English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Polymorphonuclear leukocytes (PMNs) comprise the vast majority of white blood cells and serve as the first responders during acute inflammatory responses. These cells constitute an essential component of the innate immune response, classically conceived of as antimicrobial stewards that deliver their toxic payload at the site of injury. These cells contain granules, hence their membership in the granulocyte family of leukocytes. The granules contain enzymes such as myeloperoxidase, which generates the strong oxidant hypochlorous acid, and proteinases, which degrade foreign peptides, among other functions. PMNs also possess machinery that potently produces other reactive oxygen species (ROS) such as superoxide anion. Combined with phagocytosis, the mediators elaborated by PMNs provide a bulwark of defenses to combat foreign invaders and also to aid mop up operations in injured tissues.Article, see p 1081 Yet, friendly fire from PMNs can aggravate or cause disease when these cells undergo excessive or inappropriate activation. Cardiovascular and allied conditions provide examples of the adverse consequences of collateral damage because of the unleashing of PMNs’ potent actions (Figure). The dreaded mechanical complications of myocardial infarction such as rupture of the intraventricular septum, papillary muscles, or of the ventricle itself may result, in part, from excessive extracellular matrix dissolution and extensive cell damage wrought by PMN mediators.1 Coronary microvascular damage caused by PMN can contribute to no reflow situations. PMNs …

Unfriendly Fire From Neutrophils Promiscuously Potentiates Cardiovascular Inflammation