scispace - formally typeset
J

Jan Tilmann Vollrath

Researcher at Goethe University Frankfurt

Publications -  18
Citations -  913

Jan Tilmann Vollrath is an academic researcher from Goethe University Frankfurt. The author has contributed to research in topics: Lung injury & Medicine. The author has an hindex of 6, co-authored 13 publications receiving 377 citations.

Papers
More filters
Journal ArticleDOI

Cytokines in Inflammatory Disease.

TL;DR: This review aims to briefly discuss a short list of a broad variety of inflammatory cytokines, focusing on the correlations and role of these inflammatory mediators in the genesis of inflammatory impacts.
Journal ArticleDOI

Endogenous Uteroglobin as Intrinsic Anti-inflammatory Signal Modulates Monocyte and Macrophage Subsets Distribution Upon Sepsis Induced Lung Injury.

TL;DR: In in vitro experiments, the influence of uteroglobin on monocyte functions including migratory behavior, TGF-β1 expression, cytotoxicity and viability were proven and highlight an important role of endogenous uteroglobin as intrinsic anti-inflammatory signal upon sepsis-induced early lung injury, which modules the early monocyte/macrophages driven inflammation.
Journal ArticleDOI

miR-142-3p Expression Is Predictive for Severe Traumatic Brain Injury (TBI) in Trauma Patients.

TL;DR: In this article, the authors investigated promising microRNAs (miRNA) released from affected tissue after severe trauma that have predictive values for the effects of the injury and found that miR-423-3p expression is significantly elevated after isolated traumatic brain injury and predictable for severe TBI in the first hours after trauma.
Journal ArticleDOI

Post-Traumatic Sepsis Is Associated with Increased C5a and Decreased TAFI Levels

TL;DR: Both elevated C5a and decreased TAFI may serve as promising predictive factors for the development of sepsis after polytrauma and have confirmed their potential as early sepsi biomarkers.
Journal ArticleDOI

Early Local Inhibition of Club Cell Protein 16 Following Chest Trauma Reduces Late Sepsis-Induced Acute Lung Injury.

TL;DR: The data confirmed the anti-inflammatory potential of endogenous CC16 in the murine double-hit model of ALI and confirmed that early CC16-neutralization increased the neutrophilic infiltration and lung injury at 6 h post-CLP, while 24 h later, the lung injury was reduced.