SummaryTrauma hybrid operating rooms (THORs) integrate diagnostic imaging with open surgical capabilities to provide both surgical and interventional radiology procedures, such as may be required by exsanguinating patients, in a single physical location. The world's first trauma program-designed THOR, designated the Resuscitation with Angiography, Percutaneous Treatments, and Operative Repair (RAPTOR) suite, opened in Calgary in 2013. It was considered to be paradigm shifting at the time; however, the physical space has become largely obsolete and is now disfavoured by key multidisciplinary users who are essential to RAPTOR functionality. Many health care systems worldwide are considering building such THORs, and lessons learned from early adopters may be invaluable to other planners. We critically evaluated the physical, operational, and administrative components of our RAPTOR experience in the context of the published literature. While the concept has great merit in saving lives, future-proofing such resources is critical.

Chronic venous disease (CVD) causes substantial symptom burden and healthcare cost, driven not only by venous hypertension but by a persistent molecular cascade of endothelial activation, glycocalyx degradation, and inflammation within the vein wall. Venoactive drugs (VADs) - a heterogeneous class of flavonoid, synthetic, animal-derived, and plant-derived compounds - target this cascade and are recommended by international guidelines as adjuncts to compression therapy, endovenous intervention, and wound care in venous leg ulcer (VLU) management. This review synthesizes the pharmacological rationale and clinical evidence for VADs across these three adjunct settings. The evidence base is strongest for VAD use alongside compression, supported by multiple Cochrane-grade meta-analyses; MPFF and ruscus extracts have the most robust symptom evidence, while MPFF, pentoxifylline, and sulodexide have the strongest evidence for VLU healing. Evidence in the peri-interventional setting remains the weakest, limited to open-label studies of MPFF. Priorities for future research include stratified and biomarker-guided prescribing, combination pharmacotherapy, and larger, adequately powered VLU healing trials.

Semaglutide and tirzepatide have reshaped obesity care, and aesthetic practitioners increasingly encounter patients with rapid-weight-loss-associated facial volume loss and skin changes. Nutritional deficiency may be an underrecognized contributor to impaired dermal repair during glucagon-like peptide-1 receptor agonist (GLP-1RA) therapy. The authors reviewed and synthesized evidence across metabolic pharmacology, facial anatomy and aesthetics, dermatologic histology, and clinical nutrition. PubMed, Embase, and the Cochrane Library were searched from January 2019 to March 2026, supplemented by foundational studies in collagen biology and post-weight-loss skin histology. GLP-1RA-mediated caloric restriction can reduce intake of micronutrient cofactors required for collagen biosynthesis and wound repair. Vitamin D deficiency reaches 13.6% at 12 months, and ∼22.4% of patients have at least one documented deficiency within 1 year. Deficiencies in vitamin D, iron, vitamin B12, folate, zinc, copper, and protein may plausibly compound rapid fat-compartment depletion and collagen remodeling. Direct GLP-1RA effects on dermal cells remain preclinical and should be interpreted cautiously. In summary, GLP-1RA-associated facial aging changes are multifactorial. The authors propose a risk-stratified framework for aesthetic practitioners emphasizing dietary optimization, selective supplementation, targeted laboratory assessment in at-risk patients, coordination with prescribing clinicians, and procedural timing when nutritional status is optimized. Prospective studies are needed to determine whether correcting deficiencies improves aesthetic or surgical outcomes. Level of Evidence: 5 (Therapeutic) For image description, please refer to the figure legend and surrounding text.

Here, we report the management of a severe necrotizing soft-tissue infection involving the entire lower limb of a man in his 70s. The infection originated from a lower leg hematoma that developed during anticoagulant therapy for deep vein thrombosis. Necrosis extended from the deep thigh to the lower leg, involving areas surrounding critical structures such as the femoral artery, sciatic nerve, and tibia. Limb salvage was achieved through multiple debridement procedures and skin grafts performed in collaboration with orthopedic and cardiovascular surgery teams. The exposed cortical bone on the anterior midtibia was covered using a distally pedicled gracilis muscle flap in combination with negative-pressure wound therapy to avoid the need for a distal flap. The flap survived sufficiently to avoid a distal flap, and the patient was able to ambulate without a cane 6 months postoperatively.

[This corrects the article DOI: 10.1093/schizbullopen/sgag012.].

Liver fibrosis, driven by metabolic dysfunction-associated steatohepatitis (MASH) and other chronic injuries, represents a global health crisis without approved pharmacological therapies. The Rho-associated coiled-coil kinases (ROCK1 and ROCK2), the principal effectors of Rho GTPases, have emerged as central nodes in fibrogenesis, yet the isoform-specific mechanisms and their translational potential remain incompletely defined. This review systematically dissects the divergent roles of ROCK1 and ROCK2 across the hepatic cellular landscape. We synthesize current knowledge on isoform-specific functions across major hepatic cell types, including hepatic stellate cells (HSCs), liver sinusoidal endothelial cells (LSECs), hepatocytes, macrophages, and immune cells, with emphasis on the evidence quality underlying each claim. ROCK2 appears to play a predominant role in the profibrotic vascular niche in several contexts, particularly in LSEC capillarization and HSC contraction; however, the contributions of both isoforms are fundamentally cell- and context-dependent. We discuss the evidence for ROCK isoform-specific functions, distinguishing among genetic, pharmacological, expression-based, and activation-based evidence. We further synthesize the complex crosstalk between ROCK signaling and the TGF-β/Smad, Wnt/β-catenin, Hippo/YAP, and NOX4/ROS networks. Crucially, we critically evaluate the translational pipeline-from pan-ROCK inhibitors limited by systemic hypotension to next-generation selective ROCK2 inhibitors. A notable development in clinical translation is the selective ROCK2 inhibitor TDI01, which targets endothelial ROCK2 to attenuate fibrosis. In an extended, single-arm, open-label study of TDI01 in patients with liver fibrosis, fibrosis improvement was observed in five of six patients; however, given the small sample size, absence of a control group, and exploratory endpoints, these findings represent early signals that require validation in adequately powered randomized controlled trials. We further address unresolved controversies, including the dual hepatoprotective versus pro-steatotic functions of ROCK and the dose-dependent bidirectional regulation of HSCs migration, which challenge systemic inhibition strategies. Looking forward, we spotlight emerging frontiers such as cell-specific nanodelivery systems (vitamin A-liposomes, M6PHSA), PROTAC-mediated ROCK degradation, non-coding RNA therapeutics, and synergistic combinations with FXR, PPAR, and GLP-1 receptor agonists. This review provides a comprehensive blueprint for translating ROCK isoform biology into precision antifibrotic therapies.