Systemic Oxidative Stress Research Articles

Short-term inhalation exposure to cigarette smoke induces oxidative stress and inflammation in lungs without systemic oxidative stress in mice.

Smoking is a well-established risk factor for various pathologies, including pulmonary diseases, cardiovascular disorders, and cancers. The toxic effects of cigarette smoke (CS) are mediated through multiple pathways and diverse mechanisms. A key pathogenic factor is oxidative stress, primarily induced by excessive formation of reactive oxygen species. However, it remains unclear whether smoking directly induces systemic oxidative stress or if such stress is a secondary consequence. This study aimed to determine whether short-term inhalation exposure to CS induces oxidative stress in extrapulmonary organs in addition to the lung in a murine model. In the experiment, 3R4F reference cigarettes were used to generate CS, and 8-week-old male BALB/c mice were exposed to CS at a total particulate matter concentration of either 0 or 800µg/L for four consecutive days. CS exposure led to an increase in neutrophils, eosinophils, and total cell counts in bronchoalveolar lavage fluid. It also elevated levels of lactate dehydrogenase and malondialdehyde (MDA), markers indicative of tissue damage and oxidative stress, respectively. Conversely, no significant changes were observed in systemic oxidative stress markers such as total oxidant scavenging capacity, MDA, glutathione (GSH), and the GSH/GSSG ratio in blood samples. In line with these findings, CS exposure elevated NADPH oxidase (NOX)-dependent superoxide generation in the lung but not in other organs like the liver, kidney, heart, aorta, and brain. Collectively, our results indicate that short-term exposure to CS induces inflammation and oxidative stress in the lung without significantly affecting oxidative stress in extrapulmonary organs under the current experimental conditions. NOX may play a role in these pulmonary-specific events.

Hyperuricemia is Equivalent to Type 2 Diabetes - Transforming Myth into Reality

Hyperuricemia is a metabolic disorder characterized by a high level of uric acid in the blood and was commonly thought to be associated with gout and nephrolithiasis. While hyperuricemia and T2D (Type 2 diabetes) are distinct medical conditions, they share certain similarities, and both have significant detrimental effects on humans. The prevalence of hyperuricemia and T2D has been alarmingly rising in the past two decades, and the development of these two conditions among young adults is worrisome for healthcare professionals. Research and debates have recently focused on a possible link between hyperuricemia and T2D. Individuals with persistent hyperuricemia are more likely to develop T2D. The underlying mechanisms contributing to these associations may involve chronic systemic inflammation, oxidative stress, and endothelial dysfunction. They are almost identical in etiology, pathophysiology, complications, and management. Recent studies have revealed an intricate relationship between these two conditions, suggesting hyperuricemia may be equivalent to T2D. Screening for hyperuricemia at an early stage can prevent the development of prediabetes and later overt T2D. This review article aims to explore the concept of hyperuricemia as an equivalent of T2D and shed light on the transforming perception of this association. Keywords: Uric acid, prehyperuricemia, hyperuricemia, type 2 diabetes, metabolic disorder, non-communicable disorder, endothelial dysfunction, systemic inflammation, oxidative stress, and preventive measures.

31. PHARMACOLOGICAL PREVENTION OF ISCHEMIA REPERFUSION INJURY IN RATS SUBJECTED TO LOWER LIMB ISCHEMIA

Abstract Introduction The use of tourniquet to achieve a blood-free surgical field is a common practice in orthopedic surgery. Blood flow restoration may lead to systemic inflammatory and oxidative stress damage known as ischemia/reperfusion injury (IRI). The aim of this work is to evaluate whether the administration of dexketoprofen (DEX) before reperfusion contributes to the prevention of IRI-related damage. Methods Male WAG/RijHsd rats were divided into 3 groups: two of them underwent 3h of ischemia and were administered either dexketoprofen (1 mg/kg) or vehicle; the third group was used as control, not subjected to ischemia/reperfusion. The treatment was given orally 30 minutes before reperfusion. Systemic affectation was evaluated 3h, 24h and 14 days after ischemia; at the anatomopathological level, limb edema was measured after 24h; finally, functional recovery was evaluated during the 14 days following ischemia by the rotarod and treadmill tests. Results IRI-related hepatic and muscular damage was significantly reduced by dexketoprofen, although its effect on hepatic damage was seen earlier. However, the treatment had no beneficial effect on renal damage, nor did it reduce limb edema with respect to the vehicle group (63±7.8 vs 73±10mm; p>0.05). In addition, dexketoprofen anticipated functional recovery between 2 and 9 days compared to untreated animals, as assessed by rotarod and treadmill tests. Conclusion Dexketoprofen treatment proved to be effective, reducing both hepatic and muscular damage secondary to IRI, as well as hastening the functional recovery of treated animals.

Effects of training flights of combat jet pilots on parameters of airway function, diffusing capacity and systemic oxidative stress, and their association with flight parameters

BackgroundFighter aircraft pilots are regularly exposed to physiological challenges from high acceleration (Gz) forces, as well as increased breathing pressure and oxygen supply in the support systems. We studied whether effects on the lung and systemic oxidative stress were detectable after real training flights comprising of a wide variety of exposure conditions, and their combinations.MethodsThirty-five pilots of the German Air Force performed 145 flights with the Eurofighter Typhoon. Prior to and after flight lung diffusing capacity for carbon monoxide (DLCO) and nitric oxide (DLNO), alveolar volume (VA), and diffusing capacities per volume (KCO, KNO) were assessed. In addition, the fractional concentration of exhaled nitric oxide (FeNO) was determined, and urine samples for the analysis of molecular species related to 8-hydroxy-2’-deoxyguanosine (8-OHdG) were taken. For statistical analysis, mixed ANOVA models were used.ResultsDLNO, DLCO, KNO, KCO and VA were reduced (p < 0.001) after flights, mean ± SD changes being 2.9 ± 5.0, 3.2 ± 5.2, 1.5 ± 3.7, 1.9 ± 3.7 and 1.4 ± 3.1%, respectively, while FeNO decreased by 11.1% and the ratio of 8-OHdG to creatinine increased by 15.7 ± 37.8%. The reductions of DLNO (DLCO) were smaller (p < 0.001) than those of KNO (KCO). In repeated flights on different days, baseline values were restored. Amongst various flight parameters comprising Gz-forces and/or being indicative of positive pressure breathing and oxygenation support, the combination of long flight duration and high altitude appeared to be linked to greater changes in DLNO and DLCO.ConclusionsThe pattern of reductions in diffusing capacities suggests effects arising from atelectasis and increased diffusion barrier, without changes in capillary blood volume. The decrease in exhaled endogenous NO suggests bronchial mucosal irritation and/or local oxidative stress, and the increase in urinary oxidized guanosine species suggests systemic oxidative stress. Although changes were small and not clinically relevant, their presence demonstrated physiological effects of real training flights in a modern 4th generation fighter jet.

The Role of Gut Microbiota and the Potential Effects of Probiotics in Heart Failure.

Heart failure (HF) remains a significant global health challenge, affecting millions of individuals worldwide and posing a substantial burden on healthcare systems. HF is a syndrome of intricate pathophysiology, involving systemic inflammation, oxidative stress, metabolic perturbations, and maladaptive structural changes in the heart. It is influenced by complex interactions between cardiac function, systemic physiology, and environmental factors. Among these factors, the gut microbiota has emerged as a novel and intriguing player in the landscape of HF pathophysiology. The gut microbiota, beyond its role in digestion and nutrient absorption, impacts immune responses, metabolic processes, and, as suggested by evidence in the literature, the development and progression of HF. There is a bidirectional communication between the gut and the heart, often known as the gut-heart axis, through which gut microbiota-derived metabolites, immune signals, and microbial products exert profound effects on cardiovascular health. This review aims to provide a comprehensive overview of the intricate relationship between the gut microbiota and HF. Additionally, we explore the potential of using probiotics as a therapeutic strategy to modulate the gut microbiota's composition and attenuate the adverse effects observed in HF. Conventional therapeutic approaches targeting hemodynamic and neurohormonal dysregulation have substantially improved the management of HF, but emerging research is exploring the potential implications of harnessing the gut microbiota for innovative approaches in HF treatment.

Abstract WMP23: Tobacco Cigarette Smoking Causes Cognitive Impairment Through Cerebrovascular Oxidative Damage

Introduction: Tobacco cigarette smoking (TCS) has been established as a risk factor for cardiovascular disease. Recent epidemiological studies have identified an association between TCS and cognitive impairment. However, the underlying mechanisms are yet to be established. We hypothesize that chronic TCS induces systemic and cerebrovascular oxidative stress that leads to cognitive impairment. Methods: Male C57BL6 mice were exposed to cigarette smoke or air (two hours per day, five days per week) for up to 60 weeks, n =10/group. The vascular reactivity of the carotid artery (CA) was assessed using a wire myograph. The CA blood flow was measured by Doppler ultrasonography. Dihydroethidium and diaminofluorescein were used to measure superoxide and nitric oxide. Endothelial nitric oxide synthase (eNOS), tight junction proteins (occludin and caudine-5), β-amyloid, and phosphorylated Tau were measured by immunoblotting and immunofluorescence microscopy. We assessed the cognitive function using Barnes Maze and fear conditioning testing. Results: Vascular endothelial dysfunction occurred in the CA after 16 weeks of TCS exposure, followed by a 23% reduction in CA blood flow (P=0.0006). Superoxide was significantly elevated in the CA and subsequently in the brain of TCS-exposed mice by 181% (P&lt;0.0001), compared to air-exposed mice. Reduction in eNOS and tight junction proteins were observed in the cerebrovascular endothelial cells. At 60 weeks of exposure, the brain of TCS-exposed mice showed higher levels of β-amyloid and phosphorylated-tau (352% and 260%, P=0.0032 and P&lt;0.0001, respectively), compared to air-exposed mice. At this time, TCS-exposed mice exhibited impaired spatial learning and memory. Conclusions: TCS causes progressive systemic and cerebrovascular oxidative damage, leading to cognitive impairment. Targeting vascular oxidative stress is a potential strategy to mitigate cognitive function impairment.

Extrapulmonary Comorbidities Associated with Chronic Obstructive Pulmonary Disease: A Review.

Most patients with chronic obstructive pulmonary disease (COPD) suffer from at least one additional, clinically relevant chronic disease. To a degree, the high global prevalence and mortality rate of COPD is closely related to its extrapulmonary effects. Moreover, the various of comorbidities of COPD and itself interact with each other, resulting in diverse clinical manifestations and individual differences, and thus further influencing the prognosis as well as healthcare burden of COPD patients. This is closely related to the common risk factors of chronic diseases (aging, smoking, inactivity, etc.). Additionally, some pathophysiological mechanisms caused by COPD, including the systemic inflammatory response, hypoxia, oxidative stress, and others, also have an impact on other systems. But comprehensive management and medical interventions have not yet been established. The clinicians should improve their knowledge and skills in diagnosing as well as treating the comorbidities of COPD, and then aim to develop more individualized, efficient diagnostic and therapeutic strategies for different patients to achieve greater clinical benefits. In this article, we will review the risk factors, mechanisms, and treatment strategies for extrapulmonary comorbidities in chronic obstructive pulmonary disease, including cardiovascular diseases, diabetes, anemia, osteoporosis, emotional disorders, and gastroesophageal reflux disease.

Air pollution and cardiovascular diseases

This comprehensive literature review explores the intricate relationship between air pollution and cardiovascular diseases, emphasizing the global significance of this environmental concern. The study delves into key air pollutants, including Particulate Matter (PM), Nitrogen Dioxide (NO2), Ozone (O3), and Sulfur Dioxide (SO2), revealing their associations with cardiovascular morbidity and mortality. The detrimental effects involve systemic inflammation, oxidative stress, endothelial dysfunction, and atherosclerosis. The review meticulously analyzes epidemiological studies, such as the UK Biobank study, linking long-term exposure to ambient air pollution, specifically PM2.5, PM10, NO2, and NOx, with increased risks of all-cause and cardiovascular mortality. Specific populations, characterized as susceptible or vulnerable, are identified, including adults over 60 and individuals with pre-existing health conditions. Studies examining genetic variations, blood pressure changes, and meteorological variables contribute to understanding individual susceptibility. The review highlights the role of air pollution in influencing sleep patterns, physical activity, and temperature-related cardiovascular strain. Furthermore, it emphasizes the importance of recognizing air pollution as a modifiable risk factor, providing evidence of its association with cardiovascular risk factors and Dyslipidemia. The impact of air pollution on diverse cardiovascular outcomes, including heart failure, stroke, and ischemic heart disease, is discussed. The review underscores the urgent need for public health interventions and policy recommendations to mitigate air pollution's adverse effects. Recognizing air pollution as a significant risk factor for cardiovascular diseases, the study advocates for proactive measures to reduce pollution, promoting cardiovascular health and creating a cleaner environment for future generations.

Structural characterization of DNA amplicons by ATR-FTIR spectroscopy as a guide for screening metainflammatory disorders in blood plasma

Attenuated total reflectance (ATR) Fourier transform infrared (FTIR) spectroscopy is a promising rapid, reagent-free, and low-cost technique considered for clinical translation. It allows to characterize biofluids proteome, lipidome, and metabolome at once. Metainflammatory disorders share a constellation of chronic systemic inflammation, oxidative stress, aberrant adipogenesis, and hypoxia, that significantly increased cardiovascular and cancer risk. As a result, these patients have elevated concentration of cfDNA in the bloodstream. Considering this, DNA amplicons were analyzed by ATR-FTIR at 3 concentrations with 1:100 dilution: (IU/mL): 718, 7.18, and 0.0718. The generated IR spectrum was used as a guide for variable selection. The main peaks in the biofingerprint (1800–900 cm−1) give important information about the base, base-sugar, phosphate, and sugar-phosphate transitions of DNA. To validate our method of selecting variables in blood plasma, 38 control subjects and 12 with metabolic syndrome were used. Using the wavenumbers of the peaks in the biofingerprint of the DNA amplicons, was generated a discriminant analysis model with Mahalanobis distance in blood plasma, and 100 % discrimination accuracy was obtained. In addition, the interval 1475–1188 cm−1 showed the greatest sensitivity to variation in the concentration of DNA amplicons, so curve fitting with Gaussian funcion was performed, obtaining adjusted-R2 of 0.993. PCA with Mahalanobis distance in the interval 1475–1188 cm−1 obtained an accuracy of 96 % and PLS-DA modeling in the interval 1475–1088 cm−1 obtained AUC = 0.991 with sensitivity of 95 % and specificity of 100 %. Therefore, ATR-FTIR spectroscopy with variable selection guided by DNA IR peaks is a promising and efficient method to be applied in metainflammatory disorders.

Air Pollution: A Challenge to Public Health and Healthcare Systems

Air Pollution: A Challenge to Public Health and Healthcare Systems

Application of Electrolyzed Hydrogen Water for Management of Chronic Kidney Disease and Dialysis Treatment-Perspective View.

Chronic kidney disease (CKD), which is globally on the rise, has become an urgent challenge from the perspective of public health, given its risk factors such as end-stage renal failure, cardiovascular diseases, and infections. The pathophysiology of CKD, including dialysis patients, is deeply associated with enhanced oxidative stress in both the kidneys and the entire body. Therefore, the introduction of a safe and widely applicable antioxidant therapy is expected as a measure against CKD. Electrolyzed hydrogen water (EHW) generated through the electrolysis of water has been confirmed to possess chemical antioxidant capabilities. In Japan, devices producing this water have become popular for household drinking water. In CKD model experiments conducted to date, drinking EHW has been shown to suppress the progression of kidney damage related to hypertension. Furthermore, clinical studies have reported that systemic oxidative stress in patients undergoing dialysis treatment using EHW is suppressed, leading to a reduction in the incidence of cardiovascular complications. In the future, considering EHW as one of the comprehensive measures against CKD holds significant importance. The medical utility of EHW is believed to be substantial, and further investigation is warranted.

House sparrows are heavier on organic and integrated-production farms than on conventional farms

The negative impact of conventional farming on avian biodiversity has been increasingly documented. However, the potential effects of different farming practices on bird populations' health remain unclear. We aimed to investigate whether different farming practices (organic, integrated production, conventional/intensive) have differential effects on the body mass - as a proxy for body condition - and biomarkers of oxidative stress in house sparrows (Passer domesticus), a model species strongly associated with human activities and still abundant in Switzerland. We captured a total of 681 birds in 19 organic farms, 20 integrated-production farms (labelled “IP-Suisse”) and 18 conventional farms, and measured bird body mass and tarsus length, as well as levels of malondialdehydes (MDA, a marker of oxidative damage to lipids), superoxide dismutase (SOD, a first-line antioxidant enzyme) activity, and the ratio of oxidized over reduced glutathione (GSSG/GSH, a marker of cellular oxidative stress) in blood and sperm as biomarkers of the systemic oxidative stress endured by birds. Our findings show that house sparrows living in integrated and organic farms were 2.39 % and 4.33 % heavier than birds living in conventional farms, but we did not find any difference in tarsus length, suggesting that birds were of similar size. In addition, we did not find any difference in oxidative stress markers across farming practices. Our results highlight the potential benefits of sustainable farming practices, such as organic and integrated farming, for bird populations and emphasize the need for mitigating the negative impact of agricultural intensification on biodiversity through practices that may enhance the birds’ health and thus lead to positive population dynamics.

Systemic and Lung Inflammation and Oxidative Stress Associated With Behavioral Changes Induced by Inhaled Paraquat Are Ameliorated by Carvacrol.

Paraquat (PQ) is an herbicide toxin that induces injury in different organs. The anti-inflammatory and antioxidant effects of carvacrol were reported previously. The effects of carvacrol and pioglitazone (Pio) alone and their combination on inhaled PQ-induced systemic and lung oxidative stress and inflammation as well as behavioral changes were examined in rats. In this study, animals were exposed to saline (control [Ctrl]) or PQ (PQ groups) aerosols. PQ-exposed animals were treated with 0.03 mg/kg/day dexamethasone (Dexa), 20 and 80 mg/kg/day carvacrol (C-L and C-H), 5 mg/kg/day Pio, and Pio+C-L for 16 days. Inhaled PQ markedly enhanced total and differential white blood cell (WBC) counts, nitric oxide (NO), and malondialdehyde (MDA) levels but decreased catalase (CAT) and superoxide dismutase (SOD) activities and thiol levels both in the bronchoalveolar lavage fluid (BALF) and blood and increased interferon-gamma (INF-γ) and interleukin-10 (IL-10) levels in the BALF (p < 0.001 for all cases) except lymphocyte count in blood which was not significantly changed. The escape latency and traveled distance were increased in the PQ group. However, the time spent in the target quadrant in the Morris water maze (MWM) test and the duration of time latency in the dark room in the shuttle box test were reduced after receiving an electrical shock (p < 0.05-p < 0.001). Inhaled PQ-induced changes were significantly improved in carvacrol, Pio, Dexa, and especially in the combination of the Pio+C-L treated groups (p < 0.05-p < 0.001). Carvacrol and Pio improved PQ-induced changes similar to Dexa, but ameliorative effects produced by combination treatments of Pio+C-L were more prominent than Pio and C-L alone, suggesting a potentiating effect for the combination of the two agents.

Effects of Crocus sativus and its constituent, safranal, and pioglitazone, on systemic inflammation and oxidative stress induced by paraquat aerosol in rats.

The effects of Crocus sativus, safranal, and pioglitazone on aerosolized paraquat (PQ)-induced systemic changes were examined. Control (Ctrl) and PQ groups of rats were exposed to saline or PQ (27 and 54 mg/m3, PQ-L and PQ-H) aerosols eight times on alternate days. Nine PQ-H groups were treated with dexamethasone (0.03 mg/kg/day, Dexa), two doses of C. sativus extract (20 and 80 mg/kg/day, CS-L and CS-H), safranal (0.8 and 3.2 mg/kg/day, Saf-L and Saf-H), pioglitazone (5 and 10 mg/kg/day, Pio-L and Pio-H), and the combination of low dose of the pioglitazone and extract or safranal (Pio + CS and Pio + Saf) after the end of PQ exposure. Interferon-gamma (INF-γ), interleukin 10 (IL-10), superoxide dismutase (SOD), catalase (CAT), and thiol serum levels were reduced, but tumor necrosis factor (TNF-α), malondialdehyde (MDA), and total and differential WBC were increased in both PQ groups (P<0.05 to P<0.001). All measured variables were improved in all treated groups (P<0.05 to P<0.001). The effects of high dose of C. sativus and safranal on measured parameters were higher than dexamethasone (P<0.05 to P<0.001). The effects of Pio + CS and Pio + Saf treatment on most variables were significantly higher than three agents alone (P<0.05 to P<0.001). C. sativus and safranal improved inhaled PQ-induced systemic inflammation and oxidative stress similar to those of dexamethasone and showed synergic effects with pioglitazone suggesting the possible PPARγ receptor-mediated effects of the plant and its constituent.

Reappraisal of Adipose Tissue Inflammation in Obesity.

Chronic low-grade inflammation is a central component in the pathogenesis of obesity-related expansion of adipose tissue and complications in other metabolic tissues. Five different signaling pathways are defined as dominant determinants of adipose tissue inflammation: These are increased circulating endotoxin due to dysregulation in the microbiota-gut-brain axis, systemic oxidative stress, macrophage accumulation, and adipocyte death. Finally, the nucleotide-binding and oligomerization domain (NOD) leucine-rich repeatfamily pyrin domain-containing 3 (NLRP3) inflammasome pathway is noted to be a key regulator of metabolic inflammation. The NLRP3 inflammasome and associated metabolic inflammation play an important role in the relationships among fatty acids and obesity. Several highly active molecules, including primarily leptin, resistin, adiponectin, visfatin, and classical cytokines, are abundantly released from adipocytes. The most important cytokines that are released by inflammatory cells infiltrating obese adipose tissue are tumor necrosis factor-alpha (TNF-α), interleukin 6 (IL-6), monocyte chemoattractant protein 1 (MCP-1) (CCL-2), and IL-1. All these molecules mentioned above act on immune cells, causing local and then general inflammation. Three metabolic pathways are noteworthy in the development of adipose tissue inflammation: toll-like receptor 4 (TLR4)/phosphatidylinositol-3'-kinase (PI3K)/Protein kinase B (Akt) signaling pathway, endoplasmic reticulum (ER) stress-derived unfolded protein response (UPR), and inhibitor of nuclear factor kappa-B kinase beta (IKKβ)-nuclear factor kappa B (NF-κB) pathway. In fact, adipose tissue inflammation is an adaptive response that contributes to a visceral depot barrier that effectively filters gut-derived endotoxin. Excessive fatty acid release worsens adipose tissue inflammation and contributes to insulin resistance. However, suppression of adipose inflammation in obesity with anti-inflammatory drugs is not a rational solution and paradoxically promotes insulin resistance, despite beneficial effects on weight gain. Inflammatory pathways in adipocytes are indeed indispensable for maintaining systemic insulin sensitivity. Cannabinoid type 1 receptor (CB1R) is important in obesity-induced pro-inflammatory response; however, blockade of CB1R, contrary to anti-inflammatory drugs, breaks the links between insulin resistance and adipose tissue inflammation. Obesity, however, could be decreased by improving leptin signaling, white adipose tissue browning, gut microbiota interactions, and alleviating inflammation. Furthermore, capsaicin synthesized by chilies is thought to be a new and promising therapeutic option in obesity, as it prevents metabolic endotoxemia and systemic chronic low-grade inflammation caused by high-fat diet.

Feto-Maternal Interface Organ-on-Chip: A New Technology to Study Ascending Infection.

Modeling human pregnancy is challenging as two subjects, the mother and fetus, must be evaluated in tandem. To understand pregnancy, parturition, and adverse pregnancy outcomes, the two feto-maternal interfaces (FMi) that form during gestation (i.e., the placenta and fetal membrane) need to be investigated to understand their biological roles, and organ dysfunction can lead to adverse outcomes. Adverse pregnancy outcomes such as preterm rupture of the membranes, spontaneous preterm birth, preeclampsia, intra-uterine growth restriction, and gestational diabetes rates are on the rise worldwide, highlighting the need for future studies and a better understanding of molecular and cellular pathways that contribute to disease onset. Current in vivo animal models nor in vitro cell culture systems can answer these questions as they do not model the function or structure of human FMis. Utilizing microfabrication and soft-lithography techniques, microfluidic organ-on-chip (OOC) devices have been adapted by many fields to model the anatomy and biological function of complex organs and organ systems within small in vitro platforms.These techniques have been adapted to recreate the fetal membrane FMi (FMi-OOC) using immortalized cells and collagen derived from patient samples. The FMi-OOC is a four-cell culture chamber, concentric circle system, that contains both fetal (amniochorion) and maternal (decidua) cellular layers and has been validated to model physiological and pathological states of pregnancy (i.e., ascending infection, systemic oxidative stress, and maternal toxicant exposure). This platform is fully compatible with various analytical methods such as microscopy and biochemical analysis. This protocol will outline this device's fabrication, cell loading, and utility to model ascending infection-related adverse pregnancy outcomes.

Antioxidant insights: investigating the protective role of oxidative balance in inflammatory bowel disease.

Limited studies have investigated the relationship between systemic oxidative stress and inflammatory bowel disease (IBD). The purpose of this study was to explore the relationship between oxidative balance score (OBS) and IBD. We included 175,808 participants from the UK Biobank database from 2006 to 2010. OBS scores were calculated based on 22 lifestyle and dietary factors. Multiple variable Cox proportional regression models, as well as gender stratification and subgroup analysis, were utilized to investigate the relationship between OBS and IBD. There is a significant negative correlation between OBS and the occurrence of IBD, ulcerative colitis (UC), and Crohn's disease (CD). Additionally, OBS is significantly negatively correlated with intestinal obstruction in CD patients. Gender stratified analysis suggest a significant correlation between OBS and CD in female patients, particularly pronounced in those under 60 years old. Sensitivity analysis indicates a significant negative correlation between lifestyle-related OBS and diet-related OBS with the occurrence of CD in females, diet-related OBS is negatively correlated with CD in males. OBS showed a significant negative correlation with IBD, especially in female CD patients. This study underscores the importance of antioxidant diet and lifestyle, which may provide a greater advantage for female CD patients.

The Monocyte-to-High-Density Lipoprotein Cholesterol Ratio as a Novel Predictor of the Prevalence of Senile Osteoporosis.

The prevalence of osteoporosis in elderly individuals is high, and osteoporosis is strongly associated with chronic inflammation. The monocyte-to-high-density lipoprotein ratio (MHR) is acknowledged as a marker for assessing systemic inflammation and oxidative stress, and changes in the MHR are associated with many chronic disease prevalent among the elderly population. This study investigated the relationships between the MHR and the incidence of osteoporosis in older adults, along with its predictive value. Data from 563 participants aged ≥70 years were retrospectively analysed. The haematological parameters were evaluated via established methodologies, utilizing fasting blood samples collected from the participants. The absolute monocyte count was used to calculate the MHR (MHR=monocyte/HDL-C). BMD was measured by dual-energy X-ray absorptiometry. The results were evaluated via comparative statistical analyses, Spearman correlation, logistic regression analyses, and receiver operating characteristic (ROC) curve analysis. The differences in the MHR were statistically significant among the osteoporosis groups (p < 0.001). Spearman correlation analysis revealed a positive correlation between the MHR and BMD. Furthermore, stratifying the sample into four groups on the basis of quartiles of MHR (M1, M2, M3, and M4) revealed a decreased risk of osteoporosis in the highest quartile compared with the lowest quartile (p <0.001). Multiple logistic regression analysis revealed that BMI and the MHR were independent risk factors for osteoporosis. The area under the ROC curve and the cut-off value of the MHR were 0.710 and 0.308(109/mmol), with specificity and sensitivity of 0.599 and 0.735, respectively (95% CI: 0.668~0.752, p < 0.0001). A low MHR was associated with a greater risk of senile osteoporosis. In clinical practice, the MHR has shown predictive value for senile osteoporosis, contributing to early intervention and treatment of this disease.

Коморбидный неврологический пациент: в фокусе метаболический синдром

INTRODUCTION. The article discusses the problem of managing patients suffering from metabolic syndrome and chronic cerebrovascular disorders. Metabolic syndrome is an important interdisciplinary problem. Metabolic syndrome significantly increases the incidence of strokes. Systemic metabolic disorders, insulin resistance and oxidative stress, as well as large vessel damage and microangiopathy play an important role. In addition, special attention is paid to low-grade chronic inflammation, which may be associated with the patient’s age. The most important risk factor for the development of acute cerebral ischemia is the combination of components of the metabolic syndrome, in particular, the combination of insulin resistance and arterial hypertension, which increase the likelihood of developing atrial fibrillation and increase the risk of an unfavorable outcome. CONCLUSION. Cognitive impairment is quite common in metabolic syndrome. When treating cognitive impairment as part of metabolic syndrome, it is advisable to use neuroprotectors. The use of citicoline (the drug “Ronocit”) has a clinically significant effect in restoring cognitive functions and reducing the risk of developing post-infarction and post-stroke dementia in patients with metabolic syndrome. The use of various approaches to the treatment of cognitive impairment in metabolic syndrome increases the likelihood of a favorable outcome. It is recommended to use the drugs “Ronocit” and “Cocarnit®” together in the treatment of patients with a predominance of cognitive and asthenic impairments and a clinical symptom complex of diabetic polyneuropathy. KEYWORDS: comorbidity, cognitive disorders, metabolic syndrome

Association between short-term exposure to ambient air pollutants and biomarkers indicative of inflammation and oxidative stress: a cross-sectional study using KoGES-HEXA data.

Air pollution-induced systemic inflammation and oxidative stress are hypothesized to be the major biological mechanisms underlying pathological outcomes. We examined the association between short-term exposure to ambient air pollutants and biomarkers of inflammation and oxidative stress in 2199 general middle-aged Korean population residing in metropolitan areas. Serum levels of inflammatory cytokines (interleukin [IL]-1β, IL-6, IL-8, IL-10, and tumor necrosis factor [TNF]-α) and urinary levels of 8-hydroxy-2'-deoxyguanosine (8-OHdG) were measured. Daily concentrations of a series of air pollutants (particulate matter [PM]10, PM2.5, SO2, NO2, CO, and O3) were predicted using the Community Multiscale Air Quality modeling system, and participant-level pollutant exposure was determined using geocoded residential addresses. Short-term exposure was defined as the 1- to 7-day moving averages. The multivariable-adjusted linear models controlling for the sociodemographic, lifestyle, temporal, and meteorological factors identified positive associations of PM with IL-1β, IL-8, IL-10, TNF-α, and 8-OHdG levels; SO2 with IL-10 levels, CO with IL-1β, IL-10, and TNF-α levels; and O3 with IL-1β, IL-8, and 8-OHdG levels. O3 levels were inversely associated with IL-10 levels. For each pollutant, the strongest associations were observed for the 7-day average PM and CO with IL-1β (per 10-µg/m3 increase in PM10: 2.7%, 95% confidence interval [CI] = 0.6-4.8; per 10-µg/m3 increase in PM2.5: 6.4%, 95% CI = 2.4-10.5; per 0.1-ppm increase in CO: 3.3%, 95% CI = 0.3-6.5); the 2-day average SO2 with IL-10 levels (per 1-ppb increase in SO2: 1.1%, 95% CI = 0.1-2.1); and the 7-day average O3 with IL-8 levels (per 1-ppb increase in O3: 1.3%, 95% CI = 0.7-1.9). Short-term exposure to ambient air pollutants may induce oxidative damage and pro-inflammatory roles, together with counter-regulatory anti-inflammatory response.