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The increasing prevalence of viral infections and the emergence of drug-resistant or mutant strains necessitate the exploration of novel antiviral strategies. Accumulating evidence suggests that natural plant products have significant potential to enhance the human antiviral response. Various plant natural products (PNPs) known for their antiviral properties have been evaluated for their ability to modulate immune responses and inhibit viral infections. Research has focused on understanding the mechanisms by which these PNPs interact with the human immune system and their potential to complement existing antiviral therapies. PNPs control compounds such as alkaloids, flavonoids, terpenoids, and polyphenols to promote antiviral cytokine synthesis, increase T-cell and macrophage activity, and activate antiviral genes. Studies have investigated the molecular interactions between PNPs, viruses, and host cells, exploring the potential of combining PNPs with conventional antiviral drugs to enhance efficacy. However, several challenges remain, including identifying, characterizing, and standardizing PNP extracts, optimizing dosages, improving bioavailability, assessing long-term safety, and navigating regulatory approval. The promising potential of PNPs is being explored to develop new, effective, and natural antiviral therapies. This review outlines a framework for an integrative approach to connect the full potential of PNPs in combating viral infections and improving human health. By combining natural plant products with conventional antiviral treatments, more effective and sustainable management of viral diseases can be achieved. [ABSTRACT FROM AUTHOR]

Atherosclerotic cardiovascular disease (ASCVD) causes significant morbidity and mortality globally. Most of the chemicals specifically target certain pathways and minimally impact other diseases associated with ASCVD. Moreover, interactions of these drugs can cause toxic reactions. Consequently, the exploration of multi-targeted and safe medications for treating and preventing ASCVD has become an increasingly popular trend. Gallic acid (GA), a natural secondary metabolite found in various fruits, plants, and nuts, has demonstrated potentials in preventing and treating ASCVD, in addition to its known antioxidant and anti-inflammatory effects. It alleviates the entire process of atherosclerosis (AS) by reducing oxidative stress, improving endothelial dysfunction, and inhibiting platelet activation and aggregation. Additionally, GA can treat ASCVD-related diseases, such as coronary heart disease (CHD) and cerebral ischemia. However, the pharmacological actions of GA in the prevention and treatment of ASCVD have not been comprehensively reviewed, which limits its clinical development. This review primarily summarizes the in vitro and in vivo pharmacological actions of GA on the related risk factors of ASCVD, AS, and ASCVD. Additionally, it provides a comprehensive overview of the toxicity, extraction, synthesis, pharmacokinetics, and pharmaceutics of GA,aimed to enhance understanding of its clinical applications and further research and development. [ABSTRACT FROM AUTHOR]

Introduction: The choroid plexus is located in the cerebral ventricles. It consists of a stromal core and a single layer of cuboidal epithelial cells that forms the blood-cerebrospinal barrier. The main function of the choroid plexus is to produce cerebrospinal fluid. Subarachnoid hemorrhage due to aneurysm rupture is a devastating type of hemorrhagic stroke. Following subarachnoid hemorrhage, blood and the blood degradation products that disperse into the cerebrospinal fluid come in direct contact with choroid plexus epithelial cells. The aim of the current study was to elucidate the pathophysiological cascades responsible for the inflammatory reaction that is seen in the choroid plexus following subarachnoid hemorrhage. Methods: Subarachnoid hemorrhage was induced in rats by injecting non-heparinized autologous blood to the cisterna magna. Increased intracranial pressure following subarachnoid hemorrhage was modeled by using artificial cerebrospinal fluid instead of blood. Subarachnoid hemorrhage and artificial cerebrospinal fluid animals were left to survive for 1, 3, 7 and 14 days. Immunohistochemical staining of TLR4, TLR9, FPR2, CCL2, TNFα, IL-1β, CCR2 and CX3CR1 was performed on the cryostat sections of choroid plexus tissue. The level of TLR4, TLR9, FPR2, CCL2, TNFα, IL-1β was detected by measuring immunofluorescence intensity in randomly selected epithelial cells. The number of CCR2 and CX3CR1 positive cells per choroid plexus area was manually counted. Immunohistochemical changes were confirmed by Western blot analyses. Results: Immunohistochemical methods and Western blot showed increased levels of TLR9 and a slight increase in TLR4 and FRP2 following both subarachnoid hemorrhage as well as the application of artificial cerebrospinal fluid over time, although the individual periods were different. The levels of TNFα and IL-1β increased, while CCL2 level decreased slightly. Accumulation of macrophages positive for CCR2 and CX3CR1 was found in all periods after subarachnoid hemorrhage as well as after the application of artificial cerebrospinal fluid. Discussion: Our results suggest that the inflammation develops in the choroid plexus and blood-cerebrospinal fluid barrier in response to blood components as well as acutely increased intracranial pressure following subarachnoid hemorrhage. These pro-inflammatory changes include accumulation in the choroid plexus of pro-inflammatory cytokines, innate immune receptors, and monocyte-derived macrophages. [ABSTRACT FROM AUTHOR]

Effective stormwater management is increasingly vital due to climate change impacts, such as intensified rainfall and flooding. Urban expansion, water scarcity, and intensified agriculture demand innovative solutions like Green Stormwater Infrastructure (GSI), including vegetated biofilters, green roofs, wetlands, bioretention systems, and high-rate filtration. These systems, enhanced by natural and engineered filter materials, improve contaminant removal across diverse contexts. Modern practices prioritize retention, infiltration, and groundwater recharge over traditional rapid drainage, reframing stormwater as a resource amid rising extreme weather events. In water-scarce regions, stormwater management offers dual-use potential for drinking and non-drinking applications, addressing freshwater scarcity exacerbated by population growth and climate change. Targeting the "first flush" of pollutants after rainfall allows for more efficient, cost-effective treatment. This paper identifies three key objectives: addressing GSI limitations and exploring new technologies, evaluating treatment train combinations for cost-effective reuse, and advancing urban stormwater treatment research. Various filter media, such as those in green roofs, bioretention systems, and swales, effectively remove pollutants like nutrients, heavy metals, PAHs, and micropollutants. Granular activated carbon (GAC) filters excel at reducing heavy metals and dissolved organic carbon (DOC), with pre-screening via anthracite filters to extend GAC lifespan by trapping sediments and pollutants. Managing emerging contaminants and microplastics remains underexplored and requires further investigation. [ABSTRACT FROM AUTHOR]

Type 2 diabetes mellitus (T2DM), a serious metabolic disorder, is a worldwide health problem due to the alarming rise in prevalence and elevated morbidity and mortality. Chronic hyperglycemia, insulin resistance, and ineffective insulin effect and secretion are hallmarks of T2DM, leading to many serious secondary complications. These include, in particular, cardiovascular disorders, diabetic neuropathy, nephropathy and retinopathy, diabetic foot, osteoporosis, liver damage, susceptibility to infections and some cancers. Polyphenols such as flavonoids, phenolic acids, stilbenes, tannins, and lignans constitute an extensive and heterogeneous group of phytochemicals in fresh fruits, vegetables and their products. Various in vitro studies, animal model studies and available clinical trials revealed that flavonoids (e.g., quercetin, kaempferol, rutin, epicatechin, genistein, daidzein, anthocyanins), phenolic acids (e.g., chlorogenic, caffeic, ellagic, gallic acids, curcumin), stilbenes (e.g., resveratrol), tannins (e.g., procyanidin B2, seaweed phlorotannins), lignans (e.g., pinoresinol) have the ability to lower hyperglycemia, enhance insulin sensitivity and improve insulin secretion, scavenge reactive oxygen species, reduce chronic inflammation, modulate gut microbiota, and alleviate secondary complications of T2DM. The interaction between polyphenols and conventional antidiabetic drugs offers a promising strategy in the management and treatment of T2DM, especially in advanced disease stages. Synergistic effects of polyphenols with antidiabetic drugs have been documented, but also antagonistic interactions that may impair drug efficacy. Therefore, additional research is required to clarify mutual interactions in order to use the knowledge in clinical applications. Nevertheless, dietary polyphenols can be successfully applied as part of supportive treatment for T2DM, as they reduce both obvious clinical symptoms and secondary complications. [ABSTRACT FROM AUTHOR]

Diabetic cardiomyopathy is a significant and severe complication of diabetes that affects a large portion of the global population, with its prevalence continuing to rise. Secondary metabolites, including quercetin, have shown promising effects in mitigating the progression of diabetic cardiomyopathy by targeting multiple pathological mechanisms, including impaired insulin signaling, glucotoxicity, lipotoxicity, oxidative stress, inflammation, fibrosis, apoptosis, autophagy, mitochondrial dysfunction, cardiac stiffness, and disrupted calcium handling. Addressing these mechanisms is crucial to prevent left ventricular diastolic and systolic dysfunction in advanced stages of diabetic heart disease. Scientific evidence has highlighted the cardioprotective properties of quercetin at both the myocardial and cellular/molecular levels in diabetic models. Therefore, this review aims to present a comprehensive overview of the proposed mechanisms underlying quercetin's beneficial effects, providing valuable insights that could inform future drug discovery efforts specific to diabetic cardiomyopathy. [ABSTRACT FROM AUTHOR]

This study aims to identify how Nicole Galland's novel I, Iago is considered an adaptation of William Shakespeare's play Othello in terms of race, class, and the representation of women. Additionally, the study attempts to compare and contrast the adaptation and the source play in terms of the themes of race, class, and the representation of women. To achieve the objectives of the study, the novel is analyzed through the theory of adaptation. The study concludes with an examination of how Galland's I, Iago adhered faithfully to the events portrayed in Shakespeare's play Othello, while also illuminating the ambiguities inherent in Shakespeare's titular work. [ABSTRACT FROM AUTHOR]

Pain during movement screens is a risk factor for musculoskeletal injury (MSKI). Movement screens often require specialized or clinical expertise and large amounts of time to administer. Evaluate if self-reported pain (1) with movement clearing screens is a risk factor for any MSKI, (2) with movement clearing screens is a risk factor for body region–specific MSKIs, and (3) with a greater number of movement clearing screens progressively increases MSKI risk. Retrospective cohort study. Field-based. Military service members (n = 4222). Active-duty service members self-reported pain during movement clearing screens (Shoulder Clearing, Spinal Extension, Squat-Jump-Land). Musculoskeletal injury data were abstracted up to 180 days post-screening. A traffic light model grouped service members if they self-reported pain during 0 (Green), 1 (Amber), 2 (Red), or 3 (Black) movement clearing screens. Cox proportional hazards models adjusted for age, gender, body mass index, and prior MSKI determined the relationships between pain during movement clearing screens with any and body region–specific MSKIs. Service members self-reporting pain during the Shoulder Clearing (adjusted hazard ratio and 95% confidence interval [HRadj (95% CI)] = 1.58 [1.37, 1.82]), Spinal Extension (HRadj = 1.48 [1.28, 1.87]), or Squat-Jump-Land (HRadj = 2.04 [1.79, 2.32]) tests were more likely to experience any MSKI than service members reporting no pain. Service members with pain during the Shoulder Clearing (HRadj = 3.28 [2.57, 4.19]), Spinal Extension (HRadj = 2.80 [2.26, 3.49]), or Squat-Jump-Land (HRadj = 2.07 [1.76, 2.43]) tests were more likely to experience an upper extremity, spine, back, and torso, or lower extremity MSKI, respectively, than service members reporting no pain. The Amber (HRadj = 1.69 [1.48, 1.93]), Red (HRadj = 2.07 [1.73, 2.48]), and Black (HRadj = 2.31 [1.81, 2.95]) cohorts were more likely to experience an MSKI than the Green cohort. Self-report movement clearing screens in combination with a traffic light model provide clinician- and nonclinician-friendly expedient means to identify service members at MSKI risk. [ABSTRACT FROM AUTHOR]

Background: Skeletal muscle undergoes significant atrophy in Type 2 diabetic patients and animal models. We aimed to determine if atrophy of Zucker rat skeletal muscle was due to the activation of intracellular damage pathways induced by excess reactive oxygen species production (specifically those associated with the peroxidation of lipid membranes) and calpain activity. 14 week old obese Zucker rats and littermate lean controls were injected with 1% Evan's Blue Dye. Animals were anaesthetised and extensor digitorum longus and soleus muscles were dissected, snap frozen and analysed for ROS-mediated F2-isoprostane production and calpain activation/autolysis. Contralateral muscles were histologically analysed for markers of muscle membrane permeability and atrophy., Results: Muscle mass was lower in extensor digitorum longus and soleus of obese compared with lean animals, concomitant with reduced fibre area. Muscles from obese rats had a higher proportional area of Evan's Blue Dye fluorescence, albeit this was localised to the interstitium/external sarcolemma. There were no differences in F2-isoprostane production when expressed relative to arachidonic acid content, which was lower in the obese EDL and soleus muscles. There were no differences in the activation of either μ-calpain or calpain-3., Conclusions: This study highlights that atrophy of Zucker rat skeletal muscle is not related to sarcolemmal damage, sustained hyperactivation of the calpain proteases or excessive lipid peroxidation. As such, establishing the correct pathways involved in atrophy is highly important so as to develop more specific treatment options that target the underlying cause. This study has eliminated two of the potential pathways theorised to be responsible.

Background & Aims: Ischemia-reperfusion injury (IRI) can cause hepatic failure after liver surgery or transplantation. IRI causes oxidative stress, which injures sinusoidal endothelial cells (SECs), leading to recruitment and activation of Kupffer cells, platelets and microcirculatory impairment. We investigated whether injured SECs and other cell types release microparticles during post-ischemic reperfusion, and whether such microparticles have pro-inflammatory, platelet-activating and pro-injurious effects that could contribute to IRI pathogenesis., Methods: C57BL6 mice underwent 60 min of partial hepatic ischemia followed by 15 min-24 hrs of reperfusion. We collected blood and liver samples, isolated circulating microparticles, and determined protein and lipid content. To establish mechanism for microparticle production, we subjected murine primary hepatocytes to hypoxia-reoxygenation. Because microparticles express everted phosphatidylserine residues that are the target of annexin V, we analyzed the effects of an annexin V-homodimer (Diannexin or ASP8597) on post-ischemia microparticle production and function., Results: Microparticles were detected in the circulation 15-30 min after post-ischemic reperfusion, and contained markers of SECs, platelets, natural killer T cells, and CD8+ cells; 4 hrs later, they contained markers of macrophages. Microparticles contained F2-isoprostanes, indicating oxidative damage to membrane lipids. Injection of mice with TNF-α increased microparticle formation, whereas Diannexin substantially reduced microparticle release and prevented IRI. Hypoxia-re-oxygenation generated microparticles from primary hepatocytes by processes that involved oxidative stress. Exposing cultured hepatocytes to preparations of microparticles isolated from the circulation during IRI caused injury involving mitochondrial membrane permeability transition. Microparticles also activated platelets and induced neutrophil migration in vitro. The inflammatory properties of microparticles involved activation of NF-κB and JNK, increased expression of E-selectin, P-selectin, ICAM-1 and VCAM-1. All these processes were blocked by coating microparticles with Diannexin., Conclusions: Following hepatic IRI, microparticles circulate and can be taken up by hepatocytes, where they activate signaling pathways that mediate inflammation and hepatocyte injury. Diannexin prevents microparticle formation and subsequent inflammation.

The zebrafish is a versatile model organism with the potential to contribute to our understanding of the molecular pathological mechanisms underlying Alzheimer's disease (AD). An early characteristic of AD brain pathology is lipid peroxidation resulting from oxidative stress. However, changes in lipid peroxidation have not yet been assessed in zebrafish brains, and an earlier attempt to observe changes in F₂-isoprostane levels in the brains of zebrafish exposed to hypoxia was unsuccessful. In this article, we examine the utility of various assays of lipid peroxidation and more general assays of intracellular oxidative stress to detect the changes in oxidative stress in the brains of adult zebrafish exposed to hypoxia or explanted into a sodium azide solution for chemical mimicry of hypoxia. Levels of F₂-isoprostanes and F₄-neuroprostanes were low and variable in zebrafish brains such that statistically significant changes due to hypoxia or chemical mimicry of hypoxia could not be observed. However, measurement of lipid hydroperoxides did reveal significant changes in lipid peroxidation under these conditions, while analyses of catalase gene expression and an assay based on 2',7'-dicholorofluorescein oxidation also revealed changes in oxidative stress levels.

The present randomized, placebo-controlled, double-blind, parallel-groups clinical trial examined the effects of fish oil and multivitamin supplementation on the incorporation of n-3 and n-6 fatty acids into red blood cells. Healthy adult humans (n = 160) were randomized to receive 6 g of fish oil, 6 g of fish oil plus a multivitamin, 3 g of fish oil plus a multivitamin or a placebo daily for 16 weeks. Treatment with 6 g of fish oil, with or without a daily multivitamin, led to higher eicosapentaenoic acid (EPA) composition at endpoint. Docosahexaenoic acid (DHA) composition was unchanged following treatment. The long chain LC n-3 PUFA index was only higher, compared to placebo, in the group receiving the combination of 6 g of fish oil and the multivitamin. Analysis by gender revealed that all treatments increased EPA incorporation in females while, in males, EPA was only significantly increased by the 6 g fish oil multivitamin combination. There was considerable individual variability in the red blood cell incorporation of EPA and DHA at endpoint. Gender contributed to a large proportion of this variability with females generally showing higher LC n-3 PUFA composition at endpoint. In conclusion, the incorporation of LC n-3 PUFA into red blood cells was influenced by dosage, the concurrent intake of vitamin/minerals and gender.

Overall there is good evidence that alcohol consumption induces oxidative stress, and leads to lipid peroxidation, effects which have been linked to alcohol-related toxicity and disease and may be relevant to alcoholatherosclerosis interrelationships. On the other hand, a protective effect of light to moderate alcohol consumption against cardiovascular disease is well recognized, with the further hypothesis that red wine offers extra cardiovascular protection due to its rich content of antioxidant phenolic compounds. Although this hypothesis is given some credence from in vitro data, controlled studies in humans have produced conflicting results. Clearly, the equally well described pro-oxidant effects of alcohol and its metabolism have been insufficiently considered in the pursuit of what to many is an intuitively attractive hypothesis. Further studies are required to determine if red wine phenolics are actually absorbed from the gut and whether they offer any overall antioxidant protection in vivo. The hypothesis that red wine offers extra cardiovascular protection compared to other alcoholic beverages is not proven and must await the outcome of studies in which the full spectrum of the pro-oxidant and antioxidant effects of alcoholic beverages are duly considered. In the absence of such studies, there are no grounds at present for the promotion of the consumption of alcoholic beverages on the basis of their putative "antioxidant" properties. [ABSTRACT FROM AUTHOR]

Isoflavonoids are a class of flavonoids that are derived in the human diet mainly from soybean-based foods. The major dietary isoflavonoids, genistein and daidzein, have estrogen-like activity and are classed as phytoestrogens. Because estrogens can lower serum LDL cholesterol and raise HDL cholesterol, the objective of this study was to determine if isoflavonoids could improve serum lipids in healthy subjects. Forty-six men and 13 postmenopausal women not receiving hormone replacement therapy completed a randomized, double-blind, placebo-controlled trial of two-way parallel design and 8 wk duration. One tablet containing 55 mg of isoflavonoids (predominantly in the form of genistein) or one placebo tablet was taken daily with the evening meal. Subjects maintained their usual diet and physical activity, which were unchanged throughout the intervention. Measurement of isoflavonoids and their metabolites in 24-h urine samples provided an assessment of compliance and of isoflavonoid metabolism. Serum total, LDL, HDL and HDL subclass cholesterol, triglycerides and lipoprotein (a) were assessed at baseline and during the last week of intervention. After adjustment for baseline values, no significant differences in postintervention serum lipid and lipoprotein (a) concentrations between groups were identified. Further adjustment for age, gender and weight change did not alter the results. In addition, changes in urinary isoflavonoids were not significantly correlated with changes in serum lipids and lipoprotein (a). Therefore, this study does not support the hypothesis that isoflavonoid phytoestrogens can improve the serum lipids, at least in subjects with average serum cholesterol concentrations. [ABSTRACT FROM AUTHOR]

Chlorogenic acid (CGA), also known as 3-caffeioylquinic acid or coffee tannin, is a water-soluble polyphenol phenylacrylate compound produced through the shikimate pathway by plants during aerobic respiration. CGA widely exists in higher dicotyledons, ferns and many Chinese medicinal materials, and enjoys the reputation of 'plant gold'. Here, we summarized the source, chemical structure, biological activity functions of CGA and its research progress in pigs, aiming to provide a more comprehensive understanding and theoretical basis for the prospect of CGA replacing antibiotics as a pig feed additive., (© 2023 Wiley-VCH GmbH. Published by John Wiley & Sons Ltd.)

Deliberate hypotension is an important technique for use in select anesthetics for procedures such as orthognathic surgery, specifically LeFort I maxillary osteotomy. We present a case report of an anesthetic involving deliberate hypotension for a 17-year-old female patient who presented for a LeFort I osteotomy, bilateral sagittal split of the mandible, and a genioplasty in order to correct a skeletal class III malocclusion. After reaching a steady-state general anesthetic, deliberate hypotension was induced solely with a bolus and subsequent continuous infusion of the ultrashort acting calcium channel blocker, clevidipine. The preoperative, intraoperative, and postoperative course and anesthetic management are discussed.

Oxidative stress caused by reactive oxygen species is proposed to cause age related muscle wasting (sarcopenia). Reversible oxidation of protein thiols by reactive oxygen species can affect protein function, so we evaluated whether muscle wasting in normal aging was associated with a pervasive increase in reversible oxidation of protein thiols or with an increase in irreversible oxidative damage to macromolecules. In gastrocnemius muscles of C57BL/6J female mice aged 3, 15, 24, 27, and 29 months there was no age related increase in protein thiol oxidation. In contrast, there was a significant correlation (R (2) = 0.698) between increasing protein carbonylation, a measure of irreversible oxidative damage to proteins, and loss of mass of gastrocnemius muscles in aging female mice. In addition, there was an age-related increase in lipofuscin content, an aggregate of oxidised proteins and lipids, in quadriceps limb muscles in aging female mice. However, there was no evidence of an age-related increase in malondialdehyde or F2-isoprostanes levels, which are measures of oxidative damage to lipids, in gastrocnemius muscles. In summary, this study does not support the hypothesis that a pervasive increase in protein thiol oxidation is a contributing factor to sarcopenia. Instead, the data are consistent with an aging theory which proposes that molecular damage to macromolecules leads to the structural and functional disorders associated with aging.

Dentists often treat swellings from odontogenic periapical pathologies. One management option involves immediate treatment with antibiotics, followed by surgical intervention. We report a clinical case in which an 8-year-old patient sought care for such a lesion and received pharmacological therapy alone. The lesion expanded into multiple facial spaces approximating the ocular organ and other vital cranial structures. Eventual treatment of the lesion required a CT-scan, followed by an intubated general anesthetic, incision and drainage, extraction of the involved dentition and an overnight hospital admission. This case report is meant to highlight appropriate courses of action in management of rapidly progressing periapical pathologies.

The association between consumption of full-fat dairy foods and CVD may depend partly on the nature of products and may not apply to low-fat dairy foods. Increased circulating levels of inflammatory biomarkers after consumption of dairy product-rich meals suggest an association with CVD. In the present study, we tested the effects of low-fat and full-fat dairy diets on biomarkers associated with inflammation, oxidative stress or atherogenesis and on plasma lipid classes. Within full-fat dairy diets, we also compared fermented v. non-fermented products. In a randomised cross-over study, twelve overweight/obese subjects consumed during two 3-week periods two full-fat dairy diets containing either yogurt plus cheese (fermented) or butter, cream and ice cream (non-fermented) or a low-fat milk plus yogurt diet, with the latter being consumed between and at the end of the full-fat dairy dietary periods. The concentrations of six inflammatory and two atherogenic biomarkers known to be raised in CVD were measured as well as those of plasma F2-isoprostanes and lipid classes. The concentrations of six of the eight biomarkers tended to be higher on consumption of the low-fat dairy diet than on that of the fermented dairy diet and the concentrations of two plasmalogen lipid classes reported to be associated with increased oxidisability were also higher on consumption of the low-fat dairy diet than on that of the fermented dairy diet (P< 0.001), although plasma F2-isoprostane concentrations did not differ on consumption of any of the diets. On the other hand, the concentrations of plasma sphingomyelin and IL-6 were significantly higher on consumption of the non-fermented dairy diet than on that of the low-fat dairy diet (P< 0.02). In conclusion, short-term diets containing low-fat dairy products did not lead to a more favourable biomarker profile associated with CVD risk compared with the full-fat dairy products, suggesting that full-fat fermented dairy products may be the more favourable.

This investigation explored the influence of supplemental oxygen administered during the recovery periods of an interval-based running session on the post-exercise markers of reactive oxygen species (ROS) and inflammation. Ten well-trained male endurance athletes completed two sessions of 10 × 3 min running intervals at 85 % of the maximal oxygen consumption velocity (vVO(2)peak) on a motorised treadmill. A 90-s recovery period was given between each interval, during which time the participants were administered either a hyperoxic (HYP) (Fraction of Inspired Oxygen (FIO2) 99.5 %) or normoxic (NORM) (FIO2 21 %) gas, in a randomized, single-blind fashion. Pulse oximetry (SpO(2)), heart rate (HR), blood lactate (BLa), perceived exertion (RPE), and perceived recovery (TQRper) were recorded during each trial. Venous blood samples were taken pre-exercise, post-exercise and 1 h post-exercise to measure Interleukin-6 (IL-6) and Isoprostanes (F2-IsoP). The S(p)O(2) was significantly lower than baseline following all interval repetitions in both experimental trials (p < 0.05). The S(p)O(2) recovery time was significantly quicker in the HYP when compared to the NORM (p < 0.05), with a trend for improved perceptual recovery. The IL-6 and F2-IsoP were significantly elevated immediately post-exercise, but had significantly decreased by 1 h post-exercise in both trials (p < 0.05). There were no differences in IL-6 or F2-IsoP levels between trials. Supplemental oxygen provided during the recovery periods of interval based exercise improves the recovery time of SPO(2) but has no effect on post-exercise ROS or inflammatory responses.

Background: One of the major challenges associated with our ageing population is the increasing incidence of age-associated cognitive decline, which has significant implications for an individual's ability to lead a productive and fulfilling life. In pure economic terms the costs of ageing reflects decreased productivity and engagement with the workforce. The maintenance of brain health underpinning intact cognition is a key factor to maintaining a positive, engaged, and productive lifestyle. In light of this, the role of diet, including supplementation with nutritional and even pharmacological interventions capable of ameliorating the neurocognitive changes that occur with age constitute vital areas of research., Methods: In order to reduce cognitive ageing, the ARC longevity intervention (ARCLI) was developed to examine the effects of two promising natural pharmacologically active supplements on cognitive performance. ARCLI is a randomized, placebo-controlled, double-blind, 3-arm clinical trial in which 465 participants will be randomized to receive an extract of Bacopa monnieri (CDRI08 300 mg/day), Pycnogenol (150 mg/day), or placebo daily for 12 months. Participants will be tested at baseline and then at 3, 6 and 12 months post-randomization on a wide battery of cognitive, neuropsychological and mood measures, cardiovascular (brachial and aortic systolic and diastolic blood pressures as well as arterial stiffness), biochemical (assays to measure inflammation, oxidative stress and safety) as well as genetic assessments (telomere length and several Single Nucleotide Polymorphisms). The primary aim is to investigate the effects of these supplements on cognitive performance. The secondary aims are to explore the time-course of cognitive enhancement as well as potential cardiovascular and biochemical mechanisms underpinning cognitive enhancement over the 12 months of administration.ARCLI will represent one of the largest and most comprehensive experimental clinical trials in which supplements are administered to elderly participants. Results from ARCLI may help develop novel preventative health practices and nutritional/pharmacological targets in the elderly for cognitive and brain health., Trial Registration: Australia and New Zealand Clinical Trials Register (ANZCTR): ACTRN12611000487910.

This study evaluated methods of enhancing college students' retention of information provided to them in a computer-delivered personalized drinking feedback intervention and whether enhanced retention reduced alcohol consumption during the two-week period following the intervention. Participants were 98 college students who reported at least one heavy drinking episode in the past two weeks. After participating in an online, personalized drinking feedback intervention, students were randomly assigned to one of three experimental conditions: 1) typical, in which they were simply sent home, 2) reading, in which they were asked to spend the next 20 minutes re-reading the feedback, and 3) recall, in which they were asked to spend the next 20 minutes writing down as much of the information from the feedback as they could remember. Two weeks following the intervention, participants completed a recall test and provided information on their alcohol use during the previous two weeks. Results indicated that participants in the reading and recall conditions retained more of the feedback information than did participants in the typical condition. In addition, participants in the reading and recall conditions reported reduced alcohol consumption in the two-week period following the intervention, compared to those in the typical condition. Information retention partially mediated the effects of the reading and recall conditions on drinking outcomes., ((PsycINFO Database Record (c) 2010 APA, all rights reserved).)

Background: Monocyte subpopulations distinguished by differential expression of chemokine receptors CCR2 and CX3CR1 are difficult to track in vivo, partly due to lack of CCR2 reagents., Methodology/principal Findings: We created CCR2-red fluorescent protein (RFP) knock-in mice and crossed them with CX3CR1-GFP mice to investigate monocyte subset trafficking. In mice with experimental autoimmune encephalomyelitis, CCR2 was critical for efficient intrathecal accumulation and localization of Ly6C(hi)/CCR2(hi) monocytes. Surprisingly, neutrophils, not Ly6C(lo) monocytes, largely replaced Ly6C(hi) cells in the central nervous system of these mice. CCR2-RFP expression allowed the first unequivocal distinction between infiltrating monocytes/macrophages from resident microglia., Conclusion/significance: These results refine the concept of monocyte subsets, provide mechanistic insight about monocyte entry into the central nervous system, and present a novel model for imaging and quantifying inflammatory myeloid populations.

HSCs are BM-derived, self-renewing multipotent cells that develop into circulating blood cells. They have been implicated in the repair of inflamed parenchymal tissue, but the signals that regulate their trafficking to sites of inflammation are unknown. As monocytes are recruited to sites of inflammation via chemoattractants that activate CCR2 on their surface, we investigated whether HSCs are also recruited to sites of inflammation through CCR2. Initial analysis indicated that in mice, CCR2 was expressed on subsets of HSCs and hematopoietic progenitor cells (HPCs) and that freshly isolated primitive hematopoietic cells (Lin-c-Kit+ cells) responded to CCR2 ligands in vitro. In vivo analysis indicated that after instillation of thioglycollate to cause aseptic inflammation and after administration of acetaminophen to induce liver damage, endogenous HSCs/HPCs were actively recruited to the peritoneum and liver, respectively, in WT but not Ccr2-/- mice. HSCs/HPCs recovered from the peritoneum successfully engrafted into the BM of irradiated primary and secondary recipients, confirming their self renewal and multipotency. Importantly, administration of exogenous WT, but not Ccr2-/-, HSCs/HPCs accelerated resolution of acetaminophen-induced liver damage and triggered the expression of genes characteristic of the macrophage M2 or repair phenotype. These findings reveal what we believe to be a novel role for CCR2 in the homing of HSCs/HPCs to sites of inflammation and suggest new functions for chemokines in promoting tissue repair and regeneration.

Recent studies report that depletion and repletion of muscle taurine (Tau) to endogenous levels affects skeletal muscle contractility in vitro. In this study, muscle Tau content was raised above endogenous levels by supplementing male Sprague-Dawley rats with 2.5% (wt/vol) Tau in drinking water for 2 wk, after which extensor digitorum longus (EDL) muscles were examined for in vitro contractile properties, fatigue resistance, and recovery from fatigue after two different high-frequency stimulation bouts. Tau supplementation increased muscle Tau content by approximately 40% and isometric twitch force by 19%, shifted the force-frequency relationship upward and to the left, increased specific force by 4.2%, and increased muscle calsequestrin protein content by 49%. Force at the end of a 10-s (100 Hz) continuous tetanic stimulation was 6% greater than controls, while force at the end of the 3-min intermittent high-frequency stimulation bout was significantly higher than controls, with a 12% greater area under the force curve. For 1 h after the 10-s continuous stimulation, tetanic force in Tau-supplemented muscles remained relatively stable while control muscle force gradually deteriorated. After the 3-min intermittent bout, tetanic force continued to slowly recover over the next 1 h, while control muscle force again began to decline. Tau supplementation attenuated F(2)-isoprostane production (a sensitive indicator of reactive oxygen species-induced lipid peroxidation) during the 3-min intermittent stimulation bout. Finally, Tau transporter protein expression was not altered by the Tau supplementation. Our results demonstrate that raising Tau content above endogenous levels increases twitch and subtetanic and specific force in rat fast-twitch skeletal muscle. Also, we demonstrate that raising Tau protects muscle function during high-frequency in vitro stimulation and the ensuing recovery period and helps reduce oxidative stress during prolonged stimulation.

There is considerable evidence that chronic moderate-to-high alcohol consumption increases blood pressure. The mechanisms by which this occurs are not clear. Alcohol consumption can induce oxidative stress and cytochrome P450 (CYP450) isoforms that are associated with oxidative stress and may influence vascular tone. To study the role of such mechanisms we examined whether reducing alcohol intake in moderate-to-heavy drinkers (40-110 g/day) resulted in changes in urinary excretion of 20-HETE, a CYP450 metabolite of arachidonic acid, and plasma and urinary F(2)-isoprostanes as markers of lipid peroxidation. After a 4-week run-in period during which healthy men maintained their usual drinking pattern they were randomized to a two-way crossover intervention study. In each of the 4-week treatment periods subjects either substituted their usual alcohol intake with a 0.9% alcohol beer or maintained their usual alcohol intake. Plasma and urinary F(2)-isoprostanes and urinary 20-HETE were measured by gas chromatography mass spectrometry, and serum gamma-glutamyl transpeptidase (gamma-GT) was measured as a biomarker of alcohol consumption, at the end of each study period. Sixteen healthy men age 51.0+/-2.7 years and with a BMI of 26.4+/-0.61 kg/m(2) completed the study. The reductions in alcohol intake (72.4+/-5.0 vs 7.9+/-1.6 g/day, p<0.001) and serum gamma-GT (geometric mean 24.4 U/L (95% CI 19.7, 30.2) vs 18.6 U/L (95% CI 15.5, 22.2, p<0.01) were accompanied by a significant fall in blood pressure as well as urinary 20-HETE excretion (158+/-23 vs 109+/-19 pmol/mmol creatinine, p<0.001) and plasma F(2)-isoprostanes (3438+/-158 vs 2929+/-145 pmol/L, p=0.01). A substantial reduction in alcohol consumption in healthy men lowered plasma F(2)-isoprostanes and urinary 20-HETE. Increased oxidative stress and 20-HETE production may be linked, at least in part, to the pathogenesis of alcohol-related hypertension.

Central nervous system (CNS) resident memory CD8 T cells (TRM) that express IFN-γ contribute to neurodegenerative processes, including synapse loss, leading to memory impairment. Here, we show that CCR2 signaling in CD8 TRM that persist within the hippocampus after recovery from CNS infection with West Nile virus (WNV) significantly prevents the development of memory impairments. Using CCR2-deficient mice, we determined that CCR2 expression is not essential for CNS T cell recruitment or virologic control during acute WNV infection. However, transcriptomic analyses of forebrain CCR2+ versus CCR2− CD8 TRM during WNV recovery reveal that CCR2 signaling significantly regulates hippocampal CD8 TRM phenotype and function via extrinsic and intrinsic effects, limiting expression of CD103, granzyme A and IFN-γ, respectively, and increasing the percentages of virus-specific CD8 T cells. Consistent with this, WNV-recovered Cd8acreCcr2fl/fl mice exhibit decreased recognition memory. Overall, these data implicate CCR2 signaling in the regulation of CD8 TRM phenotype, including antiviral specificity and IFN-γ expression, highlighing a neuroprotective role for CCR2 in limiting CD8 T cell-mediated neuroinflammation and cognitive deficits, providing insights into potential therapeutic targets for CNS infections. [ABSTRACT FROM AUTHOR]

Background: Acid-sensing ion channels are activated during myocardial ischemia and are implicated in the mechanism of myocardial ischemia-reperfusion injury (MIRI). Acid-sensing ion channel 3 (ASIC3), the most pH-sensitive member of the ASIC family, is highly expressed in myocardial tissues. However, the role of ASIC3 in MIRI and its precise effects on the myocardial metabolome remain unclear. These unknowns might be related to the cardioprotective effects observed with APETx2 post-conditioning. Method: Rat hearts subjected to Langendorff perfusion were randomly assigned to the normal (Nor) group, ischemia/reperfusion (I/R) group, ASIC3 blockade (AP) group. Rat hearts in group AP were treated with the ASIC3-specific inhibitor APETx2 (630 nM). Molecular and morphological changes were observed to elucidate the role of ASIC3 in MIRI. Bioinformatics analyses identified differential metabolites and pathways associated with APETx2 post-conditioning. Results: APETx2 post-conditioning stabilized hemodynamics in the isolated rat heart model of MIRI. It also reduced myocardial infarct size, mitigated mitochondrial damage at the ultrastructural level, and improved markers of myocardial injury and oxidative stress. Further more, we observed that phosphatidylcholine, phosphatidylethanolamine, citric acid, cyanidin 5-O-beta-D-glucoside, and L-aspartic acid decreased after MIRI. The levels of these metabolites were partially restored by APETx2 post-conditioning. These metabolites are primarily involved in autophagy and endogenous cannabinoid signaling pathways. Conclusion: ASIC3 is potentially a key player in MIRI. APETx2 post-conditioning may improve MIRI through specific metabolic changes. This study provides valuable data for future research on the metabolic mechanisms underlying the effects of APETx2 post-conditioning in MIRI. [ABSTRACT FROM AUTHOR]

Myelin sheath, as the multilayer dense structure enclosing axons in humans and other higher organisms, may rupture due to various injury factors after spinal cord injury, thus producing myelin debris. The myelin debris contains a variety of myelin-associated inhibitors (MAIs) and lipid, all inhibiting the repair after spinal cord injury. Through summary and analysis, the present authors found that the inhibition of myelin debris can be mainly divided into two categories: firstly, the direct inhibition mediated by MAIs; secondly, the indirect inhibition mediated by lipid such as cholesterol. It is worth noting that phagocytes are required in the latter indirect inhibition, such as professional phagocytes (macrophages et al.) and non-professional phagocytes (astrocytes et al.). Moreover, complement and the immune system also participate in the phagocytosis of myelin debris, working together with phagocytes to aggravate spinal cord injury. In conclusion, this paper focuses on the direct and indirect effects of myelin debris on spinal cord injury, aiming to provide new inspiration and reflection for the basic research of spinal cord injury and the conception of related treatment. [ABSTRACT FROM AUTHOR]

Introduction: The wound healing in diabetes is hindered and prolonged due to long-term inflammation, oxidative stress damage, and angiogenesis disorders induced by high glucose status. The management of such difficult-to-treat wounds continues to pose a significant challenge in clinical treatment. Dietary nitrate, commonly found in greens such as beets and spinach, acts as a nutritional supplement and is metabolized in the body through the salivary nitrate-nitrite-NO pathway. This pathway plays a crucial role in various physiological functions, including enhancing blood flow and attenuating inflammation. Methods: In this study, we established a diabetic rat wound model. Forty-eight rats were randomly divided into six groups (n = 8): the Con group, the Con + Nitrate group, the STZ group, the STZ + NaCl group, the STZ + rhEGF group, and the STZ + Nitrate group. Skin wound healing was assessed on the day of surgery and on postoperative days 3, 7, 10, and 14. Specimens were taken on days 7 and 14 post-surgery for relevant tests. Results: We found that dietary nitrate could accelerate skin wound healing by promoting angiogenesis and increasing blood perfusion. Significantly, dietary nitrate also regulated glucose and lipid metabolism and exhibited anti-inflammatory and antioxidant properties. Discussion: These findings provide a novel theoretical basis for managing wounds in diabetic individuals, indicating the broad potential of dietary nitrate in future clinical applications. [ABSTRACT FROM AUTHOR]

Background: In today's society, low levels of physical activity are observed in the child and adolescent population, which can cause numerous pathologies, such as obesity and mental health problems. Objective: This article aims to compile all the contexts and scenarios where it is possible to increase the levels of daily physical activity of children and young people, and which have significant scientific support. Method. To do so, a literature review was carried out examining four key contexts for intervention: school, extracurricular, family, and socio-community. Results: The results indicate that the school context, with strategies such as physical education classes and active breaks, is crucial but insufficient on its own, so it is essential to complement it with interventions in extracurricular, family, and socio-community environments. The involvement of families, access to adequate infrastructure such as parks and green areas, and the responsible use of technology, including active video games and the role of influencers on social networks, are presented as key elements to combat a sedentary lifestyle. Conclusions: It is important to highlight the importance of establishing socio-educational programs that adopt a comprehensive approach to promote physical activity in children and youth, highlighting the scientific evidence that supports the effectiveness of intervening in multiple scenarios. This review concludes that a coordinated approach between different actors (schools, families, communities) is necessary to ensure that children and youth reach adequate levels of physical activity, which not only improves their physical health, but also their mental well-being and cognitive development. [ABSTRACT FROM AUTHOR]

In the current study, two cultivars of pepper (Capsicum annuum and Capsicum frutescens) at two maturity stages (green and red) were evaluated for their contents of some bioactive compounds and antibacterial activities for their ethanolic and aqueous extracts in both raw and heat-treated forms (boiling). Boiling treatment was performed under the Egyptian household conditions. Proximate analyses of the tested samples were determined, and the resulted data showed that ash and crude protein were declined after boiling treatment, while crude fat and total carbohydrate increased. Vitamin C, β-carotene and vitamin E as well as capsaicin contents were also estimated by HPLC, and the obtained data showed that all of those components were lowered by boiling treatment. Antioxidant activity of fresh and heattreated pepper samples was carried out by using of 2,2-azinobis-3-ethylbenzothiazoline-6-sulfonic acid (ABTS•) assay. Data showed that all pepper samples had high antioxidant activities which were increased because of boiling treatment. Finally, the antibacterial activity of all ethanolic and aqueous extracts as well as capsaicin standard was tested against both Gram-positive and Gram-negative pathogenic bacteria. Only, ethanolic extracts partially inhibited all the tested organisms except, Bacillus cereus which was completely inhibited by both ethanolic and aqueous extracts. [ABSTRACT FROM AUTHOR]

Plant-derived phenolic compounds are recognized to provide several health benefits for humans, including anticancer, anti-inflammatory, and antioxidant proprieties. Their bioavailability in the human body has a significant impact on these outcomes. Their bioaccessibility and bioavailability are highly dependent on the structure and manner in which phenolics enter into the organism, through a complex food matrix, for instance, or as pure isolates. Furthermore, the bioaccessibility of phenolic compounds in the body is greatly impacted by interactions with a broad range of other macromolecules (such as proteins, lipids, dietary fibers, and polysaccharides) in food or during digestion. Encapsulation is a process that can improve bioaccessibility and bioavailability by guaranteeing coating of the active ingredients, controlled release, and targeted distribution to specific parts of the digestive system. However, this field has not yet received enough attention, due to the complex mechanisms through which phenolics act in the body. This review attempts to shed light on the results of research that has been performed on the potential and therapeutic benefits of encapsulated polyphenols in both health and disease. [ABSTRACT FROM AUTHOR]

Background: This study aimed to determine the factors associated with feeling ashamed of disclosing HIV‐positive status among females who self‐reported to health facilities for HIV testing in Kenya. Method: This study used the Kenya Demographic Health Survey data set for 2022. A total of 18,506 women aged 15–49 years were selected from the sample clusters; 13,815 had ever tested for HIV and 332 had positive results for HIV. The chi‐squared test was applied to determine the association between the selected variables of interest and the outcome variable. Furthermore, to identify the explanatory variables that were associated with the outcome variable of interest, logistic binary regression was performed. A p > 0.05 and all statistical analyses were conducted using Microsoft Excel (xlsx) and STATA15. Results: The analysis included 332 women who had tested positive during the survey out of which 125(38%) women agreed to have felt ashamed to disclose their HIV+ status. Agreed to stigma (AOR = 1.92, 95% CI: 1.15, 3.22; p < 0.05) and being intimidated by health workers (AOR = 2.49, 95% CI: 1.05, 5.93; p < 0.05) were significantly associated with feeling ashamed of disclosing HIV+ status. The remaining variables, such as age category, residence, marital status, educational attainment, total number of children born, access to information, sex partners excluding spouses in the last 12 months, and number of lifetime sex partners, were not associated with feeling ashamed. Conclusion: Health stigmatization and intimidation Stigmatization had an almost two‐fold likelihood of causing shame in the disclosure of HIV status among females with HIV who were studied. [ABSTRACT FROM AUTHOR]

Introduction: Alterations in cognitive performance are associated with inadequate nutritional states and diet composition. Prebiotics, such as inulin, are substances that can modulate the gut microbiome and, consequently, brain function by producing metabolites such as short-chain fatty acids (SCFAs). This study aimed to evaluate the effect of supplementation with inulin on cognitive flexibility, body composition, and gut microbiota in a murine model exposed to a high-fat (HF) diet. Methods: CD1 mice were divided into five groups: control fed a standard diet (C), high-fat diet (HF), inulin (I), high-fat diet with inulin (HFI), and manipulation control (M). Dietary supplementation was administered for 6 weeks. Cognitive flexibility was assessed using the Attentional Set-Shifting Test (AST). In addition, body composition was measured via electrical bioimpedance and adipose tissue compartments of each mouse were removed and weighed. Finally, gut microbiota metataxonomic was analyzed through metataxonomic bacterial 16S rRNA sequencing. Results: We observed that HF group required more AST trials than the C, HFI, and I groups in the compound discrimination (CD) and extra-dimensional (ED) stages. Notably, the HFI group required fewer trials than the HF group in the ED stage (p = 0.0187). No significant differences in overall body composition were observed between the groups. However, the percentage of gonadal and peritoneal adipose tissue was significantly higher in the HF and I groups compared to the C group. Statistically significant differences in alpha diversity for gut microbiota were observed using the Shannon, Simpson, and Chao1 indices. The I group showed a decrease in bacterial diversity compared to the HF group. While no differences were observed between groups in the phyla Bacillota and Bacteroidotes, Clostridium bacteria represented a lower proportion of sequences in the I group compared to the C group. Additionally, Lactobacillus represented a lower proportion of sequences in the HF group compared to the C and I groups. Discussion: These findings suggest that supplementation with inulin could be a useful approach to mitigate the negative effects of an HF diet on cognitive flexibility and modulate gut microbiota composition. [ABSTRACT FROM AUTHOR]

Objective: State anxiety and trait anxiety are differentially mapped in brain function. However, the genetic and neurobiological basis of anxiety-related functional changes remain largely unknown. Methods: Participants aged 18–30 from the community underwent resting-state fMRI and were assessed with the State-Trait Anxiety Inventory. Using a general linear regression model, we analyzed the effects of state and trait anxiety, as well as their sum and difference (delta), on regional homogeneity (ReHo) in cortical areas. ReHo patterns denote the spatial distribution of ReHo associated with anxiety scores. We further explored the spatial correlations between ReHo patterns and neuromaps, including gene expression, neurotransmitter receptor density, myelination, and functional connectivity gradients, to elucidate the genetic and molecular substrates of these ReHo patterns. Results: Our findings demonstrated robust spatial correlations between whole-brain ReHo patterns for state and trait anxiety, with trait anxiety and the delta value exhibiting stronger network correlations, notably in the dorsal attention, salience, visual, and sensorimotor networks. Genes highly correlated with ReHo patterns exhibited unique spatiotemporal expression patterns, involvement in oxidative stress, metabolism, and response to stimuli, and were expressed in specific cell types. Furthermore, ReHo patterns significantly correlated with neuromaps of neurotransmitter receptor density, myelination, and functional connectivity gradients. Conclusions: The ReHo patterns associated with anxiety may be driven by genetic and neurobiological traits. Our findings contribute to a deeper understanding of the pathogenesis of anxiety from a genetic and molecular perspective. [ABSTRACT FROM AUTHOR]