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Background: This study aimed to investigate the association between relative fat mass (RFM) and asthma, as well as to explore the mediating role of Systemic Immune-Inflammation Index (SII) and Systemic Inflammation Response Index (SIRI). Methods: This cross-sectional study utilized data from the National Health and Nutrition Examination Survey from 2007 to 2018. Associations between RFM and asthma were tested using multivariable logistic regressions, restricted cubic splines, subgroup analyses, and interaction tests, with mediation analysis for SII and SIRI. The inflection point was determined by the two-piecewise linear regression. Sensitivity analysis and propensity score matching (PSM) was applied to validate the stability of the associations. Results: Higher RFM was positively associated with asthma, with an inflection point at 34.08. Below this threshold, each unit increase in RFM was positively associated with a 2% increase in the odds of asthma (Odds ratio (OR) 1.02, 95% Confidence interval (CI): 1.00—1.03), while above it, the association strengthened, with a 5% increase in the odds per unit (OR 1.05, 95% CI: 1.04—1.07). The association was consistent across subgroups. The association between RFM and asthma is stronger in current asthma patients than in ever had asthma ones. Mediation analyses showed that SII and SIRI partially mediated 7.48% and 3.88% of the RFM-asthma association, respectively. The findings remained robust after sensitivity analyses and adjusting for confounding bias using PSM. Conclusions: RFM is positively associated with the prevalence of asthma in the U.S., particularly among individuals with current asthma, with systemic inflammation partially mediating this relationship. [ABSTRACT FROM AUTHOR]

Background: Circulating rare cells participate in breast cancer evolution as systemic components of the disease and thus, are a source of theranostic information. Exploration of cancer-associated rare cells is in its infancy. Objectives: We aimed to investigate and classify abnormalities in the circulating rare cell population among early-stage breast cancer patients using fluorescence marker identification and cytomorphology. In addition, we sought to determine the dependency of these markers on the presence of tumors. Design: We evaluated the validity of a multi-rare-cell detection platform and demonstrated the utility of a specific rare cell subset as a novel approach to characterize the breast cancer system. Sampling was conducted both before and after tumor resection. Methods: Linearity of the Rarmax platform was established using a spike-in approach. The platform includes red blood cell lysis, leukocyte depletion and high-resolution fluorescence image recording. Rare cell analysis was conducted on 28 samples (before and after surgery) from 14 patients with breast cancer, 20 healthy volunteers and 9 noncancer control volunteers. In-depth identification of rare cells, including circulating tumor cells, endothelial-like cells, erythroblasts, and inflammation-associated cells, was performed using a phenotype and morphology-based classification system. Results: The platform performed linearly over a range of 5 to 950 spiked cells, with an average recovery of 84.6%. Circulating epithelial and endothelial-like cell subsets have been demonstrated to be associated with or independent of cancer with tumor presence. Furthermore, certain cell profile patterns may be associated with treatment-related adverse effects. The sensitivity in detecting tumor-presence and cancer-associated abnormality before surgery was 43% and 85.7%, respectively, and the specificity was 100% and 96.6%, respectively. Conclusion: This study supports the idea of a cancer-associated rare cell abnormality to represent tumor entities as well as systemic cancer. The latter is independent of the apparent clinical cancer. [ABSTRACT FROM AUTHOR]

Introduction: Cardiac tamponade is a life-threatening condition resulting from fluid accumulation in the pericardial sac, leading to decreased cardiac output and shock. Various etiologies can cause cardiac tamponade, including liver cirrhosis, which may be induced by autoimmune hepatitis. Autoimmune hepatitis is a chronic inflammatory liver disease characterized by interface hepatitis, elevated transaminase levels, autoantibodies, and increased immunoglobulin G levels. This case report details a 60-year-old male with autoimmune hepatitis-induced cirrhosis presenting with severe pericardial effusion and cardiac tamponade, emphasizing the interplay between liver and cardiac pathologies. Methods: A 60-year-old Persian man presented with progressive dyspnea, chest pain, and significant weight gain due to fluid retention. Physical examination revealed pallor, jaundice, elevated jugular venous pressure, muffled heart sounds, and tachycardia. Laboratory tests indicated severe hepatic and renal dysfunction, with elevated liver enzymes, bilirubin, and blood urea nitrogen. Imaging studies, including electrocardiogram, computed tomography angiography, and transthoracic echocardiogram, confirmed large pericardial effusion with signs of cardiac tamponade. Emergency pericardiocentesis was performed, aspirating 500 mL of serosanguinous fluid. Post-procedural management included continuous monitoring, repeat echocardiography, and a comprehensive pharmacological regimen addressing fluid overload, autoimmune hepatitis, and cardiac function. Conclusion: This case underscores the importance of timely diagnosis and management of cardiac tamponade, particularly in patients with concomitant conditions like autoimmune hepatitis and cirrhosis. Multidisciplinary management involving hepatologists, cardiologists, and critical care specialists is crucial for improving patient outcomes. Early recognition and treatment contribute substantially to the prevention of recurrence and better long-term management of underlying conditions. Clinical key points: Prompt recognition and intervention are critical for life-threatening cardiac tamponade. Autoimmune hepatitis can lead to severe complications, including cirrhosis and pericardial effusion. A multidisciplinary approach involving collaboration among cardiothoracic surgeons, interventional cardiologists, and other specialists is essential for managing complex cases involving multiple organ systems. Continuous monitoring and long-term management of autoimmune hepatitis and cirrhosis are crucial to prevent recurrence and improve patient outcomes. [ABSTRACT FROM AUTHOR]

The objective of this study is to investigate the association between the Systemic Immune-Inflammation Index (SII) and cataracts. This cross-sectional study analyzed data from the 2005–2008 NHANES to examine the relationship between the SII and cataract prevalence. Covariates included age, race/ethnicity, gender, education level, marital status, Body Mass Index (BMI), smoking, alcohol consumption, hypertension, hyperlipidemia, and diabetes. Multivariable logistic regression was used to assess the association, while spline curve fitting explored potential non-linear relationships. Threshold analysis identified critical inflection points. To address age-related bias, Propensity Score Matching (PSM) was performed, aligning cataract patients with comparable non-cataract individuals for further evaluation. Our study included 3,623 participants, of whom 730 (20.15%) were diagnosed with cataracts. After adjusting for all covariates, multivariable logistic regression analysis demonstrated that elevated levels of the SII were significantly associated with increased odds of cataracts (Model1: OR = 1.56; 95%CI [1.33–1.85]; Model2: OR = 1.55; 95%CI [1.32–1.84]; Model3: OR = 1.57; 95%CI [1.33–1.86]). In the spline curve fitting model, the relationship between ln-SII and cataract prevalence was non-linear (P < 0.001), with a critical inflection point identified at an SII of 428.38. SII levels remained significantly associated with cataract prevalence following PSM adjustments (Model 1: OR = 1.48; 95% CI [1.21–1.80]; Model 2: OR = 1.48; 95% CI [1.21–1.80]; Model 3: OR = 1.46; 95% CI [1.20–1.78]). Elevated SII levels are associated with a higher prevalence of cataracts, underscoring the pivotal role of systemic inflammation in cataract development. These findings indicate that SII could serve as a valuable biomarker for assessing cataract risk, further emphasizing the significance of managing systemic inflammation as a potential strategy for cataract prevention. [ABSTRACT FROM AUTHOR]

Development of overt hepatic encephalopathy (oHE) is a particularly feared complication when considering treatment with transjugular intrahepatic portosystemic shunt (TIPS). However, the pathophysiology of HE, in particular after TIPS-insertion, is complex and valid predictors remain scarce. We aimed to investigate whether systemic inflammation markers (SIM) are linked to minimal (mHE) and overt HE (oHE) development before and after TIPS. 62 prospectively recruited patients undergoing TIPS-insertion were included and monitored for oHE occurrence two years thereafter. Patients underwent psychometric testing including the portosystemic encephalopathy syndrome test (PSE), yielding the psychometric hepatic encephalopathy score (PHES), and Animal Naming Test (ANT) before TIPS (baseline) and during structured follow-up 1, 3, 6 and 12 months afterwards. SIM (IL-6, TNF-α and IL-1β) were measured at corresponding timepoints. Patients were predominantly male (64.5%) with a median age of 58 years and MELD of 11. The majority (75.8%) received a TIPS for treatment of refractory ascites. 67.9% presented with mHE before TIPS. No link between the investigated SIM and PHES or ANT at baseline or during any follow-up was documented. 19 (30.6%) patients developed oHE during follow-up. Neither baseline SIM levels nor test results were significantly associated with risk for oHE. We demonstrated a significant decline of all SIM during follow-up, which did not translate to an ameliorated risk for oHE. In patients undergoing TIPS-insertion, the selected SIM have neither a strong link to post-TIPS-oHE development nor to subclinical changes in psychometric tests for mHE. [ABSTRACT FROM AUTHOR]

Severe intestinal mucositis (IM) increases the risk of bloodstream infections (BSI) and inflammatory toxicity during acute lymphoblastic leukaemia (ALL) induction treatment. However, the implications of IM in subsequent ALL therapy phases after achieving remission remain unknown. This study investigated the relationship between IM (measured by plasma citrulline and the chemokine CCL20) and the development of BSI and systemic inflammation (reflected by C‐reactive protein, CRP) in children with ALL during high‐dose methotrexate (HDMTX) treatment, an important part of ALL consolidation therapy. The study compared patients treated according to the NOPHO ALL 2008 protocol (n = 52) and the ALLTogether1 protocol (n = 42), both with identical HDMTX procedures but different scheduling. One week post‐HDMTX, citrulline dropped to median levels of 14.5 and 16.9 μM for patients treated according to the NOPHO ALL 2008 and ALLTogether1 protocols, respectively (p = 0.11). In a protocol and neutrophil count‐adjusted analysis, hypocitrullinaemia (<10 μmol/L) was associated with increased odds of BSI within 3 weeks from HDMTX (OR = 26.2, p = 0.0074). Patients treated according to the NOPHO ALL 2008 protocol exhibited increased mucosal‐ and systemic inflammation post‐HDMTX compared to patients treated according to ALLTogether1, with increased CCL20 (14.6 vs. 3.7 pg/mL, p < 0.0001) and CRP levels (10.0 vs. 1.0 mg/L, p < 0.0001). Both citrulline and CCL20 correlated with CRP for these patients (rs = −0.44, p = 0.0016 and rs = 0.35, p = 0.016, respectively). These results suggest that hypocitrullinaemia following HDMTX increases the risk of BSI, confirming previous observations from more intensive treatments. Moreover, these data indicate that the patients' vulnerability to mucositis and inflammatory toxicity after chemotherapy varies with treatment protocol. [ABSTRACT FROM AUTHOR]

Introduction: Glucocorticoids (GCs) are widely used as a treatment for rheumatoid arthritis (RA), leading to high cumulative doses in long-term treated patients. The impact of a high cumulative GC dose on the systemic inflammatory response in RA remains poorly understood. Methods: We investigated long-treated patients with RA (n = 72, median disease duration 14 years) through blood counts and the serum levels of 92 inflammation-related proteins, and disease activity was assessed using the Simple Disease Activity Index (SDAI). Patients were grouped based on the cumulative GC dose, with a cut-off value of 20 g (low/high, n = 49/23). Results and discussion: Patients with a high cumulative GC dose within the active RA group had elevated serum levels in 23 inflammation-related proteins compared with patients with a low dose (cytokines/soluble receptors: CCL3, CCL20, CCL25, IL-8, CXCL9, IL-17A, IL-17C, IL-18, sIL-18R1, IL-10, sIL-10RB, OSM and sOPG; growth factors: sTGFα and sHGF; other inflammatory mediators: caspase 8, STAMBP, sCDCP1, sirtuin 2, 4E-BP1, sCD40, uPA and axin-1; pcorr < 0.05). In non-active RA, the high and low GC groups did not differ in analysed serum protein levels. Moreover, patients with active RA with a high GC dose had an increased white blood cell count, increased neutrophil–lymphocyte and platelet–lymphocyte ratios and a decreased lymphocyte–monocyte ratio compared with the low dose group (p < 0.05). This is the first study to report elevated serum levels in inflammation-related proteins and deregulated blood counts in patients with active RA with a high cumulative GC dose. The elevated systemic inflammation highlights the importance of improving care for patients receiving high cumulative GC doses. [ABSTRACT FROM AUTHOR]

Heart failure with preserved ejection fraction (HFpEF) is a heterogeneous syndrome with various phenotypes, and obesity is one of the most common and clinically relevant phenotypes of HFpEF. Obesity contributes to HFpEF through multiple mechanisms, including sodium retention, neurohormonal dysregulation, altered energy substrate metabolism, expansion of visceral adipose tissue, and low-grade systemic inflammation. Glucagon-like peptide-1 (GLP-1) is a hormone in the incretin family. It is produced by specialized cells called neuroendocrine L cells located in the distal ileum and colon. GLP-1 reduces blood glucose levels by promoting glucose-dependent insulin secretion from pancreatic β cells, suppressing glucagon release from pancreatic α cells, and blocking hepatic gluconeogenesis. Recent evidence suggests that GLP-1 receptor agonists (GLP-1 RAs) can significantly improve physical activity limitations and exercise capacity in obese patients with HFpEF. The possible cardioprotective mechanisms of GLP-1 RAs include reducing epicardial fat tissue thickness, preventing activation of the renin–angiotensin–aldosterone system, improving myocardial energy metabolism, reducing systemic inflammation and cardiac oxidative stress, and delaying the progression of atherosclerosis. This review examines the impact of obesity on the underlying mechanisms of HFpEF, summarizes the trial data on cardiovascular outcomes of GLP-1 RAs in patients with type 2 diabetes mellitus, and highlights the potential cardioprotective mechanisms of GLP-1 RAs to give a pathophysiological and clinical rationale for using GLP-1 RAs in obese HFpEF patients. [ABSTRACT FROM AUTHOR]

Brain white matter disruptions have been implicated in contributing to fatigue, brain fog and other central symptoms commonly reported in inflammatory diseases. In this study, we included 252 RA patients with 756 age and sex matched controls and 240 UC patients with 720 age and sex matched controls using the UK Biobank imaging dataset. We looked for differences in total volume of white matter hyperintensities (WMH) between patients compared to controls. Then, using voxelwise analysis, we explored the spatial distribution of these white matter hyperintensities and differences in these between patients and controls and between disease groups. A significantly higher volume of WMH was observed in both the RA (p = 1.9 × 10−8, β = − 0.36, 95% CI = − 0.48, − 0.23) and UC (p = 0.003, β = − 0.18 95% CI = − 0.31, − 0.06) patients compared to their respective control groups. Voxelwise analysis revealed only a small cluster of RA associated WMH compared to controls. These results indicate an increased risk of white matter hyperintensities in patients with RA and UC. These findings help quantify the effect of inflammation from autoimmune diseases on cerebrovascular health and white matter integrity. [ABSTRACT FROM AUTHOR]

Telomere length (TL) is a recognized biomarker for ageing in multiple species. In dairy cattle, the transition period is considered a very stressful period. We hypothesized that TL shortens during this period. Holstein cows (n = 61) were followed during the transition period. Blood and milk samples were collected at − 7, 3, 6, 9, 21d relative to calving to determine concentrations of oxidative, energetic metabolic, and inflammatory markers. Average relative leukocyte TL was measured by a modified qPCR protocol 7d before and 21d after parturition. We confirmed TL attrition during the transition period (P = 0.02), as TL was 1.05 ± 0.229 (mean ± SD) before, and 0.97 ± 0.191 (mean ± SD) after parturition. Univariable analyses assessed associations between blood markers and TL shortening. Greater plasma oxidative parameters, including oxidized glutathione and glutathione peroxidase, were positively and negatively (respectively) associated with TL attrition. Higher blood α- and β-globulin were all positively associated, while IGF-1, albumin-globulin ratio and albumin were negatively associated with TL attrition. Greater serum amyloid A and haptoglobin were linked with greater TL shortening. This study reveals significant TL shortening during the transition period in dairy cows and identifies significant associations with oxidative stress, metabolic stress, and inflammation. While these associations are observed, no causality can be established. Our findings suggest the need for further research to explore the effects of transition-related stress on TL dynamics. [ABSTRACT FROM AUTHOR]

Unregulated, systemic inflammation negatively impacts health and production in dairy cows. Soluble mediators and platelets have been studied for their expansive role in mediating inflammation. Our objectives were to compare the plasma oxylipin and endocannabinoid profiles, and the platelet and plasma proteomic profiles of healthy cows to cows experiencing elevated systemic inflammation as indicated by plasma haptoglobin (Hp) concentrations. Postpartum cows at 3 DIM with plasma Hp concentrations 0.50 g/L and no clinical disease were enrolled into the high-inflammation group (n = 8). Cows with plasma Hp concentrations 0.1 g/L and no clinical disease were enrolled into the low-inflammation group (n = 8). Targeted lipidomic analysis revealed differences in the plasma oxylipin and endocannabinoid profile between high- and low-inflammation cows. Cows in the high-inflammation group had increased plasma concentrations of the oxylipins 9(S)-HpOTrE, 9(S)-HOTrE, 13(S)-HpOTrE, and 9,10-EpOME, and the endocannabinoid anandamide. In-depth proteomic analysis of platelets between the high- and low-inflammation groups revealed significant differences in protein categories related to platelet granule release and cellular iron uptake. Proteomic outputs from plasma revealed 24 proteins to be different between high and low-inflammation groups, including proteins involved in autophagy and immune mediation. Together, our results indicate that cows experiencing an exacerbated systemic inflammatory response in the postpartum may have impaired disease resistance, and platelets could be contributors to their inflammatory state. [ABSTRACT FROM AUTHOR]

Periodontitis is closely related to lifestyle habits. Our objective was to examine the relationship between the Life's Essential 8 (LE8) and the prevalence of periodontitis in American adults. This study used data from the 2009–2014 National Health and Nutrition Examination Survey (NHANES). LE8 scores (range 0–100) were measured according to the definition by the American Heart Association (AHA) and were categorized as low (0–49), medium (50–79), and high (80–100). The NHANES database on periodontal health was used to data to determine the prevalence of periodontitis. Multivariate regression models and restricted cubic spline (RCS) models were used to assess correlations. Weighted quantile sum (WQS) regression was used to explore the association of LE8 and its components with periodontitis risk. Stratified analysis and interaction analysis were conducted to assess the consistency of the results. In addition, mediation analyses were performed to investigate the role of systemic inflammation in mediating the association of LE8 with periodontitis risk. Participants with moderate (LE8 score 50–79) and high (LE8 score 80–100) scores had 58% (95% CI 0.43–0.79, P < 0.001) and 55% (95% CI 0.37–0.84, P = 0.010) less periodontitis prevalence, respectively, compared with adults with lower total scores. Among all 8 indicators, nicotine exposure (62.3%), blood glucose (18.2%), sleep heath (8.2%), and blood pressure (7.7%) had the most significant impact on periodontitis. Notably, no statistically significant interactions were observed in all subgroup analyses except age (P for interaction < 0.05), indicating that the protective effect of LE8 on periodontitis was shown to be more pronounced in individuals between 40 and 60 years of age. In addition, neutrophil, white blood cell (WBC), and albumin levels mediated the association between LE8 and periodontitis risk, mediating proportions of 13.3%, 21.4%, and 8.3%, respectively. These findings suggest that poorer LE8 scores increase the risk of periodontitis, which may be partly mediated by systemic inflammation. [ABSTRACT FROM AUTHOR]

Background: Long-term air pollution exposure and inflammation are considered to be associated with cognitive decline. However, whether air pollution exposure related cognitive decline is dependent on inflammation remains uncertain. Materials and methods: The present study collected data from China Health and Retirement Longitudinal Study (CHARLS) at baseline in 2011, with a follow up period in 2015. Concentration of air pollutants (particles with diameters ≤ 1.0 μm [PM1], ≤ 2.5 μm [PM2.5], ≤ 10 μm [PM10], nitrogen dioxide [NO2] and ozone [O3]) were obtained from China High Air Pollutants (CHAP) dataset. Hypersensitive C-reactive protein (hs-CRP), a systemic inflammation marker, was measured in blood of subjects and cognitive function was assessed by standardized questionnaire. Results: A total of 6434 participants were included in the study. Lower exposure to PM2.5, PM1, PM10 and NO2 were associated with mitigated cognitive decline. The odds ratios (ORs) for air pollutants changes and cognitive decline and 95% confidence intervals (CIs) were as follows: PM2.5-0.934(0.925, 0.943), PM1- 0.945 (0.935,0.955), PM10-0.977(0.972,0.982) and NO2-0.962(0.950,0.975), respectively. Hs-CRP showed no significant correlation with cognitive decline or change in levels of air pollution. The interaction regression analyses, both unadjusted and adjusted, did not uncover any significant correlation between hs-CRP and air pollution with respect to cognitive decline. Bootstrap test exhibited no significant mediating effect of hs-CRP on the relationship between any air pollutants and cognitive decline, the indirect effects of hs-CRP in conjunction with exposure to different air pollutants were all found to be non-significant, with the following bootstrap CIs and p-values: PM2.5-1.000([1.000,1.000], P = 0.480),PM1-1.000([1.000,1.000], P = 0.230),PM10-1.000([1.000,1.000], P = 0.650), O3-1.000([1.000,1.000], P = 0.470), ΔNO2-1.000([1.000,1.000], P = 0.830). Conclusion: Ambient air pollution exposure was linked to cognitive decline independent of hs-CRP level. [ABSTRACT FROM AUTHOR]

Background/Objectives: Psoriasis is a chronic dermatological condition with systemic implications, especially with metabolic syndrome (MS). This study evaluated the vicious cycle where obesity and MS exacerbate systemic inflammation that complicates the efficacy of psoriasis therapies by examining the PASI score over a one-year period. Patients were classified into two subgroups: those with psoriasis alone (PSO) and those with both psoriasis and metabolic syndrome (PSO-MS). Methods: A total of 150 patients, half of whom also concomitantly presented with metabolic syndrome, received biologic therapies comprising anti-IL-17, anti-IL-23, and anti-TNF-a, or methotrexate, with PASI scores assessed at baseline and at 3, 6, and 12 months. Results: All treatments showed significant reductions in PASI; however, patients with PSO showed more marked reductions in PASI score than those in the PSO-MS group. Anti-IL-17 treatments produced the greatest sustained long-term improvements, whereas anti-IL-23 produced prompt early improvements. Increases in BMI and leptin concentrations were associated with a modest rate of reduction in PASI score, underlining the impact of obesity and metabolic dysfunction on treatment efficacy. Conclusions: This study highlights the importance of managing comorbidities such as MS in the treatment of psoriasis, as the interplay between systemic inflammation and metabolic health further complicates therapeutic outcomes. [ABSTRACT FROM AUTHOR]

Obstructive sleep apnea syndrome (OSAS) is prevalent among children and is associated with elevated blood pressure (BP), posing a risk for future hypertension and cardiovascular diseases. While the roles of gut microbiota and systemic inflammation in OSAS pathogenesis are recognized in adults and animal models, their impact on pediatric BP remains less understood. This cross-sectional study explored the relationships between polysomnographic parameters, gut microbiota, systemic inflammation, and BP in 60 children with OSAS. Significant associations between specific microbial profiles—including beta diversity and 31 marker microbes—and BP variations were observed. These microbial profiles correlated with significant alterations in systemic inflammation markers like interleukin-17 and tumor necrosis factor-α. Notably, the relative abundance of Acinetobacter was related to fluctuations in these inflammatory markers and BP levels. The research further highlighted the unique microbial and cytokine profiles exhibited by children with different BP levels, indicating a substantial role of gut microbiota and systemic inflammation in influencing pediatric cardiovascular health. The findings suggest integrating gut microbiota management into comprehensive cardiovascular risk strategies for children with OSAS. This initiative underscores the need for further investigations to decode the mechanisms behind these associations, which could lead to innovative treatments for pediatric OSAS. [ABSTRACT FROM AUTHOR]

Background: Systemic inflammation (SI) and insulin resistance (IR) are correlated to the progression of gastrointestinal (GI) cancer. Therefore, this study aimed to analyze the potential clinical value of the C-reactive protein-triglyceride-glucose index (CTI) in relation to SI and IR in patients with GI cancer. Methods: This prospective cohort study included patients with GI cancer. Patient data were collected from Fujian Cancer Hospital as an external validation cohort. Prognostic AUC, time-dependent ROC curve, C-index, and calibration curve analyses were used to predict the efficacy and accuracy of CTI survival prediction. Multivariate survival analysis was performed to evaluate the potential prognostic value of the CTI. Multiple logistic regression was performed to evaluate the relationship between the CTI and 90-day and 180-day mortalities. Results: We divided 1520 patients with GI cancer (mean age, 60.39 ± 11.3 years; male sex, 67%) into a training cohort and internal validation cohort; the external validation cohort included 476 patients. Prognostic AUC, time-dependent ROC curve, C-index, and calibration curve analyses of all cohorts indicated that the CTI could reliably and accurately predict the short- and long-term survival outcomes of patients with GI cancer. Multivariate survival analysis showed that for each standard deviation increase in the CTI, the risk of death increased by 32%, 21%, and 40% in the training, internal validation, and external validation cohorts, respectively. A high CTI was correlated to worse survival in patients with GI cancer (training cohort, hazard ratio [HR]=1.67, 95% confidence interval [CI]=1.35–2.08; internal validation cohort, HR=1.51, 95% CI=1.07–2.14, and external validation cohort, HR=1.59, 95% CI=1.18–2.13). In different tumor subgroups, a high CTI predicted worse survival outcomes for upper GI cancer (HR=1.54, 95% CI=1.18–2.01) and lower GI cancer (HR=1.98, 95% CI=1.36–2.86). Multivariate logistic regression analysis showed that a high CTI was positively correlated with 90-day (odds ratio [OR]=3.25, 95% CI=1.75–6.23) and 180-day mortalities (OR=2.66, 95% CI=1.72–4.15). Conclusions: The CTI is related to SI and IR and can predict the short- and long-term prognosis of patients with GI cancer. Evaluation of the CTI could provide clinicians with an effective tool for predicting the prognosis of patients with GI cancer. Clinical trial registration: https://www.chictr.org.cn/showproj.html?proj=31813 , identifier ChiCTR1800020329. [ABSTRACT FROM AUTHOR]

Background: Serum C-reactive protein (CRP) levels are correlated with patient outcomes in cancer. This study aimed to determine associations between the CRP level and the dietary intake, symptoms, and eating-related distress (ERD). Methods: We conducted a multicenter survey among advanced cancer patients. Information on patient characteristics was retrieved from the electronic medical records. Data on patient outcomes were obtained through the questionnaire. Patients were categorized into the low CRP group (<5 mg/dL) and the high CRP group (≥5 mg/dL). Comparisons were calculated using the Mann–Whitney U test or chi-squared test. To assess associations between CRP levels and ERD, multivariate logistic regression analysis was performed. Results: A total of 191 patients were enrolled and divided into the low CRP group (n = 117) and the high CRP group (n = 74). The high CRP group had a more reduced dietary intake (p = 0.002) and more severe appetite loss (p = 0.008). The total scores of the ERD questionnaire (both the long and short versions) were significantly higher in the high CRP group (p = 0.040 and 0.029). The high CRP group also had significantly higher risks for ERD, as assessed using the long and short versions of the questionnaire (odds ratio [OR] 2.13, 95% confidence interval [CI] 1.10–4.11; OR 2.06, 95% CI 1.05–4.05). Conclusions: High CRP levels were significantly associated with reduced dietary intake, appetite loss, and ERD. A serum CRP value of 5 mg/dL may be a useful indicator for initiating cancer cachexia care. [ABSTRACT FROM AUTHOR]

Mood disorders include a set of psychiatric manifestations of increasing prevalence in our society, being mainly represented by major depressive disorder (MDD) and bipolar disorder (BD). The etiopathogenesis of mood disorders is extremely complex, with a wide spectrum of biological, psychological, and sociocultural factors being responsible for their appearance and development. In this sense, immune system dysfunction represents a key mechanism in the onset and pathophysiology of mood disorders, worsening mainly the central nervous system (neuroinflammation) and the periphery of the body (systemic inflammation). However, these alterations cannot be understood separately, but as part of a complex picture in which different factors and systems interact with each other. Psychoneuroimmunoendocrinology (PNIE) is the area responsible for studying the relationship between these elements and the impact of mind–body integration, placing the immune system as part of a whole. Thus, the dysfunction of the immune system is capable of influencing and activating different mechanisms that promote disruption of the psyche, damage to the nervous system, alterations to the endocrine and metabolic systems, and disruption of the microbiota and intestinal ecosystem, as well as of other organs and, in turn, all these mechanisms are responsible for inducing and enhancing the immune dysfunction. Similarly, the clinical approach to these patients is usually multidisciplinary, and the therapeutic arsenal includes different pharmacological (for example, antidepressants, antipsychotics, and lithium) and non-pharmacological (i.e., psychotherapy, lifestyle, and electroconvulsive therapy) treatments. These interventions also modulate the immune system and other elements of the PNIE in these patients, which may be interesting to understand the therapeutic success or failure of these approaches. In this sense, this review aims to delve into the relationship between immune dysfunction and mood disorders and their integration in the complex context of PNIE. Likewise, an attempt will be made to explore the effects on the immune system of different strategies available in the clinical approach to these patients, in order to identify the mechanisms described and their possible uses as biomarkers. [ABSTRACT FROM AUTHOR]

AbstractObjective: Physical exercise in treatment of asthma is scarcely studied with no clear exercise guidelines for asthmatics. We aimed to investigate the associations between physical exercise frequency, systemic inflammation and asthma control. This has not been previously studied in adult-onset asthma.Methods: This study is part of Seinäjoki Adult Asthma Study (SAAS), where 203 patients with adult-onset asthma were evaluated in 2012–2013. Exercise frequency was recorded with a structured lifestyle questionnaire. Study population was divided into two categories by exercise frequency: Low-frequency group exercised ≤2 times/week and high frequency group >2 times/week. Blood inflammatory markers were measured and IL-6 > 1.55 pg/ml and hs-CRP > 4.12 mg/l indicated systemic inflammation.Results: High-exercise frequency group had lower levels of hs-CRP (p = 0.007), IL-6 (p = 0.015), suPAR (p = 0.008) and adipsin (p = 0.031) and higher levels of adiponectin (p = 0.010) than low-exercise frequency group. In logistic multivariate regression models, higher-exercise frequency lowered odds for elevated hs-CRP (OR = 0.37, 95% CI 0.15–0.94) and IL-6 levels (OR = 0.43, 95% CI 0.20–0.91), after adjusting for possible confounding factors. There was no difference in lung function tests, asthma control test or airways questionnaire 20 scores between the exercise frequency groups. However, differences were found in single symptom questions; high-exercise frequency group had less symptoms during light housework and laughing but experienced more limitation of activity in self-reports.Conclusions: Higher-exercise frequency is associated with lower level of systemic inflammation in patients with adult-onset asthma but no clear association was found to asthma outcomes. Exercise frequency may be associated with lesser amount of some individual asthma symptoms. [ABSTRACT FROM AUTHOR]

Background: Obesity is associated with a systemic inflammatory state that contributes to neuroinflammation and increases the risk of stroke at an early age. Stroke is the third leading cause of death worldwide and the leading cause of permanent disability. This work aimed to assess whether obesity-induced neuroinflammation can be a prognostic stroke factor that can be improved with oral administration of silymarin, an anti-inflammatory and neuroprotective drug. Methods: Male C57/Bl6 mice were used to establish an obesity model through a high-fat diet (HFD) for 12 weeks. Cerebral ischemia was performed with photothrombosis in the left motor cortex at the end of the diet. Following the induction of ischemia, silymarin (100 mg/kg) was administered orally for 14 days. Levels of pro-inflammatory (IL1β, TNFα, and MCP1) and anti-inflammatory markers (IL4, IL10), neurotrophic factors (IGF1, BDNF), and CX3CL1 were assessed in the cortex and striatum using ELISA. Results: Mice on the HFD gained significantly more weight than control subjects and exhibited altered glucose metabolism, which was improved after silymarin treatment. The survival rate was significantly lower in HFD mice (52.2%) compared to control mice (86%). Silymarin treatment improved survival in both ischemic groups (non-diet control: 95.7%, HFD: 78.3%). Silymarin raised cortical TNFα, IL4, IL10, IGF1, BDNF, and CX3CL1 levels in the HFD group with stroke, while the striatum did not present relevant differences. Conclusion: Our findings suggest that silymarin improves glucose metabolism, possibly impacting post-stroke survival in obese mice. The increased levels of neurotrophic factors BDNF and IGF1, along with microglial regulatory factor CX3CL1, may contribute to the improved survival observed. These results indicate that silymarin could be a potential therapeutic option for managing neuroinflammation and enhancing post-stroke outcomes in obese individuals. [ABSTRACT FROM AUTHOR]

This study explored the link between clinical features, immune markers, and asthma-chronic obstructive pulmonary disease overlap (ACO), aiming to enhance diagnostic precision and tailor treatment. The study included 60 patients per group: COPD patients, ACO patients, and healthy controls. Biological indicators such as fractional exhaled nitric oxide (FeNO), eosinophils, immunoglobulin E (IgE), T helper (Th) 17 cell counts, regulatory T-cell (Treg) counts, and cytokine levels of interleukin-17 (IL-17) and interleukin-10 (IL-10) were measured using standard enzyme-linked immunosorbent assay and flow cytometry techniques. Elevated Th17 cells, IL-17, and Th17/Treg ratio, alongside reduced IL-10 and Treg levels, were observed in COPD and ACO patients. ACO patients showed worse lung function, with a negative correlation between FeNO, Th17 cells, Th17/Treg ratio, IL-17, and lung function indices, and a positive correlation with residual volume/total lung capacity (RV/TLC) ratio. The study suggests that Th17/Treg imbalance, FeNO, eosinophils, and IgE could be key in ACO pathogenesis, potentially aiding early diagnosis and targeted treatment. Future research may utilize these findings to develop preventative and therapeutic strategies for ACO. [ABSTRACT FROM AUTHOR]

Tattooing has become a popular global trend in industrialised countries, with the highest prevalence rates of up to 30–40 % in the adult population younger than 40 years. Common tattoo inks may contain heavy metals, polycyclic aromatic hydrocarbons, and primary aromatic amines, toxic if exceeding permissible limits. It is estimated that about 14.36 mg of ink is injected per cm2 of skin, at a depth of 1–3 mm. The injected pigment is internalised by neutrophils, fibroblasts, and macrophages or dendritic cells. About 60–90 % of the pigment is then transported to the lymph nodes via the lymphatic system and to other organs, such as the liver, spleen, and lung, through blood. Adverse reactions can be immediate (irritation, infection, inflammation of the skin), delayed (hypersensitivity reactions), and can result in long-term complications (fibrosis, granulomatous changes, systemic inflammation, and sometimes malignant diseases such as lymphoma). Pigments in tattooed skin can be identified by skin biopsy, chemical imaging, and histochemical and immunohistochemical analyses. Harmful effects of tattoo inks have been investigated ex vivo, in vitro, in vivo, and recently in silico. Studies in humans mainly refer to case reports, but there are no epidemiological studies that would evaluate the potential links between tattoos and cancer or other disorders. As the safety of people getting tattoos primarily depends on the quality of tattooing products, it is necessary to create a general regulatory framework. [ABSTRACT FROM AUTHOR]

Background: Numerous studies have linked the inflammatory pathway in psoriasis and metabolic disease, while no specific marker defined it. It is worth exploring the association of β2-microglobulin (β2M) in psoriasis severity and comorbidities. Objectives: To investigate the correlation between blood β2M level and psoriasis severity, to explore the inflammatory factors influencing the occurrence of psoriasis comorbidities such as arthritis, diabetes, and hypertension. Methods: Ninety-seven psoriasis patients were analyzed in the cohort retrospective study during 12 weeks. Results: Significantly higher levels of blood β2M and ESR were observed in the group that patients' PASI ≥10 than in the group that PASI <10. Blood β2M level had strong significantly positive correlations with the PASI in Pearson's correlation analysis. In the model that systemic inflammatory factors to find psoriasis comorbidity risk factors, logistic regression analysis showed that blood β2M level was the significant risk factor associated with diabetes and hypertension. High-sensitivity C-reactive protein (hsCRP) was the significant risk factor associated with arthritis. Conclusions: Patients with a severer psoriasis tended to have higher blood β2M levels and severer inflammatory state. In the systemic inflammation indexes, the level of blood β2M affected the risk of hypertension and diabetes, and hsCRP affected the risk of arthritis in patients with psoriasis. [ABSTRACT FROM AUTHOR]

Background: The effect of air pollution, a major global health issue, on the immune system, particularly on white blood cell (WBC) counts, remains underexplored. Methods: This study utilized data from 54,756 participants in the Korean National Health and Nutrition Examination Survey to investigate the effects of short- (day of examination and 7-day averages), mid- (30- and 90-day averages), and long-term (one-, three-, and five-year averages) air pollutant exposure on WBC counts. We assessed exposure to particulate matter (PM10, PM2.5), sulfur dioxide (SO2), nitrogen dioxide (NO2), ozone (O3), and carbon monoxide (CO). Results: Linear regression with log-transformed WBC counts, adjusted for confounders, showed that PM10 was positively associated with long-term exposure, PM2.5 was negatively associated with short- and mid-term exposures, SO2 was consistently negatively associated with short- and mid-term exposures, NO2 and CO were positive across most periods, and O3 was negatively associated with short- and mid-term exposures. Logistic regression analysis confirmed these findings, showing that short- and mid-term exposure to PM10, PM2.5, and SO2 was negatively associated with the risk of belonging to the high-WBC group, while long-term exposure to PM10, PM2.5, NO2, and CO showed positive associations with risk. Conclusions: Our findings highlight the time- and pollutant-specific associations between air pollution exposure and WBC counts, underscoring air pollution's potential impact on systemic inflammation. [ABSTRACT FROM AUTHOR]

The list of standard abbreviations for JDS is available at adsa.org/jds-abbreviations-24. Nonstandard abbreviations are available in the Notes. The objective of this study was to assess the effects of prepartum administration of anti-inflammatory therapies on BCS, BHB concentration, haptoglobin (HP) concentration, milk yield, milk components, rumination time, clinical health events, and reproductive performance in Holstein dairy cows. At 14 d before the expected calving date, cows (parous [PAR]; n = 170) and heifers (nulliparous [NUL]; n = 63) were blocked by BCS group (optimal [OPT] = 3–3.5; over-conditioned cows [OVERC; BCS ≥3.75 points]) and parity (NUL; PAR) and randomly allocated to 1 of 3 treatment groups: (1) ASA (n = 78): receive one oral administration of acetylsalicylic acid (4 boluses; 480 grain/bolus); (2) MEL (n = 76): receive one oral administration with meloxicam (1 mg/kg BW), or (3) PLC (n = 77): receive one oral treatment with gelatin capsules filled with water. Body condition score was assessed, and blood samples were collected, weekly starting 1 wk before treatment until 3 wk after calving. Daily milk yields and daily rumination times were collected from on-farm computer records. Dairy Herd Improvement Association monthly test data were collected to assess milk yield, SCC, and milk components. Furthermore, health events, culling rate, and reproductive performance data were collected from on-farm computer records. The data were analyzed using MIXED, GLIMMIX, and LIFETEST procedures of SAS as a randomized complete block design. On average, MEL-NUL cows produced 4.77 ± 0.93 kg/d and 4.81 ± 0.92 kg/d more milk from wk 6 to 21 of lactation compared with ASA-NUL and PLC-NUL cows, respectively. Similarly, a week by treatment by body condition group interaction was present, where OVERC cows treated with MEL produced more milk from wk 10 to 15 of lactation compared with ASA-OVERC and PLC-VERC cows. Parous cows treated with ASA had lower BCS compared with PAR cows treated with MEL or PLC. A lower percentage of OVERC cows treated with ASA became sick in the first 60 DIM compared with MEL-OVERC and PLC-OVERC cows (ASA = 23.88% ± 7.26%, MEL = 46.36% ± 8.57%; PLC = 46.74% ± 8.53%). Parous cows treated with ASA had a higher hazard ratio to become pregnant by 300 DIM compared with PAR MEL cows. Although the study was not sized for finding treatment differences in blocking criteria groups, these results suggest that treatment with prepartum anti-inflammatory therapies may have positive effects on milk yield and postpartum health in specific groups of cows, such as NUL and OVERC cows, although it may not be recommended for other animal categories, such as parous cows and cows with optimal BCS. Larger studies are needed to strengthen the associations observed in this study. [ABSTRACT FROM AUTHOR]

Background: In this study, we aimed to investigate whether there is a relationship between aortic arch calcification (AAC) and hidradenitis suppurativa (HS) in HS patients without cardiovascular disease. Methods: In this study, patients over 18 years of age who applied to the dermatology outpatient clinic between January 2023 and February 2024 were followed up with the diagnosis of HS without cardiovascular disease, and a healthy control group matched in terms of age and gender were included retrospectively. Results: In total, 130 patients with HS without cardiovascular disease and 130 control patients were included in the study. AAC was significantly higher in the HS group compared to the control group (p = 0.028). In the multivariate analysis, we found that age and HS were independent predictors of AAC (OR: 1.048 (1.009–1.089); p = 0.015, OR: 3.158 (1.181–8.445); p = 0.022, respectively). When we divided the groups as having AAC (grade 1–3) and not having AAC (grade 0), the rate of HS disease was significantly higher in the group with AAC compared to the group without AAC (75.0% vs. 47.5% p = 0.010). Conclusions: AAC is observed more frequently in patients with HS without cardiovascular disease than in healthy individuals. Moreover, HS can be considered as an independent predictor of AAC. AAC may contribute to developing treatment strategies in HS patients without cardiovascular disease. [ABSTRACT FROM AUTHOR]

Purpose: Systemic inflammation biomarkers, derived from routine blood tests, have been demonstrated to be associated with prognosis of patients undergoing peritoneal dialysis (PD). However, studies focusing on the comparisons of their role on predictive efficacy for prognosis of PD patient are limited and results are inconsistent. The purpose of this study was to evaluate the prognostic value of various systemic inflammation biomarkers and to identify the optimal one in PD patients. Patients and Methods: This longitudinal study involved 3,225 patients undergoing PD across China. The prognostic accuracy of systemic inflammatory biomarkers was evaluated using C-statistics. Independent prognostic biomarkers of outcomes were determined using multivariate Cox proportional hazards regression analysis. Results: During a 46-month follow-up, 829 (25.7%) patients died, with 458 (55.3%) deaths attributed to cardiovascular disease (CVD). The highest C-statistics were observed for the IBI, with 0.619 and 0.621 for all-cause and CVD mortality, respectively. The optimal threshold of the IBI for predicting prognosis in patients undergoing PD was 50.0. An elevated IBI was a significant independent predictor of all-cause mortality, with a 1-SD increase associated with higher risks of all-cause and CVD mortality. Participants in the upper two quartiles of IBI exhibited increased risks of all-cause mortality by 41.2% and 67.6%, respectively, compared to those in the lowest quartile. Similar results were observed for CVD mortality. Conclusion: The IBI is a superior prognostic indicator of survival and could be broadly applied for prognosis of patients undergoing PD. Elevated IBI is an independent risk factor for all-cause and CVD mortality. [ABSTRACT FROM AUTHOR]

Aim: To assess the potential association between the TyG index and the risk of abnormal UACR. Additionally, we aimed to determine the role and degree of influence of inflammatory biomarkers between the TyG index and abnormal UACR. Materials and Methods: A cross-sectional study recruited 1021 participants from a health management center between 2021 and 2022. Logistic or linear regression models, as well as mediation analysis, were employed to investigate the associations between the TyG index, inflammatory biomarkers (total and differential white blood cell counts, platelet, mean platelet volume(MPV), C-reactive protein(CRP)), and the risk of abnormal UACR. Results: The study included 1021 participants, of whom 55.0% were men. The median age (interquartile range [IQR]) was 61.0 (53, 70) years. In multivariable-adjusted logistic regression models, both with and without the inclusion of smoking, alcohol drinking, BMI, Lipid-lowering drugs using, TC, SUA, ALT, and AST as potential covariates, the TyG index was associated with the risk of UACR, both with the odds ratios (ORs) per 1-standard deviation (SD) increase were 1.32 (95% CI, 1.08– 1.62) and 1.27 (95% CI, 1.05– 1.52), respectively. This study also demonstrated a significant indirect effect of the TyG index on the risk of abnormal UACR through total white blood cell counts, neutrophil counts and platelet (P values < 0.05); The proportions mediated was 11.2%, 3.5% and 29.6% for each respective variable. Conclusion: Insulin resistance and inflammation are associated with an increased risk of kidney insufficiency. And indicators of inflammation weakly mediate insulin resistance and risk of kidney insufficiency. [ABSTRACT FROM AUTHOR]

In recent years, probiotics, as a class of biologically active microorganisms, have increasingly attracted attention for their potential in treating neurodegenerative diseases (NDDs). To comprehensively assess the effects of probiotics on clinical symptoms and systemic inflammation regulation in various NDDs, this systematic review conducted a detailed search of the Cochrane Library, Embase, PubMed, and Web of Science databases, ultimately including 22 eligible randomized controlled trials (RCTs), with 4 RCTs for Alzheimer's Disease (AD), 10 RCTs for Parkinson's Disease (PD), 2 RCTs for Multiple Sclerosis (MS), and 2 RCTs for Mild Cognitive Impairment (MCI), and intervention durations ranging from 4 to 16 weeks. The comprehensive analysis indicates that probiotics help improve clinical symptoms related to NDDs, including gastrointestinal function, cognitive function, quality of life, and mental health. Additionally, probiotics generally have a positive effect on reducing systemic inflammation and enhancing antioxidant capacity in patients. In conclusion, existing evidence supports the promising potential of probiotics in treating NDDs. However, further large-scale, high-quality studies are needed to explore specific differences in efficacy among various probiotic strains, dosages, and modes of administration. Moreover, considering that lifestyle and dietary habits may modulate the effects of probiotics, these external factors should also be included in research considerations to gain a more comprehensive understanding of the mechanisms and application strategies of probiotics in NDDs treatment. [ABSTRACT FROM AUTHOR]

Background/Objectives: Hypertriglyceridaemia and systemic inflammation are prevalent in patients with schizophrenia and contribute to an increased risk of cardiovascular disease. Although elevated triglycerides (TGs) and remnant cholesterol are linked to inflammation in the general population and individuals with metabolic syndrome, whether they are associated in patients with schizophrenia remains unclear. Methods: Fasting levels of TG, cholesterol (total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C) and remnant cholesterol)), and markers of systemic inflammation including high-sensitivity C-reactive protein (hsCRP), leukocyte counts and their differentials (neutrophils, monocytes and lymphocytes) were determined in 147 patients diagnosed with schizophrenia on long-term antipsychotic regimens and compared with 56 age- and sex-matched healthy controls. Apolipoprotein B and glycosylation of acute phase reactant (GlycA) signatures were assessed by NMR. Circulating cytokine levels were measured by a cytokine/chemokine multiplex assay. Results: Patients with schizophrenia had markedly elevated TG and remnant cholesterol relative to controls and had evidence of systemic inflammation with increased circulating hsCRP, GlycA, leukocyte, neutrophil counts and neutrophil-to-lymphocyte ratio (NLR). Unexpectedly TG and remnant cholesterol did not correlate with systemic inflammatory markers in patients with schizophrenia, and differences in inflammatory markers between controls and patients persisted after adjusting for the lipid profile. Interleukin (IL)-10 levels were increased in patients with schizophrenia, suggesting an anti-inflammatory signature. Conclusions: The discordance between TG, remnant cholesterol and systemic inflammation in patients with schizophrenia suggests these are likely independent contributors to cardiovascular risk in this population. [ABSTRACT FROM AUTHOR]

Background: Intestinal barrier dysfunction and systemic inflammation are common in obstructive sleep apnoea (OSA). We aimed to investigate the role of melatonin, an anti-inflammatory mediator, in mediating the relationships between OSA, intestinal barrier dysfunction and systemic inflammation. Methods: Two hundred and thirty-five male participants who complained with sleep problems and underwent whole night polysomnography at our sleep centre between 2017 and 2018 were enrolled. Polysomnographic data, anthropometric measurements and biochemical indicators were collected. Serum melatonin, intestinal barrier function biomarker zonula occludens-1 (ZO-1) and inflammatory biomarkers C-reactive protein (CRP) with lipopolysaccharide (LPS) were detected. Spearman's correlation analysis assessed the correlations between sleep parameters, melatonin and biomarkers (ZO-1, LPS and CRP). Mediation analysis explored the effect of OSA on intestinal barrier dysfunction and systemic inflammation in moderate-severe OSA patients. Results: As OSA severity increased, serum melatonin decreased, whereas ZO-1, LPS and CRP increased. Spearman's correlation analysis showed that serum melatonin was significantly negatively correlated with ZO-1 (r = -0.19, p < .05) and LPS (r = -0.20, p < .05) in the moderate-OSA group; serum melatonin was significantly negatively correlated with ZO-1 (r = -0.46, p < .01), LPS (r = -0.35, p < .01) and CPR (r = -0.30, p < .05) in the severe-OSA group. Mediation analyses showed melatonin explain 36.12% and 35.38% of the effect of apnoea-hypopnea index (AHI) on ZO-1 and LPS in moderate to severe OSA patients. Conclusions: Our study revealed that melatonin may be involved in mediating intestinal barrier dysfunction and systemic inflammation in moderate-to-severe OSA patients. [ABSTRACT FROM AUTHOR]

Background/Objectives: Despite advancements in antiretroviral therapy (ART), HIV-positive individuals face heightened risks of cardiovascular and gastrointestinal (GI) complications, often linked to persistent systemic inflammation. Left ventricular diastolic dysfunction (LVDD), prevalent in HIV patients, exacerbates this inflammatory state and may contribute to worsened GI symptoms. This study aims to explore the association between LVDD, systemic inflammation, and gastrointestinal symptoms in HIV-positive patients undergoing ART. The primary objective is to analyze how LVDD contributes to the inflammatory burden and its impact on gastrointestinal health in this population. Methods: This cross-sectional study included 320 participants divided into three groups: HIV-positive with LVDD (n = 80), HIV-positive without LVDD (n = 120), and HIV-negative controls (n = 120). Levels of inflammatory biomarkers—CRP, IL-6, TNF-α, fibrinogen, IL-1β, IFN-γ, and D-dimer—were measured, and GI symptoms were assessed. Echocardiographic evaluations were performed to determine LVDD presence and severity, while multivariate logistic regression identified predictors of GI complications. Results: Patients in the HIV + LVDD group exhibited significantly elevated levels of TNF-α, CRP, and D-dimer compared to other groups, correlating with higher incidences of nausea, diarrhea, and abdominal pain. TNF-α emerged as the strongest predictor of GI symptoms, underscoring its role in the pathophysiology linking cardiovascular and GI distress in this population. Persistent inflammation and coagulation abnormalities in the ART + LVDD group suggest that ART alone may not fully mitigate these complications. Conclusions: Our findings emphasize the compounded inflammatory burden in HIV patients with LVDD, highlighting the need for integrated approaches that address both cardiovascular and GI symptoms. Anti-inflammatory therapies targeting specific biomarkers like TNF-α could improve clinical outcomes, supporting a more comprehensive strategy to managing HIV-related comorbidities beyond viral suppression. [ABSTRACT FROM AUTHOR]

With the rationale that the oxidative potential of particulate matter (PM-OP) may induce oxidative stress and inflammation, we conducted the ASTHMA-FENOP study in which 44 asthmatic patients and 37 matched controls wore a personal sampler for 24 h, allowing the collection of fine and coarse PM fractions separately, to determine PM-OP by the dithiothreitol (DTT) and ascorbic acid (AA) methods. The levels of Interleukin 6 (IL-6) and the IL-6/IL-10 ratio, as indicators of pro- and anti-inflammatory statuses, were determined by calculating the mean differences (MDs), odds ratios (ORs) and p-trends adjusted for sex, age, study level and body mass index. Positive associations for IL-6 levels in the form of adjusted MDs and ORs were obtained for all PM-OP metrics, reaching statistical significance for both OP-DTT and OP-AA in the fine fraction, with adjusted OR = 5.66; 95%CI (1.46 to 21.92) and 3.32; 95%CI (1.07 to 10.35), respectively, along with statistically significant dose–response patterns when restricting to asthma and adjusted also for clinical variables (adjusted p-trend = 0.029 and 0.01). Similar or stronger associations and dose–response patterns were found for the IL-6/IL-10 ratio. In conclusion, our findings on the effect of PM-OP on systemic inflammation support that asthma is a heterogeneous disease at the molecular level, with PM-OP potentially playing an important role. [ABSTRACT FROM AUTHOR]

ABSTRACT Periodontal diseases, particularly periodontitis, are complex inflammatory conditions caused by interactions between oral microbiota and the host immune response. Lipopolysaccharides (LPSs) from Gram‐negative bacteria like Tannerella forsythia, Treponema denticola, and Porphyromonas gingivalis are key in pathogenesis. This review examines how LPS impacts systemic health through direct invasion, compromised oral barriers, increased vascular permeability, and immune cell transport. LPS triggers inflammation in periodontal tissues, leading to tissue destruction and disease progression. In the bloodstream, LPS contributes to conditions, such as cardiovascular diseases, diabetes, respiratory diseases, and rheumatoid arthritis. Current treatments include mechanical debridement, antibiotics, antimicrobial mouthwashes, and anti‐inflammatory therapies. Despite progress, gaps remain in understanding the molecular mechanisms of LPS in systemic diseases. Future research should focus on longitudinal studies, the gut–oral axis, biomarkers for early detection, and the lymphatic system's role in LPS dissemination. Maintaining periodontal health is crucial for overall systemic well‐being. [ABSTRACT FROM AUTHOR]

Although serum uric acid (SUA) is a risk factor for cardiometabolic outcome, but it remains unclear which patients with coronary artery disease (CAD) benefit the most from SUA lowering therapy (ULT). The association of SUA level, systemic inflammation and cardiometabolic risk is still unclear. The current study is aimed to examine whether SUA-associated cardiometabolic risk is modulated by systemic inflammation in CAD patients. A total of 16,598 CAD patients with baseline high-sensitivity C-Reactive Protein (hsCRP) and SUA available were included. Baseline and follow-up data were collected. The primary endpoint was major adverse cardiovascular and cerebrovascular events (MACCE), including death, myocardial infarction and stroke. In patients with hsCRP ≥ 2 mg/L, increasing quintiles of SUA were significantly associated with increased rates of 2-year MACCE (adjusted p < 0.001 for trend, p = 0.037 for interaction). Each unit increase in SUA levels was associated with a 11.3% increased risk of MACCE (adjusted p < 0.001, p = 0.002 for interaction). However, in patients with hsCRP < 2 mg/L, increasing quintiles of SUA were not associated with increased MACCE (adjusted p = 0.120). Elevated SUA levels are related to MACCE when hsCRP levels are 2 mg/L or more but not less than 2 mg/L. This finding suggests a potential benefit of combined ULT and anti-inflammation therapy in patients with hyperuricemia and greater systemic inflammation. [ABSTRACT FROM AUTHOR]

Simple Summary: In this study we examined whether a specific blood test score, the Scottish Inflammatory Prognostic Score (SIPS), could help predict outcomes in people with advanced lung cancer receiving immunotherapy. Immunotherapy, which uses the body's immune system to fight cancer, is effective for some patients but not all. SIPS is based on two common blood measures: albumin (a protein) and neutrophils (a type of immune cell). Our findings suggest that patients with low SIPS scores, indicating lower inflammation, generally lived longer and had slower cancer progression. SIPS could become a helpful tool for doctors to decide on treatments and guide patients about their prognosis. Using SIPS alongside other health information may improve care by helping select the most suitable therapies for people with advanced lung cancer. Further studies could confirm these findings and support SIPS as a standard measure in clinical care. Background: The Scottish Inflammatory Prognostic Score (SIPS), combining albumin (≥/<35 g/L) and neutrophil count (≤/>7.5 × 109/L), has been identified as a prognostic biomarker for patients with non-small cell lung cancer (NSCLC) undergoing treatment with pembrolizumab monotherapy. We sought to validate this biomarker of systemic inflammation in an external cohort. Methods: Patients treated with first-line pembrolizumab for advanced NSCLC with programmed death-ligand 1 (PD-L1) expression ≥ 50% at an English cancer centre were identified. Pre-treatment clinicopathological characteristics and the SIPS were recorded. The relationship between these and progression-free survival (PFS) and overall survival (OS) was examined. Results: Among 257 patients evaluated, 56% (n = 144) were classified as SIPS 0, 36% (n = 93) as SIPS 1, and 8% (n = 20) as SIPS 2. Factors such as age, performance status (PS) and brain metastases presence were significantly correlated with SIPS categories. Multivariate analysis revealed that both SIPS and PD-L1 status were independently associated with PFS and OS. The combination of SIPS with either PS or PD-L1 expression enhanced the ability to detect patients with the most favourable or poorest survival. Conclusions: Our study confirms the prognostic significance of the SIPS in patients with advanced NSCLC treated with pembrolizumab in the context of high PD-L1 expression. SIPS offers a straightforward, clinically applicable approach to patient stratification, potentially guiding therapeutic decisions and enhancing outcomes in advanced NSCLC. Future research should focus on validating these findings in prospective studies and exploring the integration of SIPS into clinical practice, alongside other prognostic markers, to optimize treatment strategies. [ABSTRACT FROM AUTHOR]

The prevalence of adolescent myopia is remarkably increasing. Previous studies have indicated that an unhealthy diet is a risk factor for myopia. However, the link between diet-related inflammation and myopia is unclear. To explore their correlation, we used dietary inflammation index (DII) that is a parameter to quantify the inflammatory potential of diet, to reveal the relationship between DII and myopia in adolescents. We extracted sociodemographic data, information of diets and eye refractive status of adolescents from National Health and Nutrition Examination Survey (NHANES) for period 1999–2008. Dietary intake data was used to calculate DII scores, which were then categorized into quartiles. Multivariable regression models and subgroup analyses were conducted to investigate the association between DII and myopia. Subsequently, smoothed curve analyses were conducted to discern the trend of correlation between DII and myopia across diverse population. A total of 7191 juveniles aged at 12 to 18 years with complete information were included in our study, consisting 3367 participants with diagnosis of myopia. Among these participants, a trend towards an increasing prevalence of myopia was observed with a higher DII. After adjusting for all covariates, stratified logistic regression analyses showed that among the population aged in 16 to 18 years old or with 9-11th grade educational level, the prevalence of myopia was significantly increased with higher DII score (OR = 1.06, 95% CI = 1.01, 1.11, P = 0.006; OR = 1.06, 95% CI = 1.01, 1.11, P = 0.010). In the two subgroups, participants in the highest quartile of DII had a 31.00% higher risk of myopia and a higher 27.00% risk of myopia respectively, compared to those in the lowest quartile of DII. Our results revealed an increasing trend in the prevalence of myopia with increased DII score in adolescents. Particularly, DII was positively associated with the risk of myopia among the population aged in 16 to 18 years old and with 9-11th grade educational level. [ABSTRACT FROM AUTHOR]