ライフサイエンスコーパス: bladder infection

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1 o adapt to the rapidly changing niche during bladder infection.

2 bgroup of mice that progressed to high-titer bladder infections.

3 095 in two independent experiments), but not bladder, infection.

4 conditions and were assessed for kidney and bladder infection 48 h after inoculation.

5 train recovered from a patient with an acute bladder infection and compare it with six other finished

6 S. agalactiae CovR promotes bladder infection and inflammation, as well as adhesion

7 s as virulent as its parent, CP9, in causing bladder infection and nearly as virulent in causing rena

8 ings may explain the prevalent recurrence of bladder infections and suggest the bladder as a site exh

9 l observations that antibody responses after bladder infections are not detectable suggest defects in

10 intracellular biofilm-like pods explains how bladder infections can persist in the face of robust hos

11 Within 12 h of murine bladder infection, half of the bacteria are intracellula

12 ke structure, were attenuated during chronic bladder infection, implying that FimH's ability to switc

13 al reflex (VUR) yet still produce kidney and bladder infection in a substantial proportion of mice.

14 ial adhesion to epithelial cells and urinary bladder infection in mice.

15 i- s-FimH1-25) significantly reduced E. coli bladder infections in the experimental mouse model of ur

16 In vivo, overexpression of HlyA during acute bladder infection induces more rapid and extensive exfol

17 e associated with a low, but defined risk of bladder infection, it is imperative that the appropriate

18 High bladder infection levels persisted over the 14-day study

19 y infection levels generally correlated with bladder infection levels, especially in C3H/HeJ and C3H/

20 vantage of a new, transparent zebrafish swim bladder infection model.

21 d a history of physician-diagnosed kidney or bladder infection (odds ratio (OR) = 1.9, 95% confidence

22 2, and AKR) showed progressive resolution of bladder infections over a 14-day period.

23 e, vasculitis, diabetic nephropathy, urinary bladder infections, prostatitis, gastric paresis, and im

24 e (F(1) x C3H/HeJ) backcross mice had severe bladder infections, similar to the susceptible C3H/HeJ p

25 Twenty-four hours following bladder infection, the kidneys of C3H/HeN and C3H/HeJ mi

26 chestrating the early innate immunity during bladder infection, they subsequently play a tissue-speci

27 me bladder enlargement, dribbling urination, bladder infection, urinary stones, and widely dilated oc

28 highly significant QTL for susceptibility to bladder infection was identified on chromosome 4, and C3

29 A constant, low-level bladder infection was observed in SWR and SJL mice.

30 n be used to effectively combat recalcitrant bladder infections without causing lasting harm to the u

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