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1 lung disease developed after infection with M. pulmonis.
2 amide (CYP) and inoculated with 10(7) CFU of M. pulmonis.
3 e could demonstrate that it was expressed in M. pulmonis.
4 ious Bcg and H-2 genotypes for resistance to M. pulmonis.
5 hmatic airways to facilitate colonization by M. pulmonis and the capacity of M. pulmonis to exacerbat
6 erior to single PCR or culture for detecting M. pulmonis, and that M. pulmonis is present in all but
8 Rats were inoculated with 3 X 10(7) CFU of M. pulmonis at 10 days prior to breeding (-10) or at ges
9 model clearly provides a mechanism by which M. pulmonis can alter its surface architecture and also
13 of 61 (34%) CAR bacillus samples from which M. pulmonis could not be cultured and identified 2 addit
19 We report here that a single recombinase in M. pulmonis, HvsR, catalyses independent DNA inversions
22 licated as a virulence determining factor in M. pulmonis-induced murine respiratory disease, the prec
30 r, AX102 exaggerated leakage at 7 days after M. pulmonis infection and increased vascular remodeling
31 lymphangiogenesis in inflamed airways after M. pulmonis infection because expression of the integrin
32 clude that the polarized stimulus created by M. pulmonis infection differentially changes the size, s
33 t in mice genetically predisposed to asthma, M. pulmonis infection elicits an inflammatory milieu in
35 ymphangiogenesis occurs in mouse lungs after M. pulmonis infection through a mechanism involving sign
39 culture for detecting M. pulmonis, and that M. pulmonis is present in all but four CAR bacillus isol
41 nduced both humoral and cellular immunity to M. pulmonis, largely prevented infection (vaccination),
42 nst two MnuA peptide sequences identified an M. pulmonis membrane protein of approximately 42 kDa by
46 that when encased within a biofilm, cells of M. pulmonis producing a short form of the Vsa protein we
53 oculated with an avirulent, poorly infective M. pulmonis strain, 14 (19%) were positive by nested PCR
57 ate the Vsa proteins nonspecifically mediate M. pulmonis surface interactions and function to sterica
59 fected by the bacterium Mycoplasma pulmonis (M. pulmonis), the segment of the microvasculature that s
61 onization by M. pulmonis and the capacity of M. pulmonis to exacerbate symptoms associated with acute
62 ough release of IFN-gamma and the ability of M. pulmonis to trigger the production of Th2-type cytoki
63 re inoculated intranasally with 10(4) CFU of M. pulmonis UAB CT and evaluated at 21 days postinfectio
64 nd characterized genes encoding V-1 from two M. pulmonis UAB CT V-1 variants that differ in hemadsorp
65 were infected intranasally with 10(5) CFU of M. pulmonis UAB CT, and their lungs were quantitatively
71 with CAR bacillus isolates known to contain M. pulmonis, whereas single PCR gave no positive results
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