Timeline

Nadira Frescaline

Post-doc

02 Oct 2024

publication

Infected wound repair correlates with collagen I induction and NOX2 activation by cold atmospheric plasma.

22 Feb 2023

publication

Complete Genome Sequences of Bioluminescent Staphylococcus aureus Strains Xen31 and Xen36, Derived from Two Clinical Isolates.

09 Sep 2022

project

NOVOPLASM – Novel perspective for cold plasma application in the treatment of severe and infected burn wounds

01 Jan 2022

publication

Danger signals in traumatic hemorrhagic shock and new lines for clinical applications.

16 Jun 2021

publication

Cold Atmospheric Plasma Promotes Killing of Staphylococcus aureus by Macrophages.

01 Dec 2020

publication

Physical plasma therapy accelerates wound re-epithelialisation and enhances extracellular matrix formation in cutaneous skin grafts.

28 Aug 2020

team

Group : Bacterial Pathogenesis and Antibacterial Agents

08 Aug 2020

publication

A Murine Model of a Burn Wound Reconstructed with an Allogeneic Skin Graft.

01 Nov 2019

publication

Cold atmospheric plasma modulates endothelial nitric oxide synthase signalling and enhances burn wound neovascularisation.

01 Jan 2018

publication

Mesenchymal Stromal Cells Based Therapy in Systemic Sclerosis: Rational and Challenges.

01 Dec 2016

publication

Pan PPAR agonist IVA337 is effective in prevention and treatment of experimental skin fibrosis.

01 Dec 2016

publication

Treatment with abatacept prevents experimental dermal fibrosis and induces regression of established inflammation-driven fibrosis.

05 Jul 2016

publication

OX40L blockade protects against inflammation-driven fibrosis.

21 Mar 2015

publication

Identification of NF-κB and PLCL2 as new susceptibility genes and highlights on a potential role of IRF8 through interferon signature modulation in systemic sclerosis.

01 Jan 2015

publication

Inflammation as a Keystone of Bone Marrow Stroma Alterations in Primary Myelofibrosis.

01 Nov 2014

publication

The nuclear receptor constitutive androstane receptor/NR1I3 enhances the profibrotic effects of transforming growth factor β and contributes to the development of experimental dermal fibrosis.

01 Feb 2014

publication

Attenuation of flightless I improves wound healing and enhances angiogenesis in a murine model of type 1 diabetes.

01 Oct 2013

publication

Venous ulceration contaminated by multi-resistant organisms: larval therapy and debridement.

01 Apr 2013

publication

Topically applied flightless I neutralizing antibodies improve healing of blistered skin in a murine model of epidermolysis bullosa acquisita.

01 Jan 2013

publication

The influence of Flightless I on Toll-like-receptor-mediated inflammation in a murine model of diabetic wound healing.

01 Nov 2012

publication

Lysosomal secretion of Flightless I upon injury has the potential to alter inflammation.

15 Sep 2012

publication

Flightless, secreted through a late endosome/lysosome pathway, binds LPS and dampens cytokine secretion.

12 Sep 2012

publication

Cytoskeletal protein Flightless (Flii) is elevated in chronic and acute human wounds and wound fluid: neutralizing its activity in chronic but not acute wound fluid improves cellular proliferation.

01 Aug 2009

publication

Attenuation of Flightless I, an actin-remodelling protein, improves burn injury repair via modulation of transforming growth factor (TGF)-beta1 and TGF-beta3.

A little guide for advanced search:

Infected wound repair correlates with collagen I induction and NOX2 activation by cold atmospheric plasma.

Complete Genome Sequences of Bioluminescent Staphylococcus aureus Strains Xen31 and Xen36, Derived from Two Clinical Isolates.

NOVOPLASM – Novel perspective for cold plasma application in the treatment of severe and infected burn wounds

Danger signals in traumatic hemorrhagic shock and new lines for clinical applications.

Cold Atmospheric Plasma Promotes Killing of Staphylococcus aureus by Macrophages.

Physical plasma therapy accelerates wound re-epithelialisation and enhances extracellular matrix formation in cutaneous skin grafts.

Group : Bacterial Pathogenesis and Antibacterial Agents

A Murine Model of a Burn Wound Reconstructed with an Allogeneic Skin Graft.

Cold atmospheric plasma modulates endothelial nitric oxide synthase signalling and enhances burn wound neovascularisation.

Mesenchymal Stromal Cells Based Therapy in Systemic Sclerosis: Rational and Challenges.

Pan PPAR agonist IVA337 is effective in prevention and treatment of experimental skin fibrosis.

Treatment with abatacept prevents experimental dermal fibrosis and induces regression of established inflammation-driven fibrosis.

OX40L blockade protects against inflammation-driven fibrosis.

Identification of NF-κB and PLCL2 as new susceptibility genes and highlights on a potential role of IRF8 through interferon signature modulation in systemic sclerosis.

Inflammation as a Keystone of Bone Marrow Stroma Alterations in Primary Myelofibrosis.

The nuclear receptor constitutive androstane receptor/NR1I3 enhances the profibrotic effects of transforming growth factor β and contributes to the development of experimental dermal fibrosis.

Attenuation of flightless I improves wound healing and enhances angiogenesis in a murine model of type 1 diabetes.

Venous ulceration contaminated by multi-resistant organisms: larval therapy and debridement.

Topically applied flightless I neutralizing antibodies improve healing of blistered skin in a murine model of epidermolysis bullosa acquisita.

The influence of Flightless I on Toll-like-receptor-mediated inflammation in a murine model of diabetic wound healing.

Lysosomal secretion of Flightless I upon injury has the potential to alter inflammation.

Flightless, secreted through a late endosome/lysosome pathway, binds LPS and dampens cytokine secretion.

Cytoskeletal protein Flightless (Flii) is elevated in chronic and acute human wounds and wound fluid: neutralizing its activity in chronic but not acute wound fluid improves cellular proliferation.

Attenuation of Flightless I, an actin-remodelling protein, improves burn injury repair via modulation of transforming growth factor (TGF)-beta1 and TGF-beta3.