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1 susceptibility to and severity of kidney and bladder infection.
2  to and severity of kidney and to an extent, bladder infection.
3 uced CL-11 for protection against kidney and bladder infection.
4 o adapt to the rapidly changing niche during bladder infection.
5 bgroup of mice that progressed to high-titer bladder infections.
6 095 in two independent experiments), but not bladder, infection.
7  conditions and were assessed for kidney and bladder infection 48 h after inoculation.
8                We found that, following each bladder infection, a highly T helper type 2 (T(H)2)-skew
9 train recovered from a patient with an acute bladder infection and compare it with six other finished
10                  S. agalactiae CovR promotes bladder infection and inflammation, as well as adhesion
11 s as virulent as its parent, CP9, in causing bladder infection and nearly as virulent in causing rena
12 ings may explain the prevalent recurrence of bladder infections and suggest the bladder as a site exh
13 l observations that antibody responses after bladder infections are not detectable suggest defects in
14 intracellular biofilm-like pods explains how bladder infections can persist in the face of robust hos
15  associated with asymptomatic bacteriuria or bladder infection (cystitis).
16                        Within 12 h of murine bladder infection, half of the bacteria are intracellula
17 ke structure, were attenuated during chronic bladder infection, implying that FimH's ability to switc
18 al reflex (VUR) yet still produce kidney and bladder infection in a substantial proportion of mice.
19 ial adhesion to epithelial cells and urinary bladder infection in mice.
20 significantly reduces UPEC IBC formation and bladder infection in mice.
21 i- s-FimH1-25) significantly reduced E. coli bladder infections in the experimental mouse model of ur
22 In vivo, overexpression of HlyA during acute bladder infection induces more rapid and extensive exfol
23 e associated with a low, but defined risk of bladder infection, it is imperative that the appropriate
24                                         High bladder infection levels persisted over the 14-day study
25 y infection levels generally correlated with bladder infection levels, especially in C3H/HeJ and C3H/
26 vantage of a new, transparent zebrafish swim bladder infection model.
27 ts, which increased K. pneumoniae fitness in bladder infection models, suggesting that long-term resi
28 d a history of physician-diagnosed kidney or bladder infection (odds ratio (OR) = 1.9, 95% confidence
29 2, and AKR) showed progressive resolution of bladder infections over a 14-day period.
30 e, vasculitis, diabetic nephropathy, urinary bladder infections, prostatitis, gastric paresis, and im
31 inary tract infection and found that a prior bladder infection resulted in an earlier onset of tumor
32 e (F(1) x C3H/HeJ) backcross mice had severe bladder infections, similar to the susceptible C3H/HeJ p
33                  Twenty-four hours following bladder infection, the kidneys of C3H/HeN and C3H/HeJ mi
34 chestrating the early innate immunity during bladder infection, they subsequently play a tissue-speci
35 me bladder enlargement, dribbling urination, bladder infection, urinary stones, and widely dilated oc
36 highly significant QTL for susceptibility to bladder infection was identified on chromosome 4, and C3
37                        A constant, low-level bladder infection was observed in SWR and SJL mice.
38 tor of host defense mechanisms in kidney and bladder infection with therapeutic potential for human a
39 n be used to effectively combat recalcitrant bladder infections without causing lasting harm to the u