Objective: This study aimed to evaluate the association between the triglyceride–glucose index (TGI) and the risk of cardiovascular disease in patients with type 2 diabetes mellitus. Methods: This study included 1348 type 2 diabetic patients who attended the endocrinology clinic at Jordan University Hospital between March 2023 and September 2023. Medical records were reviewed to identify patients with documented cardiovascular disease, and the triglyceride–glucose index (TGI) was calculated for each patient. Results: Our results showed that the TGI was higher among patients who developed any major adverse cardiovascular event (MACE), coronary artery disease (CAD), congestive heart failure (CHF), and/or myocardial infarction (MI) compared to those who did not (p < 0.001 for all comparisons). Significantly higher TGI values in males were associated with higher odds of a MACE, stroke, and CHF; higher TGI values in females were associated with higher odds of a MACE, CAD, and MI. Higher TGI values in patients younger than 60 were associated with higher odds of a MACE, CAD, CHF, and MI, while in patients older than 60, higher TGI values were associated with higher odds of CAD and MI. The TGI value that was the most predictive of a MACE in our population was >9.36, >9.39 for CAD, and >9.40 and >9.39 for CHF and MI, respectively. Conclusion: The TGI was shown to be associated with a significantly higher risk of a MACE, CAD, CHF, and MI in the whole population, along with stroke in males only. The TGI was more strongly associated with MACEs in patients younger than 60 years compared to older patients. In conclusion, the TGI was associated with cardiovascular outcomes in this diabetic cohort; however, its discriminative ability was modest (AUC 0.55–0.64). This indicates that the TGI alone is insufficient as a predictive tool and should be interpreted alongside established risk factors. Prospective studies are needed to clarify its incremental value in risk prediction.

Autism Spectrum Disorder (ASD) is a complex neurodevelopmental condition with diverse behavioral, genetic, and structural characteristics. Due to its heterogeneous nature, early diagnosis of ASD is challenging, and conventional unimodal approaches often fail to capture cross-modal dependencies. To address this, this study introduces an adaptive multimodal fusion framework that integrates behavioral, genetic, and structural MRI (sMRI) data, addressing the limitations of unimodal approaches. Each modality undergoes a dedicated preprocessing and feature optimization phase. For behavioral data, an ensemble of classifiers using a stacking technique and attention mechanism is applied for feature extraction, achieving an accuracy of 95.5%. The genetic data is analyzed using Gradient Boosting, which attained a classification accuracy of 86.6%. For the sMRI data, a Hybrid Convolutional Neural Network–Graph Neural Network (Hybrid-CNN-GNN) architecture is proposed, demonstrating a strong performance with an accuracy of 96.32%, surpassing existing methods. To unify these modalities, fused using an adaptive late fusion strategy implemented with a Multilayer Perceptron (MLP), where adaptive weighting adjusts each modality’s contribution based on validation performance. The integrated framework addresses the limitations of unimodal approaches by creating a unified diagnostic model. The transfer learning framework achieves superior diagnostic accuracy (98.7%) compared to unimodal baselines, demonstrating strong generalization across heterogeneous datasets and offering a promising step toward reliable, multimodal ASD diagnosis.

Pertussis, a highly contagious disease, contributes to a great number of hospitalizations among children, with an increased risk of morbidity and mortality. The aim of the study was to investigate the epidemiological and clinical features of B. pertussis infections among hospitalized children and to compare the clinical course according to vaccination status and the presence of co-infections. We performed a retrospective study, which included patients positive for B. pertussis detected by multiplex RT-PCR panels, from September 2022 to May 2025. Out of 2493 samples, 84 tested positive for B. pertussis (3.37%). Age-appropriate immunization was achieved in 19.1% (16/84) cases, 10.7% (9/84) were incompletely vaccinated, 9.5% (8/84) did not meet the age criteria and 60.7% (51/84) were not vaccinated. Infants ≤ 3 months were more susceptible to mixed co-infections (52%), had a more severe course, with transfers to the ICU (32%) and a prolonged average length of stay (9.2 days). Co-infections were found in 39.3% cases, rhinovirus being the most common agent (17.9%). B. pertussis and rhinovirus co-infection was associated with a decreased SpO2 level (<92%) and increased CRP and Ferritin levels.

Background: Studying the genetic characteristics and molecular mechanisms of immune regulation in horses is of great significance for protecting their genetic resources, improving breeding strategies, and enhancing their disease resistance, thereby ensuring their healthy performance in both sports and production. Aims/objectives: This study investigates the genetic characteristics and molecular mechanisms underlying immune regulation in Yili horses, comparing them with Thoroughbreds and Kazakh horses. Methods: Blood samples from each breed were analyzed for physiological, biochemical, and immune indices alongside transcriptome sequencing to identify differentially expressed genes (DEGs). Results: The results revealed significant differences in neutrophil counts, monocytes, red blood cell parameters, glucose levels, and immunoglobulins (IgA, IgG, IgM) among breeds. Yili horses exhibited intermediate values for most parameters, aligning more closely with Thoroughbreds. Transcriptomic analysis identified 3574 DEGs, enriched in immune-related pathways such as platelet activation, antigen processing, and cytokine signaling. Key genes, including TNFRSF14, IFIT3, and IL21R, correlated with immune traits, highlighting hybrid vigor in Yili horses. Functional enrichment underscored pathways like IL-17 signaling and NF-κB regulation, linking genetic differences to immune adaptability. Conclusions: These findings provide molecular insights into breed-specific immune traits, supporting strategies to enhance disease resilience in Yili horses while preserving their athletic performance. This study underscores the importance of integrating transcriptomic and phenotypic data for informed breeding practices in equine conservation and improvement.

Background and Objectives: Lupus nephritis (LN) is a major cause of mortality and morbidity in patients with systemic lupus erythematosus (SLE). Biomarkers derived from blood, urine, and multi-omics techniques are essential for enabling access to less invasive methods for LN evaluation and personalized precision medicine. Materials and Methods: The purpose of this work was to review the studies that addressed the potential role of urinary and serological biomarkers for the diagnosis, disease activity, response to treatment, and renal outcome of adult patients with LN, published over the past decade, and summarize their results with a particular emphasis being directed towards the available traditional tools. Results: Traditional biomarkers used for the diagnosis and surveillance of LN are proteinuria, urinary sediment, estimated glomerular filtration rate (eGFR), anti-double-stranded deoxyribonucleic acid (anti-dsDNA), anti-C1q, and serum complement levels. Anti-dsDNA, serum C3, and proteinuria are the conventional biomarkers with the strongest clinical evidence, with overall moderate ability in predicting LN from non-renal SLE, disease activity, renal flares, response to therapy, and prognosis. The last decade has brought significant progress in our understanding regarding the pathogenesis of LN and, consequently, several molecules, either alone or in combination panels, have emerged as potential novel biomarkers, some of them outperforming conventional biomarkers. Promising results have been suggested for urinary activated leukocyte cell adhesion molecule (ALCAM), soluble cluster of differentiation 163 (CD163), C-X-C motif chemokine ligand 10 (CXCL10), monocyte chemoattractant protein 1 (MCP-1), neutrophil gelatinase-associated lipocalin (NGAL), tumor necrosis factor-like weak inducer of apoptosis (TWEAK), and vascular cell adhesion molecule 1 (VCAM-1). Conclusions: Despite the intensive research of the last decade, no novel biomarker has entered clinical practice, and we continue to rely on traditional biomarkers to assess non-invasively LN and guide its treatment. Novel biomarkers should be validated in multiple longitudinal independent cohorts, compared with conventional biomarkers, and integrated with renal histology information in order to optimize the management of LN patients.

This study evaluated six supervised machine learning (ML) models for early detection of subclinical ketosis and low-grade ruminal acidosis in dairy cows during the transition period. Ninety-four Holstein cows were monitored for 21 days postpartum using in-line milk analyzers and intraruminal sensors that continuously recorded milk composition, behavioral, and physiological parameters. Based on clinical examination, blood β-hydroxybutyrate concentration, and fat-to-protein ratio, cows were classified as healthy (n = 44), subclinical ketosis (n = 24), or subclinical acidosis (n = 26). Among the tested models, Random Forest and XGBoost achieved perfect accuracy within this dataset, while Logistic Regression reached 89.5%, Decision Tree 84.2%, and both Naive Bayes and Support Vector Machine 78.9%. These results suggest that ensemble approaches, particularly Random Forest and XGBoost, show strong potential for integration with precision livestock technologies, but their apparent performance should be interpreted cautiously and confirmed in larger, multi-farm studies.

Background: Deep gluteal syndrome (DGS) is an underdiagnosed cause of sciatica-like pain, involving the entrapment of the sciatic nerve by various structures within the subgluteal space. While cases of ossification or calcification in the context of severe pelvic imbalance have been rarely reported, isolated SSL calcification as a primary cause of DGS remains largely unexplored and undocumented. This case report presents the first documented instance of sacrospinous ligament (SSL) calcification identified as the primary cause of DGS and its successful management with ultrasound-guided prolotherapy. Case Presentation: A 51-year-old female presented with severe, worsening left-sided sciatica of several months’ duration. Physical examination revealed an antalgic gait, positive sacroiliac joint tests, and multiple positive DGS-specific provocative tests (FAIR, Pace sign, Seated Piriformis Stretch). Radiographs and musculoskeletal ultrasound (MSK-US) confirmed calcification within the left sacrospinous ligament, with associated sciatic nerve swelling. The patient underwent three sessions of ultrasound-guided prolotherapy (dextrose 10% with lidocaine) targeting the calcification site, followed by a structured rehabilitation program. Results: The patient reported a significant reduction in pain, from a Visual Analog Scale (VAS) score of 10/10 to 1/10 within one month. All previously positive provocative tests converted to negative, indicating a resolution of the nerve entrapment. Functional mobility was fully restored. Conclusions: This case highlights isolated sacrospinous ligament calcification as a potential and previously overlooked pathological entity responsible for deep gluteal syndrome. To our knowledge, this is the first report to implicate ligamentous calcification as a primary etiological factor in DGS. Musculoskeletal ultrasound proved indispensable for both diagnosis and treatment guidance. Furthermore, ultrasound-guided prolotherapy emerged as a successful and minimally invasive therapeutic option in this case, potentially by stabilizing the ligament and reducing neurogenic inflammation. This case expands the differential diagnosis of sciatica, introduces a new target for intervention in refractory cases, and underscores the need for future studies in larger patient cohorts to validate these findings.

Anomalous origin of the Left Coronary Artery from the Pulmonary Artery (ALCAPA), also known as Bland-White-Garland syndrome, is a rare congenital coronary anomaly with an estimated incidence of 1 in 300,000 live births. While commonly diagnosed in infancy, adult presentations are exceedingly rare and pose significant diagnostic challenges. Delayed diagnosis may result in progressive myocardial ischemia, heart failure, arrhythmias, or sudden cardiac death. Surgical correction is the definitive treatment, with the goal of restoring a dual coronary artery system and preventing irreversible myocardial damage. We present the case of a 30-year-old male with a prior history of non–ST-elevation myocardial infarction who was referred for evaluation of exertional angina and symptoms of heart failure. Transthoracic echocardiography revealed a dilated left ventricle with an ejection fraction (LVEF) of 35%. Coronary angiography and cardiac MDCT identified an anomalous origin of the left circumflex artery (LCx) from the right pulmonary artery (RPA) and a coronary–pulmonary artery fistula involving the LAD. The patient underwent successful surgical correction with reimplantation of the LCx into the ascending aorta. Postoperative recovery was uneventful. At 3-month follow-up the patient was symptom-free, though echocardiography revealed persistent LV dilation and reduced LVEF, necessitating continued pharmacologic therapy and monitoring. This case highlights the importance of maintaining a high index of suspicion for ALCAPA in adult patients with unexplained cardiomyopathy or ischemic symptoms. Early diagnosis and surgical intervention remain crucial for improving long-term outcomes and preventing life-threatening complications.

Traumatic brain injury (TBI) is a major global health concern and a leading cause of long-term disability and mortality. While the primary mechanical insult is often the focus of acute care, secondary injury mechanisms—particularly cerebrovascular dysfunction—play a critical role in ongoing neural damage and poor outcomes. Increasing research highlights the role of neurovascular changes in TBI pathophysiology. This narrative review compiles evidence from the past decade on mechanisms, diagnostic methods, and treatments related to cerebrovascular dysfunction after TBI. A structured search of PubMed and Embase identified relevant clinical and preclinical studies. Key mechanisms include blood–brain barrier disruption, impaired cerebral autoregulation, microthrombosis, and oxidative stress. Diagnostic tools discussed include perfusion imaging, cerebrovascular reactivity testing, and blood-based biomarkers of vascular injury. Therapeutic strategies targeting the neurovascular unit are categorized by mechanism: anti-inflammatory agents (e.g., celecoxib, minocycline), mitochondrial protectors (e.g., Tanshinone IIA), and vasomodulators (e.g., sildenafil). We propose an integrated therapeutic approach for a multimodal treatment plan that integrates these interventions. The findings emphasize the importance of patient-specific vascular therapies to reduce secondary ischemic injury and enhance neurological recovery. Although promising preclinical data exist, clinical application remains limited. More well-designed trials are needed to confirm the safety and effectiveness of emerging therapies.

Fibromyalgia (FM) is characterized by widespread musculoskeletal pain and tenderness, cognitive dysfunction, fatigue, and insomnia. Electroacupuncture (EA) has documented efficacy against FM-associated pain, while cannabinoid receptor 1 (CB1) plays a critical role in endogenous analgesia. Herein, we examined whether pain relief initiated by EA was linked with differing cerebellar CB1 levels and signaling in an intermittent cold stress (ICS) mouse model of FM. FM-like hyperalgesia and recovery were assessed by measuring mechanical and thermal nociceptive thresholds. Compared to control mice, ICS-induced FM-model mice exhibited a significantly reduced mechanical withdrawal threshold (2.3 ± 0.1 g) and shorter thermal withdrawal latency (4.0 ± 0.5 s), indicative of mechanical and thermal hyperalgesia. Both conditions were reversed by 2 Hz EA but not sham EA. Hyperalgesia was associated with reduced CB1 receptor expression and the enhanced activity of multiple nociceptive signaling pathways (PKA, PI3K, Akt, mTOR, ERK, and NF-kB) in the mouse cerebellum. The 2 Hz EA treatment reliably reversed these abnormalities, while the sham EA treatment did not. Intracerebroventricular injection of the CB1 agonist anandamide (AEA) recapitulated the effects of EA on pain thresholds, while the analgesic effects of EA were blocked by the CB1 antagonist AM251. Precise chemogenetic stimulation at the paraventricular nucleus (PVN) of the hypothalamus reliably induced FM pain. Chemogenetic inhibition at the PVN diminished FM through the CB1 pathway in the cerebellum. Our findings suggest that dysregulation of CB1 expression and aberrant hyperactivity of nociceptive signaling pathways in the cerebellum contribute to the etiology of FM and that the upregulation of CB1 signaling mediates the analgesic efficacy of EA.