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 Tools annual

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 monthly

Global: Zendy Plus monthly

Presents the access of premium content as premium feature

Premium Content

Global: Zendy Plus annual

Global: Zendy Free Plan

Introduction In human, within the RAAS endocrine pathway somatic two domain angiotensin converting enzyme (s-ACE) primarily function in processing Angiotensin-I into Angiotensin-II that causes vasoconstriction. Simultaneously s-ACE enzymatically inactivates the vasodilator bradykinin. Hitherto, s-ACE functions in instant blood pressure upregulation. As Angiotensin-II evokes release of the mineralocorticoid aldosterone from the adrenal cortex, ACE turned out to be an excellent target for the therapeutic regulation of blood pressure [1,2]. However, worldwide use of ACE inhibitors such as “Captopril” soon highlighted side effects including a reduced inflammatory response mainly by down regulation of pro-inflammatory cytokines as IL-6 and upregulation of anti-inflammatory TGF-β [3]. Already in 1994 the occurrence in circulation of a Captopril/Lisinopril sensitive Angiotensin converting enzyme activity was described in insects as flies and Jpn J Med 2018,1:1

Angiotensin converting enzyme, a negative moderator of the innate immune response in both mammals and insects