scispace - formally typeset
S

Steven S. Witkin

Researcher at University of São Paulo

Publications -  547
Citations -  23143

Steven S. Witkin is an academic researcher from University of São Paulo. The author has contributed to research in topics: Antibody & Pregnancy. The author has an hindex of 65, co-authored 524 publications receiving 20451 citations. Previous affiliations of Steven S. Witkin include University of California, Los Angeles & University of North Carolina at Chapel Hill.

Papers
More filters
Journal ArticleDOI

Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

Daniel J. Klionsky, +2522 more
- 21 Jan 2016 - 
TL;DR: In this paper, the authors present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macro-autophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
Journal ArticleDOI

Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)

Daniel J. Klionsky, +2983 more
- 08 Feb 2021 - 
TL;DR: In this article, the authors present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes.
Journal Article

The relationship of amniotic fluid cytokines and preterm delivery, amniotic fluid infection, histologic chorioamnionitis, and chorioamnion infection.

TL;DR: The hypothesis that infection is one cause of preterm delivery, operating via a mechanism involving induction of cytokine production, is supported.
Journal ArticleDOI

An experimental model for intraamniotic infection and preterm labor in rhesus monkeys

TL;DR: In the rhesus monkey, after intraamniotic infection, there is a predictable and sequential increase in amniotic fluid tumor necrosis factor-alpha, interleukin-1 beta, and interleucin-6, followed by increases in prostaglandin E2 and prostaglandsin F2 alpha.