Rheumatoid arthritis (RA) and osteoarthritis (OA) are prevalent chronic joint diseases characterized by persistent inflammation, progressive cartilage degeneration, and impaired tissue repair mechanisms. While inflammatory pathways have been extensively studied, increasing attention has been directed toward the failure of inflammation resolution as a key contributor to chronic joint pathology. Specialized pro-resolving mediators (SPMs), including Maresin-1 (MaR1), play an active role in terminating inflammation and promoting tissue homeostasis. However, the relationship between MaR1 and cartilage-specific biomarkers such as Cartilage Oligomeric Matrix Protein (COMP) and Wnt1-inducible signaling pathway protein-1 (WISP-1) has not been sufficiently elucidated. This study investigated circulating MaR1 levels in RA and OA and examined their associations with serum COMP and WISP-1 as well as clinical inflammatory parameters. This cross-sectional, biomarker-based study included a total of 150 participants, comprising 50 patients with RA, 50 patients with OA, and 50 sex-matched healthy controls. Serum levels of MaR1, COMP, and WISP-1 were measured using enzyme-linked immunosorbent assay (ELISA). Demographic characteristics and inflammatory parameters, including erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), and rheumatoid factor (RF), were recorded. Intergroup comparisons were performed using one-way analysis of variance (ANOVA) followed by appropriate post-hoc tests. Serum MaR1 levels were significantly reduced in both RA (44.1 ± 2.2 ng/L) and OA (42.2 ± 3.2 ng/L) compared with controls (78.5 ± 7.5 ng/L; p < 0.001). COMP levels were significantly lower in the RA group than in the OA and control groups ( p < 0.05 and p < 0.001, respectively). Similarly, WISP-1 concentrations were decreased in both RA and OA compared with healthy controls ( p < 0.05). The marked reduction in MaR1 levels in RA and OA is consistent with altered inflammation-resolution biology. Concurrent decreases in COMP and WISP-1 may reflect changes in cartilage remodeling dynamics. Overall, MaR1 appears to be a candidate biomarker associated with inflammation-resolution pathways in arthritic diseases.

Background: Knee osteoarthritis (KOA) is a progressive degenerative joint disease characterized by extracellular matrix (ECM) degradation and dysregulated inflammatory signaling. Identifying serum biomarkers associated with radiographic severity may improve early diagnosis, staging, and monitoring of progression. Objective: To evaluate stage-dependent and non-linear changes in serum transforming growth factor-β3 (TGF-β3), ADAMTS-4, ADAMTS-5, and matrix metalloproteinase-13 (MMP-13) across Kellgren–Lawrence (KL) grades of KOA. Methods: In this cross-sectional study, 200 participants were classified into five groups according to KL grade (KL0–KL4; n = 40 per group). Individuals with systemic inflammatory, metabolic, autoimmune, renal, cardiovascular, or bone metabolism–related disorders, and those using medications affecting cartilage or bone metabolism, were excluded. After overnight fasting, serum TGF-β3, ADAMTS-4, ADAMTS-5, and MMP-13 levels were measured by ELISA. Between-group comparisons were performed using one-way ANOVA or Kruskal–Wallis tests with appropriate post-hoc analyses, and data are presented as mean ± standard deviation, unless otherwise stated. Results: ADAMTS-4 differed significantly across KL grades (overall p < 0.00001), showing a non-linear pattern with higher levels in KL1–KL3. ADAMTS-5 demonstrated a pronounced stage-dependent pattern (overall p < 0.00002), peaking in KL1 and declining toward advanced stages. Serum MMP-13 levels did not differ significantly across KL grades ( p > 0.05). TGF-β3 levels differed significantly across KL grades (overall p = 0.0015), with lower levels in KL1–KL2 compared with KL0 and intermediate levels in KL3–KL4. Conclusions: ADAMTS-4 and ADAMTS-5 exhibit biphasic, stage-dependent changes during KOA progression, consistent with early enzymatic activation followed by late-stage reduction. Early declines in TGF-β3 may reflect impaired cartilage homeostasis. The observed non-linear, stage-dependent serum patterns—particularly for ADAMTS-4, ADAMTS-5, and TGF-β3—highlight dynamic extracellular matrix remodeling during KOA progression and support the potential value of serum biomarkers as adjuncts to radiographic staging, especially in early disease.

Background/Objectives: Lightweight CNNs for medical imaging remain limited. We propose TurkerNeXtV2, a compact CNN that introduces two new blocks: a pooling-based attention with an inverted bottleneck (TNV2) and a hybrid downsampling module. These blocks improve stability and efficiency. The aim is to achieve transformer-level effectiveness while keeping the simplicity, low computational cost, and deployability of CNNs. Methods: The model was first pretrained on the Stable ImageNet-1k benchmark and then fine-tuned on a collected plantar-pressure OA dataset. We also evaluated the model on a public blood-cell image dataset. Performance was measured by accuracy, precision, recall, and F1-score. Inference time (images per second) was recorded on an RTX 5080 GPU. Grad-CAM was used for qualitative explainability. Results: During pretraining on Stable ImageNet-1k, the model reached a validation accuracy of 87.77%. On the OA test set, the model achieved 93.40% accuracy (95% CI: 91.3–95.2%) with balanced precision and recall above 90%. On the blood-cell dataset, the test accuracy was 98.52%. The average inference time was 0.0078 s per image (≈128.8 images/s), which is comparable to strong CNN baselines and faster than the transformer baselines tested under the same settings. Conclusions: TurkerNeXtV2 delivers high accuracy with low computational cost. The pooling-based attention (TNV2) and the hybrid downsampling enable a lightweight yet effective design. The model is suitable for real-time and clinical use. Future work will include multi-center validation and broader tests across imaging modalities.

This case describes a woman in her mid-40s with recurrent colorectal cancer who developed severe dermatologic toxicity during panitumumab-based therapy. Three months after treatment initiation, she developed a diffuse acneiform eruption, pronounced xerosis and painful periungual inflammation with exuberant granulation tissue consistent with epidermal growth factor receptor (EGFR)-inhibitor–induced paronychia. Multidisciplinary, guideline-concordant supportive care (including prompt topical measures and short-course systemic therapy) achieved symptom control and allowed continuation of anticancer treatment. This report underscores the importance of early recognition and structured management of EGFR-inhibitor toxicities to prevent treatment disruption and preserve quality of life.

Renal cell carcinoma (RCC) comprises a heterogeneous group of neoplasms with variable prognoses. Chromophobe RCC, a relatively uncommon subtype, generally follows an indolent clinical course but may occasionally exhibit aggressive or metastatic behaviour. This report describes a woman in the mid 60s with a history of partial nephrectomy for chromophobe RCC who subsequently developed metastatic disease. Systemic treatment with cabozantinib was initiated, resulting in dermatological toxicity. Serial imaging over 4 years demonstrated progressive metastatic involvement, including hepatic lesions. This account underscores the challenges of managing metastatic chromophobe RCC, differentiating true recurrence from potential second primary malignancies and addressing the adverse effects of targeted therapies such as cabozantinib.