Sendai model

Tarko A.M. (2001). Investigation of global biosphere processes with the aid of a global spatial carbon dioxide cycle model. Proceedings of the Sixth International Carbon Dioxide Conference, Extended Abstracts (October 1-2, 2001, Tohoku University, Sendai, Japan), Yol. 2, pp. 899-902. 

In the following sections we will describe the reagents and methodology for setting up and examining two models of respiratory inflammation in the rat. The first is a live Sendai virus model and the second is a model of acute bacte-... 

Cheetham, J. J., Hpand, R. M., Andrews, M., and Flanagan, T. D. (1990). Cholesterol sulfate inhibits the fusion of Sendai virus to biological and model membranes. /. BieJ. Cfjcw. 265,12404-12409. 

Figure 2.3-3 Mole fraction (jc) of P-carotene in the liquid phase for the system CO2—toluene-p-carotene at 298 K. Comparison between experimental data and calculations performed by models of Chang and Randolph [10] and of Kikic et al. [12]. Adapted from Kikic et al. Proc. of The 4 Int. Symp. on Supercritical Fluids, Sendai, Japan, 1997, p. 42 5.

At least two environmental factors may contribute to the development of HP as a promoting factor viral infections and inhalation injury. Experimental models of HP have shown that animals challenged with respiratory syncytial virus or Sendai virus exhibit a more severe inflammatory response to subsequent Saccharopolyspora rectivirgula exposure, which may persist long after the viral infection has declined (11,12). Also, studies in humans have revealed that common respiratory vimses, primarily Influenza A, are often present in the lower airways of patients with HP (13). The reasons why viral infections may potentiate HP are unknown, but it may be related to vims-induced mucociliary dysfunction, increased expression of costimulatory molecules by alveolar macrophages, and increased secretion of chemokines, enhancing the recruitment of lymphocytes to the lungs (13,14). 

Lipoamino acids are also particularly attractive as antiviral agents. Certain acylamino acid derivatives have been found to produce inhibition on influenza neuraminidase [30]. A number of V -palmitoylated amino acids/peptides have been incorporated into model membranes affecting the transition temperature between the bilayer to hexagonal aggregation, a property associated with antiviral activity. Epand et al. [31] demonstrated the inhibition action of A -palmitoyltryptophan against the Cantell strain of Sendai virus (parainfluenza type 1). 

The paramyxoviruses, largely because of their profound cell-fusing activity, have served as an important model of membrane perturbation by viruses. During Sendai virus-mediated fusion of mouse ascites cells, Pasternak and Micklem (1973) detected loss of intracellular metabolites coincident with inhibition of their accumulation from the medium. This failure to maintain selective permeability did not occur at 0°C and was unaffected by cytochalasin B which inhibits fusion by the virus. Chick embryo fibroblasts infected with Newcastle disease virus were found to release cellular enzymes, such as lactate dehydrogenase, glutamic oxaloacetic transaminase, and lysosomal enzymes (Katzman and Wilson, 1974). These cells also became... 

Haywood, A. M., 1974, Fusion of Sendai virus with model membranes, J. Mol. Biol. 87 625. 

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