scispace - formally typeset
W

Wieslaw Kozak

Researcher at Nicolaus Copernicus University in Toruń

Publications -  94
Citations -  4167

Wieslaw Kozak is an academic researcher from Nicolaus Copernicus University in Toruń. The author has contributed to research in topics: Inflammation & Prostaglandin E2. The author has an hindex of 31, co-authored 94 publications receiving 3944 citations. Previous affiliations of Wieslaw Kozak include University of Michigan & Lovelace Respiratory Research Institute.

Papers
More filters
Journal ArticleDOI

Resistance to fever induction and impaired acute-phase response in interleukin-1β-deficient mice

TL;DR: A central role for IL-1 beta as a pyrogen and a mediator of the acute-phase response in a subset of inflammatory disease models is highlighted, and the notion that blocking the action of a single key cytokine can alter the course of specific immune and inflammatory responses is supported.
Journal ArticleDOI

Immunomodulatory effects of cigarette smoke

TL;DR: Chronic exposure to cigarette smoke or nicotine causes T cell unresponsiveness, which may account for or contribute to the immunosuppressive and anti-inflammatory properties of cigarette smoke/nicotine.
Journal ArticleDOI

The adaptive value of fever

TL;DR: There is overwhelming evidence in favor of fever being an adaptive host response to infection that has persisted throughout the animal kingdom for hundreds of millions of years and it is probable that the use of antipyretic/anti-inflammatory/analgesic drugs, when they lead to suppression of fever, results in increased morbidity and mortality during most infections.
Journal ArticleDOI

Role of Fever in Disease

TL;DR: It is speculated that patients who would not have survived severe sepsis in the past are now being kept alive and that the occasionally high fevers seen in these patients may be maladaptive.
Journal ArticleDOI

IL-6 and IL-1 beta in fever. Studies using cytokine-deficient (knockout) mice.

TL;DR: The data demonstrate that in the mouse, IL‐1β and IL‐6 are critical for the induction of fever during local inflammation, whereas in systemic inflammation they appear only to contribute to fever.