Red blood cell (RBC) clearance by macrophages maintains blood homeostasis and is dysregulated in the hemolytic disorder sickle cell disease (SCD) and the lysosomal storage disorder Gaucher disease (GD), where biophysical and biochemical alterations promote premature phagocytosis. We develop a multiscale hybrid modeling framework integrating signaling dynamics, biophysical simulations, and machine learning to investigate the mechanisms governing RBC phagocytosis in these diseases. Our approach couples a systems biology model of macrophage-RBC signaling with Dissipative Particle Dynamics (DPD) simulations of molecular diffusion and membrane interactions, and leverages Physics-Informed Neural Networks (PINNs) for robust parameter inference. The DPD framework provides mechanistic insight into antibody diffusion, receptor engagement, and membrane-level interactions during macrophage-RBC contact, generating spatially resolved trajectories of CD47-SIRP α signaling and antibody-receptor binding that serve as intermediate observables constraining the signaling model. The model accurately captures differential phagocytic responses between healthy and altered RBCs, revealing diminished inhibitory signaling and changes in SHP1-mediated pathways in both SCD and GD. Identifiability analysis combining Fisher Information Matrix diagnostics and profile likelihood confirms that parameters governing the CD47-SIRP α -SHP1 axis are among the most robustly recoverable, and simulations of therapeutic perturbations with anti-SIRP α antibodies demonstrate modulation of engulfment outcomes. We further employ Physics-Informed Kolmogorov-Arnold Networks (PIKANs) as an alternative to standard PINNs, demonstrating improved robustness under noise and sampling variability. More broadly, our multiscale platform linking biophysical simulation with systems-level inference is generalizable, offering mechanistic insights and computational tools for therapeutic exploration in diseases involving dysregulated phagocytosis.

Patient Blood Management (PBM) has evolved from a transfusion-centered practice to a structured, patient-focused perioperative strategy aimed at improving surgical outcomes while preserving blood resources. In the operating room, where bleeding risk is anticipated and modifiable, PBM requires proactive intervention rather than reactive transfusion. This review synthesizes current evidence on perioperative blood conservation strategies specifically relevant to surgeons and anesthesiologists. Preoperative optimization begins with systematic identification and correction of anemia, most commonly iron deficiency, using appropriately timed oral or intravenous iron therapy and, in selected cases, erythropoiesis-stimulating agents. Careful management of anticoagulant and antiplatelet therapies, early recognition of acquired or inherited coagulopathies, and protocol-driven reversal strategies further reduce perioperative hemorrhagic risk. Intraoperatively, blood conservation depends on meticulous surgical technique, respect for anatomical planes, minimally invasive approaches, and the judicious use of advanced energy devices and topical hemostatic agents. Pharmacologic interventions-particularly tranexamic acid administered with appropriate timing and dosing-have demonstrated consistent reductions in blood loss and transfusion requirements across multiple surgical disciplines. Goal-directed coagulation management guided by viscoelastic testing allows targeted correction of specific hemostatic deficits while minimizing unnecessary blood product exposure. Acute normovolemic hemodilution and intraoperative cell salvage provide additional benefit in selected high-blood-loss procedures. Collectively, these multimodal strategies shift perioperative care from product-driven transfusion toward physiology-based blood conservation. When embedded within institutional protocols and supported by multidisciplinary collaboration, perioperative PBM reduces transfusion exposure, decreases morbidity, shortens hospital stay, and promotes sustainable stewardship of blood resources without compromising patient safety.

Emergencies cause disruption to the normal flow of the working day in a busy veterinary practice, requiring diversion of resources from routine cases to assist with the medical priority. Assessments and decisions have to be made rapidly, which can be challenging if the particular medical condition is not dealt with on a regular basis.

Emergencies cause disruption to the normal flow of the working day in a busy veterinary practice, requiring diversion of resources from routine cases to assist with the medical priority. Assessments and decisions have to be made rapidly, which can be challenging if the particular condition is not dealt with on a regular basis.

Adult gastric inflammatory myofibroblastic tumors (IMT) are rare mesenchymal neoplasms that often mimic gastrointestinal stromal tumors (GIST). This systematic review with pooled individual patient data aimed to define their clinical presentation, diagnostic work-up, and surgical management. Electronic databases (PubMed/MEDLINE, Embase, Scopus, Cochrane Library) were searched for adult (≥18 years) cases of histologically confirmed gastric IMT. Individual patient data on demographics, tumor characteristics, treatment, and outcomes were extracted from eligible case reports and series. Continuous variables were summarized as means with standard deviations and categorical variables as proportions with 95% confidence intervals, with prespecified comparisons by tumor location and surgical approach. Thirty-one patients were identified, with a female predominance and a mean age of 47.7 years. Most were symptomatic, presenting with abdominal pain or upper gastrointestinal bleeding/anemia. Tumors most frequently involved the middle third of the stomach and showed wide size variability. Distal tumors were larger and predominantly associated with pain, whereas proximal tumors more often presented with hemorrhage and less pain, suggesting distinct location-dependent clinical phenotypes. Surgical resection was the mainstay of treatment. Stomach-preserving resections were feasible in most cases, and minimally invasive surgery (MIS) was increasingly used for smaller, well-circumscribed lesions, while larger or locally invasive tumors more often required open major gastrectomy. Preoperative EUS-guided biopsy with immunohistochemistry, including ALK-1, is critical to avoid misdiagnosis. Complete surgical resection offers excellent short-to mid-term outcomes, and MIS stomach-preserving techniques appear safe for tumors under 5 cm when negative margins can be achieved.

Wilms tumor is the most common pediatric renal malignancy, while skull metastasis is rare, occurring in fewer than 2% of cases. We report a five-year-old girl with stage II anaplastic nephroblastoma who developed skull metastasis two months after radical nephrectomy. She received 24 weeks of regimen I chemotherapy. The skull mass regressed by week six and completely resolved by week ten, with full closure of the exposed area by week eighteen. Adverse effects included alopecia, nausea, anemia, and leukopenia. Post-treatment imaging showed no residual skull lesion. Regimen I demonstrated an effective therapeutic response in this rare presentation.

Anemia of chronic disease (ACD), also referred to as anemia of inflammation, is a prevalent and clinically significant complication of chronic infection, autoimmune disease, malignancy, and chronic kidney disease. It is characterized by inflammation-driven iron sequestration, impaired erythropoietin (EPO) production and signaling, and suppression of effective erythropoiesis. Current therapies (iron supplementation and erythropoiesis-stimulating agents) often address downstream consequences and may be limited by hepcidin-driven functional iron deficiency, cytokine-mediated EPO resistance, and safety concerns in vulnerable populations. This review re-examines ACD through an integrated framework of hepcidin dysregulation, iron sequestration, and inflammatory inhibition of the EPO axis. We then synthesize emerging evidence that sodium-glucose cotransporter 2 (SGLT2) inhibitors produce sustained increases in hemoglobin/hematocrit beyond transient hemoconcentration across cardiovascular and kidney disease trials, including in non-diabetic populations. Mechanistic studies suggest a coordinated biologic response that may include reduced hepcidin, improved iron mobilization, physiologic augmentation of endogenous EPO, and attenuation of systemic inflammation-pathways directly relevant to ACD. We critically re-appraise current ACD paradigms by contrasting downstream "replacement" strategies (iron and ESAs) with pathway-level approaches (HIF-PHIs and SGLT2 inhibition), and we outline biomarker-guided study designs to test whether SGLT2 inhibition may act as an adjunctive physiologic modulator of iron-erythropoietic crosstalk in well-phenotyped inflammatory anemia cohorts, while emphasizing that current evidence remains hypothesis-generating rather than practice-changing.