Key Points: Bacterial sepsis from contaminated platelet transfusions continues to occur despite recent interventions; additional measures are needed. STR to platelet transfusion is frequently not recognized or reported; use of recent AABB criteria showed highest diagnostic sensitivity.

Parkinson's disease (PD) is the second most common neurodegenerative condition and intracellular deposition of Lewy bodies in the substantia nigra (SN), which can cause dopaminergic neuronal death, is the hallmark of this syndrome. α-synuclein (syn) is a small protein expressed mainly in neurons but can also be found in a number of tissues. It can be present as a soluble monomer under normal physiological conditions, but can be toxic in its oligomeric or fibrillary forms. Most of the available literature has focused on the effects of α-syn pathology in the mechanisms leading to PD. However, the normal functions of α-syn still remain to be fully elucidated. Notably, α-syn in the hematopoietic system seems to mediate important functions as indicated by anemia and incomplete cell maturation when this protein is absent. This review will summarize basic genetic and structural findings, and critical information that suggests an essential role of α-syn in the development and activation of the hematopoietic system and immunity.

Circulating immature platelet fraction (IPF) reflects real-time thrombopoiesis and correlates with platelet recovery from thrombocytopenic presentations. To understand the dynamics of IPF in platelet transfusions, we quantified the %-IPF in single-donor platelet components (SDP) during prolonged storage. %-IPF significantly increased from baseline by day 5 post-donation. Absolute IPF counts (A-IPC) had similar significant increments. However, gamma-irradiation suppressed the increments of %-IPF and A-IPC by >50%. Ultrastructural analysis of SDP units at day 10 showed well preserved morphology of immature platelets. Our findings suggest that IPF might actively expand ex-vivo and may have a longer shelf life than their mature counterparts. Closer study of IPF may be of critical clinical importance for transfusion practices.

Platelets, traditionally known for their role in hemostasis, have emerged as key players in immune response and inflammation. Sepsis, a life-threatening condition characterized by systemic inflammation, often presents with thrombocytopenia, which at times, can be significant. Platelets contribute to the inflammatory response by interacting with leukocytes, endothelial cells, and the innate immune system. However, excessive platelet activation and consumption can lead to thrombocytopenia and exacerbate the severity of sepsis. Understanding the multifaceted roles of platelets in sepsis is crucial for developing effective therapeutic strategies. Targeting platelet-mediated inflammatory responses and promoting platelet production may offer potential avenues for improving outcomes in septic patients with thrombocytopenia. Future research should focus on elucidating the mechanisms underlying platelet dysfunction in sepsis and exploring novel therapeutic approaches to optimize platelet function and mitigate inflammation. This review explores the intricate relationship between platelets, inflammation, and thrombosis in the context of sepsis.