Dale E. Hammerschmidt

TL;DR: Embolization of granulocyte aggregates might be a previously unsuspected cause of leukostasis and pulmonary damage in various clinical situations where intravascular complement activation occurs.

TL;DR: Recommendations of a two-year project group funded by NIH to study how to manageIFs in genetic and genomic research, as well as imaging research are reported, which conclude that researchers have an obligation to address the possibility of discovering IFs in their protocol and communications with the IRB and research participants.

TL;DR: Techniques newly developed or under development may allow the predictive value of the WBC count to be refined by combining it with measures of cell activation and/or activatability.

TL;DR: The capacity of blood cells to aggregate, best exemplified by the response of platelets to vascular injury, is generally thought to be beneficial, however, if aggregation occurs inappropriately—particularly if it involves large numbers of cells—it can be harmful.

TL;DR: In this paper, the authors found that aggregation of polymorphonuclear granulocytes (PMN) in response to activated complement (C) might contribute to the genesis of the adult respiratory distress syndrome (ARDS), aggregating PMNs causing pulmonary dysfunction by becoming lodged in the lung as leucoemboli.