Faculty Bibliography
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14322
Enhancing gastroenterology education through e-learning
E-learning has revolutionized medical education by providing flexible, accessible, and interactive learning opportunities. This article explores the transformative impact of e-learning on gastroenterology education, highlighting the advancements and benefits brought by the American Society for Gastrointestinal Endoscopy (ASGE) platforms. ASGE's e-learning platforms offer specialized content, interactive tools, and continuous updates, enhancing the learning experience for gastroenterologists.
PMID: 41632049
ISSN: 1097-6779
CID: 5999722
The International Guideline for the Definition, Classification, Diagnosis and Management of Urticaria
This update and revision of the international guideline for urticaria was developed in accordance with the methods recommended by Cochrane and the Grading of Recommendations Assessment, Development and Evaluation (GRADE) working group. It is an initiative of the Global Allergy and Asthma Excellence Network (GA2LEN) and its Urticaria and Angioedema Centers of Reference and Excellence (UCAREs and ACAREs), with the participation of 210 delegates from 107 national and international societies, from 59 countries. The consensus conference was held on December 6th, 2024. This guideline was acknowledged and accepted by the European Union of Medical Specialists (UEMS). Urticaria is a frequent, mast cell-driven disease, defined by a rapid appearance of wheals, angioedema, or both. The lifetime prevalence of acute urticaria is estimated to be approximately 20%. Chronic urticaria, categorized as either chronic spontaneous urticaria or chronic inducible urticaria, is disabling, impairs quality of life, and affects performance at work and school, however, novel therapies are available. This updated version of the international guideline for urticaria covers the definition and classification of urticaria and outlines expert-guided and evidence-based diagnostic and therapeutic approaches for the different subtypes of urticaria.
PMID: 41649409
ISSN: 1398-9995
CID: 6000592
Multisystem Imaging Manifestations of Fibromuscular Dysplasia
Fibromuscular dysplasia (FMD) is a rare idiopathic, noninflammatory, nonatherosclerotic arteriopathy that leads to wall abnormalities in medium- and small-caliber arteries, typically resulting in alternating areas of stenosis and dilatation, or "beading" at angiography. Stenosis, dissection, and aneurysm can also be seen, and clinical manifestations depend on the vascular territory affected by FMD, with the renal and carotid arteries being most frequently involved. The diagnosis of FMD is made based on imaging features of FMD classified according to the angiographic appearance as focal FMD or multifocal FMD. Early diagnosis is often challenging, as mimics of FMD must first be excluded. The presence of aneurysm, dissection, or tortuosity alone is inadequate to establish the diagnosis, as these are variant manifestations; however, if a patient has focal or multifocal manifestations such as stenosis or stenosis and dilatation in one vascular bed, establishing the diagnosis of FMD, the presence of aneurysm, dissection, or tortuosity in additional vascular beds is considered multivessel involvement of all affected vascular beds. The cerebrovascular system, coronary arteries, renal and mesenteric arteries, and extremities should be evaluated for FMD involvement. The most serious potential complications of FMD are hypoperfusion secondary to aneurysm, dissection, or arterial occlusion, which can lead to hypertension, stroke, or myocardial infarction, as well as subarachnoid hemorrhage. Prompt intervention, blood pressure management, and revascularization are necessary to avoid devastating complications. Radiologists play an important role in timely identification of diverse FMD-associated morbidities and thus may contribute to early diagnosis and treatment of FMD. ©RSNA, 2026 Supplemental material is available for this article.
PMID: 41642726
ISSN: 1527-1323
CID: 6000382
Impact of community recruitment and inclusion initiatives on enrollment in the biomarker-driven MyTACTIC trial
AIMS/UNASSIGNED:Lack of diversity in clinical trial populations often results in healthcare inequity. This retrospective analysis presents the impact of implementing inclusive research practices on the diversity of the MyTACTIC trial population. PATIENTS & METHODS/UNASSIGNED:Adult patients with advanced solid tumors were enrolled from large academic centers or community cancer clinics and a number of inclusive research practices were implemented to diversify patient recruitment. We summarized race/ethnicity data of the study population related to the sites' catchment area. RESULTS/UNASSIGNED:Overall, 252 patients were enrolled (83% White). Community clinics represented 95% of screening sites (enrolled 249/252 patients). The proportion of patients from racial/ethnic minorities was generally higher in study centers from ethnically diverse catchment areas. Streamlining the protocol and implementing a free transport scheme to improve patient recruitment yielded positive feedback from site staff; 14 patients (5.5%) used the transportation service. CONCLUSION/UNASSIGNED:Findings from the MyTACTIC trial suggest that running trials at community oncology sites does not, by itself, increase patient diversity; other efforts are also necessary. NCT04632992.
PMCID:12773618
PMID: 41392942
ISSN: 1744-8301
CID: 5999222
Platelet defects in patients and mice with Ehlers-Danlos syndrome
Ehlers-Danlos syndrome (EDS) is a group of connective tissue disorders characterized by joint hypermobility, skin hyperelasticity, perivascular tissue fragility, easy bruising, and increased bleeding risk. Abnormal bleeding in EDS ranges from mild ecchymoses to life-threatening hemorrhage. Platelet function abnormalities have been reported in people with EDS, but the broad nature and extent of these defects remain poorly defined. Herein, we evaluated blood samples from people with the hypermobile, classical, classical-like, and vascular types of EDS and utilized a Col5a1+/- mouse model of classical EDS to characterize the extent of platelet dysfunction. Our findings suggest that platelet dysfunction in EDS is an outcome of reduced integrin αIIbβ3 activation resulting from decreased phosphorylation of talin-1, leading to defects in aggregation and spreading. The observed platelet dysfunction was associated with reduced expression of the platelet surface receptors GPVI and PAR1 and impaired downstream signaling. Col5a1+/- mice demonstrated increased tail bleeding time, reproduced the signaling defects observed in platelets from people with EDS, and exhibited decreased susceptibility to FeCl3-induced carotid artery thrombosis. Collectively, our data indicate that platelet dysfunction in EDS is likely contributing to hemorrhagic complications.
PMID: 41284637
ISSN: 1528-0020
CID: 5997792
Evaluating tocilizumab in ischemic stroke: Findings from the SPAN multicenter trial
UNLABELLED:Inflammation, particularly mediated through interleukin-6 (IL-6) signaling, plays a critical role in stroke pathophysiology. High levels of IL-6 are associated with poor outcomes in stroke patients. Therapeutic inhibition of IL-6 signaling may offer a novel strategy to mitigate post-stroke damage and improve recovery. This study evaluated the efficacy of tocilizumab (TCZ), a clinically approved monoclonal antibody that blocks IL-6 receptor signaling, using data from the Stroke Preclinical Assessment Network (SPAN), a multi-center, randomized, blinded, placebo-controlled trial in preclinical stroke models. METHODS:We analyzed behavioral and MRI morphometry data from 701 rodents (both males and females; 1:1), including healthy young mice, diet-induced obese mice, aging mice, and spontaneously hypertensive rats (SHR) treated with saline (N = 348) or TCZ (N = 353) at a dose of 100 mg/kg for mice, 10 mg/kg for rats after middle cerebral artery occlusion (MCAO). RESULTS:In the overall mouse cohort, TCZ did not significantly improve long-term sensorimotor recovery or reduce brain tissue loss measured by MRI. However, aging mice exhibited modest motor function improvements. In SHRs, TCZ treatment resulted in improved sensory-motor function, particularly in male rats, as demonstrated by enhanced corner test scores on days 7 and 28 post-MCAO. While TCZ in SHRs provided early (day 2) cerebroprotection with reduced lesion volume, it did not alter subsequent tissue loss, as measured by tissue atrophy at day 30. CONCLUSIONS:These results suggest that IL-6R blockade with TCZ was associated with functional improvement in aging mice (modest) and hypertensive rats (notably males), without durable effect of brain tissue loss. No benefit was observed in the overall mouse cohort. These findings support IL-6 signaling as a viable therapeutic target and warrant further investigation into IL-6 receptor inhibition as a potential treatment strategy for stroke recovery.
PMID: 41354124
ISSN: 1873-7064
CID: 5997802
Exploring Sex Differences in Stroke Outcomes: A Comprehensive Analysis From the SPAN 1 Trial
BACKGROUND:Stroke is a sexually dimorphic disease, with different risk factors, incidence, outcomes, and treatment responses in men and women. While sex differences have been documented in preclinical studies, these findings often come from single-site studies with small sample sizes and require validation across diverse research settings. METHODS:We used data from the SPAN (Stroke Preclinical Assessment Network), a randomized, placebo-controlled, blinded, multilaboratory trial, to determine if sex differences in neurological outcomes are present in preclinical stroke models. We analyzed data from 665 stroke animals treated with saline, including young mice, diet-induced obese mice, aging mice, young rats, and spontaneously hypertensive rats. We compared the corner test index and brain morphology between the sexes using linear random effect models and assessed the mortality rate using Cox proportional hazard regression models. RESULTS:No significant sex differences were found in neurological outcome measured with the corner test on either day 7 or day 30 after stroke, regardless of the mouse or rat stroke model used. Additionally, female and male mice exhibited similar infarct sizes on day 2 magnetic resonance imaging and on brain atrophy measures on day 30 after stroke, indicating a lack of sex differences in brain injury. Similarly, no sex differences were observed in acute or chronic sensorimotor or tissue outcomes in young rats. In 1 subanalysis, sex differences were seen in the spontaneously hypertensive rats cohort. Female rats exhibited a higher corner test index on day 30 than males, indicating more severe sensorimotor injury. CONCLUSIONS:In this multicenter preclinical study, we did not detect sex differences in stroke outcomes in mice, although sex differences in behavioral outcomes were observed in spontaneously hypertensive rats. These findings highlight that sex differences may be model-specific and subtle, emphasizing the need for methodological consistency and thoughtful inclusion of diverse animal models in translational stroke research to better understand if sex-specific responses contribute to stroke outcomes.
PMID: 41631765
ISSN: 2047-9980
CID: 5997812
The mitochondrial calcium uniporter regulates calcium dynamics to drive platelet function, bioenergetics, and thrombosis
BACKGROUND:handling in platelet function and thrombosis is not well understood. OBJECTIVES/OBJECTIVE:flux could attenuate platelet activation and arterial thrombosis. METHODS:levels were measured in Rhod-2- and Fura-2-loaded platelets by fluorometry, and platelet bioenergetics were analyzed using a Seahorse extracellular flux analyzer. RESULTS:platelets. CONCLUSION/CONCLUSIONS:MCU facilitates platelet activation and thrombosis by regulating calcium flux (mitochondrial and cytosolic), thereby establishing its potential as a target for antithrombotic therapeutic intervention.
PMID: 41197806
ISSN: 1538-7836
CID: 5997782
Pyruvate kinase M2 promotes venous thrombosis by enhancing SNAP23-mediated platelet exocytosis and consequent NETosis
Little is known about the role of metabolic regulatory mechanisms in the pathobiology of deep vein thrombosis (DVT). Recent studies have demonstrated the involvement of the metabolic enzyme pyruvate kinase M2 (PKM2) in platelet function; however, whether platelet PKM2 contributes to DVT has not yet been investigated. Using platelet-specific PKM2-/- (PKM2Plt-KO) or wild-type (WT) mice orally administered ML265 (a small molecule that limits PKM2 dimers by stabilizing PKM2 tetramers), we found reduced thrombus burden at 48 hours after surgery in the inferior vena cava (IVC) stenosis model compared with littermate controls. This reduction was associated with lower levels of citrullinated histone H3, a marker of neutrophil extracellular traps (NET), in the harvested thrombi and improved IVC wall contraction and relaxation responses (assessed by myography). Mechanistically, thrombin-stimulated platelets from PKM2Plt-KO mice or ML265-pretreated platelets from WT mice showed reduced SNAP23 phosphorylation and diminished PF4 release (a marker of α-granule exocytosis). The releasate collected from thrombin-stimulated platelets was less effective at inducing NETosis compared to respective controls. Using ML265-pretreated human whole blood perfused over a tissue factor-coated surface at a venous shear rate, we found that the area covered by platelet-leukocyte aggregates was profoundly reduced compared to vehicle control. Consistent with murine data, human platelets pretreated with ML265 and stimulated with thrombin exhibited decreased PF4 release and generated releasates that were less potent in inducing NETosis. These findings, to our knowledge, reveal for the first time that targeting PKM2 genetically or pharmacologically reduces SNAP23-mediated α-granule exocytosis in platelets, platelet releasate-induced NETosis, and susceptibility to DVT.
PMCID:12804119
PMID: 41118613
ISSN: 2473-9537
CID: 5997772
Body Roundness Index is a Stronger Predictor of Cardiometabolic Risk than Body Mass Index in Children between Ages 8 to 17 years
ISI:001594237300006
ISSN: 0022-3476
CID: 5992532
