A5012696893- Trauma, Hemostasis, Coagulopathy, Resuscitation
- Traumatic Brain Injury and Neurovascular Disturbances
- Cardiac Ischemia and Reperfusion
- Autoimmune and Inflammatory Disorders
- Caveolin-1 and cellular processes
- Dermatological and Skeletal Disorders
- Cardiac, Anesthesia and Surgical Outcomes
- Hypertrophic osteoarthropathy and related conditions
- Barrier Structure and Function Studies
- Signaling Pathways in Disease
- GABA and Rice Research
- Sepsis Diagnosis and Treatment
- Vascular Tumors and Angiosarcomas
- Tuberous Sclerosis Complex Research
- Neurogenesis and neuroplasticity mechanisms
- Autoimmune Bullous Skin Diseases
- Skin and Cellular Biology Research
- Cancer-related molecular mechanisms research
- Cardiac Arrest and Resuscitation
- Nerve injury and regeneration
- Trauma and Emergency Care Studies
- Inflammatory Myopathies and Dermatomyositis
- Soft tissue tumor case studies
- Nicotinic Acetylcholine Receptors Study
- Mechanical Circulatory Support Devices
Tulane University
2020-2025
Columbia University Irving Medical Center
2020
University of Virginia
2017
The endothelial glycocalyx is an anti-inflammatory, anti-coagulant coating of cells which participates in many physiologic processes. Damage to the occurs secondary several disease states, and especially pronounced ischemia-reperfusion (I/R) injury. In models trauma hemorrhage, this damage has been shown occur disordered succinate metabolism leading increased mitochondrial reactive oxygen species (mitoROS). Aortic occlusion also associated with I/R injury vascular endothelium, though precise...
Acute hemorrhage commonly leads to coagulopathy and organ dysfunction or failure. Recent evidence suggests that damage the endothelial glycocalyx contributes these adverse outcomes. The physiological events mediating acute shedding are undefined, however. Here, we show succinate accumulation within cells drives degradation through a membrane reorganization-mediated mechanism. We investigated this mechanism in cultured cell hypoxia-reoxygenation model, rat model of hemorrhage, trauma patient...
ABSTRACT Introduction: Hemorrhagic shock has recently been shown to cause shedding of a carbohydrate surface layer endothelial cells known as the glycocalyx. This glycocalyx is thought be mediator coagulopathy seen in trauma patients. Clinical studies have demonstrated increases shed blood after trauma, and animal measured disruption vessels lung, skeletal muscle, mesentery. However, no study across wide range vascular beds quantify primary locations this shedding. Methods: In present study,...
Succinate (SI) is a citric acid cycle metabolite that accumulates in tissues during hemorrhagic shock (HS) due to electron transport chain uncoupling. Dimethyl malonate (DMM) competitive inhibitor of SI dehydrogenase, which has been shown reduce accumulation and protect against reperfusion injury. Whether DMM can be therapeutic after severe HS unknown. We hypothesized would prevent buildup resuscitation (RES) swine model HS, leading better physiological recovery RES.The carotid arteries...
Angiomyomatous hamartoma (AMH) of the lymph node (LN) is an uncommon, benign vascular proliferation unknown etiology. Histologically, it characterized by replacement nodal architecture with blood vessels, smooth muscle cells, and variable amounts fibrous adipose tissue in a collagenous stroma.1,2 First described 1992, there are now 30 cases reported literature, primarily involving inguinal femoral LNs; rarely, cervical submandibular involvement have been described.
A 69-year-old woman with a history of relapsed acute lymphocytic leukemia presented for evaluation diffuse, asymptomatic scaly rash appearing 15 days after initiating inotuzumab ozogamicin 0.5 mg/m2 infusions and ponatinib 45 mg daily, which were started 2 months previously. Review systems, including pruritus flu-like symptoms, was negative. The patient received prednisone 20 daily triamcinolone 1% topical treatment without improvement the rash. only improved upon cessation ponatinib, while...
The endothelial glycocalyx forms an anti-thrombotic layer on the apical surface of cells and maintains selective permeability barrier blood vessels. Ischemia reperfusion injury like hemorrhagic shock is shown to cause damage. We have previously that mitochondrial reactive oxygen species (mitoROS) mediate damage in cultured cells. Of note, angiotensin II elevates mitoROS, suggesting a possible exacerbation hypertensive patients. It unknown, however, whether mitoROS vivo . hypothesize rat...