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Background: Several studies have revealed the positive healthy impacts of branched-chain fatty acids (BCFAs). However, most of these studies evaluated the serum BCFAs in humans, or treatment with exogenous BCFAs in animal or in-vitro models and the health impacts of dietary BCFAs have not yet been studied. Due to positive effects of BCFAs in sport, in the current study, we aimed to investigate the association between dietary BCFAs and metabolic and inflammatory parameters among elite and subelite soccer players. Methods: A cross-sectional study was carried out among 335 elite and subelite soccer players (196 male), aged between 20 and 45 years old. Soccer players were enrolled from 32 teams under the directive of The Chinese Football Association. Demographic, anthropometric, and dietary assessments were performed and laboratory measurement including serum lipids, glycemic markers, and high-sensitivity C-reactive protein was measured. Results: Those with the highest dietary BCFAs consumption had higher appetite (p =.009). Also, high consumption of dietary BCFAs was associated with lower diastolic blood pressure (odds ratio: 0.958; confidence interval: 0.918–0.999; p =.046) and low high-sensitivity C-reactive protein concentrations in the third tertile of dietary BCFAs (odds ratio: 0.431; confidence interval: 0.300–0.618; p <.001). No other association between biochemical variables and dietary BCFAs was found. Conclusion: As shown in the current study, higher dietary BCFAs consumption was associated with lower diastolic blood pressure and inflammation. Due to very limited number of studies, further studies are needed to have a better perspective of these associations and their underlying mechanisms. [ABSTRACT FROM AUTHOR]

Systemic low-grade inflammation is a feature of chronic disease. C-reactive protein (CRP) is a common biomarker of inflammation and used as an indicator of disease risk; however, the role of inflammation in disease is not completely understood. Methylation is an epigenetic modification in the DNA which plays a pivotal role in gene expression. In this study we evaluated differential DNA methylation patterns associated with blood CRP level to elucidate biological pathways and genetic regulatory mechanisms to improve the understanding of chronic inflammation. The racially and ethnically diverse participants in this study were included as 50% White, 41% Black or African American, 7% Hispanic or Latino/a, and 2% Native Hawaiian, Asian American, American Indian, or Alaska Native (total n = 13,433) individuals. We replicated 113 CpG sites from 87 unique loci, of which five were novel (CADM3, NALCN, NLRC5, ZNF792, and cg03282312), across a discovery set of 1,150 CpG sites associated with CRP level (p

Weight-inducing psychotropic treatments are risk factors for age-related diseases such as cardiovascular disorders, which are associated with both inflammation and telomere length shortening. With a longitudinal design, the present study evaluates telomere length trajectories after 1 year of weight-inducing psychotropic medication, accounting for weight changes and the inflammatory biomarker high-sensitivity C-Reactive Protein (CRP). Among 200 patients, an overall median telomere shortening of -41.2 bp was observed (p = 0.014), which is comparable with the general populations yearly telomere attrition. Linear regression showed on average -93.1 and -58.9 bp of further telomere shortening per five units of BMI for BMI values < or ≥30 kg/m2, respectively (p = 0.003 and p = 0.009, respectively). Importantly, the overall telomere shortening was predicted to be increased four-fold among patients with low baseline weight (i.e., 50 kg) and with clinically relevant weight gain (≥ 7%) after 1 year of treatment (interaction term between relevant weight gain and baseline weight: +6.3 bp, p = 0.016). Patients with relevant weight gain showed greater CRP levels (+ 49%; p = 0.016), and a telomere shortening of -36.2 bp (p = 0.010) was estimated whenever CRP level doubled. Mendelian randomization using UKBiobank data showed a causal effect of BMI on telomere shortening, notably stronger among patients receiving weight-inducing psychotropic treatments (n = 9798) than among psychiatric patients without such drugs (n = 16228) and non-psychiatric controls (n = 252932) (beta: -0.37, -0.12, -0.06, respectively; p = 0.004, p

BackgroundChronic pain leads to tau accumulation and hippocampal atrophy, which may be moderated through inflammation. In older men, we examined associations of chronic pain with Alzheimer's disease (AD)-related plasma biomarkers and hippocampal volume as moderated by systemic inflammation.MethodsParticipants were men without dementia. Chronic pain was defined as moderate-to-severe pain in 2+ study waves at average ages 56, 62, and 68. At age 68, we measured plasma amyloid-beta (Aβ42, n = 871), Aβ40 (n = 887), total tau (t-tau, n = 841), and neurofilament light chain (NfL, n = 915), and serum high-sensitivity C-reactive protein (hs-CRP, n = 968), a marker of systemic inflammation. A subgroup underwent structural MRI to measure hippocampal volume (n = 385). Analyses adjusted for medical morbidities, depressive symptoms, and opioid use.ResultsChronic pain was related to higher Aβ40 (β = 0.25, p = .009), but hs-CRP was unrelated to AD-related biomarkers (ps > .05). There was a significant interaction such that older men with both chronic pain and higher levels of hs-CRP had higher levels of Aβ42 (β = 0.36, p = .001) and Aβ40 (β = 0.29, p = .003). Chronic pain and hs-CRP did not interact to predict levels of Aβ42/Aβ40, t-tau, or NfL. Furthermore, there were significant interactions such that Aβ42 and Aβ40 were associated with lower hippocampal volume, particularly when levels of hs-CRP were elevated (hs-CRP × Aβ42: β = -0.19, p = .002; hs-CRP × Aβ40: β = -0.21, p = .001), regardless of chronic pain status.ConclusionsChronic pain was associated with higher plasma Aβ, especially when hs-CRP was also elevated. Higher hs-CRP and Aβ levels were both related to smaller hippocampal volumes. Chronic pain, when accompanied by systemic inflammation, may elevate the risk of neurodegeneration in AD-vulnerable regions.

Objective: Polycystic ovary syndrome (PCOS) is widely reported among young females, and anti-androgens are used for treating hirsutism and acne in these patients. The protective effects of myo-inositol, oral contraceptives, and insulin sensitizers have been reported on the periodontium and high-sensitivity C-reactive protein (hsCRP) levels in PCOS females. However, cyproterone acetate/ethinyl estradiol (CPA/EE) has not yet been studied. This cross-sectional study explores the periodontal status and systemic inflammation in PCOS women on CPA/EE drug combination compared to females not on medication. Method and materials: A total of 150 participants were enrolled into three groups: 50 newly diagnosed PCOS females not on medication (N-PCOS); 50 PCOS females consuming CPA/EE combination for the last 6 months (PCOS+CPA/EE); and 50 systemically healthy females (control group). Anthropometric, biochemical, periodontal parameters, and health-related quality of life questionnaires were recorded. Results: N-PCOS and PCOS+CPA/EE groups showed a nonsignificant difference in hsCRP levels, Gingival Index, bleeding on probing, waist circumference, and waist-hip ratio (P > .05). Gingival thickness and keratinized tissue width were significantly greater in the PCOS+CPA/EE than the N-PCOS group (P = .05); however, these were comparable with the control group (P > .05). Regression analysis showed significant association of bleeding on probing with Gingival Index, clinical attachment level, and hsCRP (P = .05). Conclusions: CPA/EE combination does not influence the periodontal and systemic inflammatory status in PCOS females, as similar levels of local and systemic inflammation were observed in CPA/EE consumers compared with PCOS females not on medication. However, it might play a role in increasing gingival thickness and keratinized tissue width in these patients. [ABSTRACT FROM AUTHOR]

OBJECTIVES: Chronic inflammation promotes cardiovascular risk in rheumatoid arthritis (RA). Biological disease-modifying antirheumatic drugs (bDMARDs) improve disease activity and cardiovascular disease outcomes. We explored whether bDMARDs influence the impact of disease activity and inflammatory markers on long-term cardiovascular risk in RA. METHODS: We studied 4370 participants without cardiovascular disease in a 10-country observational cohort of patients with RA. Endpoints were (1) major adverse cardiovascular events (MACE) encompassing myocardial infarction, stroke and cardiovascular death; and (2) any ischaemic cardiovascular events (iCVE) including MACE plus revascularisation, angina, transient ischaemic attack and peripheral arterial disease. RESULTS: Over 26 534 patient-years, 239 MACE and 362 iCVE occurred. The interaction between 28-joint Disease Activity Score with C-reactive protein (DAS28-CRP) and bDMARD use was significant for MACE (p=0.017), suggesting the effect of DAS28-CRP on MACE risk differed among bDMARD users (n=515) and non-users (n=3855). DAS28-CRP (per unit increase) is associated with MACE risk in bDMARD non-users (HR 1.21 (95% CI 1.07 to 1.37)) but not users (HR 0.69 (95% CI 0.40 to 1.20)). The interaction between CRP (per log unit increase) and bDMARD use was also significant for MACE (p=0.011). CRP associated with MACE risk in bDMARD non-users (HR 1.16 (95% CI 1.04 to 1.30)), but not users (HR 0.65 (95% CI 0.36 to 1.17)). No interaction was observed between bDMARD use and DAS28-CRP (p=0.167) or CRP (p=0.237) for iCVE risk. CONCLUSIONS: RA activity and inflammatory markers associated with risk of MACE in bDMARD non-users but not users suggesting the possibility of biological-specific benefits locally on arterial wall independently of effects on systemic inflammation.

The objective of the present study was to evaluate the interdependency of parent-adolescent inflammation trends across time and to examine whether shared family socioeconomic characteristics explained between-family differences in parents and adolescents risk for inflammation. A total of N = 348 families, consisting of one parent and one adolescent child, were followed every two years in a three-wave longitudinal study. Sociodemographic questionnaires were used to determine parental educational attainment and family income-to-needs ratio (INR). At each time point, parents and adolescents collected dried blood spot (DBS) samples that were assayed for circulating CRP and log-transformed prior to analysis by longitudinal dyadic models. Models revealed significant differences in parents and adolescents inflammation trends over time (bint = - 0.13, p

Purpose: To investigate the effect of full-mouth disinfection on the sizes of the periodontal wound and periodontal inflammatory burden and whether it leads to a decrease in C-reactive protein (CRP) levels. Materials and Methods: The study included 20 systemically healthy subjects (11 women and 9 men) 30 to 68 years old with localised or generalised periodontitis (stage III, grade C). The sizes of the periodontal wound and periodontal inflammatory burden were measured with the web application “Periodontalwound”, which is based on measurements of average tooth cervices, as well as probing depths and bleeding on probing assessed at six sites around each tooth present in the oral cavity. The levels of hsCRP (high-sensitivity CRP) were measured with an immunochemical method. All three parameters were measured before initial treatment and 3 months after therapy. Full-mouth disinfection included removal of plaque and calculus with ultrasonic and hand instruments in one session. Results: The results showed a statistically significant decrease in the size of the periodontal wound (p < 0.001), a statistically significant decrease in the size of periodontal inflammatory burden (p < 0.001), and a decrease in hsCRP levels 3 months after therapy. Conclusion: Full-mouth disinfection leads to a decrease in the periodontal wound and periodontal inflammatory burden size, as well as a decrease in the levels of hsCRP in patients with localised or generalised periodontitis (stage III, grade C) [ABSTRACT FROM AUTHOR]

Tryptophan (TRP) metabolites along the kynurenine (KYN) pathway (KP) have been found to influence muscle. Pro-inflammatory cytokines are known to stimulate the degradation of TRP down the KP. Given that both inflammation and KP metabolites have been connected with loss of muscle, we assessed the potential mediating role of KP metabolites on inflammation and muscle mass in older men. 505 men (85.0±4.2yrs) from the Osteoporotic Fractures in Men cohort study with measured D3-creatine dilution (D3Cr) muscle mass, KP metabolites, and inflammation markers (C-reactive protein (CRP), alpha-1-acid glycoprotein (AGP) and a subsample (n=305) with interleukin (IL-6, IL-1β, IL-17A) and tumor necrosis factor-α (TNF-α)) were included in the analysis. KP metabolites and inflammatory markers were measured using liquid chromatography-tandem mass spectrometry and immunoassays, respectively. 23-92% of the inverse relationship between inflammatory markers and D3Cr muscle mass was mediated by KP metabolites (indirect effect p0.05). KP metabolites, particularly higher ratios of KYN/TRP, 3-HK/XA, 3-HK/3-HAA, QA/3-HAA and a lower ratio of NAM/QA, mediated the relationship between inflammation and low muscle mass. Our preliminary cross-sectional data suggest that interventions to alter D3Cr muscle mass may focus on KP metabolites rather than inflammation per se.

BackgroundFecal microbiota transplantation (FMT) is increasingly used for gastrointestinal and extra-gastrointestinal diseases in veterinary medicine. However, its effects on immune responses and possible adverse events have not been systematically investigated.Hypothesis/objectivesDetermine the short-term safety profile and changes in the peripheral immune system after a single FMT administration in healthy dogs.AnimalsTen client-owned, clinically healthy dogs as FMT recipients, and 2 client-owned clinically healthy dogs as FMT donors.MethodsProspective non-randomized clinical trial. A single rectal enema of 5 g/kg was given to clinically healthy canine recipients. During the 28 days after FMT administration, owners self-reported adverse events and fecal scores. On Days 0 (baseline), 1, 4, 10, and 28 after FMT, fecal and blood samples were collected. The canine fecal dysbiosis index (DI) was calculated using qPCR.ResultsNo significant changes were found in the following variables: CBC, serum biochemistry, C-reactive protein, serum cytokines (interleukins [IL]-2, -6, -8, tumor necrosis factor [TNF]-α), peripheral leukocytes (B cells, T cells, cluster of differentiation [CD]4+ T cells, CD8+ T cells, T regulatory cells), and the canine DI. Mild vomiting (n = 3), diarrhea (n = 4), decreased activity (n = 2), and inappetence (n = 1) were reported, and resolved without intervention.Conclusions and clinical importanceFecal microbiota transplantation did not significantly alter the evaluated variables and recipients experienced minimal adverse events associated with FMT administration. Fecal microbiota transplantation was not associated with serious adverse events, changes in peripheral immunologic variables, or the canine DI in the short-term.

Observational studies suggest that posttraumatic stress disorder (PTSD) increases risk for various autoimmune diseases. Insights into shared biology and causal relationships between these diseases may inform intervention approaches to PTSD and co-morbid autoimmune conditions. We investigated the shared genetic contributions and causal relationships between PTSD, 18 autoimmune diseases, and 3 immune/inflammatory biomarkers. Univariate MiXeR was used to contrast the genetic architectures of phenotypes. Genetic correlations were estimated using linkage disequilibrium score regression. Bi-directional, two-sample Mendelian randomization (MR) was performed using independent, genome-wide significant single nucleotide polymorphisms; inverse variance weighted and weighted median MR estimates were evaluated. Sensitivity analyses for uncorrelated (MR PRESSO) and correlated horizontal pleiotropy (CAUSE) were also performed. PTSD was considerably more polygenic (10,863 influential variants) than autoimmune diseases (median 255 influential variants). However, PTSD evidenced significant genetic correlation with nine autoimmune diseases and three inflammatory biomarkers. PTSD had putative causal effects on autoimmune thyroid disease (p = 0.00009) and C-reactive protein (CRP) (p = 4.3 × 10-7). Inferences were not substantially altered by sensitivity analyses. Additionally, the PTSD-autoimmune thyroid disease association remained significant in multivariable MR analysis adjusted for genetically predicted inflammatory biomarkers as potential mechanistic pathway variables. No autoimmune disease had a significant causal effect on PTSD (all p values > 0.05). Although causal effect models were supported for associations of PTSD with CRP, shared pleiotropy was adequate to explain a putative causal effect of CRP on PTSD (p = 0.18). In summary, our results suggest a significant genetic overlap between PTSD, autoimmune diseases, and biomarkers of inflammation. PTSD has a putative causal effect on autoimmune thyroid disease, consistent with existing epidemiologic evidence. A previously reported causal effect of CRP on PTSD is potentially confounded by shared genetics. Together, results highlight the nuanced links between PTSD, autoimmune disorders, and associated inflammatory signatures, and suggest the importance of targeting related pathways to protect against disease and disability.

BACKGROUND: Suicide is the second leading cause of death in 12- to 17-year-old adolescents in the USA. Research on biological mechanisms contributing to self-harm risk that could be targeted in treatment could help to prevent suicide and self-harm episodes. AIMS: We aimed to evaluate whether markers of inflammation, interleukin-6 (IL-6) and C-reactive protein (CRP), predict self-harm over 3 months within a sample selected for elevated suicide/self-harm risk at project entry. METHOD: Fifty-one adolescents aged 12-19 years selected for elevated suicide/self-harm risk completed three clinical interviews about suicide attempts and non-suicidal self-injury, 3 months apart. At baseline and 3 months, youth also provided blood samples, from which we assayed levels of IL-6 and CRP. RESULTS: Using generalised mixed models, we found that greater levels of IL-6 predicted more self-harm episodes (odds ratio [OR] = 3.3, 95% CI: 1.1, 10.0) and specifically, non-suicidal self-injury (OR = 3.5, 95% CI: 1.1, 11.2), over 3 months. CONCLUSIONS: The study findings increase our understanding of whether and how inflammation may be implicated in risk of self-harm. IL-6 may be a viable biological marker of short-term risk for self-harm.

BACKGROUND: In contrast to fine particles, less is known of the inflammatory and coagulation impacts of coarse particulate matter (PM10-2.5, particulate matter with aerodynamic diameter ≤10μm and>2.5μm). Toxicological research suggests that these pathways might be important processes by which PM10-2.5 impacts health, but there are relatively few epidemiological studies due to a lack of a national PM10-2.5 monitoring network. OBJECTIVES: We used new spatiotemporal exposure models to examine associations of both 1-y and 1-month average PM10-2.5 concentrations with markers of inflammation and coagulation. METHODS: We leveraged data from 7,071 Multi-Ethnic Study of Atherosclerosis and ancillary study participants 45-84 y of age who had repeated plasma measures of inflammatory and coagulation biomarkers. We estimated PM10-2.5 at participant addresses 1 y and 1 month before each of up to four exams (2000-2012) using spatiotemporal models that incorporated satellite, regulatory monitoring, and local geographic data and accounted for spatial correlation. We used random effects models to estimate associations with interleukin-6 (IL-6), C-reactive protein (CRP), fibrinogen, and D-dimer, controlling for potential confounders. RESULTS: Increases in PM10-2.5 were not associated with greater levels of inflammation or coagulation. A 10-μg/m3 increase in annual average PM10-2.5 was associated with a 2.5% decrease in CRP [95% confidence interval (CI): -5.5, 0.6]. We saw no association between annual average PM10-2.5 and the other markers (IL-6: -0.7%, 95% CI: -2.6, 1.2; fibrinogen: -0.3%, 95% CI: -0.9, 0.3; D-dimer: -0.2%, 95% CI: -2.6, 2.4). Associations consistently showed that a 10-μg/m3 increase in 1-month average PM10-2.5 was associated with reduced inflammation and coagulation, though none were distinguishable from no association (IL-6: -1.2%, 95% CI: -3.0 , 0.5; CRP: -2.5%, 95% CI: -5.3, 0.4; fibrinogen: -0.4%, 95% CI: -1.0, 0.1; D-dimer: -2.0%, 95% CI: -4.3, 0.3). DISCUSSION: We found no evidence that PM10-2.5 is associated with higher inflammation or coagulation levels. More research is needed to determine whether the inflammation and coagulation pathways are as important in explaining observed PM10-2.5 health impacts in humans as they have been shown to be in toxicology studies or whether PM10-2.5 might impact human health through alternative biological mechanisms. https://doi.org/10.1289/EHP12972.

BackgroundTobacco smoke exposure (TSE) has inflammatory and immunosuppressive effects which may be associated with altered levels of inflammatory markers and pediatric illnesses.ObjectiveThe primary objective was to examine the associations of cotinine-confirmed and parent-reported child TSE patterns and discharge diagnoses with C-reactive protein (CRP), IL-8, and IL-10 in 0-11-year-old pediatric emergency department (PED) patients who lived with ≥ 1 smoker.MethodsSaliva samples were obtained from 115 children with a mean (SD) age of 3.5 (3.1) years during the PED visit (T0). Saliva was analyzed for cotinine, CRP, IL-8, and IL-10. Parents self-reported their children's TSE patterns; children's medical records were reviewed to identify and categorize discharge diagnoses. Linear regression models were utilized to find T0 associations of cotinine-confirmed and parent-reported child TSE patterns, and PED diagnoses with each inflammatory marker. All models were adjusted for child race/ethnicity, child sex, annual household income, and housing type. The TSE models also adjusted for child discharge diagnosis.ResultsAt T0, the geometric mean (GeoM) of cotinine was 4.1 ng/ml [95 %CI = 3.2-5.2]; the GeoMs of CRP, IL-8, and IL-10 were 3,326 pg/ml [95 %CI = 2,696-4,105], 474 pg/ml [95 %CI = 386-583], and 1.1 pg/ml [95 %CI = 0.9-1.3], respectively. Parent-reported child TSE patterns were positively associated with ln-transformed CRP levels, while adjusting for the covariates (β^ = 0.012 [95 %CI:0.004-0.020], p = 0.037). In the parent-reported child TSE pattern model, there were significant positive associations between the covariate of child age with CRP and IL-8 levels (p = 0.028 and p

AİM: Late-onset neonatal sepsis has a high mortality rate in premature infants. To date, no single test in the evaluation of neonatal sepsis has been demonstrated to be both sensitive and specific enough to assist in timely decision making. The aim of our study is to develop a predictive model that can be applied to all premature babies, using clinical and laboratory findings in premature babies, to recognize late-onset neonatal sepsis. STUDY DESİGN: 65 premature patients diagnosed with culture-proven late-onset neonatal sepsis and hospitalized in Dr. Behcet Uz Pediatric Diseases and Surgery Training and Research Hospital neonatal intensive care unit between January 2018 and December 2020, and 65 premature newborns of similar age and gender who did not have sepsis were included in the study retrospectively. RESULTS: In our study, feeding difficulties, worsening in clinical appearance and fever were found to be significant among clinical findings, while thrombocytopenia and high C-reactive protein among laboratory findings are the strongest data supporting late-onset neonatal sepsis. In multiple regression analysis, thrombocytopenia, mean platelet volume, C-reactive protein, lymphocyte count and feeding difficulties had the highest odds ratio (p < 0.05). By converting these data into a scoring system, a nomogram was created that can be easily used by all clinicians. CONCLUSION: In our study, we developed a scoring system that can be easily applied to all premature patients by evaluating the clinical and laboratory findings in late-onset neonatal sepsis. We think that it will help in recognizing late-onset neonatal sepsis and strengthening the treatment decision. Predicting the individual probability of sepsis in preterm newborns may provide benefits for uninfected newborns to be exposed to less antibiotics, not to be separated from mother and baby, and to reduce healthcare system expenditures. The nomogram can be used to assess the likelihood of sepsis and guide treatment decision. [ABSTRACT FROM AUTHOR]

C-reactive protein (CRP) levels have been implicated in the severity and symptomatology of major depressive disorder (MDD). The aim of this study was to explore the structure of depressive symptoms in patients with MDD according to different groups of CRP levels using network analysis. The study included 864 individuals (mean age = 54.05, 67.48 % male) diagnosed with MDD from the 2015–2020 National Health and Nutrition Examination Survey (NHANES). Analyses examined how depressive symptoms and CRP level were related to each other, and how the network structure of depressive symptoms differed across groups with different CRP levels. A direct positive correlation was observed between CRP levels and specific depressive symptoms (e.g., appetite change, energy loss, and feelings of worthlessness). Moreover, there was a stronger correlation between depressive symptoms in the medium CRP and high CRP groups compared to the low CRP group. Furthermore, it was observed that there were notable structural differences between the high-CRP and moderate-CRP groups. The study is based on cross-sectional data, which precludes the drawing of causal conclusions. Furthermore, it does not take into account confounding factors such as body mass index (BMI) and lifestyle. The findings underscore the pivotal role of CRP as a marker of the severity of depressive symptoms. Routine CRP level testing and anti-inflammatory therapies may be beneficial for depressed patients with elevated CRP levels in clinical practice. • CRP levels were directly associated with some specific depressive symptoms. • A higher density structure of depressive symptoms was observed in the elevated CRP groups. • The groups with high and moderate CRP levels had different symptom's structure. • Regular CRP levels testing and anti-inflammatory treatments may be useful for depression. [ABSTRACT FROM AUTHOR]

C-reactive protein (CRP) is a protein made by the liver, which is released into the bloodstream in response to inflammation. Furthermore, CRP is a potential risk factor for heart disease. Hence, it is of great importance to develop a rapid, sensitive, accurate, and cost-effective method for CRP detection. Herein, we report an enzyme-free fluorescent assay for the rapid and ultra-sensitive detection of CRP with a limit of detection (LOD) reaching as low as 3.08 pg/mL (i.e., ~ 27 fM). The high sensitivity of our method was simply achieved via dual-functionalized gold nanoparticles (AuNPs). By regulating the molar ratio of DNA to CRP antibody immobilized on the AuNP surface, hundreds to thousands-fold amplification in the analyte signal could be instantly accomplished. Furthermore, our sensor was selective: non-target proteins such as interleukin-6, interleukin-1β, procalcitonin, bovine serum albumin, and human serum albumin did not interfere with the target CRP detection. Moreover, simulated serum samples were successfully analyzed. Given the excellent sensitivity, selectivity, and high resistance to complicated matrices, the enzyme-free CRP detection strategy developed in this work can be used as a generic platform to construct sensors for a wide variety of protein biomarkers and hence offers potential as a tool for rapid, accurate, and low-cost medical diagnosis. [ABSTRACT FROM AUTHOR]

The document titled "Contents list" from the journal Analyst, published by The Royal Society of Chemistry, features a range of research articles on topics such as CO2-based micro-respirometry, magnetic droplets in microfluidic chips, molecularly imprinted polymer sensors for biomarker detection, and more. The journal aims to connect the world with the chemical sciences and reinvest profits back into the chemistry community. The articles cover diverse areas of research, including energy storage, cardiovascular diseases, cancer diagnosis algorithms, and pesticide exposure assessments, among others. [Extracted from the article]

LaNiO3 perovskite nanoparticles, especially nanospheres (LNNS), show great promise in biomedical assays due to their peroxidase-like catalytic properties. However, LNNS-based diagnostic reagents have not been tested in nanozyme enzyme-linked immunosorbent assay (NLISA) or other enzyme-linked immunosorbent assays, and there is limited data on their synthesis. To fill this gap, it is necessary to develop a method for creating LNNS conjugates with monoclonal antibodies and to investigate the reproducibility, scalability, and applicability of these diagnostic reagents in NLISA. We have successfully developed a method for producing novel diagnostic reagents utilizing LaNiO3 nanospheres. Our research demonstrates the application of these nanospheres in a NLISA specifically designed for the detection of C-reactive protein (CRP) in real serum samples. This method is both reproducible and scalable, allowing for the efficient production of nanospheres that are functionalized with monoclonal antibodies targeting CRP, with a mean diameter of approximately 270 nm. Based on the promising results obtained from our experiments, we have developed and optimized a sandwich-format NLISA for CRP detection. This assay achieved a lower limit of detection at 0.178 μg L−1, with a dynamic range from 12.5 to 0.195 μg L−1 and a linear detection range extending from 0.195 to 6.25 μg L−1, showcasing its potential for clinical applications. The new NLISA method, utilizing LaNiO3 nanospheres in a sandwich format for the detection of CRP, significantly enhances sensitivity compared to similar use horseradish peroxidase-based ELISA. In this study for the first time, the functionalization of lanthanum nickelate nanospheres with recognition elements has been demonstrated. This advancement also sheds light on the technological challenges involved in synthesizing diagnostic reagents, identifying areas that need further exploration. [ABSTRACT FROM AUTHOR]

ABSTRACT Introduction Objective Methods Results Conclusions Inflammation is a marker of immune activation. Inflammation may have an effect on both ovarian function and luteal function, both essential to pregnancy. High inflammation may also signal dysregulated processes within the ovary, which could be in part measured through Anti‐Müllerian hormone, follicle‐stimulating hormone, and inhibin B levels.To determine the relationship between inflammation, measured by C‐reactive protein, and three biomarkers of ovarian function during the early follicular phase: Anti‐Müllerian hormone, follicle‐stimulating hormone, and inhibin B.Secondary cross‐sectional analysis of data and serum obtained in Time to Conceive, a prospective cohort study sample of 843 women attempting pregnancy in central North Carolina from 2008 to 2016. Participants were aged 30 and 44 years, had no history of infertility, endometriosis, or polycystic ovarian syndrome, and were not currently breastfeeding. Serum samples were obtained on days 2, 3, or 4 of the menstrual cycle. C‐reactive protein (natural‐log transformed), Anti‐Müllerian hormone (natural‐log transformed), follicle‐stimulating hormone (natural‐log transformed), and inhibin B (untransformed) were measured in serum. Diminished ovarian reserve was examined dichotomously and defined as an Anti‐Müllerian hormone level below 0.7 ng/mL.The analysis included 703 participants with C‐reactive protein measured. In an adjusted linear regression model, a 20% increase in C‐reactive protein was associated with a 0.57 pg/mL decrease in inhibin B (95% CI: −0.84 to −0.29 pg/mL) and a 0.535% decrease in follicle‐stimulating hormone (95% CI: −1.01 to −0.06). Although there was not a significant relationship between Anti‐Müllerian hormone and C‐reactive protein, a 20% increase in C‐reactive protein was associated with a 0.87% increase in Anti‐Müllerian hormone (95% CI: −0.27 to 2.01). C‐reactive protein was not associated with the odds of diminished ovarian reserve in an adjusted logistic regression model (OR: 0.97, 95% CI: 0.77–1.20).Inflammation, as measured by C‐reactive protein, is associated with early follicular phase follicle‐stimulating hormone and inhibin B, although this is not true of AMH. Inflammation may exert an effect on ovarian function. [ABSTRACT FROM AUTHOR]

Background: Research suggests that systemic inflammation may link loneliness to adverse health outcomes, yet there is a gap in comprehensively reviewing recent evidence on the relationship between loneliness and biological measures of inflammation in adults. This scoping review synthesizes current research to address the question: Is there a definitive link between loneliness and biological markers of inflammation in adults? Methods: Following the methods outlined by Arksey and O'Malley, we developed a protocol, defined our research question, and systematically searched PubMed, CINAHL, Embase, and Scopus for English-language studies conducted from 2018 to 2023 exploring the relationship between loneliness and biomarkers of inflammation in adults. Results: Twelve studies meeting the inclusion criteria displayed heterogeneity in terms of sample characteristics, loneliness scales, and inflammatory biomarkers. The UCLA Loneliness Scale, in various forms, emerged as the predominant tool for measuring loneliness, while C-reactive protein and interleukin-6 were the most frequently evaluated inflammatory biomarkers. Notably, all 12 studies reported an association between loneliness and at least 1 biological marker of inflammation. Conclusion: Research consistently associates loneliness with poor health outcomes in aging adults, but the underlying mechanisms remain unclear. This scoping review suggests that inflammation may serve as a pathway linking loneliness to adverse health outcomes. However, the variability across studies highlights the need for standardized measurement methods and a consideration of both the duration and extent of loneliness. Enhancing our understanding of how loneliness affects systemic inflammation may help clarify why loneliness is associated with negative health outcomes. [ABSTRACT FROM AUTHOR]

Tracheobronchial chondritis is a rare immune-related adverse event (irAE) associated with immune checkpoint inhibitors. We report a case wherein tracheobronchial chondritis occurred while administering nivolumab for recurrent hypopharyngeal squamous cell carcinoma (SCC) in a man diagnosed with T2N3bM0 stage IVB hypopharyngeal SCC. After treatment with cisplatin and radiotherapy followed by left and right neck dissection, local recurrence was observed in the hypopharynx. Because of the difficulty of salvage surgery, we administered 240 mg/body of nivolumab. After 9 cycles of nivolumab, the patient was judged to have complete response. After 10 cycles, he had cough and sputum, for which prompting us to perform imaging tests. Computed tomography (CT) showed edematous thickening around the trachea and bilateral bronchi and elevated amounts of adjacent subcutaneous fat tissue. Positron emission tomography-CT showed diffuse fluorodeoxyglucose uptake in the trachea and bilateral bronchi, bronchial endoscopy showed redness and swelling throughout the bronchi, and biopsy showed partial mucosal erosion, inflammatory cell (lymphocyte) infiltration, interstitial edema, and desmoplasia. The patient was diagnosed with tracheobronchial chondritis as an irAE resulting from administering anti-programmed death-1 monoclonal antibody. After four-day prednisolone treatment, his cough and sputum disappeared; after two weeks, tracheobronchial chondritis no longer appeared on CT. [ABSTRACT FROM AUTHOR]

Introduction: To evaluate the demographic, clinical, diagnostic, and treatment data of pediatric patients with ventriculoperitoneal shunt infection and risk factors for ventriculoperitoneal shunt infection and recurrence of ventriculoperitoneal shunt infection. Methods: Patients aged 0–18 years who were diagnosed with ventriculoperitoneal shunt infection at Cukurova University Faculty of Medicine Hospital between 2016 and 2021 were included in the study. Demographic, clinical, laboratory, and treatment data of the patients were evaluated retrospectively. Risk factors for the development and recurrence of ventriculoperitoneal shunt infection were evaluated. Patients who underwent ventriculoperitoneal shunt but did not develop any shunt infection were selected as the control group. Results: Eighty-five patients with a diagnosis of ventriculoperitoneal shunt infection were included in the study. Fever (58.8%), anorexia (58.8%), vomiting (56.5%), and altered consciousness (54.1%) were the most common complaints at admission. The control group consisted of 48 patients. The number of shunt revisions was statistically significantly higher in the group that developed ventriculoperitoneal shunt infection compared to the control group (p < 0.001). In patients with ventriculoperitoneal shunt infection, C-reactive protein and cerebrospinal fluid protein values before shunt insertion were found to be statistically significantly higher than the control group (p < 0.001). Conclusion: Ventriculoperitoneal shunt infection occurs most frequently in the first months after shunt application. Therefore, it is extremely important to prevent colonization and contamination during surgery in preventing the development of ventriculoperitoneal shunt infection. In the present study, cerebrospinal fluid protein elevation and C-reactive protein elevation before shunt application were found to be significant in terms of the development and recurrence of ventriculoperitoneal shunt infection. [ABSTRACT FROM AUTHOR]

Atopic dermatitis (AD) is a chronic recurrent inflammatory skin disease. Fucoidans are reportedly effective in treating AD; however, their clinical efficacy requires further exploration. This study aimed to investigate the clinical efficacy of low-molecular-weight fucoidan (LMF) supplementation in patients with AD and reveal the underlying mechanism of its effects; this is a randomized, double-blind, placebo-controlled trial. Participants were randomly assigned to a study or control group to receive conventional AD therapy with oral supplementation of either LMF or placebo for 12 weeks. Symptom severity was measured by the SCORing Atopic Dermatitis (SCORAD) index. Each participant used a diary to record daily medication use. Blood samples were collected at three time points for assessing AD-related cytokines, immunoglobulin E (IgE), C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), white blood cell (WBC) count, the percentage of eosinophils, and biochemical profiles of hepatic and renal functions. The study group showed significant symptom relief, whereas the control group showed no significant improvements. The frequency of steroid ointment application significantly decreased, and the frequency of oral antihistamine use decreased in the study group, whereas no significant changes were observed in the control group. The AD-related immune parameters serum IgE, eosinophils, CD8+ T cells, interferon-γ (IFN-γ), ESR, and CRP significantly decreased in the study group but not the control group. There were no severe adverse events in either group. This study is the first to demonstrate the effectiveness and safety of LMF as a supplemental therapy for patients with AD via its anti-inflammatory activity. [ABSTRACT FROM AUTHOR]

Background: Inflammatory processes can trigger acute coronary syndromes (ACS) which may increase core body temperature (BT), a widely available low‐cost marker of systemic inflammation. Herein, we aimed to delineate baseline characteristics of ST‐segment elevation myocardial infarction (STEMI) and non‐ST‐segment elevation ACS (NSTE‐ACS) patients stratified by initial BT and to assess its predictive utility towards major adverse cardiovascular events (MACE) after the index ACS. Methods: From 2012 until 2017, a total of 1044 ACS patients, 517 with STEMI and 527 with NSTE‐ACS, were prospectively recruited at the University Hospital Zurich. BT was measured by digital tympanic thermometer along with high‐sensitivity C‐reactive protein (hs‐CRP) and cardiac troponin‐T (hs‐cTnT) levels prior to coronary angiography. Patients were stratified according to initial BT and uni‐ and multivariable regression models were fit to assess associations of BT with future MACE risk. Results: Among patients with STEMI, BT was not predictive of 1‐year MACE, but a U‐shaped relationship between BT and MACE risk was noted in those with NSTE‐ACS (p =.029), translating into a 2.4‐fold (HR, 2.44, 95% CI, 1.16–5.16) increased 1‐year MACE risk in those with BT >36.8°C (reference: 36.6–36.8°C). Results remained robust in multivariable‐adjusted analyses accounting for sex, age, diabetes, renal function and hs‐cTnT. However, when introducing hs‐CRP, the BT‐MACE association did not prevail. Conclusions: In prospectively recruited patients with ACS, initial BT shows a U‐shaped relationship with 1‐year MACE risk among those with NSTE‐ACS, but not in those with STEMI. BT is a broadly available low‐cost marker to identify ACS patients with high inflammatory burden, at high risk for recurrent ischaemic events, and thus potentially suitable for an anti‐inflammatory intervention. Registration: ClinicalTrials.gov Identifier: NCT01000701. [ABSTRACT FROM AUTHOR]

Background: Dyslipidaemia, inflammation and elevated Lp(a) levels are associated with the progression of atherosclerosis. This study investigates whether patients with a first‐time presentation of chest pain and on‐target LDL‐C levels and intermediate FRS/ESC‐Score risks, display a high inflammatory burden linked to myocardial injury and whether inflammation at admission affects the re‐event rate up to 6 years follow‐up. Methods: Blind assessments of novel inflammatory markers such as Glycoprotein A and B via nuclear magnetic resonance (NMR), cytokines, hsCRP, Neutrophil‐to‐Lymphocyte ratio (NLR) and Lipoprotein(a) levels were examined. Out of 198 chest pain patients screened, 97 met the inclusion criteria at admission. Results: cTnI(+) patients (>61 ng/L) with elevated Lipoprotein(a), showed significantly increased levels of Glycoprotein A and B, hsCRP, IL‐6, a high NLR and a reduced left ventricular ejection fraction (%) compared to cTnI(−) individuals. Those patients, with a higher inflammatory burden at hospital admission (hsCRP, IL‐6, Glycoprotein A and B, and Lipoprotein(a)) had a higher re‐event rate at follow‐up. Conclusions: Inflammation and Lipoprotein(a) levels were particularly prominent in patients presenting with reduced left ventricular ejection fraction. Notably, Glycoproteins A/B emerge as novel markers of inflammation in these patients. Our study highlights the significantly higher impact of inflammatory burden in patients with chest pain and high level of myocardial damage than in those with lower myocardial affectation, even when they all had lipid levels well controlled. Inflammation at the time of admission influenced the re‐event rate over a follow‐up period of up to 6 years. [ABSTRACT FROM AUTHOR]

The value of C-reactive protein point-of-care testing (CRP POCT) to guide antibiotic prescriptions in adults has previously been emphasized. The aim of this study was to assess the impact of CRP POCT on antibiotic prescriptions by general practitioners (GPs) for suspected lower respiratory tract infections in children ≥3 years old and in adults. This was an open-label randomized trial (NCT03540706) conducted in 26 GPs in France between October 2019 and March 2023. Of the 404 participating patients, 207 (51.2%) were randomized to the CRP POCT group and 197 (48.8%) to the control group (i.e. no CRP POCT). During consultations, GPs measured CRP levels in patients randomized to the CRP POCT group. The primary endpoint was the proportion of patients in each group who were prescribed antibiotics by their GP during the consultation. Z-tests were used for comparisons. The overall proportion of patients treated with antibiotics was similar in the CRP POCT (n = 89/207, 43% CI: 36.2, 50.0) and in the control group (n = 94/197, 47.7% CI: 40.6, 54.9), difference: −4.7 CI: −14.4, 5.0; p 0.3. Overall, 75% of the GPs followed CRP-based antibiotic prescription recommendations in the CRP POCT group. CRP POCT did not reduce antibiotic prescriptions in this trial. [ABSTRACT FROM AUTHOR]

Xenotransplantation has made significant advances recently using pigs genetically engineered to remove carbohydrate antigens, either alone or with addition of various human complement, coagulation, and anti-inflammatory "transgenes". Here we evaluated results associated with gene-edited (GE) pig hearts transplanted in baboons using an established costimulation-based immunosuppressive regimen and a cold-perfused graft preservation technique. Eight baboons received heterotopic abdominal heart transplants from 3-GE (GalKO.β4GalNT2KO.hCD55, n = 3), 9-GE (GalKO.β4GalNT2KO.GHRKO.hCD46.hCD55. TBM.EPCR.hCD47. HO-1, n = 3) or 10-G (9-GE + CMAHKO, n = 2) pigs using Steen's cold continuous perfusion for ischemia minimization. Immunosuppression (IS) included induction with anti-thymocyte globulin and αCD20, ongoing αCD154, MMF, and tapered corticosteroid. All three 3-GE grafts functioned well initially, but failed within 5 days. One 9-GE graft was lost intraoperatively due to a technical issue and another was lost at POD 13 due to antibody mediated rejection (AMR) in a baboon with a strongly positive pre-operative cross-match. One 10-GE heart failed at POD113 with combined cellular and antibody mediated rejection. One 9-GE and one 10-GE hearts had preserved graft function with normal myocardium on protocol biopsies, but exhibited slowly progressive graft hypertrophy until elective necropsy at POD393 and 243 respectively. Elevated levels of IL-6, MCP-1, C-reactive protein, and human thrombomodulin were variably associated with conditioning, the transplant procedure, and clinically significant postoperative events. Relative to reference genetics without thrombo-regulatory and anti-inflammatory gene expression, 9- or 10-GE pig hearts exhibit promising performance in the context of a clinically applicable regimen including ischemia minimization and αCD154-based IS, justifying further evaluation in an orthotopic model. [ABSTRACT FROM AUTHOR]

Introduction: ORAL Surveillance, a post-authorisation safety study of patients with rheumatoid arthritis (RA) enriched for cardiovascular (CV) risk, demonstrated increased risk of major adverse CV events (MACE) and malignancies (excluding non-melanoma skin cancer [NMSC]) for tofacitinib versus tumour necrosis factor inhibitors (TNFi). This analysis of a real-world Canadian observational study evaluated tofacitinib safety/effectiveness in patients meeting or not meeting CV risk criteria. Methods: CANTORAL included patients with moderate-to-severe RA initiating tofacitinib (10/2017–07/2020; N = 504). Interim data (data-cut: 07/2021) were stratified as CV risk-enriched (CV+ ; patients ≥ 50 years with ≥ 1 additional CV risk factor) or not CV risk-enriched (CV−; ≥ 50 years without additional CV risk factors and 18–49 years with/without CV risk factors). Safety and persistence were evaluated to month (M) 36. Effectiveness outcomes to M18 included Clinical Disease Activity Index (CDAI)-defined low disease activity (LDA)/remission (CANTORAL co-primary endpoints) and Disease Activity Score in 28 joints, C-reactive protein (DAS28-4[CRP]) < 3.2/ < 2.6. Results: Overall, 272/232 patients were included in CV+ /CV− cohorts (full analysis set) (435/356 patient-years [safety analysis set]). Incidence rates (events/100 patient-years) in CV+ /CV− cohorts were 138.5/112.5 for treatment-emergent adverse events (AEs); 17.0/5.6 for serious AEs; 1.2/0.3 for deaths; 5.5/1.7 for serious infections; 1.4/1.1 for herpes zoster; 1.6/0.0 for MACE; 2.1/0.3 for malignancies (excluding NMSC); 0.7/0.6 for NMSC; 0.5/0.0 for venous thromboembolic events. Persistence was generally comparable between cohorts. In CV+ /CV− cohorts, at M6, CDAI LDA and remission rates were 51.5%/54.6% and 12.0%/19.6%; DAS28-4(CRP) < 3.2/ < 2.6 rates were 44.0%/39.3% and 31.5%/28.8%, respectively; effectiveness was generally maintained to M18. Conclusions: In concordance with studies of background risk, AEs were more common in patients with CV risk enrichment, particularly those aged ≥ 65 years. Tofacitinib effectiveness/persistence were generally similar regardless of CV risk enrichment. These findings support individualised treatment benefit–risk assessment, including CV assessment/management, to optimise RA outcomes. [ABSTRACT FROM AUTHOR]

Context Carnosine and histidine-containing dipeptides (HCDs) are suggested to have anti-inflammatory and antioxidative benefits, but their effects on circulating adipokines and inflammatory and oxidative stress biomarkers remain unclear. Objectives The aim of the present systematic review and meta-analysis was to determine the impact of HCD supplementation on inflammatory and oxidative stress biomarkers. Data Sources A systematic search was performed on Medline via Ovid, Scopus, Embase, ISI Web of Science, and the Cochrane Library databases from inception to 25 January 2023. Data Extraction Using relevant key words, trials investigating the effects of carnosine/HCD supplementation on markers of inflammation and oxidative stress, including C-reactive protein (CRP), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), adiponectin, malondialdehyde (MDA), glutathione (GSH), superoxide dismutase (SOD), total antioxidant capacity (TAC), and catalase (CAT) were identified. Meta‐analyses were conducted using random‐effects models to calculate the weighted mean differences (WMDs) and 95% confidence intervals (CIs). Data Analysis A total of 9 trials comprising 350 participants were included in the present meta-analysis. Carnosine/HCD supplementation led to a significant reduction in CRP (WMD: –0.97 mg/L; 95% CI: –1.59, –0.36), TNF-α (WMD: –3.60 pg/mL; 95% CI: –7.03, –0.18), and MDA (WMD: –0.34 μmol/L; 95% CI: –0.56, –0.12) and an elevation in CAT (WMD: 4.48 U/mL; 95% CI: 2.43, 6.53) compared with placebo. In contrast, carnosine/HCD supplementation had no effect on IL-6, adiponectin, GSH, SOD, and TAC levels. Conclusion Carnosine/HCD supplementation may reduce inflammatory and oxidative stress biomarkers, and potentially modulate the cardiometabolic risks associated with chronic low-grade inflammation and lipid peroxidation. Systematic Review Registration PROSPERO registration no. CRD42017075354. [ABSTRACT FROM AUTHOR]

Gaultheria trichophylla Royle is a traditional treatment for inflammatory conditions including arthritis. The objective was to evaluate the anti-arthritic activity of the extracts and salicylate-rich fractions through adjuvant-induced arthritis, histopathological analysis, radiological imaging, hematological, biochemical parameters along with using bioinformatic tools. In vivo anti-arthritic efficacy of the extract and SRF (at 100, 200, 300, and 150 mg/kg doses) was assessed using healthy albino rats. Molecular docking of identified compounds along with network pharmacology analysis helped to determine the route of action of drug. Both the extract and SRF showed dose-dependent anti-arthritic activity by decreasing the joint diameter, increase in pain threshold and body weight compared with negative control group. Along with SRF (150 mg/kg), EEGT (300 and 200 mg/kg) shows significant (P < 0.01) anti-arthritic activity by lowering levels of WBC, platelets, serum C-reactive protein (CRP), and rheumatoid factor (RF) and raising levels of RBC and Hb. The modified biochemical measures (AST, ALT, ALP, and total protein level) further supported the anti-arthritic action. Histopathology and radiology study showed that EEGT (300 and 200 mg/kg), SRF (150 mg/kg) and diclofenac (10 mg/kg) inhibited joint destruction. GCMS analysis showed the presence of methyl salicylate, sitosterol, calcifediol, and ergosta-5,22-dien-3-ol, acetate as important bioactive constituents. Moreover, as the significant node in the pharmacology network and docking against TNF-α, a classical therapeutic target in RA showed potential of G. trichophylla in treatment of RA. The results showed that G. trichophylla have effectively reduced the inflammation of the joints. [ABSTRACT FROM AUTHOR]

Background: Although atezolizumab plus bevacizumab (Atezo/Bev) therapy has been used as the preferred first-line treatment for advanced hepatocellular carcinoma (HCC), up to 26% of patients do not achieve disease control, suggesting alternative treatments might be more beneficial for such patients. We investigated key predictors for refractoriness to Atezo/Bev therapy, particularly in the first-line setting. Methods: We retrospectively analyzed 302 patients with HCC who received Atezo/Bev therapy between October 2020 and September 2022 across nine hospitals in Japan. Refractoriness was defined as best overall response (BOR) of progressive disease or stable disease and a progression-free survival (PFS) of < 180 days (RECIST v1.1). Clinical benefit was defined as BOR of partial/complete response or stable disease with PFS of ≥ 180 days. Baseline characteristics and potential predictors, identified through literature review, were compared between these groups. Stratifications of overall survival (OS), and PFS were also assessed. Results: Refractoriness was observed in 126 (41.7%) patients, while 154 (51.0%) achieved clinical benefit. Due to a significant association between the treatment line and refractory rate, the subsequent analysis focused on the first-line cohort (n = 214; 72 [33.6%] patients showed refractoriness). Among 13 potential predictors, the CRP and AFP in immunotherapy (CRAFITY) score had the best predictive performance, with refractory rates of 24.6%, 44.6%, and 57.9% in CRAFITY-0, 1, and 2 patients, respectively (p < 0.001). OS and PFS were also well-stratified by this scoring system. Conclusions: Approximately one-third of patients were refractory to first-line Atezo/Bev therapy. The CRAFITY score demonstrated superior performance in predicting refractoriness. [ABSTRACT FROM AUTHOR]

The article presents the case study of a 4-day-old infant with a rash, fussiness, and feeding difficulties. Topics include initial symptoms and presentation; the physical examination findings, which revealed a non-febrile infant with a generalized, blanching red rash but no neurological or cardiac abnormalities; and diagnostic tests, including blood count showing low platelets and elevated procalcitonin, and cerebrospinal fluid analysis with elevated white blood cells and protein.

Enterovirus (EV) and parechovirus (HPeV) are common viruses in the neonatal period, with similar seasonality and symptomatology. They also are the main causes of aseptic meningitis in newborns and children under 1 year of age. We compared the clinical signs, laboratory data, brain, and neurodevelopmental outcome of 10 infants with HPeV and 8 with EV meningitis. In patients with EV meningitis, serum C-reactive protein (CRP) values were significantly higher than those of patients with HPeV infection. Procalcitonin values were low in both groups. White blood cell (WBC) and lymphocyte values were significantly higher in EV patients. None of the infants had a brain lesion on cerebral ultrasound neither negative neurological outcome. Based solely on symptoms, it is not possible to distinguish HPeV from EV infection. C-reactive protein, WBC, and lymphocyte values might allow the physician to assume EV infection. The gold standard test for diagnosis remains real-time polymerase chain reaction on cerebral spinal fluid. [ABSTRACT FROM AUTHOR]

Purpose: The aim of this study was to investigate the clinical and multi-slice spiral computed tomography angiography (MSCTA) characteristics for the diagnosis of infected AAA. Methods: This retrospective comparative study included patients who were diagnosed with AAA at our hospital between January 2014 and May 2023. Results: A total of 40 patients were included, comprising 20 with infected AAA and 20 with non-infected AAA. Patients with infected AAA were more likely to be younger (62.9 ± 10.1 vs. 70.0 ± 4.4 years, P = 0.007) and to present with fever [7 (35%) vs. 1 (5%), P = 0.026], pain [15 (75%) vs. 2 (10%), P < 0.001], higher C-reactive protein levels (60.4 ± 57.0 vs. 4.1 ± 2.9 mg/l, P = 0.005), and higher erythrocyte sedimentation rates (47.7 ± 23.4 vs. 15.2 ± 8.3 mm/h, P < 0.001) compared to those with non-infected AAA. Moreover, those with infected AAA exhibited significantly more eccentric saccular morphology [17 (85%) vs. 1 (5%), P = 0.002], a smaller longitudinal-transverse ratio (1.12 ± 0.33 vs. 2.33 ± 0.54, P = 0.001), thicker peri-aneurysmal soft tissue (2.29 ± 1.48 vs. 0.73 ± 0.55 cm, P < 0.001), more lobulated margins [18 (90%) vs. 1 (5%), P = 0.001], lower aortic calcification scores (49 vs. 56, P < 0.001), more pneumatosis [6 (30%) vs. 0 (0%), P = 0.014], more ruptures [15 (75%) vs. 5 (20%), P = 0.002], more blurred peri-abdominal aortic fat spaces [16 (80%) vs. 2 (10%), P = 0.001], more adjacent bone destruction [5 (25%) vs. 0 (0%), P = 0.025], more involvement of the psoas major muscle [8 (40%) vs. 1 (5%), P = 0.005], more lymphadenectasis [8 (40%) vs. 1 (5%), P = 0.020], and less tortuous aortas [2 (10%) vs. 9 (45%), P = 0.034] compared with those with non-infected AAA. Conclusion: The clinical manifestations and MSCTA characteristics may differ between infected and non-infected AAA. [ABSTRACT FROM AUTHOR]

Objective: Nephropathy is among the most pervasive complications of diabetes; it frequently results in end-stage renal disease and even death. However, current biomarkers for diabetic nephropathy (DN) have limited diagnostic utility. Thus, this present study aims to examine the associations of estimated glomerular filtration rate (eGFR) with plasma concentrations of microRNA-192 (miR-192), pentraxin-3 (PTX-3), and transforming growth factor-beta1 (TGF-β1) to identify biomarkers able to distinguish late-stage from early-stage DN. Methods: In total, 50 healthy volunteers and 271 diabetes patients were enrolled in this study. Participants were stratified into seven groups according to eGFR and glycated hemoglobin (HbA1c), healthy controls, diabetes without DN (G1), diabetes with mild renal impairment (G2), and 4 DN grades (G3a, G3b, G4, and G5). Results: DN groups exhibited increases in serum miR-192 (p < 0.05), PTX-3(p < 0.05), TGF-β1(p < 0.05), malondialdehyde (p < 0.05), and xanthine oxidase (p < 0.05) levels and reductions in glutathione-s-transferase (p < 0.05) and superoxide dismutase (p < 0.05) compared to healthy controls. Among patients, eGFR was negatively correlated with miR-192, PTX-3, and TGF-β1, and positively correlated with HbA1c. In receiver operating characteristic curve analysis, miR-192 and PTX-3 demonstrated good diagnostic performance in distinguishing early from advanced DN. Conclusion: Elevated serum miR-192 and PTX-3 are associated with lower eGFR in DN, suggesting their utility as diagnostic and prognostic biomarkers. [ABSTRACT FROM AUTHOR]

Purpose: Macronutrient intakes vary across people and economic status, leading to a disparity in diet-related metabolic diseases. This study aimed to provide insight into this by: (1) identifying dietary patterns in adults using reduced rank regression (RRR), with macronutrients as response variables, and (2) investigating the associations between economic status and macronutrient based dietary patterns, and between dietary patterns with central obesity (waist circumference) and systemic inflammation (C-reactive protein [CRP]). Methods: 41,849 US participants from the National Health and Nutrition Examination Survey (NHANES), 1999–2018 were included. The percentages of energy from protein, carbohydrates, saturated fats, and unsaturated fats were used as response variables in RRR. Multivariable generalized linear models with Gaussian distribution were employed to investigate the associations. Results: Four dietary patterns were identified. Economic status was positively associated with both the high fat, low carbohydrate [βHighVsLow = 0.22; 95% CI: 0.16, 0.28] and high protein patterns [βHighVsLow = 0.07; 95% CI: 0.03, 0.11], and negatively associated with both the high saturated fat [βHighVsLow = -0.06; 95% CI: -0.08, -0.03] and the low alcohol patterns [βHighVsLow = -0.08; 95% CI; -0.10, -0.06]. The high saturated fat pattern was positively associated with waist circumference [βQ5VsQ1 = 1.71; 95% CI: 0.97, 2.44] and CRP [βQ5VsQ1 = 0.37; 95% CI: 0.26, 0.47]. Conclusion: Macronutrient dietary patterns, which varied by economic status and were associated with metabolic health markers, may explain associations between economic status and health. [ABSTRACT FROM AUTHOR]

Purpose: To investigate longitudinal associations between the vitamin D status and inflammatory markers in children and adolescents. Methods: Children from eight European countries from the IDEFICS/I.Family cohort with repeated measurements were included in this study. A linear mixed-effect model was used to model the association of serum 25(OH)D as independent variable and z-scores of inflammatory markers [CRP, cytokines, adipokines, combined inflammation score] as dependent variables, where one level accounts for differences between individuals and the other for changes over age within individuals. Results: A total of 1,582 children were included in the study. In the adjusted model, 25(OH)D levels were positively associated with adiponectin (β = 0.11 [95% CI 0.07; 0.16]) and negatively with the inflammation score (β = − 0.24 [95% CI − 0.40; − 0.08]) indicating that the adiponectin z-score increased by 0.11 units and the inflammation score decreased by 0.24 units per 12.5 nmol/l increase in 25(OH)D. In children with overweight or obesity, only a positive association between 25(OH)D and IP-10 was observed while in children with normal weight adiponectin was positively and the inflammation score was negatively associated. Associations of vitamin D with adiponectin and the inflammation score were stronger in girls than in boys and a positive association with TNF-α was observed only in girls. Conclusion: Our results suggest that an increase in vitamin D concentrations may help to regulate inflammatory biomarkers. However, it seems to be no benefit of a better vitamin D status in children with overweight/obesity unless their weight is managed to achieve an improved inflammatory marker status. [ABSTRACT FROM AUTHOR]

Telomere length, a biomarker of human aging, is related to adverse health outcomes. Growing evidence indicates that oxidative stress and inflammation contributes to telomere shortening, whereas social support may protect from telomere shortening. Despite sex differences in telomere length and social support, little is known about whether there are sex differences in the relationship between oxidative stress/inflammation and telomere length, and sex-specific moderating roles of social support in older adults. Using data from the National Health and Nutrition Examination Survey (NHANES) 1999–2002, this study assessed whether the associations between oxidative stress/inflammation and telomere length vary with sex and explored social support as a moderator in these associations among 2289 older adults. Oxidative stress was measured based on serum Gamma-glutamyl transferase (GGT), and inflammation was measured based on C-reactive protein (CRP). After adjusting for the covariates, GGT was significantly associated with telomere length in females only (β = − 0.037, 95% CI = − 0.070, − 0.005), while CRP was associated with telomere length in males only (β = − 0.019, 95% CI = − 0.035, − 0.002). Moreover, high social support mitigated the negative association between GGT and telomere length, which was more evident in females. Furthermore, social support moderated the association between CRP and telomere length in males aged 70 and above. Our findings indicated that biological mechanisms related to telomere length may vary with sex, while social support plays a sex-specific moderating role. [ABSTRACT FROM AUTHOR]

Suicidal behavior necessitates prompt diagnosis due to its severe consequences. C-reactive protein (CRP) levels may offer insights into its pathophysiology and aid in risk assessment, potentially enhancing preventive interventions and treatment strategies. The aim of this study is to assess the CRP levels in depressed patients with and without suicidal behavior. Our systematic review was registered in Prospero (#CRD42024518477). We searched five databases (PubMed, Scopus, PsycINFO, Web of Science, and CINAHL Complete) for records in English from inception to February 2024. We included observational studies that measured CRP in depressed patients with and without suicidal behavior. We used the Newcastle–Ottawa Scale (NOS) to assess the quality of the included studies. We employed a random-effects model, and the statistical analysis was conducted using Stata software version 17. Initial 632 articles narrowed to 15 for systematic review. Fifteen studies with 3652 participants included. Fourteen studies involving 3387 depressed patients, 1269 with suicidal behavior, analyzed CRP levels. Suicidal patients exhibited higher CRP levels (SMD: 0.80 [0.37, 1.23]). Analysis of seven studies with 465 participants, including 200 depressed patients with suicidal behavior and 265 healthy controls, showed higher CRP levels in depressed patients (SMD: 1.58 [0.97, 2.19]). In summary, our systematic review and meta-analysis of CRP levels in suicidal patients revealed that those with suicidal behavior exhibited higher CRP levels, suggesting possible implications for treatment approaches. • 14 studies covering 3,387 depressed patients and 1,269 with suicidal behavior found elevated CRP levels. • Suicidal patients had significantly higher CRP levels than non-suicidal depressed patients (SMD: 0.80 [0.37, 1.23]). • Depressed patients with suicidal behavior have higher CRP levels than healthy controls (SMD: 1.58 [0.97, 2.19]). [ABSTRACT FROM AUTHOR]

Background: Chronic allograft dysfunction (CAD) represents a complex process of inflammatory response, fibrosis, and tissue restoration, mediated by a myriad of proinflammatory cytokines, enzymes, and growth factors. NOD-like receptor protein3 (NLRP3) inflammasome is one of the NLR protein families. It drives proteolysis of proinflammatory caspases which induces maturation of pro-interleukin (IL)-1β and pro-IL-18. The aim of this work is to study NLRP3 inflammasome activation in patients with renal transplantation in relation to allograft function, inflammation, and renal fibrosis. Methods: Thirty renal transplant recipients (RTR): 15 patients with stable renal function (Group I), 15 patients with CAD (Group II), and 15 healthy subjects (Group III) were included. Serum and urinary NLRP3, caspase-1, and interleukin-1β were measured using an enzyme-linked immunosorbent assay (ELISA) kit. Serum high sensitivity C-reactive protein (hs-CRP) level was measured, and neutrophil-lymphocyte ratio (NLR) was calculated. Renal function was evaluated by serum creatinine (S.Cr) and estimated glomerular filtration rate (eGFR). Resistive index (RI) was calculated with Doppler ultrasonography. In patients with CAD, renal interstitial fibrosis (RIF) was graded in renal biopsies. Results: Serum NLRP3, caspase-1, serum and urinary IL-1β, and hs-CRP showed a statistically significant increase in RTR, particularly in those with CAD compared to the controls with a positive correlation with each other, their urinary level, S. Cr, hs-CRP, NLR, RI, and RIF (p < 0.001). The receiver operating characteristic curve showed high diagnostic accuracy of serum NLRP3, caspase-1, and IL-1β in discriminating patients with CAD from patients with stable renal function. Conclusion: The NLRP3-caspase1-IL-1β cascade is activated and upregulated in renal transplant recipients, particularly those with advanced renal impairment, and thus may play a role in developing CAD and renal fibrosis. They could be potential biomarkers for post-transplant outcome, follow-up, and early diagnosis. Moreover, their cascade could be a target for future anti-inflammatory therapeutic strategies for allograft dysfunction. [ABSTRACT FROM AUTHOR]

Both tissue hypoperfusion and elevated surgical stress during surgery are involved in the pathogenesis of postoperative acute kidney injury (AKI). Although intraoperative hypotension, which evokes renal hypoperfusion, has been reported to be associated with the development of postoperative AKI, there is no consensus on the association between surgical stress responses (e.g., hypertension and inflammation) and postoperative AKI. Given that intraoperative values of nociceptive response (NR) index are reportedly associated with surgical stress responses, the present study was performed to assess associations between intraoperative NR index and postoperative AKI in patients undergoing non-cardiac surgery. In this single-institutional retrospective cohort study, data of the highest and lowest values of NR index during surgery were obtained in consecutive adult patients undergoing non-cardiac surgery under general anesthesia from February 2022 to August 2023. Data on highest and lowest mean blood pressure (MBP) during surgery were also obtained. In 5,765 patients enrolled, multivariate regression analysis revealed that the development of early postoperative AKI was significantly associated with highest NR during surgery ≥ 0.920, lowest MBP during surgery < 54 mmHg, age ≥ 48 years, male sex, ASA-PS ≥ III, emergency, and duration of surgery ≥ 226 min. In addition to intraoperative hypotension, a higher level of intraoperative NR index is likely associated with higher incidence of early postoperative AKI in adult patients undergoing non-cardiac surgery under general anesthesia. [ABSTRACT FROM AUTHOR]

Although rapidly progressive glomerulonephritis (RPGN) is the main renal phenotype of microscopic polyangiitis (MPA), we aim to clarify the clinical features of slowly progressive MPA. This retrospective observational study included 12 patients diagnosed with MPA in our hospital between January 2012 and February 2022. We investigated the differences in surrogate markers, rate of decline of estimated glomerular filtration rate (eGFR) between the slowly progressive and rapidly progressive MPA groups. Of the 12 patients with MPA, 3 (25.0%) had slowly progressive MPA: MPA within 30% decrease in eGFR 3 months pretreatment, all of whom developed RPGN during the course. Patients with slowly progressive MPA had lower levels of C-reactive protein, myeloperoxidase anti-neutrophil cytoplasmic antibodies, and interleukin-6; higher levels of sialylated carbohydrate antigen KL-6. Slowly progressive MPA is not uncommon in our hospital. A linear relationship was found between slower rate of eGFR decline and lower surrogate markers of disease activity. Some MPA cases have slowly progressive glomerulonephritis leading to RPGN, which may be clinically characterized by low disease activity. It may be useful to measure myeloperoxidase anti-neutrophil cytoplasmic antibody in chronic kidney disease with concomitant urinary abnormalities to diagnose MPA with slowly progressive glomerulonephritis. KEY LEARNING POINTS: Rapidly progressive glomerulonephritis is the main renal phenotype of microscopic polyangiitis (MPA), and slowly progressive MPA is rarely observed. Slowly progressive MPA was not rare in our hospital and was characterized clinically by low disease activity and complicated by interstitial pneumonia. When encountering patients with undiagnosed chronic kidney disease complicated by interstitial pneumonia, measuring myeloperoxidase anti-nuetrophil cytoplasmic antibody regardless of the rate of renal function decline, potentially leads to the diagnosis of slowly progressive MPA. [ABSTRACT FROM AUTHOR]

Background: This study investigates the effects of spondylodiscitis on the inflammation burden in infective endocarditis patients. Methods: A prospective, observational study was conducted between September 2018 and October 2022 in a non-surgical teaching hospital. Patients with a definite or possible and treated as infective endocarditis were recruited from the Alkmaar Endocarditis Team meetings. Spondylodiscitis was diagnosed based on symptoms and radiological findings. The inflammation burden was defined as the area under the C‑reactive protein (CRP) curve. Results: 174 consecutive patients with infective endocarditis were included (mean age 73 years, 34.5% female). Concomitant spondylodiscitis was present in 32 patients (18%), frequently associated with Streptococcus species (38%). At admission, the mean level of CRP was significantly higher in patients with concomitant spondylodiscitis (p = 0.004). The median CRP area under the curve was significantly higher in spondylodiscitis patients (4.2 × 106 min.mg/l [1.2 × 105 − 1.6 × 107 min.mg/l] vs 2.0 × 106 min.mg/l [8.7 × 104 − 1.6 × 107 min.mg/l], p < 0.001). This difference remained during the whole treatment period. At 6 months of follow-up, rates of mortality and relapse of infective endocarditis were not significantly different. Conclusion: The prevalence of spondylodiscitis in non-referred patients with infective endocarditis was 18%. Endocarditis patients with spondylodiscitis had an increased inflammation burden at and during admission. This difference in normalisation of CRP levels was particularly apparent in the final phase of antibiotic treatment but not related to infectious complications. Despite an augmented inflammation burden, spondylodiscitis was not associated with mortality, cardiac surgery or infectious relapse. [ABSTRACT FROM AUTHOR]

Background: Cytoreductive surgery (CRS) and hyperthermic intraperitoneal chemotherapy (HIPEC) can be associated with significant morbidity and prolonged hospital stay. Postoperative infections account for a high burden of these complications. This study aimed to assess the predictive value of postoperative C-reactive protein (CRP) levels for overall infectious complications and anastomotic leaks. Methods: This was a single-center prospective study of patients undergoing CRS and HIPEC for peritoneal metastases between 2018 and 2020 at Maisonneuve-Rosemont Hospital in Montreal, QC, Canada. CRP levels were measured daily for 10 days following surgery. A comparison was made between patients with infectious complications and those without. Results: Ninety-nine patients were included. Thirty patients had infectious complications (30.3%) and four patients presented an anastomotic leak (4%). CRP levels were significantly higher in patients with infectious complications from postoperative days (PODs) 2–10. Daily cut-off values most accurately predicted infectious complications on day 8 (94.3 mg/L; area under the curve [AUC] 0.85, sensitivity [SE] 76.2%, specificity [SP] 94.7%, positive predictive value [PPV] 88.9%, negative predictive value [NPV] 87.8%; p < 0.0001) and day 9 (72.7 mg/L; AUC 0.89, SE 95.2%, SP 81.8%, PPV 76.9%, NPV 96.4%; p < 0.0001). Patients with infectious complications had longer operative time, higher peritoneal cancer index, and a higher number of intestinal anastomoses, while their baseline characteristics were comparable. Conclusion: Measurement of CRP helps predict infectious complications following CRS and HIPEC, particularly on PODs 8 and 9. Cut-off values are more accurate after the first postoperative week, especially in ruling out infectious complications. [ABSTRACT FROM AUTHOR]

Purpose of review: This review focuses on the association between RA and heart failure, highlighting the role of inflammation and the prevalence of heart failure with preserved ejection fraction (HFpEF) in this population. Recent findings: The incidence of heart failure in RA patients is two to three times higher than in the general population, with inflammation playing a significant role independent of traditional cardiovascular risk factors. HFpEF accounts for about half of heart failure cases and is increasingly recognized in RA patients, although it remains underdiagnosed. Atypical presentations and non-specific symptoms further complicate diagnosis. Early control of inflammation has been shown to reduce the risk of heart failure development and progression, improving both morbidity and mortality outcomes. Summary: Rheumatoid arthritis (RA) is a systemic inflammatory disease affecting approximately 1% of the population, with cardiovascular disease being the leading cause of premature death in these patients. [ABSTRACT FROM AUTHOR]

Background: Although ERAS Program had some advantages in laparoscopic distal gastrectomy (LDG), its efficacy and safety remained unclear. We conducted a systematic review and meta-analysis to assess the efficacy and safety of the ERAS group and the traditional care (TC) group in LDG. Methods: Multiple databases were retrieved from 1 January 2000 to 30 April 2023. The risk ratio (RR), standardized mean difference (SMD) and their 95% confidence interval (CI) were used to estimate the results. Results: Our meta-analysis contained 17 randomized controlled trials (RCTs) studies, which comprised 1468 patients. Regarding efficacy, the ERAS group had significantly shorter postoperative time to first flatus (SMD=-1.29 [95% CI: -1.68, -0.90]), shorter time to first defecation (SMD=-1.26 [95% CI: -1.90, -0.61]), shorter hospital stays (SMD=-0.99 [95% CI: -1.34, -0.63]), and lower hospitalization costs (SMD=-1.17 [95% CI: -1.86, -0.48]) compared to the TC group. Furthermore, in the ERAS group, C-reactive protein levels were lower on postoperative days 1, 3 or 4, and 7; albumin levels were higher on postoperative days 3 or 4 and 7; and interleukin-6 levels were lower on postoperative days 1 and 3. Regarding safety, the overall postoperative complication rate was lower in the ERAS group (RR: 0.76 [95% CI: 0.60, 0.97]), but there was no significant difference in the individual postoperative complication rate. Other indicators were also not statistically significant. Conclusion: The combination of ERAS Program with laparoscopy surgery was safe and effective for the perioperative management of patients with distal gastric cancer. [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]