Not so once upon a time.

This story reflects a personal narrative of a graduate student who experienced a disturbing incident during Mardi Gras in New Orleans, shedding light on the enduring issue of racism. The author's journey to graduate school and the challenges faced along the way provide context for the pivotal moment of racial discrimination. The narrative then shifts to the author's decision to prioritize education over anger, highlighting the sacrifices made to protect their future as a graduate student. The incident serves as a stark reminder that, despite personal achievements and aspirations, racial prejudice persists. In conclusion, the author calls for resilience and focus in the pursuit of personal goals while acknowledging the ongoing struggle against racism and other forms of discrimination in society. This personal story serves as a poignant reminder of the challenges faced by individuals and the need for continued efforts to combat systemic intolerance.

TLT-1-CONTROLS EARLY THROMBUS FORMATION AND STABILITY BY FACILITATING AIIBB3 OUTSIDE-IN SIGNALING IN MICE.

Platelets regulate inflammation as well as hemostasis. Inflammatory insults often induce hemostatic function through mechanisms that are not always understood. The triggering receptor expressed in myeloid cells (TREM)-like transcript 1 (TLT-1) is an abundantly expressed platelet receptor and its deletion leads to hemorrhage and edema after lipopolysaccharide and TNF-α treatment. To define a role for TLT-1 in immune derived bleeding we used a CXCL-2 mediated local inflammatory reaction in the vessels of the cremaster muscle of treml1 -/- and wild type mice. Our whole mount immunofluorescent staining of the cremaster muscle demonstrated a 50% reduction in clot size and increased extravasation of plasma molecules in treml1 -/- mice compared to wild type. We demonstrate that the decreased clotting in treml1 -/- mice is associated with a 2X reduction in integrin ß3 phosphorylation on residue Y773 after platelet activation, which is consistent with treml1 -/- mice displaying reduced outside-in signaling and smaller thrombi. We further substantiate TLT-1's role in the regulation of immune derived bleeding using the reverse arthus reaction and demonstrate TLT-1's role in thrombosis using the thromboplastin initiated and collagen/epinephrine models of pulmonary embolism. Thus, the data presented here demonstrate that TLT-1 regulates early clot formation though the stabilization of αIIbß3 outside-in signaling.

Emerging Roles for Platelets in Inflammation and Disease.

Platelets and their interaction with cells of the immune system contribute through a variety of molecular mechanisms to support hemostasis and inflammation. These simple yet essential cells exert their effects in lymphocytes, monocytes, and neutrophils, both recruiting and modulating their function after activation. Emerging evidence is starting to define the mechanisms that allow platelets to also play pivotal roles in host defense. For example, platelet cell-surface expression of toll-like receptors allows platelets to direct neutrophil activation toward extracellular trap formation and facilitate the elimination of blood pathogens. In addition to these well-known receptors, two of the most recently discovered platelet receptors, C-type lectin receptor 2 (CLEC-2), and TREM-like transcript-1 (TLT-1), have been shown to modulate hemostatic and inflammation-related roles in platelets. This review will discuss the evolution of our understanding of platelet functions from hemostasis to inflammation, and highlight novel mechanisms that platelets use to mediate hemostasis under inflammatory pressure.