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1 sposition of properdin-deficient patients to meningococcal infection.
2 e and causes attenuation in a mouse model of meningococcal infection.
3 s released into serum shortly after onset of meningococcal infection.
4 ed in the sera of patients convalescing from meningococcal infection.
5 central nervous system (CNS) in response to meningococcal infection.
6 e and causes attenuation in a mouse model of meningococcal infection.
7 ve critical impact on the pathophysiology of meningococcal infections.
8 ver-represented among patients with systemic meningococcal infections.
9 broad protection against both gonococcal and meningococcal infections.
10 tic lineages caused the majority of invasive meningococcal infections.
13 important in understanding human immunity to meningococcal infections and can aid in the design of an
14 ably contributes to the early containment of meningococcal infection, and sensing defects create incr
15 before and during an outbreak of serogroup C meningococcal infection at a university in the United Ki
16 deficient patients are susceptible to lethal meningococcal infection, but the mechanism of this selec
18 se-control study of US college students with meningococcal infection from September 1, 1998, to Augus
21 es have documented the incidence of invasive meningococcal infection in college students or whether t
25 infection-related adverse events, including meningococcal infections, were observed through the exte
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