Search Results (2,050)

Background/Objectives: Traumatic brain injury (TBI) often results in heterogeneous recovery across cognitive and motor domains. However, the prognostic implications of motor–cognitive imbalance at the time of rehabilitation discharge remain unclear. This study investigated whether discharge patterns of motor–cognitive imbalance are associated with functional outcomes at 1- and 2-year follow-up in individuals with moderate-to-severe TBI. Methods: We conducted a retrospective cohort study using the Traumatic Brain Injury Model Systems (TBIMS) National Database. Adults discharged from inpatient rehabilitation with available Functional Independence Measure (FIM) motor and cognitive subscores were included (n = 8342). Participants were classified as cognitive-dominant, motor-dominant, or balanced based on standardized discrepancies between FIM motor and cognitive scores. Propensity score matching was performed against the balanced group, yielding a matched cohort of 1310 participants. Outcomes included the Disability Rating Scale (DRS), FIM (total and subscales), Glasgow Outcome Scale—Extended (GOSE), and Participation Assessment with Recombined Tools—Objective (PART-O) at 1 and 2 years. Results: The matched cohort included cognitive-dominant (n = 524), motor-dominant (n = 524), and balanced (n = 262) participants with good covariate balance. Compared with the balanced group, the cognitive-dominant group showed lower disability severity (DRS) at 1 year (β = −0.45; 95% CI, −0.81 to −0.09) and 2 years (β = −0.40; 95% CI, −0.78 to −0.03), and higher FIM total scores at both time points. The motor-dominant group demonstrated higher FIM motor scores but lower odds of favorable disability status (DRS ≤ 3) at 2 years (OR = 0.52; 95% CI, 0.31–0.88). GOSE and PART-O outcomes did not differ significantly across groups. Conclusions: Discharge motor–cognitive imbalance patterns were associated with modest but distinct differences in long-term disability severity and functional independence after moderate-to-severe TBI. The direction of imbalance may provide additional prognostic context beyond total functional scores and support domain-targeted post-acute rehabilitation planning. Full article

Background: Intracerebral hemorrhage (ICH) is a devastating subtype of stroke, in which neuroinflammation and blood–brain barrier (BBB) disruption are secondary pathophysiological events that drive progressive brain injury. Histone lysine demethylase JMJD3 (Jumonji C domain-containing protein 3) is a master epigenetic switch governing inflammatory signaling; however, its participation in ICH-induced vascular disruption and its possible mechanism remain elusive. Objective: To examine the expression patterns of JMJD3 in the context of ICH and to evaluate the therapeutic potential of its specific inhibitor, GSK-J4, in attenuating neuroinflammation and BBB disruption in a murine ICH model. Methods: Hemin treatment of a mouse C8-D1A astrocytic cell line was used to develop an in vitro ICH model. The transcript level of the Jmjd3 gene and its correlation with pro-inflammatory signaling were analyzed with or without GSK-J4 pretreatment. ICH in vivo was created experimentally in adult male C57BL/6 mice through stereotactic striatal injection of collagenase IV, and the mice were randomly assigned to sham, ICH + vehicle, and ICH + GSK-J4 (30 mg/kg intraperitoneally (i.p.), every other day starting three days before ICH) groups. At three days post-ICH, ipsilateral brain tissues were collected to detect JMJD3 cellular localization, pro-inflammatory mediator levels, tight junction protein expression, BBB ultrastructure, and hematoma volume. White matter integrity and neuronal recovery were assessed on day 7, and sensorimotor function was assessed longitudinally on days 1, 3, 5, 7, and 14. Results: Jmjd3 gene transcription was upregulated in hemin-treated astrocytes and correlated positively with IL-6 pro-inflammatory signaling activation. In vivo, the co-localization of JMJD3 with the astrocytic identifier glial fibrillary acidic protein (GFAP) was markedly increased in the area adjacent to the hematoma at three days post-ICH. GSK-J4 administration significantly suppressed the pro-inflammatory signaling cascade by decreasing the levels of inducible nitric oxide synthase (iNOS), tumor necrosis factor-α (TNF-α), and matrix metalloproteinase-9 (MMP-9), enhanced brain vascular structural and functional integrity by upregulating tight junction proteins zonula occludens protein-1 (ZO-1) and claudin-5, improved BBB ultrastructural integrity, and decreased hematoma volume at three days post-ICH. Furthermore, GSK-J4 administration promoted white matter integrity (increased myelin basic protein [MBP] expression) and neuronal recovery (increased neuron-specific nuclear protein [NeuN] expression) at seven days post-ICH and significantly improved the performance of ICH mice in sensorimotor behavioral tests. Conclusions: Astrocytic JMJD3 is upregulated following ICH and promotes neuroinflammation, which in turn mediates BBB disruption. Pharmacological inhibition of JMJD3 by GSK-J4 attenuates neuroinflammation and subsequent BBB damage, accelerates hematoma resolution, and promotes histological and functional recovery after ICH, likely by downregulating MMP-9 expression. These findings identify astrocytic JMJD3 as a novel epigenetic therapeutic target for acute ICH. Full article

Background and Clinical Significance: Chromothripsis represents a catastrophic genomic event in plasma cell myeloma (PCM) associated with poor prognosis. We report a case of newly diagnosed PCM with complex cytogenetic abnormalities indicative of genomic instability. Case Presentation: A 67-year-old man presented with acute dyspnea and was found to have severe acute kidney injury, anemia, hypercalcemia, and IgG lambda monoclonal gammopathy. Bone marrow biopsy revealed plasma cell infiltration. Comprehensive FISH analysis demonstrated a complex pattern with gain of 1q, monosomy 13, and multiple numeric and structural abnormalities affecting chromosomes 5, 9, and 15, suggestive of a chromothripsis-like pattern. Despite requiring hemodialysis, the patient achieved complete renal recovery and >99% reduction in serum-free light chains after one cycle of CyBorD plus daratumumab, which was continued for four cycles. Follow-up bone marrow evaluation at three months confirmed complete histologic, flow cytometric, and cytogenetic remission, allowing for preparation for autologous stem cell transplantation. Conclusions: This case demonstrates that exceptional clinical responses can be achieved in high-risk disease with contemporary quadruplet regimens. While the long-term durability of such responses in genomically unstable cases remains uncertain, this case highlights the importance of comprehensive cytogenetic characterization to identify and monitor genomic instability in PCM. Full article

Background: Tile C1.2 pelvic ring injuries are characterized by combined rotational and vertical instability and require reliable posterior stabilization. The aim of this exploratory biomechanical study was to compare the construct-level mechanical behavior of three posterior pelvic ring fixation strategies in a standardized Tile C1.2 injury model while maintaining identical anterior symphyseal fixation in all specimens. Methods: Nine fourth-generation composite pelvic specimens with a simulated Tile C1.2 injury pattern were allocated to three groups (n = 3 per group) according to posterior fixation method: anterior sacroiliac plating, sacroiliac screw fixation, and ilioiliac plate fixation. All specimens received the same anterior symphyseal plate. Mechanical testing was performed under monotonic axial compression using a universal testing machine and a custom acetabular support designed to ensure reproducible load transmission. A preload of 50 N was applied before data acquisition, after which displacement was zeroed. Loading was then continued up to a predefined maximum load of 1.9 kN. Axial displacement was obtained from actuator travel, and apparent axial secant stiffness was evaluated at predefined load levels. Results: Across the tested loading range, sacroiliac screw fixation demonstrated the lowest axial displacement and the highest apparent axial secant stiffness, whereas ilioiliac plate fixation showed the greatest displacement and the lowest stiffness values. Anterior sacroiliac plate fixation showed intermediate mechanical behavior. No structural failure occurred within the tested load range. Conclusions: Within the limits of this small synthetic biomechanical study, the investigated posterior fixation strategies showed different construct-level displacement and stiffness profiles under monotonic axial compression when anterior fixation was kept constant. Among the tested posterior constructs, sacroiliac screw fixation was associated with lower displacement and higher apparent stiffness within this experimental model. Full article

Diabetic retinopathy (DR) is a common cause of vision loss in diabetes, and it often progresses without early symptoms. DR reflects injury of the retinal neurovascular unit (NVU), which includes neurons, Müller glia, astrocytes, endothelial cells, pericytes, and immune cells. Chronic hyperglycemia drives oxidative stress, advanced glycation end products–receptor for advanced glycation end products (AGE–RAGE) signaling, mitochondrial injury, and low-grade inflammation. These changes disrupt endothelial junctions, promote leukostasis, weaken pericyte support, increase basement membrane thickening, and lead to capillary dropout and hypoxia. Hypoxia-related signaling increases anti-vascular endothelial growth factor (VEGF) activity, which raises vascular leakage and supports neovascular disease. Glial stress and microglial activation add cytokines and reactive oxygen species, and neural dysfunction can appear early and can weaken neurovascular coupling. Modern diabetes care changes the short-term risk landscape because potent therapies can lower HbA1c quickly. Large and rapid HbA1c reductions can trigger early worsening of diabetic retinopathy (EWDR), mainly in patients with high baseline HbA1c and moderate-to-severe baseline DR. Semaglutide’s retinopathy complication signal in SUSTAIN-6 fits an EWDR-like pattern that tracks with rapid glycemic improvement in vulnerable eyes. In parallel, surgery adds acute stress, inflammation, glucose swings, hemodynamic shifts, and medication interruptions. These factors can worsen microvascular instability during recovery. Current perioperative guidelines and regulatory recommendations describe glucose targets and medication safety considerations, including preoperative interruption of SGLT2 inhibitors to reduce euglycemic ketoacidosis risk; however, the retina-specific implications of these measures remain indirect. This review summarizes current evidence linking NVU biology, EWDR risk, and perioperative diabetes-related factors. It discusses how these factors may interact in patients with diabetes and how they may influence retinal outcomes. The review is intended to synthesize current evidence and mechanistic interpretations rather than to provide formal clinical practice recommendations. Full article

Background and Clinical Significance: Mallet finger is a common injury of the extensor mechanism at the distal interphalangeal (DIP) joint; however, open double mallet lesions are rare and may present a complex reconstruction challenge. Case Presentation: A 15-year-old male high school student who sustained an open injury to the left ring and little fingers after a high-energy buggy accident. The ring finger showed an open double mallet lesion in which the extensor tendon remained attached to a tiny avulsion fragment, and a separate dorsal base fragment was also present. The adjacent little finger had a concomitant open fracture with substantial soft tissue injury. Emergency surgery was performed on the day of the injury. For the ring finger, reduction of the tendon-attached avulsion fragment and separate dorsal base fragment was achieved using extension-block pinning, transarticular DIP pinning, and pull-out fixation over a volar button. For the little finger, cross-pinning was performed because the distal fragment was too small for stable non-transarticular fixation. Serial radiographs showed maintained alignment and progressive healing. At the final follow-up, 21 months after the injury, residual deformity and limitation of DIP motion remained; however, no infection, major skin complications, or nail deformity were observed. The little finger DIP joint became ankylosed, whereas some residual mobility remained in the ring finger DIP joint. Despite persistent functional limitations, the patient was able to continue school attendance and percussion-related activities. Conclusions: This case highlights that in an open double mallet lesion, disruption of both the tendon-attached fragment and its bony bed should be considered, and stabilization of the base may be useful in selected injury patterns before definitive tendon-side repair. Full article

The global spread of COVID-19 led to the rapid authorization of remdesivir as the first antiviral therapy. However, accumulating clinical evidence has linked its use to cardiac adverse effects. Understanding the mechanisms underlying remdesivir-induced cardiotoxicity is critical for optimizing its clinical use and ensuring patient safety. This study investigates the electrophysiological and molecular features underlying remdesivir-induced cardiac toxicity in male and female guinea pigs, aiming to elucidate the sex-dependent differences in cardiac dysfunction and the role of mitochondria in mediating these effects. A cardiac injury model was established via intraperitoneal administration of remdesivir. In vivo telemetry and ex vivo electrocardiography were used for continuous monitoring of cardiac electrical activity, while optical mapping enabled the assessment of action potential parameters and conduction properties. The histopathological alterations and mitochondrial ultrastructure were examined by hematoxylin–eosin staining and transmission electron microscopy. ELISA and Western blot analyses were performed to explore the inflammatory signaling, apoptosis, and mitochondrial dynamics. Remdesivir induced distinct sex-specific patterns of cardiac toxicity. Compared with female guinea pigs, male guinea pigs had significantly more severe myocardial injury, which was characterized by extensive inflammatory cell infiltration, marked mitochondrial disruption, and a higher incidence of sustained ventricular tachyarrhythmia. Overall, remdesivir was associated with sex-dependent cardiac toxicity, accompanied by mitochondrial impairment and inflammatory activation. Male guinea pigs were more susceptible to electrophysiological instability and mitochondrial dysfunction. These findings highlight the importance of carefully evaluating remdesivir’s cardiac effects and support the need for individualized, sex-specific considerations in its clinical administration. Full article

Titanium dioxide nanoparticles (TiO₂ NPs), widely used as food additives, frequently coexist with high-fat diets (HD) in modern dietary patterns, yet their combined in vivo toxicity remains poorly understood. This study investigated the multi-organ effects of co-exposure to TiO₂ NPs or food-grade E171 and HD in male C57BL/6J mice. Mice were randomly assigned to six groups and fed regular or high-fat diets containing 1 wt% TiO₂ NPs or E171 for 13 weeks. Histopathology, serum biochemistry, organ coefficients, and open-field behavioral tests were used to assess tissue injury and functional alterations. Co-exposure to TiO₂ NPs and HD markedly exacerbated tissue damage across multiple organs. In the liver, more severe ballooning degeneration, necrosis, and inflammatory infiltration were observed, accompanied by altered liver enzymes and reduced organ coefficients. Intestinal injury was characterized by crypt distortion and increased inflammation, particularly in the HD + TiO₂ group. Testicular tissues showed disorganized seminiferous tubules, loss of spermatogenic cells, and interstitial hyperplasia. In the brain, hippocampal neurons exhibited pyknosis and disarray, with decreased brain coefficients and impaired exploratory behavior. E171 induced similar but milder effects. These findings indicate that HD enhances TiO₂ NPs induced multi-organ toxicity, highlighting the health risks of realistic co-exposure to dietary nanoparticles and high-fat foods. Full article

Rotator cuff injuries are among the most common musculoskeletal conditions that affect shoulder function and can ultimately impact quality of life. While physical therapy is essential in the care of rotator cuff injuries, the ideal dose of therapeutic exercises continues to be a significant clinical dilemma because of the generalized nature of rehabilitation protocols. This pilot study proposes a machine learning approach to personalize rehabilitation using surface electromyography (sEMG) data collected from eight healthy individuals by testing four key shoulder movements: scaption, internal rotation, external rotation, and external rotation at 90° abduction. In this research, the XGBoost algorithm was used to model muscle activation patterns by achieving a high predictive accuracy (R² = 0.5325; MSE = 0.0084 μV²). Because sEMG reliably measures superficial muscle activity, a linear programming model was used to divide a 60 min therapy session in a way that increases activation of superficial muscles (such as deltoid and trapezius) while reducing strain on deep muscles (such as supraspinatus and infraspinatus). Three optimization scenarios were tested by reflecting a different clinical goal: prioritizing superficial muscles, minimizing deep muscle strain, or balancing both. Optimized time allocations assigned more time to external rotation at 90° abduction and scaption. This research demonstrates the potential for data-driven methods to transform rotator cuff rehabilitation through personalized and evidence-based treatment plans. The results enhance clinical practice by enabling adaptive rehabilitation planning and show that machine learning can support decision-making in complex muscle activation analysis with strong performance and low latency. Full article

Background: Distal femur fractures remain among the most challenging injuries in orthopedic trauma, particularly in elderly or osteoporotic patients and in cases involving periprosthetic or highly comminuted distal femur fracture patterns. Modern fixation strategies include retrograde intramedullary nails, locking plates, and, more recently, combined nail–plate constructs (NPC). However, the optimal fixation method remains debated, and high-quality comparative evidence is limited. This systematic review evaluates clinical outcomes, union rates, and complications associated with single versus combined fixation constructs in distal femur fractures. Materials and Methods: A systematic review was performed according to PRISMA guidelines using PubMed/MEDLINE, EMBASE, and the Cochrane Database up to June 2025. Original studies reporting surgical management of distal femur fractures, including periprosthetic distal femur fractures, with postoperative outcomes were included. Ten retrospective studies met the inclusion criteria, comprising 397 patients. Methodological quality was assessed using the Modified Coleman Methodology Score (mean: 56.5). Data collected included patient demographics, fracture type, surgical technique, union rates, complications, and follow-up duration. Descriptive statistics were used to summarize trends due to study heterogeneity. Results: Among the included fractures, 304 involved the distal femur and 55 were periprosthetic. Combined nail–plate fixation was used in 203 patients, while 185 received single-implant fixation. Across studies, union rates were consistently higher in the NPC group, with several reporting 100% union, compared with more variable results in single-construct cohorts (72–96.7%). The most frequent complication in the NPC group was infection (12 cases), whereas delayed union predominated in single-implant constructs (19 cases). Patient comorbidities, such as diabetes or smoking, were inconsistently reported but may have influenced complication patterns. Follow-up periods ranged from 5.15 to 20 months, and operative details were included in several studies. Due to heterogeneity and retrospective design, no meta-analysis was performed, but descriptive trends were consistently observed. Conclusions: Nail–plate constructs appear to offer mechanical advantages in complex or high-risk distal femur fractures, achieving superior union rates compared with single implants. However, this benefit is counterbalanced by a higher incidence of postoperative infections, likely related to greater surgical invasiveness. Single constructs remain appropriate for simpler fracture configurations or better-quality bone. High-quality prospective research with standardized radiographic and functional outcomes is needed to clarify indications and optimize fixation strategies for distal femur fractures. Full article

Sickle cell anemia (SCA) is a genetic disorder characterized by chronic hemolysis, primarily driven by red blood cell lysis. Its pathophysiology is centered, though not exclusively, on the increased release of intracellular components, such as hemoglobin degradation products, which are known to stimulate innate immune responses and promote prothrombotic states. Current therapies alleviate symptoms, yet patients remain exposed to a chronic inflammatory milieu punctuated by episodes of acute pain. The recurrence of these crises can be life-threatening due to ischemia–reperfusion injury, hypercoagulability, and respiratory complications. Central mechanisms are marked by elevated hemolysis, heightened inflammatory signaling, and increased procoagulant activity, largely driven by soluble molecules released into the plasma, such as hemoglobin, nuclear molecules and other products. These compounds are recognized from sensors on immune and endothelial cells, named Pattern Recognition Receptors (PRRs), and constitute canonical pathways for intracellular activation. Four main types have been extensively studied in the literature over recent years in both infectious and sterile inflammatory contexts; still, only a few have elucidated the mechanisms underlying acute and chronic inflammation in patients with SCA. Although Toll receptors were shown to be major in triggering immunity, other receptors were found to be important regarding this function, which suggested a multifactorial mechanism for this triggering. Therefore, here, we propose a comprehensive review of previously published findings regarding the expression, activation, and dynamics of Toll-like, NOD-like, and RIG-I–like receptors in the progression of SCA and its associated inflammatory features. Full article

Background: Fibroblast growth factor-23 (FGF23) is a key regulator of phosphate homeostasis and an emerging biomarker in cardiovascular disease. Emerging data suggest that FGF23 may also contribute to the pathophysiology of myocardial infarction (MI), but existing studies have largely focused on non-acute stages. To address this gap, we investigated early FGF23 regulation by characterizing serum concentration kinetics over the first 24 h following MI, using both a clinical MI model (TASH) and a cohort of patients with ST-elevation myocardial infarction (STEMI). Methods: Circulating FGF23 concentrations (cFGF23; RU/mL) were determined by C-terminal ELISA in patients with preserved renal function (eGFR > 30 mL/min/1.73 m²). TASH (transcoronary septal ablation) was carried out in patients with hypertrophic obstructive cardiomyopathy (n = 38). Venous serum samples were taken at baseline (pre-TASH) and at 30′, 60′, 2 h, 4 h and 24 h post-TASH. For the STEMI cohort (n = 18), serum was sampled immediately before and 3 h after coronary recanalization. All samples were processed using standardized procedures prior to analysis. Changes over time were assessed using the Friedman test with Bonferroni-corrected pairwise Wilcoxon comparisons. Results: FGF23 concentrations changed significantly over time after TASH (Friedman test, p < 0.000001, Kendall’s W = 0.518). Baseline FGF23 was 28.9 (19.4–71.0) RU/mL and increased significantly at 30′ (68.2 (36.2–178.7) RU/mL, adjusted p < 0.0001 **) after TASH. Concentrations remained elevated at 60′ (54.8 (31.6–118.3) RU/mL; adjusted p = 0.0019 *), returned to baseline at 2 h (30.9 (20–71.2) RU/mL; adjusted p = 1.0 vs. baseline) and decreased significantly below baseline at 4 h (24 (12.13–37.5) RU/mL, adjusted p = 0.0215 *). By 24 h, FGF23 had returned to baseline levels (28.8 (12.8–57.3) RU/mL; adjusted p = 1.0 vs. baseline). Although concentrations were numerically higher than at the 4 h nadir, this recovery did not reach statistical significance (adjusted p = 0.136 vs. 4 h). In STEMI patients, a non-significant decrease was observed from baseline (27 (15.5–35.75) RU/mL) to 3 h after recanalization (15.5 (6.75–34.25) RU/mL; p = 0.074, effect size r = 0.422). In an exploratory normalized analysis, the decline reached significance (p = 0.0241). Conclusions: The triphasic kinetics of circulating FGF23 in TASH patients—characterized by an early rise, transient undershoot, and a recovery toward baseline with a continuing upward trend—are consistent with a dynamic release-and-clearance pattern following myocardial injury. These findings are hypothesis-generating and warrant further investigation in larger cohorts with additional biomarkers to elucidate the source, regulation, and potential functional significance of FGF23 in the acute phase of myocardial infarction. Full article

Background and Objectives: Simultaneous bilateral scapular fractures are exceptionally rare injuries and are most commonly associated with high-energy trauma, convulsions, or electrical injury. Their occurrence following low-energy trauma is extremely uncommon. This study aimed to conduct a scoping review of the literature on simultaneous bilateral scapular fractures, with emphasis on demographic characteristics, mechanisms of injury, fracture patterns, treatment strategies, and clinical outcomes. To provide clinical context, the findings are illustrated by a case of a 43-year-old previously healthy recreational athlete who sustained simultaneous bilateral scapular fractures after a low-energy fall directly onto the back. Materials and Methods: A scoping review of the literature was conducted in accordance with PRISMA-ScR guidelines using the PubMed/MEDLINE and Scopus databases. Studies reporting simultaneous bilateral scapular fractures were identified and analyzed with respect to demographic characteristics, mechanisms of injury, fracture patterns, treatment modalities, and outcomes. Results: Thirty-seven studies published between 1946 and 2025 were included, comprising a total of 43 patients. Most cases resulted from high-energy trauma (41.9%), convulsions (25.6%), or electrical injury (16.3%). Low-energy trauma and spontaneous fractures were rare. The scapular body was the most commonly involved anatomical region. Conservative treatment predominated and was generally associated with favorable functional outcomes, while surgical intervention was reserved for displaced or intra-articular fractures. The illustrative case involved bilateral comminuted extra-articular fractures of the scapular bodies and spines without associated injuries and was managed conservatively, resulting in complete fracture healing and full, painless shoulder range of motion. Conclusions: The findings of this scoping review, illustrated by the representative clinical case, indicate that simultaneous bilateral scapular fractures may occur even after low-energy trauma in otherwise healthy individuals. Bilaterality alone should not be interpreted as an independent indication for surgical treatment when fractures are stable and minimally displaced. A high index of clinical suspicion and appropriate radiological evaluation are therefore warranted, particularly in emergency and trauma settings, in order to avoid missed or delayed diagnosis, even in cases with seemingly benign mechanisms of injury. Full article

Neonatal hypoxic ischemic encephalopathy (HIE) is a common birth complication that can cause death or lifelong disabling conditions like cerebral palsy, epilepsy, and autism. It is well established that maternal infection and inflammation are significant risk factors for HIE but reasons for this increase in neurological risk to the offspring remain unknown. Inflammation or infection are associated with epigenetic changes and may contribute to the increased risk of neurodevelopmental disability in exposed offspring. Here, we analyzed and compared DNA methylation patterns in brain monocytes isolated from control, maternal immune activation (MIA), and an inflammation sensitized HIE (IS-HIE) CF-1 mouse model at postnatal day 7. We found that maternal inflammation induced significant methylation differences in neonates relative to control samples in both MIA and IS-HIE samples with no significant differences identified between the MIA and IS-HIE groups. MIA samples showed hypermethylation at loci involving craniofacial development and transcription factors important for regulating neurodevelopment and immune function. MIA samples also demonstrated significant hypermethylation at multiple mitochondrial genome CpGs. These findings suggest that maternal inflammation induces epigenetic alterations in fetal brain immune cells that are detectable in neonates. These changes may contribute to heightened neurodevelopmental risk in offspring following hypoxic injury, highlighting potential molecular pathways for future therapeutic targeting. Full article

Kidney Injury Molecule-1 (KIM-1), a type I transmembrane glycoprotein, is emerging as a promising biomarker in the landscape of genitourinary malignancies. Initially it was described for its role in renal tubular injury, but it is currently being studied for its expression in various neoplasms, particularly renal cell carcinoma, where it correlates with tumor grade, stage and prognosis. Recent studies have demonstrated its potential usefulness as a non-invasive diagnostic tool through urinary and plasma/serum studies, offering a valuable adjunct to imaging and pathology studies. KIM-1 may also play a role in urothelial cancer, although its specificity and relevance in this context are not clearly established yet. The following review presents our current knowledge on the biology of KIM-1, its expression patterns across various genitourinary tumors and its clinical implications in early detection, prognosis and treatment monitoring. We also explore the limitations and future directions regarding the integration of KIM-1 into precision oncology approaches. Full article