Concentrations Of Inflammatory Biomarkers Research Articles

Evaluation of Hippocampal Microanatomy and Neuro-Biomarkers Following Administration of Silver Nanoparticles Conjugated with Tenofovir Disoproxil Fumarate in Experimental Diabetic Rats.

Adverse complications like metabolic disorders, neurotoxicity, and low central nervous system (CNS) penetration are associated with the long-term use of tenofovir disoproxil fumarate (TDF). Therefore, some modifications are required to enhance neurological functions using silver nanoparticles (AgNPs). This study aimed to evaluate the neuroprotective impact of silver nanoparticles (AgNPs)-conjugated TDF as AgNPs-TDF on the hippocampal microanatomy and some neuro-biomarkers of diabetic rats. Forty-two male Sprague-Dawley rats, with an average weight of 250 ± 13 g, were divided into non-diabetic and diabetic groups. They were further divided into 3 groups each (n = 7): non-diabetic control (NC), non-diabetic + TDF (NTF), and non-diabetic + TDF + silver nanoparticles (NTS), as well as diabetic control (DC), diabetic + TDF (DTF), and diabetic + TDF + silver nanoparticles (DTS). The characterization of AgNPs-TDF was assessed, and the conjugates were administered to the diabetic rats, followed by behavioral testing and biochemical, immunohistochemical, and microanatomy analyses of the hippocampus. The results showed that the administration of AgNPs-TDF significantly reduced the blood glucose level, malondialdehyde (MDA), and inflammatory biomarker concentrations in DTS compared with the DTF and DC groups. Furthermore, AgNPs-TDF administration significantly increased the levels of tissue superoxide dismutase (SOD), reduced glutathione (GSH), and insulin-like growth factor-1 in DTS compared with the DTF and DC groups. In addition, the DTS group revealed a monomorphic pattern of dark-stained neuronal nuclei similar to the control group and showed neuroprotective effects on hippocampal microanatomy compared with the DTF group. This study shows that AgNPs-TDF restores various alterations in the hippocampus and improves cognitive functions in diabetic rats.

Relationship between Diet-Related Inflammation and Hospitalization Risk and Disease Severity in Patients with COVID-19

Background: Increased serum concentrations of inflammatory biomarkers in patients indicate a strong association between COVID-19 and inflammation. However, the association between diet-related inflammation and COVID-19 has been less investigated. The aim of this study is to investigate whether the inflammatory scores of the diet are associated with the severity of COVID-19 disease and the probability of hospitalization of patients. Methods: The authors conducted a cross-sectional study involving 141 patients with COVID-19. The empirical dietary inflammatory pattern (EDIP) and dietary inflammation scores (DIS) were calculated based on a 147-item semi-quantitative food frequency questionnaire. The association between serum levels of inflammatory biomarkers and diet-related inflammation was also investigated. Results: 74 inpatients and 87 outpatients participated in this study. Higher DIS scores were significantly associated with an increased risk of COVID-related hospitalization (Tertile3 vs. tertile1: OR = 3·62; 95 % CI 1·43 to 9·14, P=0·008 after fully adjustment). This association with EDIP was also observed, but it was not significant. Conclusion: The data from this provide evidence that a pro-inflammatory diet was associated with higher risk of hospitalization due to high severity of COVID-19.

Inflammation biomarkers and neurobehavioral performance in rural adolescents.

Systemic inflammation has been associated with lower neurobehavioral performance in diverse populations, yet the evidence in adolescents remains lacking. Cytokines can alter neural network activity to induce neurocognitive changes. This work seeks to investigate the association between inflammation and neurobehavior in adolescents living in a rural region of Ecuador. We examined 535 adolescents in rural communities of Ecuador (ESPINA study), 508 of which had neurobehavioral assessments (NEPSY-II) and circulating plasma levels of inflammatory markers (CRP, IL-6, TNF-⍺, sICAM-1, sVCAM-1, SAA, and sCD14). Associations between inflammatory biomarker concentrations and neurobehavioral scores were examined using adjusted bivariate semi-parametric models with generalized estimating equations. A partial least square regression approach was used to create composite variables from multiple inflammation biomarkers and model their association with cognitive outcomes. Higher sCD14 and TNF-α concentrations were significantly associated with lower social perception scores, by -0.47 units (95% CI: -0.80, -0.13) and -0.42 (-0.72, -0.12) for every 50% increase in inflammatory marker concentration, respectively. Similarly, every 50% increase in the inflammation summary score was associated with a significantly lower Social Perception score by -0.11 units (-0.19, -0.03). A unit increase in inflammatory composites of seven markers were associated with lower scores in language (-0.11 units, p=0.04), visuospatial processing (-0.15, p= 0.09), and social perception (-0.22, p=0.005) domains. Higher levels of inflammation were associated with lower neurobehavioral performance in adolescents, especially with social perception. In addition, using a robust analytic method to examine an association between a composite inflammatory variable integrating seven markers led to additional findings, including the domains of language and visuospatial processing. A longitudinal follow-up of such investigations could unveil potential changes in inflammation-neurobehavior performance links through developmental stages and intervention opportunities.

Association between Inflammatory and Metabolic Biomarkers and Common Mental Disorders among Adults: 2015 Health Survey of São Paulo, SP, Brazil.

Recent studies suggest that plasma inflammatory biomarker concentrations may represent valuable indicators for the diagnosis and prognosis of mental disorders. At the same time, metabolic alterations may contribute to the development and progression of systemic low-grade inflammation. Background/Objectives: This study evaluated the association between plasma inflammatory biomarkers and common mental disorders (CMD), exploring the relationship between metabolic biomarkers, metabolic syndrome (MetS), and inflammatory biomarkers in younger and older adults. Methods: This cross-sectional study used data from the 2015 Health Survey of São Paulo with a Focus on Nutrition Study. The occurrence of CMD was assessed through the Self-Reporting Questionnaire (SRQ-20). Blood samples were used to measure plasma concentrations of inflammatory and cardiometabolic biomarkers. MetS was defined according to the International Diabetes Federation Consensus. The Mann-Whitney test compared inflammatory biomarker concentrations across CMD groups and cardiometabolic conditions, and logistic regression models explored associations between inflammatory biomarker concentration and CMD. Results: The sample included 575 participants, 22.6% (n = 130) of whom had CMD. Concentrations of plasminogen activator inhibitor 1, C-reactive protein (CRP), and the systemic low-grade inflammation score varied significantly among CMD groups. CRP concentrations were positively associated with the presence of CMD, independent of confounding factors. Participants with insulin resistance, dyslipidemia, and MetS exhibited significantly higher CRP concentrations than individuals without these conditions. Conclusions: The findings suggest that increased plasma CRP concentrations may be a potential risk factor for CMD. Higher CRP concentrations were observed in individuals with insulin resistance, dyslipidemia, and MetS. Future interventional studies should explore these hypotheses in diverse populations.

Relationship between biomarkers and platelet aggregation activity in presence of hydrogen sulfide in patients with coronary heart disease

Biological significance of hydrogen sulfide (H2S) in regulation of platelet functions and in development of thrombosis is being studied, but there is no consensus on the role of H2S in these physiological processes. The platelets are very sensitive to various mediators released from blood vessels and blood cells. Multiple pro-inflammatory molecules may exert direct effects on the state of cardiovascular system. Thus, an imbalance in the production of pro-inflammatory and anti-inflammatory cytokines increases the risk of thrombosis, and it can lead to endothelial dysfunction, instability and rupture of atherosclerotic plaques. The aim of our study was to determine concentrations and identify the relationships between certain biomarkers (LIGHT, PlGF, IFNá2, TNFáâ, IL-3, IL-5, IL-6, IL-8, IL-15, IL-17F, MIP-1á, CXCL16) and collagen-induced platelet aggregation in presence of hydrogen sulfide exposure in patients with coronary heart disease. We performed a simple one-step comparative study which included 22 patients with coronary artery disease (CHD). The level of biomarkers was determined by multiplex analysis (xMAP technology). Platelet aggregation activity was studied by the turbidimetric assay. All samples were examined against the background of a 30-min pre-incubation with hydrogen sulfide, with the addition of an aggregation inducer (collagen, 2 mmol/L). Sodium hydrosulfide at a concentration of 10-6 M was used as a hydrogen sulfide donor. The results of comparative and correlation analysis were considered reliable at a statistical significance level of p 0.05. The patients were divided into two groups, i.e., group 1 (n = 10) showed a reduced aggregation or a decreased size of aggregates against the background of preincubation with H2S. In group 2 (n = 12), preincubation with H2S was followed by increased degree or size of platelet aggregates. The concentrations of tumor necrosis factor ligand (LIGHT), interferon IFNá2, interleukins IL-3, IL-8, IL-15, IL-17F, chemokine CCL3/MIP-1a were significantly increased in group 2 patients, where collagen-induced platelet aggregation increased upon preincubation H2S, as compared with patients in group 1. The correlation analysis revealed positive correlations found that in the 1st group of patients between the concentrations of MIP-1a (Rs = 0.56, p = 0.03; Rs = 0.69, p = 0.01), IL-5 (Rs = 0.83, p = 0.01; Rs = 0.73, p = 0.01), and IL-8 (Rs = 0.60, p = 0.02; Rs = 0.95, p = 0.01), respectively, and with both size of aggregates and the index of the platelet aggregation degree. Moreover, distinct correlations between the aggregate size and the concentration of IL-6 (Rs = 0.53, p = 0.04) were revealed. In the 2nd group of patients, correlations were found with the size of aggregates and PIGF (Rs = 0.59, p = 0.04), and between CXCL16 values and the size of aggregates (Rs = 0.58, p = 0.04), like as with the degree of aggregation (Rs = 0.65, p = 0.04). Thus, we have found that, in 2 groups of patients with coronary heart disease with increased collagen-induced platelet aggregation, preincubated with H2S, higher concentrations of inflammatory biomarkers (IFNá2, IL-3, IL-8, IL-15, IL-17F, MIP-1á) were detected. One may suggest that the more pronounced proinflammatory state in this group of patients may cause platelet resistance to inhibitory effect of hydrogen sulfide. In the 1st group of patients, we revealed multiple correlations of aggregation parameters with values of inflammatory markers (IL-5, IL-6, IL-8, MIP- 1a), which may be a pre-requisite for different corrective therapies for the patients of these groups.

Pulmonary herpes simplex virus and cytomegalovirus in patients with acute respiratory distress syndrome related to COVID-19

PurposeHuman herpesviruses, particularly cytomegalovirus (CMV) and herpes simplex virus (HSV), frequently reactivate in critically ill patients, including those with acute respiratory distress syndrome (ARDS) related to coronavirus disease 2019 (COVID-19). The clinical interpretation of pulmonary herpesvirus reactivation is challenging and there is ongoing debate about its association with mortality and benefit of antiviral medication. We aimed to quantify the incidence and pathogenicity of pulmonary CMV and HSV reactivations in critically ill COVID-19 patients.MethodsMechanically ventilated COVID-19 patients seropositive for CMV or HSV were included in this observational cohort study. Diagnostic bronchoscopy with bronchoalveolar lavage was performed routinely and analyzed for alveolar viral loads and inflammatory biomarkers. Utilizing joint modeling, we explored the dynamic association between viral load trajectories over time and mortality. We explored alveolar inflammatory biomarker dynamics between reactivated and non-reactivated patients.ResultsPulmonary reactivation (> 104 copies/ml) of CMV occurred in 6% of CMV-seropositive patients (9/156), and pulmonary reactivation of HSV in 37% of HSV-seropositive patients (63/172). HSV viral load dynamics prior to or without antiviral treatment were associated with increased 90-day mortality (hazard ratio [HR] 1.24, 95% confidence interval [CI] 1.04–1.47). The alveolar concentration of several inflammatory biomarkers increased with HSV reactivation, including interleukin (IL)-6, IL-1β, granulocyte colony stimulating factor (G-CSF), and tumor necrosis factor (TNF).ConclusionIn mechanically ventilated COVID-19 patients, HSV reactivations are common, while CMV reactivations were rare. HSV viral load dynamics prior to or without antiviral treatment are associated with mortality. Alveolar inflammation is elevated after HSV reactivation.

Preoperative examination of inflammatory biomarkers in relation to the prognosis of postoperative complications after heart transplantation

Abstract Funding Acknowledgements Type of funding sources: Public hospital(s). Main funding source(s): Semmelweis University Heart transplantation (HTX) is the definitive therapy for end-stage heart failure. Although complications have drastically decreased with modern immunosuppressive therapy, surgical and anesthetic techniques, significant complications such as graft failure, acute rejection or infection must still be expected. The purpose of the study is to examine cytokine pathways linked to inflammation from direct preoperative serum samples, which can serve as prognostic factors in relation to septic events and mortality in the early postoperative period. The study was conducted using the blood samples of 102 patients who underwent HTX. Blood samples were taken from the patients immediately before HTX. The amounts of a total of 32 cytokines and related proteins were determined using LEGENDplex assays. After that, we correlated the biomarker amounts determined in the serum samples with the end points we indicated. In patients undergoing HTX who developed septic events during postoperative intensive care, the preoperative MMP2 serum concentration was significantly higher compared to other patients undergoing HTX (n=23, p=0.04). Independent predictors of mortality in the intensive care unit (n=5) were preoperative MRP8/14 (AUC=0.8), NGAL (AUC=0.75), IGFBP-4 (AUC=0.73), cystatin C (AUC=0.7) and the MMP2 (AUC=0.74) serum concentrations. Patients transplanted from left ventricular mechanical circulatory support (LVAD) (n=11) were examined as a separate group, where early postoperative mortality was significantly higher (n=4, p=0.02), the independent predictor of which was the concentration of IGFBP-4 (p=0.04 , AUC=0.73). Based on our results, it can be said that the differences in the preoperative concentration of certain inflammatory biomarkers that can be measured in the serum show correlations with the postoperative septic events and mortality of patients undergoing HTX.

Changes in plasma concentrations of novel vascular and inflammatory biomarkers in obstructive sleep apnea patients pre- and post-stroke

BackgroundObstructive sleep apnea (OSA) is increasingly recognized as a common condition in the general population and causes significant OSA-associated morbidities including cardiovascular and cerebrovascular events such as cerebral small vessel disease (CSVD) and stroke. MethodsIn this study, using sensitive ELISA immunoassays, we measured subset of endothelial/vascular and inflammatory biomarkers as well as neurofilament light chain (NfL), a sensitive marker for neuroaxonal injury, using plasma from OSA patients post-stroke (Acute Cerebral Infarction (ACI), N = 26) to determine their usefulness as potential prognostic markers in disease progression. ResultsOur results showed significantly increased plasma TNFα and NfL concentrations and decreased concentrations of platelet derived growth factor (PDGF-AA) in post-stroke OSA patients with more severe white matter hyperintensities (WMHs). And after separating the patients based on sex, compared to females, male post-stroke OSA patients with severe WMHs have increased circulating levels of inflammatory chemokine CXCL10 and cytokine Interleukin-10 (IL-10) and significantly decreased levels of Angiopoietin-1 (Ang-1) an important protein responsible for endothelial/vascular integrity functions. Importantly, in a subset of newly diagnosed OSA patients (without prior history of stroke), significantly increased plasma CXCL10 levels and decreased plasma Ang-1 levels were also readily observed when compared to healthy controls, indicating possible altered endothelial integrity and ongoing vascular inflammation in these newly diagnosed OSA patients. ConclusionsIn summary, our study has identified a novel set of plasma biomarkers including PDGF-AA, CXCL10 and Ang-1 for their potential prognostic value for disease outcomes pre- and post-stroke in OSA patients and use as surrogate markers to measure efficacy of treatment modalities.

Unveiling the Role of PAR 1: A Crucial Link with Inflammation in Diabetic Subjects with COVID-19.

Inflammation is a distinguished clinical manifestation of COVID-19 and type 2 diabetes mellitus (T2DM), often associated with inflammatory dysfunctions, insulin resistance, metabolic dysregulation, and other complications. The present study aims to test the hypothesis that serum concentrations of PAR-1 levels differ between COVID-19 diabetic patients (T2DM) and non-diabetic COVID-19 patients and determine their association with different biochemical parameters and inflammatory biomarkers. T2DM patients with COVID-19 (n = 50) with glycated hemoglobin (HbA1c) levels of (9.23 ± 1.66) and non-diabetic COVID-19 patients (n = 50) with HbA1c levels (4.39 ± 0.57) were recruited in this study. The serum PAR-1 levels (ELISA method) were determined in both groups and correlated with parameters such as age, BMI, inflammatory markers including CRP, interleukin 6 (IL-6), tumor necrosis factor-alpha (TNF-α), D-dimer, homocysteine, and N-terminal pro-B-type natriuretic peptide (NT-proBNP). Demographic variables such as BMI (29.21 ± 3.52 vs. controls 21.30 ± 2.11) and HbA1c (9.23 ± 1.66 vs. controls 4.39 ± 0.57) were found to be statistically elevated in COVID-19 T2DM patients compared to non-diabetic COVID-19 patients. The concentrations of several inflammatory biomarkers and PAR-1 were remarkably increased in the COVID-19 T2DM group when compared with the non-diabetic COVID-19 group. The univariate analysis revealed that increased serum PAR-1 estimations were positively correlated with enhanced HbA1c, BMI, inflammatory cytokines, D-dimer, homocysteine, and NT-proBNP. The findings in the current study suggest that increased levels of serum PAR-1 in the bloodstream could potentially serve as an independent biomarker of inflammation in COVID-19 patients with T2DM.

Pediatric sepsis inflammatory blood biomarkers that correlate with clinical variables and severity of illness scores

BackgroundSepsis is a dysregulated systemic inflammatory response triggered by infection, resulting in organ dysfunction. A major challenge in clinical pediatrics is to identify sepsis early and then quickly intervene to reduce morbidity and mortality. As blood biomarkers hold promise as early sepsis diagnostic tools, we aimed to measure a large number of blood inflammatory biomarkers from pediatric sepsis patients to determine their predictive ability, as well as their correlations with clinical variables and illness severity scores.MethodsPediatric patients that met sepsis criteria were enrolled, and clinical data and blood samples were collected. Fifty-eight inflammatory plasma biomarker concentrations were determined using immunoassays. The data were analyzed with both conventional statistics and machine learning.ResultsTwenty sepsis patients were enrolled (median age 13 years), with infectious pathogens identified in 75%. Vasopressors were administered to 85% of patients, while 55% received invasive ventilation and 20% were ventilated non-invasively. A total of 24 inflammatory biomarkers were significantly different between sepsis patients and age/sex-matched healthy controls. Nine biomarkers (IL-6, IL-8, MCP-1, M-CSF, IL-1RA, hyaluronan, HSP70, MMP3, and MMP10) yielded AUC parameters > 0.9 (95% CIs: 0.837-1.000; p < 0.001). Boruta feature reduction yielded 6 critical biomarkers with their relative importance: IL-8 (12.2%), MCP-1 (11.6%), HSP70 (11.6%), hyaluronan (11.5%), M-CSF (11.5%), and IL-6 (11.5%); combinations of 2 biomarkers yielded AUC values of 1.00 (95% CI: 1.00–1.00; p < 0.001). Specific biomarkers strongly correlated with illness severity scoring, as well as other clinical variables. IL-3 specifically distinguished bacterial versus viral infection (p < 0.005).ConclusionsSpecific inflammatory biomarkers were identified as markers of pediatric sepsis and strongly correlated to both clinical variables and sepsis severity.

СВЯЗЬ ВОСПАЛИТЕЛЬНЫХ МАРКЕРОВ И ТРЕВОЖНО-ДЕПРЕССИВНЫХ РАССТРОЙСТВ У ПАЦИЕНТОВ С ОСТРЫМ ИНФАРКТОМ МИОКАРДА

Abstract. Introduction. In recent years, the influence of anxiety and depressive disorders on the course of cardiovascular diseases has been increasingly discussed. The main psychosocial risk factors for the development of acute myocardial infarction include depression and anxiety (various anxiety syndromes and disorders). Currently, inflammation is considered as one of the leading links in myocardial infarction pathogenesis, course, and prognosis. Recent studies have linked the development of anxiety and depressive disorders with changes in the proinflammatory cytokine levels. Severity of immunoinflammatory reactions in patients with unstable forms of coronary heart disease is greater than in patients with a stable course of the disease. The aim of our investigation was to study the proinflammatory cytokine levels in patients with myocardial infarction depending on the presence of anxiety and depressive disorders. Materials and Methods. The study included 160 patients, averagely aged 56.2±1.4 years, who were admitted to the hospital with the ST-segment elevation myocardial infarction. The diagnosis of the said disease was set according to the generally accepted diagnostic criteria. In addition to the traditional clinical and instrumental studies, the patients of the groups under study underwent an assessment of the concentrations of inflammatory biomarkers in plasma and psychological tests using anxiety and depression rating scales, such as Zung Depression Scale and Spielberger-Khanin Anxiety Scale. Results and Discussion. Signs of depression were identified in 82 (51.25%) patients with acute myocardial infarction. Symptoms of mild depression were identified in 44 (53.7%) patients, moderate depression in 30 (36.6%) patients, and severe depression in 8 (9.7%) patients. It has been proven that the average depression score increases with the increase in the disease severity. The average score was 49.72+1.68 for personal anxiety in the group and 41.9±1.6 for reactive anxiety. As the class of infarction severity increased, a significant increase in anxiety levels was observed. An increase in the serum concentrations of CRP, IL-1β, IL-6, IL-8, and TNF-α was detected during the development of myocardial infarction, which was statistically significantly associated with the presence of anxiety-depressive disorders and some indicators of myocardial contractile function. Conclusions. Subclinical inflammation is one of the mechanisms of the negative impact of anxiety and depressive disorders on the prognosis for this category of patients. The presence of anxiety and depression symptoms is associated with higher levels of pro-inflammatory markers, i. e., CRP, IL-1β, IL-6, IL-8, and TNF-a. The degree of activation of proinflammatory markers depends on the severity of the myocardial damage signs and on the nature of complications.

Relationship between biomarkers of autophagy and inflammation in acute period of ischemic stroke

Postischemic neuroinflammation is a critical pathophysiological process within the entire pattern of cerebral ischemia, spanning early injury and tissue repair. According to recent experimental data, autophagy is involved in the regulation of neuroinflammation, influencing the outcome of the acute period of ischemic stroke (IS).Objective. To evaluate the relationship between autophagy biomarkers and inflammation indicators in the dynamics of the acute period of atherothrombotic IS.Materials and methods. 112 patients in the acute period of newly developed atherothrombotic IS and 56 donors (control group) were examined. Patients underwent dynamic clinical and neurological examination on the 1st, 7th and 14th days from the onset of the disease (magnetic resonance imaging, testing using the NIHSS scale, modified Rankin scale). At the same time intervals, blood was drawn for testing. The number of active autophagosomes in peripheral blood was assessed by flow cytometry using a specific Cyto-ID dye. The serum concentrations of proinflammatory cytokines IL‑1β, IL‑8, IL‑18 (interleukins‑1β, -8, -18), TNFα (tumor necrosis factor-α), autophagy biomarkers Beclin‑1, LC 3 and p62 were determined by enzyme-linked immunosorbent assay analysis. C-reactive protein was assessed by a highly sensitive immunoturbidimetric method.Results. A statistically significant increase in the studied parameters was revealed compared to the control group. The maximum increase in inflammation biomarkers was observed on the 1st day, and the maximum increase in key indicators of autophagy (LC 3, Beclin‑1, Cyto-ID) – on the 7th day after the development of ischemia. A direct relationship was established between the level of autophagy and the concentration of inflammatory biomarkers (CRP, IL‑1β, IL‑18, TNF-α) on the 1st and 7th days of acute IS.Conclusions. The identified correlations indicate the participation of activated autophagy in the regulation of post-ischemic neuroinflammation and its involvement in ischemic brain damage in the early stages of the acute period of IS (days 1–7). The results obtained confirm the literature data on the influence of autophagy on the outcome of the acute period of the disease.

Perivascular Space Burden and Cerebrospinal Fluid Biomarkers in US Veterans With Blast-Related Mild Traumatic Brain Injury.

Blast-related mild traumatic brain injury (mTBI) is recognized as the "signature injury" of the Iraq and Afghanistan wars. Sleep disruption, mTBI, and neuroinflammation have been individually linked to cerebral perivascular space (PVS) dilatation. Dilated PVSs are putative markers of impaired cerebrospinal fluid (CSF) and interstitial fluid exchange, which plays an important role in removing cerebral waste. The aim of this cross-sectional, retrospective study was to define associations between biomarkers of inflammation and MRI-visible PVS (MV-PVS) burden in Veterans after blast-related mTBI (blast-mTBI) and controls. The CSF and plasma inflammatory biomarker concentrations were compared between blast-mTBI and control groups and correlated with MV-PVS volume and number per white matter cm3. Multiple regression analyses were performed with inflammatory biomarkers as predictors and MV-PVS burden as the outcome. Correction for multiple comparisons was performed using the Banjamini-Hochberg method with a false discovery rate of 0.05. There were no group-wise differences in MV-PVS burden between Veterans with blast-mTBI and controls. Greater MV-PVS burden was significantly associated with higher concentrations of several proinflammatory biomarkers from CSF (i.e., eotaxin, MCP-1, IL-6, IL-8) and plasma (i.e., MCP-4, IL-13) in the blast-mTBI group only. After controlling for sleep time and symptoms of post-traumatic stress disorder, temporal MV-PVS burden remained significantly associated with higher CSF markers of inflammation in the blast-mTBI group only. These data support an association between central, rather than peripheral, neuroinflammation and MV-PVS burden in Veterans with blast-mTBI independent of sleep. Future studies should continue to explore the role of blast-mTBI related central inflammation in MV-PVS development, as well as investigate the impact of subclinical exposures on MV-PVS burden.

Inflammatory biomarker concentrations in dogs with gastric dilatation volvulus with and without 24-h intravenous lidocaine.

Canine gastric dilatation volvulus (GDV) is characterized by tissue ischemia, reperfusion, and systemic inflammation. Evidence exists that lidocaine exerts anti-inflammatory properties and potentially improves outcome. Prospective, randomized observational cohort study in client-owned dogs with GDV. The primary objective of the study was the determination of pro- and anti-inflammatory biomarker concentrations in dogs with GDV with and without intravenous (IV) lidocaine therapy. The second objective was the evaluation of side effects of lidocaine. Of 35 dogs included in the study, 20 dogs were assigned to receive lidocaine (LIDO) (2 mg/kg initially, followed by a continuous infusion at a rate of 50 μg/kg/min over 24 h) and 15 dogs not to receive lidocaine (NO-LIDO). Plasma concentrations of cytokines interleukin (IL)-6, IL-7, IL-8, IL-10, IL-15, IL-18, interferon gamma, keratinocyte chemotactic-like, monocyte chemotactic protein, and C-reactive protein (CRP) were measured at admission (prior any therapeutic intervention, T0), immediately after surgery (T1), at 24 h (T24), and at 48 h (T48) post-surgery. No significant differences in concentrations of any cytokines were found between the LIDO- and the NO-LIDO group. Significant lower CRP concentrations (median [range]) were found in dogs with lidocaine compared to dogs without at T24 (97.5 pg/mL [46.3-161.7] vs. 127.9 pg/mL [26.9-182.0]; p = 0.046) and T48 (73.7 pg/mL [18.4-169.4] vs. 116.3 pg/mL [71.4-176.8]; p = 0.002). Dogs receiving lidocaine exhibited significantly impaired mentation, a prolonged period of anorexia, and longer hospitalization compared to dogs without lidocaine. Lidocaine administration had no impact on the plasma levels of cytokines during the 48-h study period, but significantly lower CRP concentrations were found at T24 and T48. Lidocaine's potential side effects require careful decision making regarding its use.

Diagnostic and Prognostic Predictors for the Success of Pulpotomy in Permanent Mature Posterior Teeth with Moderate to Severe Pulpitis: A Scoping Review

A partial or complete pulpotomy is a type of vital pulp therapy (VPT) that aims to remove the inflamed, infected pulp, leaving behind healthy, vital pulp that is capable of healing. VPT has gained renewed popularity as a treatment option in permanent mature posterior teeth with irreversible, moderate to severe pulpitis; its high success rates matching that of root canal treatment (RCT). There is currently no consensus regarding diagnostic and prognostic predictors of success of pulpotomies for managing such cases. Therefore, we conducted a scoping review to identify and analyze how these factors affect the outcome of treatment. A literature search using the PRISMA guidelines was undertaken using PubMed and Scopus on 7 July 2023. A total of 22 studies met the inclusion criteria and were qualitatively analyzed by two reviewers. The following diagnostic and prognostic factors were recognized and discussed; presenting signs and symptoms, periapical diagnosis, bleeding time, indicators of inflammation (bleeding time, concentration of inflammatory biomarkers), patient age and medical status, the depth, activity and location of caries, and restorative factors. Based on the studies assessed, there is limited evidence to support their prognostic value. Further research is necessary to identify solid predictors of outcome.

Dynamic changes in inflammatory responses and 3-year clinical outcomes of XINSORB scaffolds in coronary stenting

BackgroundInflammation is known to play a crucial role in the development of coronary atherosclerosis and vascular healing after stenting. This study aimed to investigate the dynamic changes in inflammatory responses between XINSORB and TIVOLI scaffolds and their correlation with 3-year clinical outcomes. MethodA total of 140 patients in the XINSORB group and 42 patients in the TIVOLI group were included in this prospective, single-center study, conducted in Shanghai tenth People's Hospital. Blood samples were collected at baseline, 24 h, 6 months, and 12 months after stent implantation to measure high sensitivity C-reactive protein (hsCRP), fibrinogen (FBG), white blood cell count (WBC), tumor necrosis factor (TNF), and interleukin-6 (IL-6). Receiver-operating characteristic curves and proportional hazards models were generated to evaluate the relationship between 24-h postoperative inflammatory indicators and 3-year patient-oriented composite endpoints (POCE). ResultThe levels of hsCRP, FBG, WBC, TNF, and IL-6 reached their peak levels 24 h after stenting and then gradually decreased to levels comparable to baseline at 6 and 12 months. During the 3-year follow-up, 11.4 % of the XINSORB cohort and 9.5 % of the TIVOLI cohort experienced POCE (P = 0.948). High levels of hsCRP and IL-6 24 h after the procedure were associated with clinical endpoints, and the combination of these two biomarkers improved the predictive ability of prognosis. ConclusionsThere were no significant differences between the changes in the concentration of inflammatory biomarkers after XINSORB stents or drug-eluting stent implantation. Reduction in postoperative inflammatory levels may decrease the occurrence of clinical outcomes. This study provides insights into the dynamic changes of inflammatory responses and their correlation with clinical outcomes, which could have implications for the management of patients undergoing coronary stenting. Trial registrationThe study has been registered on the official website of the China Clinical Trial Registry (ChiCTR1800014966).

Adherence to Healthy and Sustainable Dietary Patterns and Long-Term Chronic Inflammation: Data from the EPIC-Potsdam Cohort

ObjectivesWe explored the prospective associations between adherence to a priori chosen dietary patterns, including EAT-Lancet (EAT-L) and Mediterranean (tMDS) diet with long-term inflammatory responses in a German population sample.Design and SettingProspective cohort study.ParticipantsA subsample of 636 predominantly healthy participants from the European Prospective Investigation into Cancer and Nutrition (EPIC)-Potsdam study who were on average 51-years old at baseline.MeasurementsData was collected repeatedly between 1994/1998–2013. At baseline (1994/1998) and 6.8-years later (2001/2005), EAT-L and tMDS scores were derived from available food frequency questionnaires. Stable high, stable low, increasing, and decreasing adherence to EAT-L and tMDS were defined as scoring above/below baseline median at baseline and 6.8-years later. Long-term chronic inflammation was assessed based on the average values of repeated measurements of two inflammatory biomarkers - chemerin and high-sensitivity C-reactive protein (hs-CRP) - in plasma samples collected between 2010/2012 and 2013. Multivariable linear regression analysis adjusted for socio-demographic and lifestyle factors at baseline and in 2010/2012 was used to assess the association between diet adherence and long-term hs-CRP and chemerin concentrations.ResultsStable high or increasing adherence to EAT-L diet compared to stable low adherence was associated with slight reduction of long-term chemerin concentrations on the long run (stable high: −4.4%; increasing: −4.0%), not reaching statistical significance. Increasing adherence to tMDS compared to stable low adherence was also associated with a minor reduction in chemerin concentrations (−3.6%). Decreasing adherence to tMDS compared stable high adherence was associated with 2.7% higher chemerin. The associations were even less pronounced when hs-CRP was used as an outcome.ConclusionsAdherence to healthy and sustainable dietary patterns defined using existing definitions for EAT-L and tMDS were associated with minor and not statistically significant reduction in the concentrations of inflammatory biomarkers on the long run. More research is needed to explore whether following these diets may represent a suitable approach for targeted prevention in the general population.

Attenuated effects of topical vinpocetine in an imiquimod-induced mouse model of psoriasis

Psoriasis is an uncontrolled, long-lasting inflammatory dermatosis distinguished by thickened, erythematous, and flaky skin lesions. Massive amounts of inflammatory cytokines are produced when immune system imbalances are driven by genetic and environmental triggers. Vinpocetine (VNP), a man-made analogue of the compound vincamine found in the dwarf periwinkle herb, has robust anti-inflammatory, immunomodulatory, and anti-oxidative effects; alleviates the epidermal penetration of immune cells, such as eosinophils and neutrophils; and abolishes the generation of pro-inflammatory molecules. ObjectiveThis study was aimed at exploring the effects of long-term topical VNP, both alone and co-administered with clobetasol propionate, in an imiquimod-induced mouse model of psoriasiform dermatitis. MethodsThe study protocol consisted of 48 Swiss albino mice, randomly divided into six groups of eight mice each. In group I, petroleum jelly was administered daily for 8 days. In group II, imiquimod was administered topically at 62.5 mg daily for 8 days. In groups III, VI, V, and VI, 0.05% clobetasol propionate, 1% VNP, 3% VNP, and 3% VNP plus 0.05% clobetasol were administered topically for an additional 8 days after the induction, thus resulting in a total trial length of 16 days. ResultsTopical VNP at various doses alleviated the severity of imiquimod-induced psoriatic lesions—including erythema, silvery-white scaling, and thickening—and reversed the histopathological abnormalities. Moreover, imiquimod-exposed animals treated with VNP showed markedly diminished concentrations of inflammatory biomarkers, including tumour necrosis factor-α, interleukin (IL)-8, IL-17A, IL-23, IL-37, nuclear factor-kappa B (NF-κB), and transforming growth factor-β1. ConclusionThis research provides new evidence that VNP, alone and in combination with clobetasol, may serve as a potential adjuvant for long-term management of autoimmune and autoinflammatory skin diseases, particularly psoriasis, by attenuating psoriatic lesion severity, suppressing cytokine generation, and limiting NF-κB-mediated inflammation.

Prenatal exposure to perfluoroalkyl substances and inflammatory biomarker concentrations.

We analyzed data from 1411 participants, recruited between 2008 and 2011, in the Maternal-Infant Research on Environmental Chemicals study. Our primary outcome was a composite inflammatory index derived by summing the z-scores of eight proinflammatory biomarkers. Using multivariable linear regression models, we quantified associations between each PFAS and the inflammatory index and individual biomarkers. We quantified the effects of the PFAS mixture using weighted quantile sum regression, and evaluated effect modification using product terms and sex-stratified models. Each doubling of PFOA and PFHxS was associated with a 0.38 (95% CI, 0.09, 0.67) and 0.21 (95% CI, 0.01, 0.41) SD increase in the proinflammatory index, respectively. A one-quartile increase in the PFAS mixture was associated with a 0.40 (95% CI, 0.09, 0.71) SD increase in the proinflammatory index. In individual models, we observed positive associations between PFAS and concentrations of monocyte chemoattractant protein-1, macrophage inflammatory protein-1β, and matrix metalloproteinases-9; however, the magnitude and precision varied according to the specific PFAS. Sex-specific findings were identified in few PFAS-biomarker associations. PFOA, PFOS, and PFHxS, individually and as a mixture, were positively associated with proinflammatory biomarkers during pregnancy.

Heart failure in erythrodermic psoriasis: a retrospective study of 225 patients.

Erythrodermic psoriasis (EP) is a severe form of psoriasis that affects multiple organs, including the cardiovascular system. However, few studies have focused on this condition.This study is aimed to assess the prevalence and factors associated with heart failure in EP patient, and to the measure the serum concentrations of fibroblast growth factor 23 (FGF23), a potential predictor of chronic heart failure. We retrospectively studied patients with EP hospitalized at Peking Union Medical College Hospital between January 2005 to October 2021. The prevalence of heart failure and associated factors was measured. In addition, peripheral blood samples were collected from 17 patients and matched with samples from eight healthy controls, and their serum concentrations of FGF23 were measured by ELISA. We studied 225 patients with EP, with a male: female ratio of 2.7:1 and a mean age of 47.6 ± 16.7 years. Twenty-five (11.1%) participants were diagnosed with heart failure during their hospital stay. The patients with EP and heart failure were older (58.2 years vs. 46.2 years, p = 0.001); had a higher prevalence of a history of coronary heart disease (32.0% vs. 21.5%, p < 0.001), fever (48.0% vs. 23.0%, p = 0.007), infection (56.0% vs. 35.5%, p = 0.046); higher hsCRP concentration (43.2 mg/L vs. 8.2 mg/L, p = 0.005); and higher prevalence of anemia (60.0% vs. 22.0%, p < 0.001), hypoalbuminemia (64.0% vs. 42.0%, p = 0.037), and hyperlipidemia (40.0% vs. 20.0%, p = 0.023) than those without heart failure. The serum FGF23 concentration was significantly higher in patients with EP than controls (493.1 pg/ml vs. 277.8 pg/ml, p = 0.027), and was significantly lower after treatment (395.7 pg/ml vs. 463.1 pg/ml, p = 0.022). Clinicians should be aware of the risk of heart failure in patients with EP, and especially those of advanced age and with a history of coronary heart disease, severe systemic symptoms, high concentrations of inflammatory biomarkers, and poor nutritional status.