Plasmids were compared in immortalised cell culture, human airway liquid interface primary cell cultures, and mouse lung models to determine which design directed optimal transgene expression.
Using rat and isolated mouse lung models, Uhlig and colleagues [ 10] found that the ERK pathway did not significantly contribute to the ventilator-induced releases of MIP-2 in spite of the increased expression of phopho-ERK1/2.
In this work, we report the refinement of copolymer design and extend our physiological studies to demonstrate that the polymers: 1) reduce both shear stress and pressure-mediated increase in hydraulic conductivity, 2) reduce nitric oxide production in response to elevated hydrostatic pressure and, 3) reduce the capillary filtration coefficient (Kfc) in an isolated perfused mouse lung model.
In this study, we have characterized neutrophil recruitment profiles of the monomer, dimer, and wild type (WT) CXCL8 in a mouse lung model.
We have used the V600EBRAF-driven mouse lung model that develop premalignant lesions to understand stroma tumour interactions during pre-cancerous development.
We established the A/J mouse lung model of B[ a]P tumorigenicity and then used B[ a]P-7,8-catechol diacetate as a bioavailable precursor of B[ a]P-7,8-dione to test its tumorigenic potential.
The A/J mouse lung model is often used, but its use to study of the role of AKRs in B[ a]P activation is made difficult since the murine AKR1C enzymes are not orthologues of the human enzymes.
Secondly, fourteen mammalian virulence-related genes are absent or truncated in M18 genome, and the competitive index analysis of the strains M18 and LESB58 indicated the strain M18 is easier to be erased than that of LESB58 in the acute infection mouse lung model.
The covalent binding of electrophilic B[ a]P-7,8-dione with DNA nucleobases was previously reported in vitro, but there was a failure to detect these adducts in the A/J mouse lung model of B[ a]P carcinogenesis, when animals were treated with B[ a]P, B[ a]P-7,8 trans-dihydrodiol, or B[ a]P-7,8-dione.
To evaluate whether the decrease in ENaC-mediated transepithelial Na+ transport observed in vitro in AEC lacking CAP1/ Prss8 could have a physiological relevance in vivo, we measured sodium-driven alveolar fluid clearance (AFC) in an in situ nonventilated mouse lung model using I-albumin as a volume marker (Randrianarison et al, 2007, 2008).
In an earlier study, Ferran et al. [ 22] referred to the later "conventional" curative treatment in a mouse-lung model of P. multocida infection studies.
