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Distal sensory polyneuropathy (DSP) is a disabling, chronic condition in people with HIV (PWH), even those with viral suppression of antiretroviral therapy (ART), and with a wide range of complications, such as reduced quality of life. Previous studies demonstrated that DSP is associated with inflammatory cytokines in PWH. Adhesion molecules, essential for normal vascular function, are perturbed in HIV and other conditions linked to DSP, but the link between adhesion molecules and DSP in PWH is unknown. This study aimed to determine whether DSP signs and symptoms were associated with a panel of plasma biomarkers of inflammation (d-dimer, sTNFRII, MCP-1, IL-6, IL-8, IP-10, sCD14) and vascular I integrity (ICAM-1, VCAM-1, uPAR, MMP-2, VEGF, uPAR, TIMP-1, TIMP-2) and differed between PWH and people without HIV (PWoH). A cross-sectional study was conducted among 143 participants (69 PWH and 74 PWoH) assessed by studies at the UC San Diego HIV Neurobehavioral Research Program. DSP signs and symptoms were clinically assessed for all participants. DSP was defined as two or more DSP signs: bilateral symmetrically reduced distal vibration, sharp sensation, and ankle reflexes. Participant-reported symptoms were neuropathic pain, paresthesias, and loss of sensation. Factor analyses reduced the dimensionality of the 15 biomarkers among all participants, yielding six factors. Logistic regression was used to assess the associations between biomarkers and DSP signs and symptoms, controlling for relevant demographic and clinical covariates. The 143 participants were 48.3% PWH, 47 (32.9%) women, and 47 (33.6%) Hispanics, with a mean age of 44.3 ± 12.9 years. Among PWH, the median (IQR) nadir and current CD4+ T-cells were 300 (178-448) and 643 (502-839), respectively. Participants with DSP were older but had similar distributions of gender and ethnicity to those without DSP. Multiple logistic regression showed that Factor 2 (sTNFRII and VCAM-1) and Factor 4 (MMP-2) were independently associated with DSP signs in both PWH and PWoH (OR [95% CI]: 5.45 [1.42-21.00], and 15.16 [1.07-215.22]), respectively. These findings suggest that inflammation and vascular integrity alterations may contribute to DSP pathogenesis in PWH, but not PWoH, possibly through endothelial dysfunction and axonal degeneration.

Objective Methods Results Conclusions The aim was to investigate the mediating role of inflammatory biomarkers in the causal effect of body composition on glycaemic traits and type 2 diabetes.A retrospective observational study and a Mendelian randomization (MR) study were used. Observational analyses were performed using data from 4717 Chinese children and adolescents aged 6–18 years who underwent dual‐energy X‐ray absorptiometry for body composition. MR analyses were based on summary statistics from UK Biobank, deCODE2021, Meta‐Analysis of Glucose and Insulin‐Related Traits Consortium (MAGIC) and other large consortiums. Inflammatory biomarkers included leptin, adiponectin, osteocalcin, fibroblast growth factor 23 (FGF23) and parathyroid hormone (PTH).In a retrospective observational study, increased fat mass had a positive effect on homeostasis model assessment of insulin resistance (HOMA‐IR) and homeostasis model assessment of pancreatic beta cell function (HOMA‐β) through FGF23, whereas fat‐free mass produced the opposite effects. PTH and osteocalcin played significant roles in the association of fat mass and fat‐free mass with fasting glucose, fasting insulin and HOMA‐IR (all p < 0.05). Mediation MR results indicated that childhood body mass index affected glycaemic traits through leptin and adiponectin. There existed a causal effect of fat‐free mass on type 2 diabetes via FGF23 (indirect effect: OR [odds ratio]: 1.14 [95% CI, confidence interval: 1.01–1.28]) and adiponectin (OR: 0.85 [95% CI: 0.77–0.93]). Leptin mediated the causal association of fat mass (indirect effect: β: −0.05 [95% CI: −0.07, −0.02]) and fat‐free mass (β: 0.03 [95% CI: 0.01, 0.04]) with fasting glucose.Our findings suggest that different body compositions have differential influences on glycaemic traits and type 2 diabetes through distinct inflammatory biomarkers. The findings may be helpful in tailoring management of body composition based on inflammatory biomarkers with different glycaemic statuses. [ABSTRACT FROM AUTHOR]

The present systematic review aimed to evaluate the effect of probiotic supplementation on gut microbiota and sport performance in athletes and physically active individuals. This review followed the recommendations of the Preferred Reporting Items for Systematic Reviews and Meta-Analysis (P RISMA). The search had no time limits and included the following databases: MEDLINE, LILACS, Scopus, Web of Science, Cochrane, and SP ORT Discus. The risk of bias was assessed through the updated version of the Cochrane tool for assessing the risk of bias in randomized trials (RoB 2). Nine randomized clinical trials (RCTs) were included, accounting for 216 participants. Of these, seven studies found positive results on sport performance. Additionally, some studies showed significant decrease in biochemical parameters linked to inflammation. It was also observed direct results in the microbiota composition of the participants, such as an increase in the abundance of probiotics and a decrease in certain pathogenic bacteria. Therefore, the use of probiotics showed improvement in inflammatory biomarkers and oxidative stress, which indirectly may contribute to the improvement of sport performance. However, the majority of the studies presented a high risk of bias, which impair the reproducibility of the results. While the field of probiotic supplementation and sport performance is emerging, the promising results from this systematic review suggest that further investigation through larger and more robust randomized clinical trials can provide valuable insights for athletes and their performance. [ABSTRACT FROM AUTHOR]

Introduction: This present research was designed to investigate the antiinflammatory and immune-modulatory effects of a 50% hydroethanolic extract of "Gola" guava fruit (GF50%) and guava leaf (GL50%) against papain-induced knee osteoarthritis (KOA). Methods: Sixty Sprague-Dawley rats were divided into five groups (10 rats/group): T0 (negative control), T1 (positive control), T2 (200 mg/kg GF50%), T3 (400 mg/kg GF50%), T4 (200 mg/kg GL50%), and T5 (400 mg/kg GL50%). Physical parameters were evaluated throughout the trial, while biochemical, histopathological, and radiographic analyses were performed at 0, 15, and 30 days. The histopathological and radiographic analyses were evaluated using the Osteoarthritis Research Society International (OARSI) score and Kellgren-Lawrence (KL) classification systems, respectively. Results and discussion: The T1 group demonstrated a significant increase in knee diameter, confirming successful OA induction. The T5 group maintained a significantly lower body weight at day 30, and the T3 group exhibited the highest weight gain. The high dose of GL50% (400 mg/kg) effectively reduced knee inflammation and significantly downregulated myeloperoxidase (MPO), interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α). In contrast, it significantly (p < 0.001) upregulated the serum and knee capsule tissue superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx). In addition, histopathological and X-ray examinations also confirmed the chondroprotective potential of GL50% extract against OA. Consequently, 400 mg/kg GL50% exhibited anti-inflammatory and chondroprotective potential by lowering oxidative stress and pro-inflammatory cytokines and elevating antioxidant status. These findings could provide a theoretical basis for understanding the mechanism and potential medicinal value of guava fruit and leaf in treating KOA. [ABSTRACT FROM AUTHOR]

Introduction: Patients with the acquired immunodeficiency syndrome (AIDS) have an increased prevalence and incidence of intermediate-stage age-related macular degeneration (AMD). Several elevated plasma inflammatory biomarkers are associated with increased incidence of intermediate-stage AMD in this population. We evaluated the association between AMD risk alleles and plasma inflammatory biomarker levels in persons with AIDS. Materials and Methods: Cryopreserved plasma specimens of 229 non-Hispanic White and 252 non-Hispanic blacks from the Longitudinal Study of the Ocular Complications of AIDS cohort were assayed for plasma levels of soluble tumor necrosis factor receptor (sTNFR) 2, interleukin (IL)-18, C × 3motif chemokine ligand 1 (CX3CL1), C-reactive protein (CRP), and soluble CD14 (sCD14). Genotyping included AMD-associated variants rs10801553 and rs800292 for complement factor H (CFH) rs9332739 and rs547154 for complement factor 2 (C2), rs2230199 for C3, rs2285714 for CFI, and rs3732379 and rs3732378 for C × 3motif chemokine receptor 1 (CX3CR1). Results: In Whites, AMD low-risk CX3CR1 variants (V249I and T280M) were associated with reduced plasma levels of IL-18. In Blacks, AMD low-risk C3 R102G and low-risk CX3CR1 T280M variants were associated with reduced CRP levels. Conclusions: Genetic variants in AMD-associated immune genes may influence AMD-associated systemic plasma inflammatory biomarker levels in patients with AIDS. [ABSTRACT FROM AUTHOR]

Neurological involvement has been widely reported in SARS-CoV-2 infection. However, viral identification in the cerebrospinal fluid (CSF) is rarely found. The aim of this study is to evaluate the accuracy of virological and immunological biomarkers in CSF for the diagnosis of neuroCOVID-19. We analyzed 69 CSF samples from patients with neurological manifestations: 14 with suspected/confirmed COVID-19, with 5 additional serial CSF samples (group A), and as a control, 50 non-COVID-19 cases (group B—26 with other neuroinflammatory diseases; group C—24 with non-inflammatory diseases). Real-time reverse-transcription polymerase chain reaction (real-time RT-PCR) was used to determine SARS-CoV-2, and specific IgG, IgM, neopterin, and protein 10 induced by gamma interferon (CXCL-10) were evaluated in the CSF samples. No samples were amplified for SARS-CoV-2 by real-time RT-PCR. The sensitivity levels of anti-SARS-CoV-2 IgG and IgM were 50% and 14.28%, respectively, with 100% specificity for both tests. CXCL-10 showed high sensitivity (95.83%) and specificity (95.83%) for detection of neuroinflammation. Serial CSF analysis showed an association between the neuroinflammatory biomarkers and outcome (death and hospital discharge) in two cases (meningoencephalitis and rhombencephalitis). The detection of SARS-CoV-2 RNA and specific immunoglobulins in the CSF can be used for neuroCOVID-19 confirmation. Additionally, CXCL-10 in the CSF may contribute to the diagnosis and monitoring of neuroCOVID-19. [ABSTRACT FROM AUTHOR]

Background: Subacute thyroiditis (SAT) is characterized by profound inflammation and fluctuations in thyroid hormones which may affect the hemostasis balance. This study investigates sex-specific associations between thyroid status, inflammation and hemostasis biomarkers in SAT. Methods: We included 52 patients (40 women and 12 men) treated with non-steroidal anti-inflammatory drugs (NSAID) or methylprednisolone (MPS). Free thyroxine (fT4), thyroid stimulating hormone, C-reactive protein, complete blood count and routine hemostasis parameters were assessed. Results: Both men and women were in hyperthyroid state and had comparable levels of inflammatory biomarkers. A shortened activated partial thromboplastin time (aPTT) was observed in 16.7% of the men and 10% of the women (p = 0.562), and a shortened prothrombin time (PT) was observed in 33% of the men and 12.5% of the women (p = 0.094). In men, aPTT positively correlated with fT4 (r = 0.627; p < 0.05), while PT positively correlated with leukocyte-based inflammatory indices in women (p < 0.05). NSAID-treated patients had lower aPTTs and platelet counts than those treated with MPS (p < 0.05). Principal component analysis extracted "proinflammatory", "prothrombotic" and "antithrombotic" factors, but the "proinflammatory" factor was the independent predictor of elevated fT4 in women (OR = 2.705; p = 0.036). Conclusions: Our data demonstrated sex-specific associations of thyroid status and inflammatory biomarkers with hemostasis parameters in SAT. Routine hemostasis screening tests may help in monitoring the changes in the hemostasis system over the course of SAT. [ABSTRACT FROM AUTHOR]

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Background: Necrotizing enterocolitis (NEC) is a life-threatening disease that affects premature infants. However, the role of inflammatory biomarkers in identifying surgical/death NEC without pneumoperitoneum remains elusive. Purpose: We aimed to verify the value of platelet-to-lymphocyte ratio (PLR) and the combination of white blood cell (WBC), absolute neutrophil count (ANC), absolute lymphocyte count (ALC), neutrophil lymphocyte ratio (NLR), PLR, C reactive protein (CRP) and procalcitonin (PCT) in predicting the severity of NEC, and to construct a model to differ surgically NEC from non-surgically NEC. Methods: A retrospective analysis was performed on 191 premature infants with NEC. Based on the inclusion and exclusion criteria, 90 infants with Stage II and IIIA NEC were enrolled in this study, including surgical/death NEC (n = 38) and medical NEC (n = 52). The values of inflammatory biomarkers were collected within 24 h of onset. Results: The univariate analysis revealed that the values of WBC (p = 0.040), ANC (p = 0.048), PLR (p = 0.009), CRP (p = 0.016) and PCT (p < 0.01) in surgical/death NEC cohort were significantly higher than medical NEC cohort. Binary multivariate logistic regression analysis indicates that ANC, PLR, CRP, and PCT are capable of distinguishing infants with surgical/death NEC, and the AUC of the regression equation was 0.79 (95% CI 0.64–0.89; sensitivity 0.63; specificity 0.88), suggesting the equation has a good discrimination. Implications for practice and research: Elevated PLR is associated with severe inflammation in surgical/death NEC patients. The prediction modelling of combination of ANC, PLR, CRP and PCT can differentiate surgical/death NEC from infants with medical NEC, which may improve risk awareness and facilitate effective communication between nurses and clinicians. However, multicentre research is needed to verify these findings for better clinical management of NEC. [ABSTRACT FROM AUTHOR]

Background: CD19-targeted chimeric antigen receptor T (CAR-T) cell therapy stands out as a revolutionary intervention, exhibiting remarkable remission rates in patients with refractory/relapsed (R/R) B-cell malignancies. However, the potential side effects of therapy, particularly cytokine release syndrome (CRS) and infections, pose significant challenges due to their overlapping clinical features. Promptly distinguishing between CRS and infection post CD19 target CAR-T cell infusion (CTI) remains a clinical dilemma. Our study aimed to analyze the incidence of infections and identify key indicators for early infection detection in febrile patients within 30 days post-CTI for B-cell malignancies. Methods: In this retrospective cohort study, a cohort of 104 consecutive patients with R/R B-cell malignancies who underwent CAR-T therapy was reviewed. Clinical data including age, gender, CRS, ICANS, treatment history, infection incidence, and treatment responses were collected. Serum biomarkers procalcitonin (PCT), interleukin-6 (IL-6), and C-reactive protein (CRP) levels were analyzed using chemiluminescent assays. Statistical analyses employed Pearson's Chi-square test, t-test, Mann–Whitney U-test, Kaplan–Meier survival analysis, Cox proportional hazards regression model, Spearman rank correlation, and receiver operating characteristic (ROC) curve analysis to evaluate diagnostic accuracy and develop predictive models through multivariate logistic regression. Results: In this study, 38 patients (36.5%) experienced infections (30 bacterial, 5 fungal, and 3 viral) within the first 30 days of CAR T-cell infusion. In general, bacterial, fungal, and viral infections were detected at a median of 7, 8, and 9 days, respectively, after CAR T-cell infusion. Prior allogeneic hematopoietic cell transplantation (HCT) was an independent risk factor for infection (Hazard Ratio [HR]: 4.432 [1.262–15.565], P = 0.020). Furthermore, CRS was an independent risk factor for both infection ((HR: 2.903 [1.577–5.345], P < 0.001) and severe infection (9.040 [2.256–36.232], P < 0.001). Serum PCT, IL-6, and CRP were valuable in early infection prediction post-CAR-T therapy, particularly PCT with the highest area under the ROC curve (AUC) of 0.897. A diagnostic model incorporating PCT and CRP demonstrated an AUC of 0.903 with sensitivity and specificity above 83%. For severe infections, a model including CRS severity and PCT showed an exceptional AUC of 0.991 with perfect sensitivity and high specificity. Based on the aforementioned analysis, we proposed a workflow for the rapid identification of early infection during CAR-T cell therapy. Conclusions: CRS and prior allogeneic HCT are independent infection risk factors post-CTI in febrile B-cell malignancy patients. Our identification of novel models using PCT and CRP for predicting infection, and PCT and CRS for predicting severe infection, offers potential to guide therapeutic decisions and enhance the efficacy of CAR-T cell therapy in the future. [ABSTRACT FROM AUTHOR]

Background: Implant dentistry has become increasingly prevalent, with complications such as peri-implantitis posing challenges. Tumor necrosis factor-alpha (TNF-α) has been implicated in the inflammatory response around dental implants, akin to its role in periodontal diseases. Evaluating TNF-α levels in peri-implant tissues compared to healthy tooth tissues could provide insights into the inflammatory environment and aid in clinical management. Materials and Methods: A cross-sectional study was conducted involving 50 participants with dental implants and healthy adjacent teeth. Peri-implant mucosal samples and gingival tissue around healthy teeth were collected. TNF-α levels were quantified using enzyme-linked immunosorbent assay (ELISA) kits. Statistical analysis was performed to compare TNF-α concentrations between peri-implant tissues and healthy tooth tissues. Results: The mean TNF-α level in peri-implant tissues was found to be 120 pg/mL (standard deviation ± 25 pg/mL), whereas in healthy tooth tissues, it was 60 pg/mL (standard deviation ± 15 pg/mL). Statistical analysis revealed a significant difference (p < 0.05) in TNF-α levels between peri-implant tissues and healthy tooth tissues. Conclusion: Elevated levels of TNF-α in peri-implant tissues suggest a heightened inflammatory response compared to healthy tooth tissues. This underscores the potential role of TNF-α in peri-implantitis pathogenesis and emphasizes the importance of monitoring inflammatory biomarkers for early detection and targeted intervention in implant dentistry. [ABSTRACT FROM AUTHOR]

The aim of this study was to evaluate the potential interplay between a carbohydrate diet and inflammation in atherosclerotic cardiovascular disease (ASCVD) development. ATTICA is a prospective observational study of 3042 adults free of cardiovascular disease (CVD) who were recruited in 2002 and followed for 20 years. Baseline data on carbohydrate intake and inflammatory biomarker levels were collected. Participants were stratified by carbohydrate intake (low vs. high: 190 g/day) and carbohydrate quality. At the 20-year follow-up in 2022, 1988 participants had complete data for CVD assessment. The overall quantity and quality of carbohydrate intake did not show a significant association with CVD incidence; inflammatory markers were positively correlated with an increased risk of CVD (p-values < 0.05). Chronic systemic inflammation seems to affect the CVD risk of participants who had a higher carbohydrate intake more substantially, as compared to those with low intake. Additionally, individuals with higher high carbohydrate/low fiber intake experienced a higher risk of inflammation-related CVD, compared to those with high carbohydrate/high fiber intake. The presented findings revealed that the effect of inflammation markers on the CVD risk is influenced both by the amount and quality of carbohydrate intake, irrespective of overall dietary habits and clinical and lifestyle characteristics. [ABSTRACT FROM AUTHOR]

Purpose: Inflammatory biomarkers associated with peripheral artery disease (PAD) have been examined separately; however, an algorithm that includes a panel of inflammatory proteins to inform prognosis of PAD could improve predictive accuracy. We developed predictive models for 2-year PAD-related major adverse limb events (MALE) using clinical/inflammatory biomarker data. Methods: We conducted a prognostic study using 2 phases (discovery/validation models). The discovery cohort included 100 PAD patients that were propensity-score matched to 100 non-PAD patients. The validation cohort included 365 patients with PAD and 144 patients without PAD (non-matched). Plasma concentrations of 29 inflammatory proteins were determined at recruitment and the cohorts were followed for 2 years. The outcome of interest was 2-year MALE (composite of major amputation, vascular intervention, or acute limb ischemia). A random forest model was trained with 10-fold cross-validation to predict 2-year MALE using the following input features: 1) clinical characteristics, 2) inflammatory biomarkers that were expressed differentially in PAD vs non-PAD patients, and 3) clinical characteristics and inflammatory biomarkers. Results: The model discovery cohort was well-matched on age, sex, and comorbidities. Of the 29 proteins tested, 5 were elevated in PAD vs non-PAD patients (MMP-7, MMP-10, IL-6, CCL2/MCP-1, and TFPI). For prognosis of 2-year MALE on the validation cohort, our model achieved AUROC 0.63 using clinical features alone and adding inflammatory biomarker levels improved performance to AUROC 0.84. Conclusion: Using clinical characteristics and inflammatory biomarker data, we developed an accurate predictive model for PAD prognosis. Plain Language Summary: Inflammatory biomarkers associated with peripheral artery disease (PAD) have been examined separately; however, an algorithm that includes an inflammatory protein panel to inform prognosis of PAD may improve predictive accuracy. We developed predictive models for 2-year major adverse limb events (MALE) using clinical characteristics (demographics, comorbidities, and medications) and a panel of 5 PAD-specific inflammatory biomarkers (MMP-7, MMP-10, IL-6, CCL2/MCP-1, and TFPI) that achieved excellent performance on an independent validation cohort (AUROC 0.84). The models developed through this study may support PAD risk-stratification and targeted management strategies. [ABSTRACT FROM AUTHOR]

Objectives: Coronavirus disease-2019 (COVID-19)-related severe acute respiratory distress syndrome (ARDS) differs pathophysiological from other pulmonary septic shock-related ARDS. Thus, we assessed whether all-cause in-hospital mortality differs for severe COVID-19-related and classical severe ARDS and which inflammatory biomarkers can predict mortality among these patients. Material and Methods: This single-center, retrospective, observational cohort study included pulmonary septic shock patients (n = 114) with COVID-19-related and classical severe ARDS admitted in the Intensive Care Unit. Results: Patients with a mean age of 73 (IQR 62– 82), predominantly male (63%), were divided into two groups based on outcomes: survivors (n = 50) and non-survivors (n = 64). COVID-19-related severe ARDS (n = 48) accounts for 75% of deaths. Present comorbidities like heart disease (p = 0.043), neurologic disorders (p = 0.018), and liver disease (p = 0.038) were associated with in-hospital mortality, as well. Regarding inflammatory biomarkers, the AUC/c-statistic was 0.656 (95% CI: 0.53– 0.759) for leukocytes, 0.613 (95% CI: 0.509– 0.717) C-reactive protein (CRP) and 0.651 (95% CI: 0.548– 0.753) for procalcitonin in predicting all-cause in-hospital mortality among patients with pulmonary septic shock and severe ARDS. Conclusion: Patients with pulmonary septic shock and with COVID-19-related severe ARDS had a higher incidence of in-hospital mortality than those with classical severe ARDS. The high value of leukocytes, C-reactive protein, and procalcitonin were predictive for all-cause in-hospital mortality in patients with pulmonary septic shock and ARDS. Infection with COVID-19 was an independent predictor of in-hospital mortality in the presence of ARDS. [ABSTRACT FROM AUTHOR]

The magnification of Western eating habits has contributed to a large increase in the development of several diseases and conditions, namely cardiovascular disease, obesity, dyslipidemia, and hyperglycemia. These are part of a cluster of metabolic factors involved in metabolic syndrome. However, there are new dietary patterns more focused on the consumption of plant-based foods. Thus, the aim of this review was to investigate the impact of plant-based diets on metabolic syndrome and to achieve the inflammatory mediators and the antioxidant effects involved in this potential health benefits effect. Advanced research was performed for articles published in the last 10 years, which were analyzed and selected according to the defined inclusion and exclusion criteria. Of the articles analyzed, the majority supported the positive impact of plant-based diets on metabolic syndrome. Furthermore, several studies also showed that these diets appear to have an anti-inflammatory and antioxidant role. Thus, plant-based diets appear to have health benefits, contributing to the prevention of metabolic syndrome, and improving the cardiovascular and metabolic markers’ profile, mainly when including healthy foods. The total exclusion of animal source foods (especially meat and fish) from the diet, as well as the consumption of processed and additive plant-based foods, may contribute to an increased prevalence of metabolic syndrome.

Abstract Background CD19-targeted chimeric antigen receptor T (CAR-T) cell therapy stands out as a revolutionary intervention, exhibiting remarkable remission rates in patients with refractory/relapsed (R/R) B-cell malignancies. However, the potential side effects of therapy, particularly cytokine release syndrome (CRS) and infections, pose significant challenges due to their overlapping clinical features. Promptly distinguishing between CRS and infection post CD19 target CAR-T cell infusion (CTI) remains a clinical dilemma. Our study aimed to analyze the incidence of infections and identify key indicators for early infection detection in febrile patients within 30 days post-CTI for B-cell malignancies. Methods In this retrospective cohort study, a cohort of 104 consecutive patients with R/R B-cell malignancies who underwent CAR-T therapy was reviewed. Clinical data including age, gender, CRS, ICANS, treatment history, infection incidence, and treatment responses were collected. Serum biomarkers procalcitonin (PCT), interleukin-6 (IL-6), and C-reactive protein (CRP) levels were analyzed using chemiluminescent assays. Statistical analyses employed Pearson’s Chi-square test, t-test, Mann–Whitney U-test, Kaplan–Meier survival analysis, Cox proportional hazards regression model, Spearman rank correlation, and receiver operating characteristic (ROC) curve analysis to evaluate diagnostic accuracy and develop predictive models through multivariate logistic regression. Results In this study, 38 patients (36.5%) experienced infections (30 bacterial, 5 fungal, and 3 viral) within the first 30 days of CAR T-cell infusion. In general, bacterial, fungal, and viral infections were detected at a median of 7, 8, and 9 days, respectively, after CAR T-cell infusion. Prior allogeneic hematopoietic cell transplantation (HCT) was an independent risk factor for infection (Hazard Ratio [HR]: 4.432 [1.262–15.565], P = 0.020). Furthermore, CRS was an independent risk factor for both infection ((HR: 2.903 [1.577–5.345], P

Background: The relationship between amniotic fluid inflammatory biomarkers and preterm birth in second- or third-trimester pregnancy has been a focus, and understanding the correlation between these markers and preterm birth is important for early identification and intervention in preterm birth. The aim of this study was to explore potential inflammatory biomarkers in second- or third-trimester pregnancy amniotic fluid associated with preterm birth. Methods: On November 30, 2023, we searched literature involved the influence of second- or third-trimester pregnancy amniotic fluid inflammatory biomarkers on preterm birth through PubMed, Web of Science, Embase, Scope, CNKI, WanFang, VIP and China Biomedical Databases. The search languages were Chinese and English. Included outcomes indexes were combined utility analysis via R software. Results: A total of 11 articles were included in the combined utility analysis. This combined analysis revealed significant differences in several inflammatory biomarkers in amniotic fluid between the two groups (MD = 6.87, 95%CI: 0.26 - 13.47, P < 0.01); the difference in amniotic fluid IL-6 between the two groups (MD = 5.73, 95%CI: 3.13-8.32, P < 0.01); the difference in amniotic fluid IL-10 between the two groups (MD = 0.11, 95%CI: -3.26-3.48, P < 0.01); the difference in amniotic fluid CRP between the two groups (MD = 21.34, 95%CI: 11.69-30.89, P < 0.01); the difference in amniotic fluid MCP-1 between the two groups (MD = 312.14, 95%CI: 211.34-412.97, P < 0.01); the difference in the amniotic fluid MMP-9 between the two groups (MD = 0.86, 95%CI: -0.10-1.82, P < 0.01); and the difference in TNF-α in amniotic fluid between the two groups (MD = 22.78, 95%CI: -5.05-50.61, P < 0.01). Conclusions: The inflammatory biomarkers IL-1β, IL-6, IL-10, CRP, TNFα, MCP-1 and MMP-9 in the amniotic fluid of patients in the second- or third-trimester pregnancy were all correlated with preterm birth. [ABSTRACT FROM AUTHOR]

One of the most common diseases causing the destruction of enamel and remaining tooth structure is dental caries which further leads to pulpal and periapical inflammation if not treated. As tools for revealing important factors in identifying targets disease and pathophysiology for the evolution of prevention and treatment strategies, molecular and cellular biology plays a pivotal role. Finding an accurate diagnosis that will serve as the foundation for effective treatment continues to be one of the key issues in endodontics. Inflammatory biomarkers play a diverse and broad role in endodontics, with the potential to become a key factor in determining treatment plans by assisting in diagnosis and prognosis. Inflammatory biomarkers have the potential to become a key factor in determining treatment plans by assisting in diagnosis and prognosis. Endodontists are still divided on issues such as vital pulp therapy versus traditional root canal therapy and retreatment versus periapical surgery. Furthermore, clinical challenges such as determining the appropriate tissue fluid to analyse, establishing a precise inflammatory threshold, and delivering results at the chairside must be overcome. Endodontists may soon be able to use chairside genetic tests to make more informed treatment decisions for their patients.

Coronavirus disease (COVID-19) is a viral infection caused by SARS-CoV-2 that has become a global health emergency with a negative impact on patient care. The evolution of patients with COVID-19 is unpredictable, with an unfavorable evolution in the case of patients with comorbidities. This state-of-the-art review focuses on the role of hematological inflammatory biomarkers: the neutrophil-to-lymphocyte ratio (NLR), monocyte-to-lymphocyte ratio (MLR), and platelet-to-lymphocyte ratio (PLR) in predicting major adverse cardiovascular events (MACE) and mortality in patients with COVID-19. In this review, we included 21 studies that investigated the role of biomarkers in the risk of mortality and MACE, reporting on a total of 7,588 patients. Regarding the clinical data, 57.49% of the patients presented hypertension (15 out of the 21 studies reported hypertensive patients), followed by ischemic heart disease in 33.56% of patients (13 studies) and diabetes in 30.37% of patients (17 studies). In additional, among the usual risk factors, 23.55% of patients presented obesity (7 studies) and 23.02% were active smokers (10 studies). We recorded an average cut-off value of 7.728 for NLR (range 2.6973–15.2), 0.594 for MLR (range 0.26–0.81), and 215.07 for PLR (range 177.51–266.9) for the risk of MACE and mortality. We also recorded an average area under the curve (AUC) of 0.783 for NLR, 0.744 for MLR, and 0.713 for PLR. Our findings suggest that these biomarkers exhibit prognostic value in predicting adverse outcomes, and that evaluating these biomarkers at admission could provide novel information in stratifying risk groups for improving patient management.

Abstract Background Inflammatory factors have increasingly become a more cost-effective prognostic indicator for gastric cancer (GC). The goal of this study was to develop a prognostic score system for gastric cancer patients based on inflammatory indicators. Methods Patients’ baseline characteristics and anthropometric measures were used as predictors, and independently screened by multiple machine learning(ML) algorithms. We constructed risk scores to predict overall survival in the training cohort and tested risk scores in the validation. The predictors selected by the model were used in multivariate Cox regression analysis and developed a nomogram to predict the individual survival of GC patients. Results A 13-variable adaptive boost machine (ADA) model mainly comprising tumor stage and inflammation indices was selected in a wide variety of machine learning models. The ADA model performed well in predicting survival in the validation set (AUC = 0.751; 95% CI: 0.698, 0.803). Patients in the study were split into two sets – “high-risk” and “low-risk” based on 0.42, the cut-off value of the risk score. We plotted the survival curves using Kaplan-Meier analysis. Conclusion The proposed model performed well in predicting the prognosis of GC patients and could help clinicians apply management strategies for better prognostic outcomes for patients.

Atherosclerosis is a chronic condition that is the main underlying cause of cardiovascular disease. Inflammation is one of the key factors in the pathogenesis of atherosclerosis and its complications. This review explains an up-to-date understanding of the immunological mechanisms of atherogenesis and biomarkers of inflammation, as well as available treatments for low-intensity chronic inflammation. Information is provided on the perspective directions of anti-inflammatory therapy for atherosclerosis being studied.

Abstract Diabetes mellitus is one of the most significant global burden diseases. It is well established that a chronic, systemic, low-grade inflammatory condition is strongly correlated with type 2 diabetes mellitus (T2D) and the development of target-organ damage (TOD). Sodium-glucose cotransporter inhibitors (SGLTis), novel oral drugs for the treatment of diabetes, act mainly by reducing glucose reabsorption in proximal renal tubules and/or the intestine. Several high-quality clinical trials and large observational studies have revealed that SGLTis significantly improve cardiovascular and renal outcomes in T2D patients. Increasing evidence suggests that this is closely related to their anti-inflammatory properties, which are mainly manifested by a reduction in plasma concentrations of inflammatory biomarkers. This review analyses the potential mechanisms behind the anti-inflammatory effects of SGLTis in diabetes and presents recent evidence of their therapeutic efficacy in treating diabetes and related TOD. Graphic Abstract

Abstract There is evidence that healthy diets improve the immune system and lessen the severity of infectious diseases such as COVID‐19. We have investigated whether the dietary total antioxidant capacity (TAC) and dietary approach to stop hypertension (DASH) score could be associated with the occurrence and clinical outcomes of COVID‐19. This case–control study included 120 adults who were admitted to the hospital. Dietary TAC and DASH diet scores were determined by a 138‐item semi‐quantitative food frequency questionnaire (FFQ). Inflammation‐related markers including C‐reactive protein (CRP) and transmembrane protease serine 2 (TMPRSS‐2) differential were measured. Also, using chest radiology criteria, the severity of the disease was evaluated. The mean CRP values in the lowest and highest tertiles of either dietary TAC or DASH diet scores were 9.44 ± 11.26 and 3.52 ± 4.83 mg/dL (p = .003) or 9.04 ± 11.23 and 4.40 ± 6.23 mg/dL (p = .013), respectively. Individuals with higher dietary TAC were at a lower risk of COVID‐19 (OR: 0.06, p 0.05). The study found that adherence to a diet with higher dietary TAC and DASH diet scores may be protective against COVID‐19 and improve outcomes of the disease. More research is needed to corroborate these findings.

This prospective study investigated the association between elevated neutrophil-to-monocyte ratio (NMR), lymphocyte-to-monocyte ratio (LMR), C-reactive protein (CRP), procalcitonin, and tumor necrosis factor-alpha (TNF-alpha) and the risk of developing neurological complications in mechanically ventilated neonates. The aim was to evaluate these biomarkers’ predictive value for neurological complications. Within a one-year period from January to December 2022, this research encompassed neonates born at ≥35 weeks of gestational age who required mechanical ventilation in the neonatal intensive care unit (NICU) from the first day of life. Biomarkers were measured within the first 24 h and at 72 h. Sensitivity, specificity, and area under the curve (AUC) values were calculated for each biomarker to establish the best cutoff values for predicting neurological complications. The final analysis included a total of 85 newborns, of which 26 developed neurological complications and 59 without such complications. Among the studied biomarkers, TNF-alpha at >12.8 pg/mL in the first 24 h demonstrated the highest predictive value for neurological complications, with a sensitivity of 82%, specificity of 69%, and the highest AUC (0.574, p = 0.005). At 72 h, TNF-alpha levels greater than 14.3 pg/mL showed further increased predictive accuracy (sensitivity of 87%, specificity of 72%, AUC of 0.593, p < 0.001). The NMR also emerged as a significant predictor, with a cutoff value of >5.3 yielding a sensitivity of 78% and specificity of 67% (AUC of 0.562, p = 0.029) at 24 h, and a cutoff of >6.1 showing a sensitivity of 76% and specificity of 68% (AUC of 0.567, p = 0.025) at 72 h. Conversely, CRP and procalcitonin showed limited predictive value at both time points. This study identifies TNF-alpha and NMR as robust early predictors of neurological complications in mechanically ventilated neonates, underscoring their potential utility in guiding early intervention strategies. These findings highlight the importance of incorporating specific biomarker monitoring in the clinical management of at-risk neonates to mitigate the incidence of neurological complications.

Post-stroke anxiety disorder （PSA） is a common psychiatric complication of stroke， which jeopardizes patients' recovery and their quality of life. Recent studies suggest that inflammation plays an important role in the pathogenesis of PSA. Therefore， this paper reviewed the related licture about the association between PSA and serum inflammatory biomarkers in order to provide references for the intervention of PSA. In this study， a comprehensive search was performed in China National knowledge Infrastructure （CNKI）， Wanfang Data， Web of Science and PubMed database to identify the well qualified literature focusing on the relationship between PSA occurrence and serum inflammatory biomarkers， and a total of 13 studies were retrieved. Analysis indicates a certain association between PSA occurrence and serum inflammatory biomarkers， and denotes that the elevation of inflammatory biomarkers may be a trigger for the disease occurrence and its progression， but the specific mechanism underlying this relationship requires further study.

Abstract Background Sodium-glucose cotransporter 2 (SGLT-2) inhibitors are increasingly recognized for their role in reducing the risk and improving the prognosis of heart failure (HF). However, the precise mechanisms involved remain to be fully delineated. Evidence points to their potential anti-inflammatory pathway in mitigating the risk of HF. Methods A two-sample, two-step Mendelian Randomization (MR) approach was employed to assess the correlation between SGLT-2 inhibition and HF, along with the mediating effects of inflammatory biomarkers in this relationship. MR is an analytical methodology that leverages single nucleotide polymorphisms as instrumental variables to infer potential causal inferences between exposures and outcomes within observational data frameworks. Genetic variants correlated with the expression of the SLC5A2 gene and glycated hemoglobin levels (HbA1c) were selected using datasets from the Genotype-Tissue Expression project and the eQTLGen consortium. The Genome-wide association study (GWAS) data for 92 inflammatory biomarkers were obtained from two datasets, which included 14,824 and 575,531 individuals of European ancestry, respectively. GWAS data for HF was derived from a meta-analysis that combined 26 cohorts, including 47,309 HF cases and 930,014 controls. Odds ratios (ORs) and 95% confidence interval (CI) for HF were calculated per 1 unit change of HbA1c. Results Genetically predicted SGLT-2 inhibition was associated with a reduced risk of HF (OR 0.42 [95% CI 0.30–0.59], P

Dialysis membranes are not hemocompatible with human blood, as the patients are suffering from the blood–membrane interactions' side effects. Zwitterionic structures have shown improved hemocompatibility; however, their complicated synthesis hinders their commercialization. The goal of the study is to achieve fast functionalization for carboxybetaine and sulfobetaine zwitterionic immobilization on PES membranes while comparing the stability and the targeted hemocompatibility. The chemical modification approach is based on an aminolysis reaction. Characterization, computational simulations, and clinical analysis were conducted to study the modified membranes. Atomic force microscopy (AFM) patterns showed a lower mean roughness for carboxybetaine-modified (6.3 nm) and sulfobetaine-modified (7.7 nm) membranes compared to the neat membrane (52.61 nm). The pore size of the membranes was reduced from values above 50 nm for the neat PES to values between 2 and 50 nm for zwitterionized membranes, using Brunauer–Emmett–Teller (BET) analysis. More hydrophilic surfaces led to a growth equilibrium water content (EWC) of nearly 6% for carboxybetaine and 10% for sulfobetaine-modified membranes. Differential scanning calorimetry (DSC) measurements were 12% and 16% stable water for carboxybetaine- and sulfobetaine-modified membranes, respectively. Sulfobetaine membranes showed better compatibility with blood with respect to C5a, IL-1a, and IL-6 biomarkers. Aminolysis-based zwitterionization was found to be suitable for the improvement of hemodialysis membranes. The approach introduced in this paper could be used to modify the current dialysis membranes with minimal change in the production facilities. [ABSTRACT FROM AUTHOR]

Low back disorder (LBD) is a major cause of disability worldwide. Inflammation results in proliferation of cytokines or consequent degradation products (collectively known as inflammatory biomarkers) that activate pain pathways which can result in non-specific LBD. This systematic review and meta-analysis aim to evaluate the relationship between inflammatory biomarkers and clinical outcomes in patients with LBD. The PRISMA guideline was followed for the systematic reivew. Three online databases were searched. Four RCTs and sixteen observational studies with 1142 LBD patients were analysed. The primary outcomes were back and leg pain scores, back-specific disability scores and expression of inflammatory biomarkers. Standardized mean difference (SMD) and their 95% confidence intervals (CI) were evaluated. The Grading of Recommendations Assessment, Development, and Evaluation (GRADE) approach was used to summarize the strength of evidence. Four RCTs and sixteen observational studies were included in the analysis of 1142 patients with LBD. There was a statistically significant reduction in back pain score and IL-1 beta and increase in the expression of CTX-1 and IL-10 levels post treatment. There was a significant relationship between increase in the expression of MCP- and reduction in the expression of hsCRP with increase in back pain. Significant relationship was also observed between increase in the expression of MCP-1 and reduction in the expression of IL-6 with increase in leg pain. Increase in the expression of IL-8 and reduction in the expression of hsCRP was also associated with increased disability score. Inflammatory biomarkers play a significant role in the pathogenesis of LBD. CTX-1, IL-10 and IL-1 beta may be responsible for the decrease in back pain scores post treatment. There is a relationship between MCP-1, IL-6, IL-8 and hsCRP with clinical and functional assessments for LBD. Further studies will improve understanding of the pathogenesis of LBD and aid in targeted management strategies. [ABSTRACT FROM AUTHOR]

This prospective study investigated the association between elevated neutrophil-to-monocyte ratio (NMR), lymphocyte-to-monocyte ratio (LMR), C-reactive protein (CRP), procalcitonin, and tumor necrosis factor-alpha (TNF-alpha) and the risk of developing neurological complications in mechanically ventilated neonates. The aim was to evaluate these biomarkers' predictive value for neurological complications. Within a one-year period from January to December 2022, this research encompassed neonates born at ≥35 weeks of gestational age who required mechanical ventilation in the neonatal intensive care unit (NICU) from the first day of life. Biomarkers were measured within the first 24 h and at 72 h. Sensitivity, specificity, and area under the curve (AUC) values were calculated for each biomarker to establish the best cutoff values for predicting neurological complications. The final analysis included a total of 85 newborns, of which 26 developed neurological complications and 59 without such complications. Among the studied biomarkers, TNF-alpha at >12.8 pg/mL in the first 24 h demonstrated the highest predictive value for neurological complications, with a sensitivity of 82%, specificity of 69%, and the highest AUC (0.574, p = 0.005). At 72 h, TNF-alpha levels greater than 14.3 pg/mL showed further increased predictive accuracy (sensitivity of 87%, specificity of 72%, AUC of 0.593, p < 0.001). The NMR also emerged as a significant predictor, with a cutoff value of >5.3 yielding a sensitivity of 78% and specificity of 67% (AUC of 0.562, p = 0.029) at 24 h, and a cutoff of >6.1 showing a sensitivity of 76% and specificity of 68% (AUC of 0.567, p = 0.025) at 72 h. Conversely, CRP and procalcitonin showed limited predictive value at both time points. This study identifies TNF-alpha and NMR as robust early predictors of neurological complications in mechanically ventilated neonates, underscoring their potential utility in guiding early intervention strategies. These findings highlight the importance of incorporating specific biomarker monitoring in the clinical management of at-risk neonates to mitigate the incidence of neurological complications. [ABSTRACT FROM AUTHOR]

Bariatric surgery is an effective treatment for severe obesity, but complications and peri-operative monitoring are important considerations. We conducted a comprehensive review of studies assessing pre-operative biomarkers and complications in patients undergoing bariatric surgery. A total of 14 studies were included. Gastric leak, infections, bleeding, obstruction or stenosis, hypoglycemia, and hypoalbuminemia were the most common complications observed. Our analysis showed a significant association between lower pre-operative albumin levels and complications (SMD [95%CI] = − 0.21 [− 0.38; − 0.04]). However, other biomarkers did not have a significant impact on complication occurrence. Changes in C-reactive protein, neutrophil–lymphocyte ratio, and white blood cell levels were observed in certain peri-operative time points and complication subgroups. These findings suggest the potential use of pre-operative biomarkers and peri-operative changes of biomarker's levels for predicting complications. [ABSTRACT FROM AUTHOR]

We aimed to study the impact of polymorphisms in the genes encoding interleukin-6 (IL6) and tumor necrosis factor receptor-2 (TNFR2), reported to be mortality risk predictors, in patients with end-stage kidney disease (ESKD) undergoing dialysis. TNFRSF1B (rs3397, rs1061624, and rs1061622) and IL6 (rs1800796, rs1800797, and rs1554606) polymorphisms were studied in patients with ESKD and controls; the genotype and allele frequencies and the associations with inflammatory and erythropoiesis markers were determined; deaths were recorded throughout the following two years. The genotype and allele frequencies for the TNFRSF1B rs3397 polymorphism were different in these patients compared to those in the controls and the global and European populations, and patients with the C allele were less common. Patients with the CC genotype for TNFRSF1B rs3397 presented higher hemoglobin and erythrocyte counts and lower TNF-α levels, suggesting a more favorable inflammatory response that seems to be associated with erythropoiesis improvement. Patients with the GG genotype for TNFRSF1B rs1061622 showed lower serum ferritin levels. None of the TNFRSF1B (rs3397, rs1061624, and rs1061622) or IL6 (rs1800796, rs1800797, and rs1554606) polymorphisms had a significant impact on the all-cause mortality rate of Portuguese patients with ESKD. [ABSTRACT FROM AUTHOR]

Diabetes mellitus is one of the most significant global burden diseases. It is well established that a chronic, systemic, low-grade inflammatory condition is strongly correlated with type 2 diabetes mellitus (T2D) and the development of target-organ damage (TOD). Sodium-glucose cotransporter inhibitors (SGLTis), novel oral drugs for the treatment of diabetes, act mainly by reducing glucose reabsorption in proximal renal tubules and/or the intestine. Several high-quality clinical trials and large observational studies have revealed that SGLTis significantly improve cardiovascular and renal outcomes in T2D patients. Increasing evidence suggests that this is closely related to their anti-inflammatory properties, which are mainly manifested by a reduction in plasma concentrations of inflammatory biomarkers. This review analyses the potential mechanisms behind the anti-inflammatory effects of SGLTis in diabetes and presents recent evidence of their therapeutic efficacy in treating diabetes and related TOD. [ABSTRACT FROM AUTHOR]

There is evidence that healthy diets improve the immune system and lessen the severity of infectious diseases such as COVID‐19. We have investigated whether the dietary total antioxidant capacity (TAC) and dietary approach to stop hypertension (DASH) score could be associated with the occurrence and clinical outcomes of COVID‐19. This case–control study included 120 adults who were admitted to the hospital. Dietary TAC and DASH diet scores were determined by a 138‐item semi‐quantitative food frequency questionnaire (FFQ). Inflammation‐related markers including C‐reactive protein (CRP) and transmembrane protease serine 2 (TMPRSS‐2) differential were measured. Also, using chest radiology criteria, the severity of the disease was evaluated. The mean CRP values in the lowest and highest tertiles of either dietary TAC or DASH diet scores were 9.44 ± 11.26 and 3.52 ± 4.83 mg/dL (p =.003) or 9.04 ± 11.23 and 4.40 ± 6.23 mg/dL (p =.013), respectively. Individuals with higher dietary TAC were at a lower risk of COVID‐19 (OR: 0.06, p < ·0001). Individuals with greater DASH diet scores were also at decreased odds of COVID‐19 (OR: 0.12, p < ·0001). No significant associations were found between dietary TAC and DASH diet scores with severity of COVID‐19 disease, CRP, or TMPRSS‐2 (p > 0.05). The study found that adherence to a diet with higher dietary TAC and DASH diet scores may be protective against COVID‐19 and improve outcomes of the disease. More research is needed to corroborate these findings. [ABSTRACT FROM AUTHOR]

Aims: The molecular mechanism of short‐sleep conditions on cognition remains largely unknown. This research aimed to investigate associations between short sleep, inflammatory biomarkers and cognitive function in the US population (NHANES data 2011–2014) and explore cellular mechanisms in mice. Methods: Systemic immune‐inflammation index (SII) was calculated using blood‐cell based biomarkers. Further, we employed integrated bioinformatics and single‐cell transcriptomics (GSE137665) to examine how short sleep exposure influenced the molecular pathways associated with inflammation in the brain. To explore the signaling pathways and biological processes of sleep deprivation, we carried out enrichment analyses utilizing the GO and KEGG databases. Results: Population results showed that, compared with normal sleep group, severe short sleep was associated with lower cognitive ability in all the four tests. Moreover, a higher SII level was correlated with lower scores of cognitive tests. In mice study, elevated activation of the inflammatory pathway was observed in cell subgroups of neurons within the sleep deprivation and recovery sleep cohorts. Additionally, heightened expression of oxidative stress and integrated stress response pathways was noted in GABAergic neurons during sleep deprivation. Conclusion: This study contributed to the understanding of the influence of short sleep on cognitive function and its cellular mechanisms. [ABSTRACT FROM AUTHOR]

Objective: To construct and validate radiomics models for hepatocellular carcinoma (HCC) grade predictions based on contrast-enhanced CT (CECT). Methods: Patients with pathologically confirmed HCC after surgery and underwent CECT at our institution between January 2016 and December 2020 were enrolled and randomly divided into training and validation datasets. With tumor segmentation and feature extraction, radiomic models were constructed using univariate analysis, followed by least absolute shrinkage and selection operator (LASSO) regression. In addition, combined models with clinical factors and radiomics scores (Radscore) were constructed using logistic regression. Finally, all models were evaluated using the receiver operating characteristic (ROC) curve with the area under the curve (AUC), calibration curve, and decision curve analysis (DCA). Results: In total 242 patients were enrolled in this study, of whom 170 and 72 formed the training and validation datasets, respectively. The arterial phase and portal venous phase (AP+VP) radiomics model were evaluated as the best for predicting HCC pathological grade among all the models built in our study (AUC = 0.981 in the training dataset; AUC = 0.842 in the validation dataset) andwas used to build a nomogram. Furthermore, the calibration curve and DCA indicated that the AP+VP radiomics model had a satisfactory prediction efficiency. Conclusions: Low- and high-grade HCC can be distinguished with good diagnostic performance using a CECT-based radiomics model. [ABSTRACT FROM AUTHOR]

Background: Sodium-glucose cotransporter 2 (SGLT-2) inhibitors are increasingly recognized for their role in reducing the risk and improving the prognosis of heart failure (HF). However, the precise mechanisms involved remain to be fully delineated. Evidence points to their potential anti-inflammatory pathway in mitigating the risk of HF. Methods: A two-sample, two-step Mendelian Randomization (MR) approach was employed to assess the correlation between SGLT-2 inhibition and HF, along with the mediating effects of inflammatory biomarkers in this relationship. MR is an analytical methodology that leverages single nucleotide polymorphisms as instrumental variables to infer potential causal inferences between exposures and outcomes within observational data frameworks. Genetic variants correlated with the expression of the SLC5A2 gene and glycated hemoglobin levels (HbA1c) were selected using datasets from the Genotype-Tissue Expression project and the eQTLGen consortium. The Genome-wide association study (GWAS) data for 92 inflammatory biomarkers were obtained from two datasets, which included 14,824 and 575,531 individuals of European ancestry, respectively. GWAS data for HF was derived from a meta-analysis that combined 26 cohorts, including 47,309 HF cases and 930,014 controls. Odds ratios (ORs) and 95% confidence interval (CI) for HF were calculated per 1 unit change of HbA1c. Results: Genetically predicted SGLT-2 inhibition was associated with a reduced risk of HF (OR 0.42 [95% CI 0.30–0.59], P < 0.0001). Of the 92 inflammatory biomarkers studied, two inflammatory biomarkers (C-X-C motif chemokine ligand 10 [CXCL10] and leukemia inhibitory factor) were associated with both SGLT-2 inhibition and HF. Multivariable MR analysis revealed that CXCL10 was the primary inflammatory cytokine related to HF (MIP = 0.861, MACE = 0.224, FDR-adjusted P = 0.0844). The effect of SGLT-2 inhibition on HF was mediated by CXCL10 by 17.85% of the total effect (95% CI [3.03%–32.68%], P = 0.0183). Conclusions: This study provides genetic evidence supporting the anti-inflammatory effects of SGLT-2 inhibitors and their beneficial impact in reducing the risk of HF. CXCL10 emerged as a potential mediator, offering a novel intervention pathway for HF treatment. [ABSTRACT FROM AUTHOR]

Background: Approximately one in four stroke patients suffer from recurrent vascular events, underlying the necessity to improve secondary stroke prevention strategies. Immune mechanisms are causally associated with coronary atherosclerosis. However, stroke is a heterogeneous disease and the relative contribution of inflammation across stroke mechanisms is not well understood. The optimal design of future randomized control trials (RCTs) of anti-inflammatory therapies to prevent recurrence after stroke must be informed by a clear understanding of the prognostic role of inflammation according to stroke subtype and individual patient factors. Aim: In this narrative review, we discuss (1) inflammatory pathways in the etiology of ischemic stroke subtypes; (2) the evidence on inflammatory markers and vascular recurrence after stroke; and (3) review RCT evidence of anti-inflammatory agents for vascular prevention. Summary of review: Experimental work, genetic epidemiological data, and plaque-imaging studies all implicate inflammation in atherosclerotic stroke. However, emerging evidence also suggests that inflammatory mechanisms are also important in other stroke mechanisms. Advanced neuroimaging techniques support the role of neuroinflammation in blood–brain barrier dysfunction in cerebral small vessel disease (cSVD). Systemic inflammatory processes also promote atrial cardiopathy, incident and recurrent atrial fibrillation (AF). Although several inflammatory markers have been associated with recurrence after stroke, interleukin-6 (IL-6) and high-sensitivity C-reactive protein (hsCRP) are presently the most promising markers to identify patients at increased vascular risk. Several RCTs have shown that anti-inflammatory therapies reduce vascular risk, including stroke, in coronary artery disease (CAD). Some, but not all of these trials, selected patients on the basis of elevated hsCRP. Although unproven after stroke, targeting inflammation to reduce recurrence is a compelling strategy and several RCTs are ongoing. Conclusion: Evidence points toward the importance of inflammation across multiple stroke etiologies and potential benefit of anti-inflammatory targets in secondary stroke prevention. Taking the heterogeneous stroke etiologies into account, the use of serum biomarkers could be useful to identify patients with residual inflammatory risk and perform biomarker-led patient selection for future RCTs. [ABSTRACT FROM AUTHOR]

Introduction. Hematologic biomarkers of inflammation may serve as valuable adjuncts in clinical practice, aiding in several aspects such as differential diagnosis, prognostic assessment for patient stratification and monitoring the efficacy of antimicrobial therapy. The aim of this study was to evaluate the efficacy of Neutrophil to Lymphocyte Ratio (NLR), Platelet to Lymphocyte Ratio (PLR), Lymphocyte to Monocyte Ratio (LMR), and Systemic Inflammatory Index (SII) in predicting bacterial sexually transmitted infections (STI). Methods. This prospective study was conducted in the north-west region of Romania and included patients from several medical special units such as dermatology, obstetrics-gynecology, urology, and general practice. The study group comprised patients with a high suspicion of STI, while the control group consisted of healthy subjects. Quantitative data are presented as medians (interquartile ranges). Results. The median values of SII, NLR, and SIRI were higher in the group of subjects with sexually transmitted diseases compared to the control group [604.06 (432.36 - 880.02) vs. 556.89 (388.63 - 874.19); 2.61 (1.57 - 3.3) vs. 2.29 (1.66 - 3.26); and 0.95 (0.53 - 1.52) vs. 0.89 (0.67 - 1.34)]. Regarding PLR, the median values were lower in the group of subjects with sexually transmitted diseases compared to the control group [138.1 (99.19 - 169.6) vs. 140.65 (117 - 190.32)]. As for LMR, the median values were equal between the two groups [4.64 (3.74 - 6.11) vs. 4.64 (3.75 - 5.45)]. Nevertheless, the differences did not reach the significance level. Conclusion. Our study suggests that inflammatory biomarkers might aid in detecting bacterial STIs, but their significance was not statistically confirmed. Further research on alternative laboratory tests is needed for improved STI diagnosis and management. [ABSTRACT FROM AUTHOR]

Simple Summary: The vaginal microbiome may play a role in racial disparities in ovarian cancer; there is evidence suggesting that it differs according to race and contributes to inflammation by producing or consuming compounds that can shape how ovarian cancer progresses. Our cross-sectional study aimed to investigate the extent to which chemical compounds, or metabolites, from vaginal fluid, also differ by race, and whether these metabolites are linked to systemic inflammation. Our study of 20 White and 16 Black patients identified 1 out of 99 metabolites, arachidonoylcarnitine (C20:4), as occurring at lower levels in Black and higher levels in White patients with ovarian cancer. More than one-third of vaginal fluid metabolites considered showed correlations with biomarkers of systemic inflammation. Our findings suggest that vaginal fluid metabolites likely differ by race, and may play an important role in inflammatory processes, which may be relevant to racial differences in ovarian cancer outcomes. These pilot findings have the potential to improve our understanding of biological mechanisms underlying racial disparities in ovarian cancer but need verification with larger sample sizes. The vaginal microbiome differs by race and contributes to inflammation by directly producing or consuming metabolites or by indirectly inducing host immune response, but its potential contributions to ovarian cancer (OC) disparities remain unclear. In this exploratory cross-sectional study, we examine whether vaginal fluid metabolites differ by race among patients with OC, if they are associated with systemic inflammation, and if such associations differ by race. Study participants were recruited from the Ovarian Cancer Epidemiology, Healthcare Access, and Disparities Study between March 2021 and September 2022. Our study included 36 study participants with ovarian cancer who provided biospecimens; 20 randomly selected White patients and all 16 eligible Black patients, aged 50–70 years. Acylcarnitines (n = 45 species), sphingomyelins (n = 34), and ceramides (n = 21) were assayed on cervicovaginal fluid, while four cytokines (IL-1β, IL-10, TNF-α, and IL-6) were assayed on saliva. Seven metabolites showed >2-fold differences, two showed significant differences using the Wilcoxon rank-sum test (p < 0.05; False Discovery Rate > 0.05), and 30 metabolites had coefficients > ±0.1 in a Penalized Discriminant Analysis that achieved two distinct clusters by race. Arachidonoylcarnitine, the carnitine adduct of arachidonic acid, appeared to be consistently different by race. Thirty-eight vaginal fluid metabolites were significantly correlated with systemic inflammation biomarkers, irrespective of race. These findings suggest that vaginal fluid metabolites may differ by race, are linked with systemic inflammation, and hint at a potential role for mitochondrial dysfunction and sphingolipid metabolism in OC disparities. Larger studies are needed to verify these findings and further establish specific biological mechanisms that may link the vaginal microbiome with OC racial disparities. [ABSTRACT FROM AUTHOR]

Introduction: The majority of dialysis patients have chronic low-grade inflammation linked to protein energy waste, early CVD, osteoporosis, and overall weakness. To minimize the risk of infections and complications, guidelines advocate for the use of arteriovenous fistulas (AVFs) whenever possible, as central venous catheters (CVCs) pose a greater risk for these issues. Objective: This study aimed to assess the impact of various hemodialysis vascular access types on the occurrence and characteristics of infections experienced by hemodialysis patients. Patients and Methods: This prospective cohort study was conducted in Ain Shams University Hospitals, Hemodialysis Units over 6 months duration. Results: We found that the average age of the patients was 49.5 ± 8.4 years and the average duration of hemodialysis (HD) was 3.2 ± 1.9 years. The proportion of males and females was nearly equal (46.0% and 54.0% respectively). Patients from El-Demerdash and ASHUSH accounted for 60.3% and 39.7% of the cases, respectively. Catheter types included temporary catheters (49.2%), AVFs (31.7%), and AVGs (19.0%). We noticed that less than one-fifth of cases had leucocytosis and elevated procalcitonin in months 2 and 3. Leucocytosis and elevated procalcitonin in months 2 and 3 were most frequent in temporary catheters, followed by AVGs, and least frequent in AVFs. Conclusion: The use of temporary catheters was linked to a higher incidence of infections. Infection episodes were accompanied by elevated inflammatory markers, a higher likelihood of catheter removal, an increased risk of thrombosis, and more frequent hospital admissions. [ABSTRACT FROM AUTHOR]

Background: The primary objective of this research is to devise a model to predict the pathologic complete response in esophageal squamous cell carcinoma (ESCC) patients undergoing neoadjuvant immunotherapy combined with chemoradiotherapy (nICRT). Methods: We retrospectively analyzed data from 60 ESCC patients who received nICRT between 2019 and 2023. These patients were divided into two cohorts: pCR-group (N = 28) and non-pCR group (N = 32). Radiomic features, discerned from the primary tumor region across plain, arterial, and venous phases of CT, and pertinent laboratory data were documented at two intervals: pre-treatment and preoperation. Concurrently, related clinical data was amassed. Feature selection was facilitated using the Extreme Gradient Boosting (XGBoost) algorithm, with model validation conducted via fivefold cross-validation. The model's discriminating capability was evaluated using the area under the receiver operating characteristic curve (AUC). Additionally, the clinical applicability of the clinical-radiomic model was appraised through decision curve analysis (DCA). Results: The clinical-radiomic model incorporated seven significant markers: postHALP, DHB, post-ALB, firstorder_Skewness, GLCM_DifferenceAverage, GLCM_JointEntropy, GLDM_DependenceEntropy, and NGTDM_Complexity, to predict pCR. The XGBoost algorithm rendered an accuracy of 0.87 and an AUC of 0.84. Notably, the joint omics approach superseded the performance of solely radiomic or clinical model. The DCA further cemented the robust clinical utility of our clinical-radiomic model. Conclusion: This study successfully formulated and validated a union omics methodology for anticipating the therapeutic outcomes of nICRT followed by radical surgical resection. Such insights are invaluable for clinicians in identifying potential nICRT responders among ESCC patients and tailoring optimal individualized treatment plans. [ABSTRACT FROM AUTHOR]

(1) Background: The advantage of using carbapenems over beta-lactam/beta-lactamase inhibitor combinations in critically ill septic patients still remains a debated issue. We aimed to assess the comparative impact of an optimized pharmacokinetic/pharmacodynamic (PK/PD) target attainment of piperacillin-tazobactam vs. meropenem on the trend over time of both Sequential Organ Failure Assessment (SOFA) score and inflammatory biomarkers in critically ill patients receiving continuous infusion (CI) monotherapy with piperacillin-tazobactam or meropenem for treating documented Gram-negative bloodstream infections (BSI) and/or ventilator-associated pneumonia (VAP). (2) Methods: We performed a retrospective observational study comparing critically ill patients receiving targeted treatment with CI meropenem monotherapy for documented Gram-negative BSIs or VAP with a historical cohort of critical patients receiving CI piperacillin-tazobactam monotherapy. Patients included in the two groups were admitted to the general and post-transplant intensive care unit in the period July 2021–September 2023 and fulfilled the same inclusion criteria. The delta values of the SOFA score between the baseline of meropenem or piperacillin-tazobactam treatment and those at 48-h (delta 48-h SOFA score) or at 7-days (delta 7-days SOFA) were selected as primary outcomes. Delta 48-h and 7-days C-reactive protein (CRP) and procalcitonin (PCT), microbiological eradication, resistance occurrence, clinical cure, multi-drug resistant colonization at 90-day, ICU, and 30-day mortality rate were selected as secondary outcomes. Univariate analysis comparing primary and secondary outcomes between critically ill patients receiving CI monotherapy with piperacillin-tazobactam vs. meropenem was carried out. (3) Results: Overall, 32 critically ill patients receiving CI meropenem monotherapy were compared with a historical cohort of 43 cases receiving CI piperacillin-tazobactam monotherapy. No significant differences in terms of demographics and clinical features emerged at baseline between the two groups. Optimal PK/PD target was attained in 83.7% and 100.0% of patients receiving piperacillin-tazobactam and meropenem, respectively. No significant differences were observed between groups in terms of median values of delta 48-h SOFA (0 points vs. 1 point; p = 0.89) and median delta 7-days SOFA (2 points vs. 1 point; p = 0.43). Similarly, no significant differences were found between patients receiving piperacillin-tazobactam vs. meropenem for any of the secondary outcomes. (4) Conclusion: Our findings may support the contention that in critically ill patients with documented Gram-negative BSIs and/or VAP, the decreases in the SOFA score and in the inflammatory biomarkers serum levels achievable with CI piperacillin-tazobactam monotherapy at 48-h and at 7-days may be of similar extent and as effective as to those achievable with CI meropenem monotherapy provided that optimization on real-time by means of a TDM-based expert clinical pharmacological advice program is granted. [ABSTRACT FROM AUTHOR]

A randomized, double-blind, and placebo-controlled study was conducted to assess the effect of dietary supplementation with high-rich docosahexaenoic acid (DHA) (Tridocosahexanoin-AOX® 70%) at 50 mg/kg/day in pediatric patients with cystic fibrosis (CF) as compared with placebo. The duration of supplementation was 12 months. A total of 22 patients were included, with 11 in the DHA group and 11 in the placebo group. The mean age was 11.7 years. The outcome variables were pulmonary function, exacerbations, sputum cellularity, inflammatory biomarkers in sputum and peripheral blood, and anthropometric variables. In the DHA group, there was a significant increase in FVC (p = 0.004) and FVE1 expressed in liters (p = 0.044) as compared with placebo, and a lower median number of exacerbations (1 vs. 2). Differences in sputum cellularity (predominantly neutrophilic), neutrophilic elastase, and sputum and serum concentrations of resolvin D1 (RvD1), interleukin (IL)-8 (IL-8), and tumor necrosis factor alpha (TNF-α) between the study groups were not found. Significant increases in weight and height were also observed among DHA-supplemented patients. The administration of the study product was safe and well tolerated. In summary, the use of a highly concentrated DHA supplement for 1 year as compared with placebo improved pulmonary function and reduced exacerbations in pediatric CF. [ABSTRACT FROM AUTHOR]

The purpose of this study was to compare the inflammatory biomarkers in postmenopausal women with osteoporosis and those with normal bone mineral density (BMD).A total of 850 postmenopausal women aged 50 to 65 were randomly selected for participation in this cross-sectional investigation. 100 women displayed normal BMD, while 101 were diagnosed with osteoporosis, as determined by dual-energy X-ray absorptiometry. Biochemical techniques were used to quantify tumor necrosis factor α (TNF-α) levels, high-sensitivity C-reactive protein (hs-CRP), and interleukin-6. The area under the curve (AUC) for the diagnosis of osteoporosis was calculated using receiver-operator characteristic (ROC) curves.A significant difference was observed between the two groups in terms of age, menopause age, education level, and BMI (p

Background: Atopic dermatitis (AD) is a chronic inflammatory skin disease resulting from the complex interplay of genetic and environmental factors, meriting exploration using temporally dynamic biomarkers. DNA methylation–based algorithms have been trained to accurately estimate biological age, and deviation of predicted age from true age (epigenetic age acceleration) has been implicated in several inflammatory diseases, including asthma. Objective: We sought to determine the role of epigenetic and biological aging, telomere length, and epigenetically inferred abundance of 7 inflammatory biomarkers in AD. Methods: We performed DNA methylation–based analyses in a pediatric AD cohort (n = 24, mean ± standard deviation [SD] age 2.56 ± 0.28 years) and age-matched healthy subjects (n = 24, age 2.09 [0.15] years) derived from blood using 5 validated algorithms that assess epigenetic age (Horvath, Skin&Blood) and biological age (PhenoAge, GrimAge), telomere length (TelomereLength), and inflammatory biomarker levels. Results: Epigenetic and biological age, but not telomere length, were accelerated in AD patients for 4 algorithms: Horvath (+0.88 years; 95% confidence interval [CI], 0.33 to 1.4; P = 2.3 × 10−3), Skin&Blood (+0.95 years; 95% CI, 0.67 to 1.2; P = 1.8 × 10−8), PhenoAge (+8.2 years; 95% CI, 3.4 to 13.0; P = 1.3 × 10−3), and GrimAge (+1.8 years 95% CI, 0.22 to 3.3; P = .026). Moreover, patients had increased levels of β2 microglobulin (+47,584.4 ng/mL; P = .029), plasminogen activation inhibitor 1 (+3,432.9 ng/mL; P = 1.1 × 10−5), and cystatin C (+31,691 ng/mL; P = 4.0 × 10−5), while levels of tissue inhibitor metalloproteinase 1 (−370.7 ng/mL; P = 7.5 × 10−4) were decreased compared to healthy subjects. Conclusion: DNA methylation changes associated with epigenetic and biological aging, and inflammatory proteins appear early in life in pediatric AD and may be relevant clinical biomarkers of pathophysiology.

IntroductionThis present research was designed to investigate the anti-inflammatory and immune-modulatory effects of a 50% hydroethanolic extract of “Gola” guava fruit (GF50%) and guava leaf (GL50%) against papain-induced knee osteoarthritis (KOA).MethodsSixty Sprague–Dawley rats were divided into five groups (10 rats/ group): T0 (negative control), T1 (positive control), T2 (200 mg/kg GF50%), T3 (400 mg/kg GF50%), T4 (200 mg/kg GL50%), and T5 (400 mg/kg GL50%). Physical parameters were evaluated throughout the trial, while biochemical, histopathological, and radiographic analyses were performed at 0, 15, and 30 days. The histopathological and radiographic analyses were evaluated using the Osteoarthritis Research Society International (OARSI) score and Kellgren–Lawrence (KL) classification systems, respectively.Results and discussionThe T1 group demonstrated a significant increase in knee diameter, confirming successful OA induction. The T5 group maintained a significantly lower body weight at day 30, and the T3 group exhibited the highest weight gain. The high dose of GL50% (400 mg/ kg) effectively reduced knee inflammation and significantly downregulated myeloperoxidase (MPO), interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α). In contrast, it significantly (p < 0.001) upregulated the serum and knee capsule tissue superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx). In addition, histopathological and X-ray examinations also confirmed the chondroprotective potential of GL50% extract against OA. Consequently, 400 mg/kg GL50% exhibited anti-inflammatory and chondroprotective potential by lowering oxidative stress and pro-inflammatory cytokines and elevating antioxidant status. These findings could provide a theoretical basis for understanding the mechanism and potential medicinal value of guava fruit and leaf in treating KOA.

IntroductionPeriodontitis is a severe oral infection that can contribute to systemic inflammation. A large body of evidence suggests a role for systemic inflammation in the initiation of neurodegenerative disease. This systematic review synthesized data from observational studies to investigate the association between periodontitis and neuroinflammation in adults.Methods and materialsA systematic literature search of PubMed, Web of Science, and Cumulative Index to Nursing and Allied Health Literature (CINAHL) was performed for studies published from the date of inception up to September 2021. Search terms for the exposure "oral disease" and outcome "dementia", "neuroinflammation" and "cognitive decline" were used. Study selection and data extraction were independently undertaken by two reviewers. The final eligible articles were included only if the exposure is periodontitis and the outcome is cognitive impairment or dementia or a topic related to this condition, and if the study was conducted in an adult population. The quality and risk of bias were assessed by Newcastle Ottawa Scale (NOS). Qualitative synthesis was used to narratively synthesize the results. Six cohort studies, three cross-sectional studies, and two case-control studies met the inclusion criteria. These eleven studies were only narratively synthesized. Meta-analysis was not performed due to the methodological heterogeneity of the studies.ResultsThe results of included studies show that chronic periodontitis patients with at least eight years of exposure are at higher risk of developing cognitive decline and dementia. Oral health measures such as gingival inflammation, attachment loss, probing depth, bleeding on probing, and alveolar bone loss are associated with cognitive impairment. The reduction of epidermal growth factor (EGF), interleukin 8 (IL-8), interferon γ-induced protein 10 (IP-10), and monocyte chemoattractant protein-1 (MCP-1) in addition to over expression of interleukin 1-β (IL-1β) are significant in patients suffering from cognitive decline with pre-existing severe periodontitis.ConclusionsAll the included studies show evidence of an association between periodontitis and cognitive impairment or dementia and Alzheimer's disease pathology. Nonetheless, the mechanisms responsible for the association between periodontitis and dementia are still unclear and warrant further investigation.

BackgroundHIV infection causes neuroinflammation and immune activation (NIIA) and systemic inflammation and immune activation (SIIA), which in turn drive neurodegeneration (ND). Cross-sectionally, higher levels of NIIA biomarkers correlate with increased biomarkers of ND. A more convincing confirmation would be a longitudinal demonstration.MethodsPWH in the US multisite CHARTER Aging project were assessed at a baseline visit and after 12 years using standardized evaluations. We measured a panel of 14 biomarkers of NIIA, SIIA, and ND in plasma and CSF at two time points and calculated changes from baseline to the 12-year visit. Factor analysis yielded simplified indices of NIIA, SIIA, and ND.ResultsThe CSF NIIA factor analysis yielded Factor1 loading on soluble tumor necrosis factor type-2 (sTNFR-II) and neopterin, and Factor2, loading on MCP1, soluble CD14, and IL-6. The SIIA factor analysis yielded Factor1 loading on CRP, D-dimer, and Neopterin; Factor2 loading on sTNFR-II. The ND analysis yielded Factor1 loading on Phosphorylated tau (p-tau) and Aβ42; Factor2 loading on NFL. NIIA Factor1, but not Factor2, correlated with increases in CSF NFL (r = 0.370, p = 0.0002).ConclusionsIncreases in NIIA and SIIA in PWH were associated with corresponding increases in ND, suggesting that reducing neuro/systemic inflammation might slow or reverse neurodegeneration.