endothelial cells and pericytes are currently used for many disease models for drug discovery. This review highlights certain recent trends in neuroinflammatory responses and iPSC-derived brain cell applications in neuroinflammatory disorders.

Introduction: Difficult airway is defined as difficulty or failure in one or more steps in upper airway management. Evaluation of the upper airway with physical examination methods and endoscopic devices is crucial in predicting difficult airway. The aim of this study was to evaluate bedside tests, Cormack Lehane (CL) and Tasli Classification (TC) scores of the patients and it was aimed to reveal the role of TC which will be performed preoperatively as a predictor of difficult tracheal intubation (DTI)., Methods: The study included a total of 98 patients who underwent surgical treatment under general anesthesia. Demographic data, including age, gender, and body mass index (BMI), and bedside tests consisting Modified Mallampati Classification (MMC), thyromental (TD) and sternomental (SD) distances, neck circumference (NC), interincisor distance (IID), CL and TC were recorded., Results: Evaluation was made of 64 (65.3%) male and 34 (34.7%) female patients ranging in age from 18 to 84 years (mean age: 50.35 ± 0.47 years). The successfully intubated patients (SIP)  group comprised 68 (69.4%) patients, and the difficult intubation patients (DIP) group, 30 (30.6%). According to CL, the numbers of SIP and DIP constituting grade 1 was 29 (42.6%) and one (3.3%); grade 2a was 29 (42.6%) and one (3.3%); grade 2b was eight (11.8%) and three (10%); grade 3a was one (1.5%) and six (20%); grade 3b was one (1.5%) and 14 (46.7%) respectively. Grade 4 was only detected in the DIP group in 5 (16.7%) patients. According to TC, the numbers of SIP and DIP constituting grade 1 was 20 (29.4%) and 1 (3.3%); grade 2a was 37 (54.4%) and seven (23.3%); grade 2b was 10 (14.7%) and 18 (60%); grade 3 was one (1.5%) and two (6.7%) respectively. Grade 4 was only detected in the DIP group in two (6.7%) patients., Conclusion: The TC, CL, NC and BMI scores were higher in the DIP group and higher TC scores (grade 2b, 3, and 4) can be a predictor of difficult airway. However, it may be more beneficial to use TC as a complementary diagnostic tool with bedside tests such as NC, SM, TM and MMC, rather than used alone., (Copyright © 2021 The Voice Foundation. Published by Elsevier Inc. All rights reserved.)

One lingering effect of the COVID-19 pandemic created by SARS-CoV-2 is the emergence of Long COVID (LC), characterized by enduring neurological sequelae affecting a significant portion of survivors. This review provides a thorough analysis of these neurological disruptions with respect to cognitive dysfunction, which broadly manifest as chronic insomnia, fatigue, mood dysregulation, and cognitive impairments with respect to cognitive dysfunction. Furthermore, we characterize how diagnostic tools such as PET, MRI, EEG, and ultrasonography provide critical insight into subtle neurological anomalies that may mechanistically explain the Long COVID disease phenotype. In this review, we explore the mechanistic hypotheses of these neurological changes, which describe CNS invasion, neuroinflammation, blood-brain barrier disruption, and gut-brain axis dysregulation, along with the novel vascular disruption hypothesis that highlights endothelial dysfunction and hypoperfusion as a core underlying mechanism. We lastly evaluate the clinical treatment landscape, scrutinizing the efficacy of various therapeutic strategies ranging from antivirals to anti-inflammatory agents in mitigating the multifaceted symptoms of LC. [ABSTRACT FROM AUTHOR]

Cerebral endothelial cells (CEC) that form the brain capillaries are the principal constituents of the blood brain barrier (BBB), the main active interface between the blood and the brain which plays a protective role by restricting the infiltration of pathogens, harmful substances and immune cells into the brain while allowing the entry of essential nutrients. Aberrant CEC function often leads to increased permeability of the BBB altering the bidirectional communication between the brain and the bloodstream and facilitating the extravasation of immune cells into the brain. In addition to their role as essential gatekeepers of the BBB, CEC exhibit immune cell properties as they can receive and transmit signals between the blood and the brain partly via release of inflammatory effectors in pathological conditions. Cerebral endothelial cells express innate immune receptors, including toll like receptors (TLRs) and inflammasomes which are the first sensors of exogenous or endogenous dangers and initiators of immune and inflammatory responses which drive neural dysfunction and degeneration. Accumulating evidence indicates that activation of TLRs and inflammasomes in CEC compromises BBB integrity, promotes aberrant neuroimmune interactions and modulates both systemic and neuroinflammation, common pathological features of neurodegenerative and psychiatric diseases and central nervous system (CNS) infections and injuries. The goal of the present review is to provide an overview of the pivotal roles played by TLRs and inflammasomes in CEC function and discuss the molecular and cellular mechanisms by which they contribute to BBB disruption and neuroinflammation especially in the context of traumatic and ischemic brain injuries and brain infections. We will especially focus on the most recent advances and literature reports in the field to highlight the knowledge gaps. We will discuss future research directions that can advance our understanding of the central contribution of innate immune receptors to CEC and BBB dysfunction and the potential of innate immune receptors at the BBB as promising therapeutic targets in a wide variety of pathological conditions of the brain. [ABSTRACT FROM AUTHOR]

Aging and age-related neurodegenerative disorders are characterized by the dysfunction or loss of brain nicotinic acetylcholine receptors (nAChRs), and these changes may be related to other senescence markers, such as oxidative stress and DNA repair dysfunction. However, the mechanism of nAChR loss in the aging brain and the modification of this process by drugs (e.g., memantine, Mem) are not yet fully understood. To study whether the differences in nAChR expression in the rat brain occur due to aging or oxidative stress and are modulated by Mem, we analyzed nAChR subunits (at RNA and protein levels) and other biomarkers by real-time quantitative polymerase chain reaction (RQ-PCR) and Western blot validation. Twenty-one female Wistar rats were divided into four groups, depending on age, and the oldest group received injections of Mem or water with the use of intragastric catheters. We studied the cerebral grey matter (CGM), subcortical white matter (SCWM), and cerebellum (Ce). Results showed an age-related decrease of α7 nAChR mRNA level in SCWM. The α7 nAChR mRNA loss was accompanied by reduced expression of 8-oxoguanine DNA glycosylase 1 (OGG1) and an increased tumor necrosis factor alpha (TNFα) level. In the water group, we observed a higher level of α7 nAChR protein in the SCWM and Ce. Biomarker levels changed, but to a different extent depending on the brain area. Importantly, the dysfunction in antioxidative status was stopped and even regressed under Mem treatment. After two weeks of treatment, an increase in TP53 protein level and a decrease in 8-oxo-2′deoxyguanosine (8-oxo-2′dG) level were observed. We conclude that Mem administration may be protective against the senescence process by antioxidative mechanisms. [ABSTRACT FROM AUTHOR]

Monitoring and assessing the progression of symptoms in neurodegenerative diseases, including Alzheimer's and Parkinson's disease, are critical for improving patient outcomes. Traditional biomarkers, such as cerebrospinal fluid analysis and brain imaging, are widely used to investigate the underlying mechanisms of disease and enable early diagnosis. In contrast, digital biomarkers derived from phenotypic changes—such as EEG, eye movement, gait, and speech analysis—offer a noninvasive and accessible alternative. Leveraging portable and widely available devices, such as smartphones and wearable sensors, digital biomarkers are emerging as a promising tool for ND diagnosis and monitoring. This review highlights the comprehensive developments in digital biomarkers, emphasizing their unique advantages and integration potential alongside traditional biomarkers. [ABSTRACT FROM AUTHOR]

Neuroinflammation is involved in various neurological and neurodegenerative disorders in which the activation of microglia is one of the key factors. In this study, we examined the anti-inflammatory effects of the flavonoids nobiletin (5,6,7,8,3′,4′-hexamethoxyflavone) and eriodictyol (3′,4′,5,7-tetraxydroxyflavanone) on human microglia cell line activation stimulated by either lipopolysaccharide (LPS), severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) full-length Spike protein (FL-Spike), or the mycotoxin ochratoxin A (OTA). Human microglia were preincubated with the flavonoids (10, 50, and 100 µM) for 2 h, following which, they were stimulated for 24 h. The inflammatory mediators interleukin-1 beta (IL-1β), chemokine (C-X-C motif) ligand 8 (CXCL8), IL-6, and matrix metalloproteinase-9 (MMP-9) were quantified in the cell culture supernatant by enzyme-linked immunosorbent assay (ELISA). Both nobiletin and eriodictyol significantly inhibited the LPS, FL-Spike, and OTA-stimulated release of IL-1β, CXCL8, IL-6, and MMP-9 at 50 and 100 µM, while, in most cases, nobiletin was also effective at 10 µM, with the most pronounced reductions at 100 µM. These findings suggest that both nobiletin and eriodictyol are potent inhibitors of the pathogen-stimulated microglial release of inflammatory mediators, highlighting their potential for therapeutic application in neuroinflammatory diseases, such as long COVID. [ABSTRACT FROM AUTHOR]

This paper provides a detailed analysis of the operation of representative forging tools (in the context of using various surface engineering techniques) used in the process of the hot forging of nickel–chromium steel elements. The influence of the microstructure and hardness of the material on the durability of the tools is also discussed, which is important for understanding the mechanisms of their wear. The research showed that the standard tools used in the process (only after nitriding) as a reference point worked for the shortest period, making an average of about 1400 forgings. In turn, the tools coated with the CrAlSiN coating allowed for the production of the largest number of forgings, reaching 2400 pieces, with uniform wear. In comparison, the tools with the CrAlBN coating made 1900 forgings. Three-dimensional scanning analysis showed that CrAlSiN- and CrAlBN-coated tools have lower volumetric wear, around 41–43 mm3, compared to 59 mm3 for nitrided tools. For a better comparison of tool life, the authors proposed the Z-factor, as the material loss to the number of forgings. The CrAlSiN coating showed the lowest material loss, despite a slightly higher Z-factor value compared to the CrAlBN coating. The use of hybrid coatings such as CrAlSiN and CrAlBN significantly reduces tool wear while increasing service life compared to tools that are nitrided only. [ABSTRACT FROM AUTHOR]

Parenting behavior comprises a variety of adult-infant and adult-adult interactions across multiple timescales. The state transition from nonparent to parent requires an extensive reorganization of individual priorities and physiology and is facilitated by combinatorial hormone action on specific cell types that are integrated throughout interconnected and brainwide neuronal circuits. In this review, we take a comprehensive approach to integrate historical and current literature on each of these topics across multiple species, with a focus on rodents. New and emerging molecular, circuit-based, and computational technologies have recently been used to address outstanding gaps in our current framework of knowledge on infant-directed behavior. This work is raising fundamental questions about the interplay between instinctive and learned components of parenting and the mutual regulation of affiliative versus agonistic infant-directed behaviors in health and disease. Whenever possible, we point to how these technologies have helped gain novel insights and opened new avenues of research into the neurobiology of parenting. We hope this review will serve as an introduction for those new to the field, a comprehensive resource for those already studying parenting, and a guidepost for designing future studies. Listen to this article's corresponding podcast at https://physrev.podbean.com/e/neurobiology-of-parenting-and-infant-evoked-aggression/. [ABSTRACT FROM AUTHOR]

Background: The Rho proteins and Rho-kinase (ROCK) enzymes are responsible for signal transduction, and cause cell permeability, contractility, differentiation, migration, proliferation or apoptosis depending on cell types. All of these functions are vital for cancer initiation and progression. In this study, the preventive and protective effects of a selective ROCK inhibitor Y-27632 against Ehrlich ascites carcinoma in Swiss albino mice were investigated., Methods: Adult male albino mice were divided into five equal groups, and Y-27632 (0.1, 1, and 10 mg/kg) was given to groups as two steps; before (pre-carcinoma) and after inoculation of carcinoma cell suspensions (post-carcinoma). At the end of the experiments (at day 15), cardiac blood samples, the ascitic fluid, and intestinal specimens were collected for histopathology and biochemical investigation., Results: Significant decreases in the body weight and immunostaining scores in small and large intestine for ROCK2, preservation of serum glutathione (GSH) levels, and an increase in tumor level of nitric oxide were recorded in groups pretreated with Y-27632. However, treatment with Y-27632 after tumor inoculation did not affect body weight and ROCK2 immunostaining scores, increased serum MDA levels, and decreased GSH levels., Conclusions: This is the first study on the effectiveness of Y-27632 in this experimental tumor model. Our findings provided direct evidence for ROCK involvement in tumor development. These data suggest that pretreatment with Y-27632 has a protective effect against tumor formation., (Copyright © 2014 Institute of Pharmacology, Polish Academy of Sciences. Published by Elsevier Urban & Partner Sp. z o.o. All rights reserved.)

The 20th century was a time for architectural change, technical innovation and the search for affordable construction and prefabrication. In this context, pneumatic concrete laminar structures represent the advances towards a new architecture that could give answers to the challenges of the century. This work identifies the systems that were explored during that period and describes the experimental designs developed by W. Neff, H. Heifetz, H. Isler, D. B. South and D. Bini. In addition, the adaptation capability of this singular type and the reasons that caused the abandonment of these structure are also analysed.

The SARS-CoV-2 virus that resulted in the COVID-19 pandemic has been implicated in a range of neurological issues, such as encephalopathy, stroke, and cognitive decline. Although the precise mechanism causing these issues is unknown, mounting evidence shows that blood–brain barrier (BBB) disruption is probable2 a major factor. The integrity of the blood–brain barrier (BBB), a highly selective barrier that divides the brain from the systemic circulation, is crucial for preserving normal brain function. By analysing the multi-transcriptome data, this work explores the neurological impacts of the SARS-CoV-2 virus and provides insight into the molecular mechanisms behind BBB breakdown and neurological symptoms in COVID-19 patients. The endothelial cells of BBB expresses inflammatory genes in response to the systemic inflammation induced due to SARS-CoV-2 remnants in the body. This raises the possibility that systemic inflammation brought on by SARS-CoV-2 and BBB integrity are correlated. Furthermore, the study highlights the pathways involved in oxidative stress and endothelial cell activation, revealing their role in COVID-19 passage through BBB and induction of systemic inflammation and advancement toward neurological disorders. The article showcases the evidence that mitochondrial dysfunction is a major aftermath associated with SARS-CoV-2 infection as the impaired Mitochondria leads to an accumulation of reactive oxygen species (ROS), triggering endothelial dysfunction, and leading to the passage of harmful molecules across the BBB. This study offers insightful information that may open up the possibilities for new treatment plans by targeting biomarkers specifically associated with inflammation and BBB dysfunctioning conditions. [ABSTRACT FROM AUTHOR]

Compared with their linear counterparts, cyclic peptides, characterized by their unique topologies, offer superior stability and enhanced functionality. In this review article, the rational design of cyclic peptide primary structures and their significant influence on self-assembly processes and functional capabilities are comprehensively reviewed. We emphasize how strategically modifying amino acid sequences and ring sizes critically dictate the formation and properties of peptide nanotubes (PNTs) and complex assemblies, such as rotaxanes. Adjusting the number of amino acid residues and side chains allows researchers to tailor the diameter, surface properties, and functions of PNTs precisely. In addition, we discuss the complex host–guest chemistry of cyclic peptides and their ability to form rotaxanes, highlighting their potential in the development of mechanically interlocked structures with novel functionalities. Moreover, the critical role of computational methods for accurately predicting the solution structures of cyclic peptides is also highlighted, as it enables the design of novel peptides with tailored properties for a range of applications. These insights set the stage for groundbreaking advances in nanotechnology, drug delivery, and materials science, driven by the strategic design of cyclic peptide primary structures. [ABSTRACT FROM AUTHOR]

Neurovascular unit (NVU) inflammation via activation of glial cells and neuronal damage plays a critical role in neurodegenerative diseases. Though the exact mechanism of disease pathogenesis is not understood, certain biomarkers provide valuable insight into the disease pathogenesis, severity, progression and therapeutic efficacy. These markers can be used to assess pathophysiological status of brain cells including neurons, astrocytes, microglia, oligodendrocytes, specialized microvascular endothelial cells, pericytes, NVU, and blood-brain barrier (BBB) disruption. Damage or derangements in tight junction (TJ), adherens junction (AdJ), and gap junction (GJ) components of the BBB lead to increased permeability and neuroinflammation in various brain disorders including neurodegenerative disorders. Thus, neuroinflammatory markers can be evaluated in blood, cerebrospinal fluid (CSF), or brain tissues to determine neurological disease severity, progression, and therapeutic responsiveness. Chronic inflammation is common in age-related neurodegenerative disorders including Alzheimer's disease (AD), Parkinson's disease (PD), and dementia. Neurotrauma/traumatic brain injury (TBI) also leads to acute and chronic neuroinflammatory responses. The expression of some markers may also be altered many years or even decades before the onset of neurodegenerative disorders. In this review, we discuss markers of neuroinflammation, and neurodegeneration associated with acute and chronic brain disorders, especially those associated with neurovascular pathologies. These biomarkers can be evaluated in CSF, or brain tissues. Neurofilament light (NfL), ubiquitin C-terminal hydrolase-L1 (UCHL1), glial fibrillary acidic protein (GFAP), Ionized calcium-binding adaptor molecule 1 (Iba-1), transmembrane protein 119 (TMEM119), aquaporin, endothelin-1, and platelet-derived growth factor receptor beta (PDGFRβ) are some important neuroinflammatory markers. Recent BBB-on-a-chip modeling offers promising potential for providing an in-depth understanding of brain disorders and neurotherapeutics. Integration of these markers in clinical practice could potentially enhance early diagnosis, monitor disease progression, and improve therapeutic outcomes. [ABSTRACT FROM AUTHOR]

Major Depressive Disorder (MDD) is a prevalent mental health condition with a complex pathophysiology involving neuroinflammation, neurodegeneration, and disruptions in neuronal and glial cell function. Microglia, the innate immune cells of the central nervous system, release inflammatory cytokines in response to pathological changes associated with MDD. Damage-associated molecular patterns (DAMPs) act as alarms, triggering microglial activation and subsequent inflammatory cytokine release. This review examines the cellular mechanisms underlying MDD pathophysiology, focusing on the lipid-mediated modulation of neuroinflammation. We explore the intricate roles of microglia and astrocytes in propagating inflammatory cascades and discuss how these processes affect neuronal integrity at the cellular level. Central to our analysis are three key molecules: High Mobility Group Box 1 (HMGB1) and S100 Calcium Binding Protein β (S100β) as alarmins, and Neuron-Specific Enolase (NSE) as an indicator of neuronal stress. We present evidence from in vitro and ex vivo studies demonstrating how these molecules reflect and contribute to the neuroinflammatory milieu characteristic of MDD. The review then explores the potential of omega-3 polyunsaturated fatty acids (ω-3 PUFAs) as neuroinflammation modulators, examining their effects on microglial activation, cytokine production, and neuronal resilience in cellular models of depression. We critically analyze experimental data on how ω-3 PUFA supplementation influences the expression and release of HMGB1, S100β, and NSE in neuronal and glial cultures. By integrating findings from lipidomic and cellular neurobiology, this review aims to elucidate the mechanisms by which ω-3 PUFAs may exert their antidepressant effects through modulation of neuroinflammatory markers. These insights contribute to our understanding of lipid-mediated neuroprotection in MDD and may inform the development of targeted, lipid-based therapies for both depression and neurodegenerative disorders. [ABSTRACT FROM AUTHOR]

In the current era of Industry 4.0 and Circular Economy, green logistics have become necessary for being sustainable. Adopting green logistics practices is a challenging task for the manufacturing industry, specifically in developing countries like India. In this study, we identified 16 barriers to implementing green logistics in the Indian manufacturing industry in reference to Industry 4.0 and circular economy. Data was collected from experts through a questionnaire-based survey. The decision-making trial and evaluation laboratory (DEMATEL) technique was applied to examine the degree of influence and interaction among the barriers. It has also helped in the classification of barriers into cause-and-effect categories. To validate the findings, a sensitivity analysis had also been carried out. The findings would help manufacturing organisations in developing strategies for implementing green logistics to achieve long-term sustainability. [ABSTRACT FROM AUTHOR]

The European olive tree, Olea europaea L., and its polyphenols hold great therapeutic potential to treat neuroinflammation and cognitive impairment. This review examines the evidence for the anti-inflammatory and neuroprotective actions of olive polyphenols and their potential in the treatment of long COVID and neurodegenerative diseases such as Alzheimer's disease (AD), Parkinson's disease (PD), and multiple sclerosis (MS). Key findings suggest that olive polyphenols exhibit antioxidant, anti-inflammatory, neuroprotective, and antiviral properties, making them promising candidates for therapeutic intervention, especially when formulated in unique combinations. Recommendations for future research directions include elucidating molecular pathways through mechanistic studies, exploring the therapeutic implications of olive polyphenol supplementation, and conducting clinical trials to assess efficacy and safety. Investigating potential synergistic effects with other agents addressing different targets is suggested for further exploration. The evidence reviewed strengthens the translational value of olive polyphenols in conditions involving cognitive dysfunction and emphasizes the novelty of new formulations. [ABSTRACT FROM AUTHOR]

Orlistat, a selective inhibitor of gastrointestinal lipases, was used to investigate triacylglycerol absorption. Using mice and a variety of emulsified dietary lipids we found that the absorption of radiolabelled tripalmitin (containing the fatty acid 16:0), but not of triolein (18:1n-9) or tri-gamma-linolenin (18:3n-6), was incomplete from meals rich in esterified palmitate. Further, the absorption of radiolabelled tri-gamma-linolenin, from both saturated and unsaturated dietary triacylglycerols, was 1.3- to 2-fold more potently inhibited by orlistat than that of triolein and tripalmitin. These radiolabelled triacylglycerols, which have the same fatty acid in all three positions, may not always be accurate markers of the absorption of dietary triacylglycerols. Orlistat was more effective at inhibiting the absorption of radiolabelled triacylglycerols with which it was codissolved than those added separately, which indicates that equilibration between lipid phases in the stomach may not always be complete. The saturation of the dietary lipid had little or no effect on the potency of orlistat. Orlistat provides a novel approach for studying the role of triacylglycerol hydrolysis in the overall process of triacylglycerol absorption.

Long COVID, also known as post-acute sequelae of SARS-CoV-2 infection, refers to a condition where individuals continue to experience a range of symptoms weeks to months after the acute phase of COVID-19 has resolved. While respiratory symptoms are commonly associated with COVID-19, emerging evidence suggests that neurological manifestations play a significant role in the long-term effects of the disease. This article explores the neurological basis of long COVID, delving into the various symptoms, pathophysiological mechanisms, impact on cognitive function, neuroimaging findings, current treatment approaches, long-term prognosis, and future research directions in understanding and managing the neurological sequelae of long COVID. [ABSTRACT FROM AUTHOR]

Aim: This study aimed to undertake an anthropometric assessment and to compare the muscular strength of elite athletes with that of a control group to predict Mallampati classification. Material and Method: The study group consisted of elite track athletes, and the control group consisted of volunteers with similar characteristics. Anthropometric measurements of the hand, fingers, and wrist were made; handgrip strength and the pinch strength of the fingers were also measured. A serum biochemical analysis was then performed. Participants were divided into two groups: those with Modified Mallampati Scores (MMS) I and II, and those with III and IV. A partial correlation test was used to examine the correlations of the variables according to the MMS groups. Results: The study included 32 elite athletes and 42 volunteer participants. Serum Na level, fingertip to root digit 3 (FTR3), and FTR4 were significantly lower in males in MMS groups 3-4. Among all cases, wrist extension angle (WEA) was found to be significantly lower in MMS group 3-4. However, hand breadth at thumb (HBT), hand depth radial (HDR), breadth at the first joint of digit 2 (BFJD2), pinch strength of thumb (PST), and PSLF were significantly higher in MMS groups 3-4. Among these variables, HBT, BFJD2, PST, and PSLF were significantly higher in elite athletes, but HDR was similar between the study groups. MMS groups showed the highest correlation with the pinch strength of the thumb. Conclusion: The pinch strength of the thumb and little finger was determined as the most important predictors for the MMS group rather than the handgrip strength (HGS). [ABSTRACT FROM AUTHOR]

This document is a special issue of the journal Cells that focuses on the role of astrocytes in central nervous system (CNS) disorders. It includes 22 articles that provide evidence implicating astrocytes in the etiology of specific disorders. The articles discuss how astrocyte dysfunction is now recognized as a factor in disorders previously thought to be solely of neuronal or oligodendrocyte origin. The document provides an overview of the papers included in the special issue, which cover various CNS disorders and explore potential therapeutic approaches. [Extracted from the article]

The leaves of Rhamnus erythroxylon Pall. are widely used as tea substitutes in northwest China for their fragrant aroma, anti-irritability, and digestion-enhancing properties. Ombuin, a main flavonoid compound found in the leaves, exhibited notable anti-inflammatory and antioxidant effects. However, its potential role in treating neuroinflammatory-related diseases remains unexplored. Thus, this study aims to evaluate the anti-neuroinflammatory effects of ombuin and to explore the underlying molecular mechanisms. According to our findings, ombuin dramatically reduced the release of interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), IL-1β, nitric oxide (NO), and reactive oxygen species (ROS) in lipopolysaccharide (LPS)-stimulated BV-2 microglia. Further analysis, including transcriptomics, network pharmacology, molecular docking, and cellular heat transfer assays, revealed that Src was a direct target of ombuin. Western blot analysis showed that ombuin effectively suppressed Src phosphorylation and inhibited the downstream expressions of p-PI3K p85, p-AKT1, p-IKKα/β, p-IκBα, and nuclear factor κB (NF-κB). Meanwhile, the repression of Src significantly reversed the anti-neuroinflammatory activity of ombuin. Our results identified Src as a direct target of ombuin and implied that ombuin exerted an anti-neuroinflammatory effect by inhibiting Src phosphorylation and suppressing the activation of the PI3K-AKT and NF-κB pathways, which might provide an alternative therapeutic strategy for neurodegenerative diseases. [ABSTRACT FROM AUTHOR]

Cognitive decline covers a broad spectrum of disorders, not only resulting from brain diseases but also from systemic diseases, which seriously influence the quality of life and life expectancy of patients. As a highly selective anatomical and functional interface between the brain and systemic circulation, the blood-brain barrier (BBB) plays a pivotal role in maintaining brain homeostasis and normal function. The pathogenesis underlying cognitive decline may vary, nevertheless, accumulating evidences support the role of BBB disruption as the most prevalent contributing factor. This may mainly be attributed to inflammation, metabolic dysfunction, cell senescence, oxidative/nitrosative stress and excitotoxicity. However, direct evidence showing that BBB disruption causes cognitive decline is scarce, and interestingly, manipulation of the BBB opening alone may exert beneficial or detrimental neurological effects. A broad overview of the present literature shows a close relationship between BBB disruption and cognitive decline, the risk factors of BBB disruption, as well as the cellular and molecular mechanisms underlying BBB disruption. Additionally, we discussed the possible causes leading to cognitive decline by BBB disruption and potential therapeutic strategies to prevent BBB disruption or enhance BBB repair. This review aims to foster more investigations on early diagnosis, effective therapeutics, and rapid restoration against BBB disruption, which would yield better cognitive outcomes in patients with dysregulated BBB function, although their causative relationship has not yet been completely established. [ABSTRACT FROM AUTHOR]

Respiratory viral infections pose a significant public health threat, particularly in children and older adults, with high mortality rates. Some of these pathogens are the human respiratory syncytial virus (hRSV), severe acute respiratory coronavirus-2 (SARS-CoV-2), influenza viruses (IV), human parvovirus B19 (B19V), and human bocavirus 1 (HBoV1). These viruses cause various respiratory symptoms, including cough, fever, bronchiolitis, and pneumonia. Notably, these viruses can also impact the central nervous system (CNS), leading to acute manifestations such as seizures, encephalopathies, encephalitis, neurological sequelae, and long-term complications. The precise mechanisms by which these viruses affect the CNS are not fully understood. Glial cells, specifically microglia and astrocytes within the CNS, play pivotal roles in maintaining brain homeostasis and regulating immune responses. Exploring how these cells interact with viral pathogens, such as hRSV, SARS-CoV-2, IVs, B19V, and HBoV1, offers crucial insights into the significant impact of respiratory viruses on the CNS. This review article examines hRSV, SARS-CoV-2, IV, B19V, and HBoV1 interactions with microglia and astrocytes, shedding light on potential neurological consequences. [ABSTRACT FROM AUTHOR]

The COVID-19 pandemic has introduced new challenges in managing neurological conditions, particularly among athletes. This paper explores the intersection of post-COVID-19 neurological syndrome (PCNS/PASC) and post-concussion syndrome (PCS), focusing on their implications in sports medicine. Our analysis covers the symptomatology, pathophysiology, and management strategies for PCNS/PASC and PPCS, with special attention paid to the unique challenges faced by athletes recovering from these conditions, including the risk of symptom exacerbation and prolonged recovery. Key findings reveal that both PCNS/PASC and PPCS present with overlapping symptoms such as cognitive difficulties, exercise intolerance, and mental health issues, but differ in specific manifestations like anosmia and ageusia, unique to COVID-19. Pathophysiological analysis reveals similarities in blood–brain barrier disruption (BBB) but differences in the extent of immune activation. Management strategies emphasize a gradual increase in physical activity, close symptom monitoring, and psychological support, with a tailored approach for athletes. Specific interventions include progressive aerobic exercises, resistance training, and cognitive rehabilitation. Furthermore, our study highlights the importance of integrating neurology, psychiatry, physical therapy, and sports medicine to develop comprehensive care strategies. Our findings underscore the dual challenge of COVID-19 and concussion in athletes, necessitating a nuanced, interdisciplinary approach to effective management. Future research should focus on the long-term neurological effects of both conditions and optimizing treatment protocols to improve patient outcomes. This comprehensive understanding is crucial for advancing the management of athletes affected by these overlapping conditions and ensuring their safe return to sports. [ABSTRACT FROM AUTHOR]