Search Results (5,499)

Background: Serum markers are commonly used to diagnose bone and joint infections; however, their accuracy for diagnosing pyogenic spondylitis remains unproven. This study aimed to validate the diagnostic accuracy of inflammatory, nutritional, and immunological serum markers for spinal infections and identify the most effective combinations. Methods: The retrospective cohort study analyzed 656 patients who visited the hospital for spinal diseases between 1 January 2004 and 31 March 2021; a total of 76 were diagnosed with pyogenic spondylitis. Blood samples were analyzed for serum albumin (Alb), total protein (TP), globulin (Glb), C-reactive protein (CRP), platelet count, white blood cell count, neutrophil count, lymphocyte count, and monocyte count. Combination markers, including albumin–globulin ratio (AGR), CRP–albumin ratio (CAR), CRP–AGR (CAGR), neutrophil–lymphocyte ratio (NLR), and platelet–lymphocyte ratio (PLR), were also evaluated. Receiver operating characteristic curves were used to determine each marker’s diagnostic performance. Furthermore, multivariate analysis was performed to examine the odds ratios. Results: Patients with pyogenic spondylitis showed significantly different levels in Alb (p < 0.0001), Glb (p < 0.0001), CRP (p < 0.0001), platelet count (p < 0.0001), WBC count (p < 0.0006), neutrophil count (p = 0.0019), lymphocyte count (p = 0.0085), AGR (p < 0.0001), CAR (p < 0.0001), CAGR (p < 0.0001), NLR (p < 0.0001), and PLR (p < 0.0001). CRP (AUC = 0.80) showed good diagnostic accuracy, while combination markers CAR (AUC = 0.82) and CAGR (AUC = 0.83) had the highest areas under the curve (AUC). Multivariate analysis indicated that decreased age and the presence of comorbidities (including chronic kidney disease, chronic liver disease, malignancy, or diabetes), were independent predictors of early pyogenic spondylitis (OR_age = 0.93, OR_comorbidities = 16.98, p_age = 0.0005, and p_comorbidities = 0.0001). In patients with low-inflammatory pyogenic spondylitis, significant differences were observed in TP (p = 0.0293), Glb (p = 0.0012), CRP (p = 0.0023), platelet count (p = 0.0108), AGR (p = 0.0044), CAR (p = 0.0006), CAGR (p = 0.0004), PLR (p = 0.0192), and NLR (p = 0.0027), with CAGR showing the highest AUC (AUC = 0.70) among them. Conclusions: Serum combination markers (AGR, CAGR, CAR, PLR, and NLR) showed diagnostic value for pyogenic spondylitis, with CAGR achieving the highest accuracy. In low-inflammatory pyogenic spondylitis patients (CRP ≤ 1.0 mg/dL), these markers may aid diagnosis. Full article

Verticillium wilt (VW), caused by Verticillium dahliae, poses a significant threat to global cotton production. Through analysis of public transcriptome databases, this study identified GhSTZ, a C2H2 zinc finger protein transcription factor gene, which was significantly induced by V. dahliae. Suppressing GhSTZ expression via virus-induced gene silencing significantly enhanced cotton resistance to VW. This resistance manifested as a 1.2-fold increase in lignin deposition, optimized ROS (reactive oxygen species) homeostasis, and a 1.3-fold elevation in glucose levels. Transcriptome analysis revealed 338 differentially expressed genes in GhSTZ-silenced plants, with 97 upregulated and 241 downregulated. Key downregulated genes included PME (pectin methylesterase) and PG1-pec (polygalacturonase) in the pentose phosphate pathway, while the key upregulated genes comprised C4H (cinnamate 4-hydroxylase) and C3H (p-coumarate 3-hydroxylase) in the phenylpropanoid biosynthesis pathway. Notably, in the plant–pathogen interaction signaling pathway, approximately half of the genes exhibited upregulated expression while the other half showed downregulation. Protein–protein interaction network analysis further revealed cooperative interaction between PME and the secoisolariciresinol dehydrogenase SIRD. This study is the first to elucidate GhSTZ as a negative regulator that compromises cotton disease resistance through a tripartite mechanism. These findings offer a novel approach to enhancing crop disease resistance by targeting the negative regulatory genes. Full article

Chronic inflammation underpins the pathogenesis of both rheumatoid arthritis (RA) and neurodegenerative conditions such as Alzheimer’s disease (AD). This narrative review explores the role of C-reactive protein (CRP), particularly its monomeric form (mCRP), as a central molecular link connecting systemic autoimmune inflammation with neuroinflammatory and vascular pathology. In RA, fibroblast-like synoviocytes (FLSs) are activated by CRP through CD32/CD64-mediated signaling, triggering proinflammatory cascades involving NF-κB and p38 MAPK. Recent studies have highlighted that locally synthesized CRP within the synovium may convert to mCRP, amplifying inflammation and tissue damage. Beyond RA, mCRP has been identified within amyloid-beta (Aβ) plaques in AD brains, suggesting a direct role in neurodegenerative pathology. Experimental models also demonstrate that mCRP is upregulated in stroke-affected brain regions and associated with complement activation and blood–brain barrier (BBB) disruption, which is central to AD progression. The convergence of pathways involving IL-6, RAGE (receptor for advanced glycation end-products), and mCRP-mediated complement activation reveals a shared axis of inflammation between RA and AD. This highlights the potential of mCRP not only as a biomarker of chronic inflammation but also as a therapeutic target. Furthermore, evidence from periodontal disease and cardiovascular comorbidities highlights the systemic nature of mCRP-driven inflammation, offering insights into the mechanisms of disease overlap. This review advocates for further mechanistic studies into mCRP signaling, particularly its role at the interface of systemic and neuroinflammation, with the goal of identifying new interventional strategies for patients with RA at elevated risk of neurodegenerative and vascular complications. Full article

The associations between sialylated anti-cyclic citrullinated peptide (anti-CCP) antibodies bearing α-2,6-sialic acid (SIA), ST6Gal1 and Neu1 enzymes, and clinical disease activity measures such as disease activity score 28 (DAS28), the Simplified Disease Activity Index (SDAI), and Clinical Disease Activity Index (CDAI) are unknown in rheumatoid arthritis (RA). To address this gap, this study included 97 patients with RA evaluated at baseline (month 0) and at 6 and 12 months. At each visit, blood cells were analyzed for B-cell ST6Gal1 and Neu1 expressions, and plasma samples were assessed for ST6Gal1 and Neu1 levels. The erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), monocyte chemotactic protein-1 (MCP-1), and IgG anti-CCP with its α-2,6-SIA modification were measured. Disease activity measures, namely DAS28-ESR, DAS28-CRP, DAS28-MCP-1, SDAI, and CDAI, were calculated. Correlations and Receiver Operating Characteristics among ST6Gal, Neu1, SIA/anti-CCP ratios, and disease activity measures were assessed. Multivariate regression analyses were performed to reveal confounding factors in such correlations. The total SIA content of anti-CCP antibodies was inversely correlated with B-cell Neu1 levels (ρ = −0.317 with p = 0.013. Plasma (free-form) Neu1 levels were inversely correlated with SIA/IgG anti-CCP ratios (ρ = −0.361, p = 0.001) in the DAS28-MCP-1 < 2.2 (remission) subgroup. No such correlation was observed for the DAS28-ESR, DAS28-CRP, SDAI, or CDAI subgroups. B-cell ST6Gal1 levels correlated inversely with SDAI ≤ 11 and DAS28-MCP-1 ≤ 3.6 combined remission and low-disease-activity subgroups (ρ = −0.315 with p = 0.001 and ρ = −0.237 with p = 0.008, respectively). The same was observed for B-cell ST6Gal1/Neu1 ratios correlating with the SDAI ≤ 11 subgroup (ρ = −0.261, p = 0.009). Nevertheless, B-cell ST6Gal1/Neu1 ratios against SDAI ≤ 11 and DAS28-MCP-1 ≤ 3.6 subgroups produced significant area-under-curve (AUC) values of 0.616 and 0.600, respectively (asymptotic p-Values 0.004 and 0.018, respectively). Through multivariate regression analyses, we found that biologics (a confounding factor) interfered with p-Values related to the B-cell ST6Gal1 enzyme but did not interfere with p-Values related to the pure B-cell Neu1 enzyme. In addition, disease duration interfered with p-Values related to the pure Neu1 enzyme on B-cells or in plasma. Moreover, plasma ST6Gal1/Neu1 ratios against the DAS28-MCP-1 < 2.2 remission subgroup produced an AUC of 0.628 and asymptotic p = 0.003. Therefore, it is suggested that B-cell ST6Gal1/Neu1 ratios can be used as clinical indicators for the combined remission and low-disease-activity subgroup of SDAI and DAS28-MCP-1 formulae. Plasma ST6Gal1/Neu1 ratios are also good indicators of DAS28-MCP-1 remission. Full article

Background: Gut microbiota dysregulation is increasingly recognized as a key contributor to the progression of liver cirrhosis and its complications, particularly hepatic encephalopathy. Fecal microbiota transplantation (FMT) has emerged as a novel therapeutic strategy aimed at restoring intestinal microbial homeostasis and modulating systemic inflammation. Methods: This prospective, single-center clinical trial evaluated the short-term safety and efficacy of FMT in patients with alcohol-related liver cirrhosis. Clinical assessment, liver stiffness (via elastography), steatosis (controlled attenuation parameter), inflammatory biomarkers, and extended biochemical panels were analyzed at baseline, one week and one month post-FMT. A control group receiving standard medical therapy was used for comparison. Results: FMT was associated with a significant reduction in hepatic encephalopathy severity (p = 0.014), sustained improvements in liver stiffness (p = 0.027) and decreased steatosis (p = 0.025). At one month, C-reactive protein and neutrophil-to-lymphocyte ratio both declined significantly (p = 0.043), indicating a measurable anti-inflammatory effect. No serious adverse events were recorded. In comparison with controls, FMT recipients showed lower systemic inflammation and improved neuropsychiatric status. Conclusions: FMT demonstrated a favorable safety profile and yielded early clinical and biochemical benefits in patients with cirrhosis. These preliminary findings support the potential utility of microbiota-based interventions in chronic liver disease and warrant validation in larger, multicenter trials. Full article

Background: Systemic lupus erythematosus (SLE) is an autoimmune disorder associated with premature atherosclerosis and vascular impairment. However, the role of endocan, a biomarker of glycocalyx injury, is not completely clarified in the detection of vascular damage. Therefore, our aim was to investigate serum endocan in comparison with conventional inflammatory markers, arterial stiffness parameters, and carotid ultrasound findings in a cohort of young patients with SLE. Methods: We enrolled 47 clinically active young SLE patients (40 females and 7 males) in the study. Arterial stiffness indicated by augmentation index and pulse wave velocity (PWV) was measured by arteriography. Brachial artery flow-mediated dilatation and common carotid intima-media thickness were detected by ultrasonography. The serum concentrations of endocan, IL-6, MPO, MCP-1, MMP-3, -7, and -9, as well as TNFα, were measured by an enzyme-linked immunosorbent assay (ELISA). Results: We found significant negative correlations between serum endocan and both CH50 and C3. Serum endocan was higher in active SLE patients compared to inactive patients, however, the difference was not statistically significant (241.4 (183–295) vs. 200.3 (167–278) pg/mL; p = 0.313). Serum TNFα and hsCRP significantly correlated with PWV. However, we did not detect significant correlations between vascular diagnostic tests and serum endocan levels. Conclusions: Based on our results, serum endocan is associated with disease activity; however, further studies are needed to clarify the value of serum endocan in the cardiovascular risk estimation of SLE patients. Measurement of serum endocan, as well as the routine assessment of arterial stiffness parameters, should be integrated into the comprehensive management plans of young patients with SLE. Full article

Excessive alcohol consumption is associated with various health complications, including liver damage and systemic inflammation. Probiotic interventions have emerged as promising strategies to mitigate alcohol-induced harm, yet their mechanisms of action remain incompletely understood. This randomized, double-blind, placebo-controlled clinical trial aimed to evaluate the protective effects of Weizmannia coagulans BC179 in chronic alcohol consumers. Seventy participants with a history of long-term alcohol intake were randomly assigned to receive either BC179 (3 g/day, 1 × 10¹⁰ CFU) or a placebo for a 30-day intervention period. Following alcohol ingestion, dynamic monitoring of blood alcohol concentration (BAC), inflammatory and oxidative stress biomarkers, and serum metabolomic profiles was conducted. BC179 supplementation significantly reduced BAC and enhanced the activities of alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH), while decreasing levels of alkaline phosphatase (ALP), high-sensitivity C-reactive protein (hs-CRP), tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6). Conversely, the anti-inflammatory cytokine interleukin-10 (IL-10), superoxide dismutase (SOD), and glutathione (GSH) were significantly upregulated. Levels of cytochrome P4502E1 (CYP2E1) and malondialdehyde (MDA) were also markedly reduced. Metabolomic analysis revealed significant modulation of taurine and hypotaurine metabolism, as well as downregulation of caffeine-related pathways. Collectively, these findings indicate that W. coagulans BC179 alleviates alcohol-induced discomfort by enhancing alcohol metabolism, attenuating inflammation, reducing oxidative stress, and modulating key metabolic pathways. This probiotic strain may represent a promising adjunctive strategy for managing alcohol-related health issues. Full article

Background/Objectives: Patients with erythropoietic protoporphyria (EPP) have a decreased activity of the ferrochelatase enzyme which converts protoporphyrin IX (PpIX) into heme, causing PpIX to accumulate in erythrocytes. The ensuing release of PpIX to the skin when exposed to visible light causes a phototoxic reaction with severe pain, erythema, and edema. Erythrocyte PpIX levels in adult EPP patients are rather stable and largely unaffected by pharmaceutical treatments. It is important to be aware of drugs causing an increase in PpIX as this may increase the risk of liver toxicity. Method: The patient had blood samples taken regularly for analyses of PpIX, znPpIX, ALT, ALP, iron, leucocytes, C-reactive protein, and hemoglobin before, during, and after treatment with teriflunomide. Additionally, we tested if teriflunomide increased PpIX in vitro. Results: A female EPP patient was treated for 7 years with teriflunomide for multiple sclerosis attacks. During treatment, her natural PpIX level increased from about 30 µmol/L to about 200 µmol/L, without significant simultaneous changes in hemoglobin, iron levels, alanine transaminase (ALT), or alkaline phosphatase (ALP). The patient experienced no increase in photosensitivity. In vitro addition of teriflunomide did not affect PpIX levels. Discussion: In patients with lead intoxication, the release of PpIX from erythrocytes is very slow. The increase in PpIX during treatment with teriflunomide compared to periods with no medication could be caused by a similar slow PpIX release from the erythrocytes. This theory is supported by the patient’s unchanged light sensitivity and stable levels of hemoglobin, iron, and liver enzymes. Full article

Background: Diagnosing and predicting outcomes in elderly patients with heart failure (HF) is challenging due to atypical symptoms and the limited value of natriuretic peptides, highlighting the need to search for new risk stratification biomarkers in this population. Aim: We aimed to analyze factors associated with the composite endpoint (all-cause mortality or decompensated HF-related hospitalization) within six months of follow-up in elderly patients with left ventricular systolic dysfunction and decompensated HF, with particular emphasis on copeptin concentration. Methods: This is a retrospective observational study based on prospectively collected data of 279 consecutive elderly patients hospitalized between 2018 and 2023 due to decompensated HF. Inclusion criteria were age > 65 years, history of HF diagnosed at least two years before the index hospitalization, and left ventricular ejection fraction < 40% on admission echocardiography. Serum copeptin levels were measured using an Enzyme-Linked Immunosorbent Assay (ELISA) (Human Copeptin ELISA kit, Sunred Biological Technology Co, Shanghai, China). The primary endpoint was all-cause mortality or decompensated HF-related hospitalization during the six-month follow-up. Results: The median age of the study population was 77 years (IQR: 69–79), and 221 (79.2%) were male. The composite endpoint occurred in 110 patients (38.1%). Multivariable analysis showed that serum concentrations of copeptin [hazard ratio (HR) 1.053 (1.042–1.064), p < 0.0001], bilirubin [HR 1.085 (1.057–1.114), p < 0.0001], uric acid [HR 1.005 (1.003–1.006), p < 0.0001], high-sensitivity C-reactive protein (hs-CRP) [HR 1.208 (1.088–1.342), p < 0.0001], and sodium [HR 1.111 (1.025–1.203), p = 0.01], as well as ischemic etiology of HF [HR 3.969 (2.396–6.575), p < 0.0001], were independently associated with worse outcomes. Conclusions: Our study demonstrated that higher concentrations of copeptin, bilirubin, hs-CRP, and uric acid, as well as lower sodium levels and ischemic etiology of HF, were independently associated with all-cause mortality or HF-related hospitalization during a six-month follow-up in elderly patients with decompensated HF. Full article

Traumatic brain injury (TBI) is a major cause of long-term neurological impairment, with aging amplifying vulnerability and worsening recovery. Older individuals face greater cognitive and motor deficits post-TBI and respond less effectively to treatments, as both aging and TBI independently elevate neuroinflammation and cognitive decline. This study evaluated the therapeutic effects of human adipose-derived stem cell small extracellular vesicles (hASC-sEVs) on neurological recovery and neuroinflammation in a mouse model of TBI. Male C57BL/6 mice (3, 15, and 20 months old) underwent controlled cortical impact (CCI) and received intranasal hASC-sEVs 48 h post-injury; control groups received PBS. A dose–response study at 7 days post injury (dpi) identified 20 µg as the optimal therapeutic dose, improving motor function, reducing neuroinflammation, and enhancing neurogenesis. This was followed by a 30-dpi study assessing cognitive function, neuroinflammation, neurogenesis, and proteomic changes in microglia and astrocytes via mass spectrometry. hASC-sEV treatment significantly improved behavioral outcomes and reduced neuroinflammatory markers (GFAP, IBA-1, and MHC-II), with reduced efficacy observed in older mice. Proteomics revealed that hASC-sEVs reduce inflammatory proteins (TNF-α, IL-1β, IFNG, CCL2) and modulated mitochondrial dysfunction and reactive oxygen species. These results highlight hASC-sEVs as a promising cell-free therapy for improving TBI outcomes, especially in aging populations. Full article

Background: Enterotoxigenic Bacteroides fragilis (ETBF) carries the bft toxin gene, which influences the host immune response and inflammatory pathways and promotes colorectal cancer (CRC). This study investigated the potential role of ETBF in CRC liver metastasis. Methods: We reviewed the records of 226 consecutive patients who underwent curative-intent (R0) resection of CRC liver metastases. ETBF DNA in fresh-frozen metastasis specimens was quantified using droplet digital PCR (ddPCR). Patients were grouped into very-low (≤80%; N = 178), low (80–90%; N = 24), and high (>90%; N = 24) ETBF-DNA groups. Three tissue cores per specimen were stained for CD8, CD4, CD20, FOXP3, CD68, and CD163, and immune-cell densities were measured digitally (cells/mm²). Results: ETBF DNA was detected in 219 of 226 lesions (96.9%). The densities of cytotoxic CD8⁺ T-cells, effector CD4⁺ T-cells, CD20⁺ B-cells, and CD163⁺ macrophages did not differ significantly by ETBF-DNA group (P_trend all > 0.12). FOXP3⁺ regulatory T-cells (Tregs) decreased (P_trend = 0.010), and CD68⁺ macrophages increased (P_trend = 0.020) as ETBF-DNA levels increased. ETBF-DNA levels in CRC liver metastases were not associated with disease-free survival or overall survival or serum C-reactive protein levels. Conclusions: ETBF was present in almost all CRC liver metastases. Higher ETBF levels were associated with a tumor-immune microenvironment enriched in CD68⁺ macrophages and deficient in FOXP3⁺ Tregs, suggesting that ETBF facilitates immune evasion without loss of effector lymphocytes. Although ETBF-DNA levels did not predict survival in this single-center cohort, the potential role of ETBF in immune remodeling and as a candidate biomarker and therapeutic target in metastatic CRC warrants further study. Full article

Background: Parapneumonic effusion is a common complication of community-acquired pneumonia and can range from a simple inflammatory transudate to an organized purulent collection, known as empyema. Progression to empyema significantly worsens the prognosis, leading to increased morbidity, longer hospital stays, and a greater need for invasive interventions. Several risk factors for pleural effusion and progression to empyema have been identified, but the absence of standardized criteria underline the need for better risk stratification. We analyzed clinical and laboratory data from a cohort of children hospitalized with pneumonia associated with pleural effusion or empyema, to identify predictive risk factors associated with these complications. Methods: We retrospectively analyzed clinical and laboratory data from patients admitted to our Pediatric Emergency Department with pneumonia complicated by pleural effusion and compared patients with simple effusion to those with empyema. Results: Seventeen children with simple pleural effusion and eighteen with empyema were enrolled. Patients with empyema had higher absolute neutrophil count, higher levels of C-reactive protein, procalcitonin, and ferritin, and lower serum albumin levels. Furthermore, they took a longer time for normalization of inflammatory markers when compared with those with pleural effusion. Invasive interventions, such as pleural drainage, and the need for intensive care were more frequent in the empyema group. Conclusions: Pleural effusion and empyema are two common complications of pediatric community-acquired pneumonia. Children developing pleural empyema have higher inflammatory markers and lower levels of serum albumin compared to patients with simple pleural effusion. Morbidity is significantly worse in children with empyema as they are more prone to require invasive interventions and intensive care. Full article

Background/Objectives: The transcription factor 7-like 2 (TCF7L2) rs7903146 polymorphism has been strongly associated with type 2 diabetes mellitus (T2DM) in various populations; however, its impact on different ethnic groups is not fully understood. Given the distinct minor allele frequency in Chinese populations, this study aimed to analyze the association of rs7903146 with the risk of T2DM in a Han Chinese cohort and its relationship with relevant clinical parameters. Methods: We conducted a case–control study including 600 patients with type 2 diabetes mellitus (T2DM) and 511 sex-matched non-diabetic controls of Han Chinese descent. The TCF7L2 rs7903146 (C/T) polymorphism was genotyped using a TaqMan™ SNP assay. Clinical parameters, including body mass index (BMI), fasting plasma glucose, hemoglobin A1c, lipid profile, and high-sensitivity C-reactive protein (hs-CRP), were compared between genotypes. Logistic regression analyses were performed under a dominant genetic model (CT/TT vs. CC), adjusting for age, sex, systolic and diastolic blood pressure, BMI, and smoking status. Subgroup analyses were conducted by sex, BMI category, age at diagnosis, and family history of T2DM. Given the exploratory nature of this study and the low frequency of the TT genotype, no formal correction for multiple testing was applied. Results: Frequencies of the CT and TT genotypes were higher in the diabetic group (p = 0.045) and were significantly associated with an increased risk of T2DM under a dominant genetic model (adjusted OR = 2.24, p = 0.025). Individuals with CT/TT genotypes had elevated fasting glucose and hs-CRP levels; these genotypes were also linked to higher BMI in the female T2DM patients. The T allele frequency varied across ethnic groups, being lowest in East Asians and highest in Latin (Brazilian/mixed ancestry) populations. Mechanistically, the T allele may contribute to T2DM via altered TCF7L2 expression, impaired insulin secretion, inflammation, and metabolic dysregulation. Conclusions: The TCF7L2 rs7903146 T allele was associated with an increased risk of T2DM and higher fasting glucose and hs-CRP levels in this Han Chinese cohort. The CT/TT genotypes were also associated with higher BMI in the female T2DM patients. While the findings are consistent with the known effects of this variant in other populations, mechanistic hypotheses such as the involvement of inflammatory or metabolic pathways remain hypothetical and warrant further functional validation. Full article

Periprosthetic joint infection (PJI) is a devastating complication of joint arthroplasty surgery that is difficult to both diagnose and treat. Misdiagnosing a prosthetic infection has terrible consequences for both the patient and healthcare system. No currently used diagnostic test fulfills the requirements to be considered a gold standard. This shortcoming has been overcome through the implementation of multi-criteria diagnostic protocols elaborated by societies including the Infectious Diseases Society of America, International Consensus Meeting and European Bone and Joint Infection Society, using a combination of clinical, paraclinical and molecular findings in order to achieve the best accuracy in diagnosing PJI. This review aims to survey the current state of the techniques and technologies used for the diagnosis of PJI, investigating the accuracies of serum biomarkers (e.g., C-reactive protein, Interleukin-6, procalcitonin, D-dimers, Serum Intercellular Adhesion Molecule-1), synovial biomarkers (e.g., Antimicrobial peptides, lipocalin-2, leukocyte esterase, calprotectin), tissue biomarkers (e.g., Toll-like receptors, CD15) and advanced molecular techniques (e.g., Polymerase chain reaction, Metagenomic next-generation sequencing), as well as describing their ongoing limitations. In the search for an accurate, inexpensive and fast diagnostic test for PJI, we conclude that the accuracies of the currently studied biomarkers could be further enhanced through the development of novel detection technologies. Full article

Background and Objectives: Carotid artery stenosis is an inflammatory vascular disease closely linked to atherosclerosis and associated with inflammatory biomarkers. The neutrophil/albumin ratio (NAR) is a novel promising biomarker in assessing cardiovascular disease severity. This study aimed to evaluate the relationship between NAR and lesion severity in patients with carotid artery stenosis. Materials and Methods: This retrospective, single-center, comparative study included 625 asymptomatic patients who underwent digital subtraction angiography (DSA) for suspected high-grade carotid artery stenosis between 2012 and 2022. Patients were classified into two groups based on stenosis severity: critical carotid artery stenosis (≥70% stenosis) and non-critical carotid artery stenosis (<70%). Only asymptomatic patients were included; patients with symptoms were excluded. NAR was calculated preoperatively as neutrophil count divided by serum albumin. Additional inflammatory markers, such as neutrophil–lymphocyte ratio (NLR) and C-reactive protein (CRP) to albumin ratio (CAR), were also analyzed. Results: Severe carotid artery stenosis was detected in 191 of the patients who underwent DSA. Individuals in the critical carotid artery stenosis group were older and had a higher prevalence of diabetes mellitus and hypertension (51 (45–57) vs. 60 (54–68), p < 0.001; 143 vs. 83, p = 0.025; 193 vs. 104, respectively, p = 0.021), as well as higher neutrophil counts (4.3 (3.2–6.2) vs. 8.1 (4.9–12.5), p < 0.001), NLR (2.2 (1.4–3.2) vs. 4.2 (2.3–8.9), p < 0.001), while CRP (3.8 (1.8–8) vs. 5.7 (3.6–7.6), p = 0.005) and CAR (0.9 (0.5–1.9) vs. 1.6 (0.8–2.1), p < 0.001) values were significantly higher. NAR was higher in patients of the critical carotid artery stenosis group than the non-critical (1.1 (0.8–1.6) vs. 2.1 (1.4–3.2), p < 0.001). Multivariate analysis identified NAR as an independent predictor of carotid artery stenosis (Odds Ratio [OR]: 3.432; 95% Confidence Interval [CI]: 2.116–5.566; p < 0.001). The best cut-off value of NAR for predicting critical carotid artery stenosis was 1.47, which provided 73.8% sensitivity and 70.5% specificity. Conclusions: NAR, which can be easily measured through a simple blood test, demonstrated moderate sensitivity and specificity in predicting critical carotid artery stenosis, suggesting its potential role as a supportive marker in clinical risk assessment. Full article