ライフサイエンスコーパス: cystic fibrosis patient

1 l and chemical makeup of a human lung from a cystic fibrosis patient.

2 The bronchial cells were obtained from a cystic fibrosis patient.

3 ssociated with more severe meconium ileus in cystic fibrosis patients.

4 c infections, such as the infections seen in cystic fibrosis patients.

5 en coexist in both the soil and the lungs of cystic fibrosis patients.

6 pathogen that infects immunocompromised and cystic fibrosis patients.

7 e may negatively impact the lung function of cystic fibrosis patients.

8 important pathogen that infects the lungs of cystic fibrosis patients.

9 the pulmonary tracts of chronically infected cystic fibrosis patients.

10 is the major infectious agent of concern for cystic fibrosis patients.

11 us associated with respiratory infections in cystic fibrosis patients.

12 oximal tubule function have been reported in cystic fibrosis patients.

13 rrect the defective airway surface liquid in cystic fibrosis patients.

14 ed alginate during infection in the lungs of cystic fibrosis patients.

15 major role in lung function deterioration in cystic fibrosis patients.

16 in a pipeline, on plants or in the lungs of cystic fibrosis patients.

17 of sputum and improving the lung function of cystic fibrosis patients.

18 es significant morbidity and mortality among cystic fibrosis patients.

19 reat in hospital-acquired infections and for cystic fibrosis patients.

20 e for Pseudomonas aeruginosa in the lungs of cystic fibrosis patients.

21 onization of this organism in the airways of cystic fibrosis patients.

22 ains causing chronic pulmonary infections in cystic fibrosis patients.

23 enotype associated with lethal infections in cystic fibrosis patients.

24 in some P. aeruginosa strains isolated from cystic fibrosis patients.

25 increases post-lung transplant mortality in cystic fibrosis patients.

26 at negatively affects the quality of life of cystic fibrosis patients.

27 nosa is the sentinel respiratory pathogen in cystic fibrosis patients.

28 hogen and a threat for immunocompromised and cystic fibrosis patients.

29 e for the formation of mucus in the lungs of cystic fibrosis patients.

30 s chronic biofilm infections in the lungs of cystic fibrosis patients.

31 with chronic lung infections as well as with cystic fibrosis patients.

32 an effective therapy for mucus hydration in cystic fibrosis patients.

33 pathogen that infects immunocompromised and cystic fibrosis patients.

34 airway infections in immune-compromised and cystic fibrosis patients.

35 primary agent of chronic lung infections in cystic fibrosis patients.

36 uces progressive respiratory inflammation in cystic fibrosis patients.

37 ommunities chronically colonize the lungs of cystic fibrosis patients.

38 pportunistic pathogen infecting the lungs of cystic fibrosis patients.

39 ons on both longevity and quality of life in cystic fibrosis patients.

40 duals and is a leading cause of mortality in cystic fibrosis patients.

41 infections and in chronic lung infections in cystic fibrosis patients.

42 sistent infection in humans, for example, in cystic fibrosis patients.

43 leading cause of morbidity and mortality in cystic fibrosis patients.

44 inflammation and progressive lung damage in cystic fibrosis patients.

45 inate and colonize the respiratory tracts of cystic fibrosis patients.

46 ections in immunocompromised individuals and cystic fibrosis patients.

47 lonization of the lower respiratory tract in cystic fibrosis patients.

48 a major cause of morbidity and mortality in cystic fibrosis patients.

49 eting isolate was cultured from one-third of cystic fibrosis patients.

50 proteins involved in the immune response of cystic fibrosis patients.

51 gen that can cause severe lung infections in cystic fibrosis patients.

52 g motility exist as biofilms in the lungs of cystic fibrosis patients.

53 for lung transplantation (n=145), and 11% of cystic fibrosis patients (16 of 145) formed gastric bezo

54 levels in bronchoalveolar lavage fluid from cystic fibrosis patients (3.6 ng/ml of lavage).

55 e concentrations in sweat from patients with cystic fibrosis, patients admitted to the emergency depa

56 Gastric bezoars are common in cystic fibrosis patients after lung transplantation.

57 indings indicate that following infection of cystic fibrosis patient airways, P. aeruginosa strains g

58 pes, indicating that as strains persisted in cystic fibrosis patient airways, their type III protein

59 but adapt to the milieu of the airway of the cystic fibrosis patient and evolve toward a common pheno

60 f Burkholderia cepacia complex infections in cystic fibrosis patients and also infect other immunocom

61 rmal subjects, small-intestinal epithelia of cystic fibrosis patients and cystic fibrosis transmembra

62 responsible for high-morbidity infections of cystic fibrosis patients and is a major agent of nosocom

63 hogen that causes chronic lung infections in cystic fibrosis patients and is a major source of nosoco

64 thogen that chronically infects the lungs of cystic fibrosis patients and is the leading cause of mor

65 nosa isolates, two from clonal infections of cystic fibrosis patients and one from an aquatic environ

66 electrolyte balance problems: older adults, cystic fibrosis patients, and persons with spinal cord i

67 Isolates from cystic fibrosis patients appear to originate from the en

68 covered from chronic pulmonary infections in cystic fibrosis patients are frequently mucoid.

69 tory isolates of Pseudomonas aeruginosa from cystic fibrosis patients are mucoid (alginate producing)

70 Cystic fibrosis patients are recommended complex, time-i

71 ly impaired hPSC-derived cholangiocytes from cystic fibrosis patients are rescued by CFTR correctors.

72 aMKII upon loss of CFTR function might leave cystic fibrosis patients at increased risk of heart dysf

73 ncrease the post-Golgi expression of CFTR in cystic fibrosis patients bearing the DeltaF508 mutation.

74 nfection by B. cepacia poses a great risk to cystic fibrosis patients because it causes accelerated l

75 jury in the P. aeruginosa-infected airway of cystic fibrosis patients by decreasing the ability of al

76 d with aggressive infections in the lungs of cystic fibrosis patients, causing disease that is often

77 on models and has been found in the lungs of cystic fibrosis patients colonized by P. aeruginosa.

78 ed the elevated sweat electrolyte content of cystic fibrosis patients compared with that of healthy c

79 aeruginosa (PA) isolated from the airways of cystic fibrosis patients constitutively add palmitate to

80 Cystic fibrosis patients depend on their caregiver's abi

81 coccus aureus-specific serum IgG compared to cystic fibrosis patients despite recurrent S. aureus inf

82 ed longitudinal data on approximately 90% of cystic fibrosis patients diagnosed in the United States

83 type III proteins, only 12% of isolates from cystic fibrosis patients did so, with nearly all of thes

84 The optimal timing for listing of cystic fibrosis patients for lung transplantation is con

85 omonas aeruginosa, the principal pathogen of cystic fibrosis patients, forms antibiotic-resistant bio

86 Pseudomonas aeruginosa in the lungs of cystic fibrosis patients grows to high densities in muco

87 idly growing mycobacteria from the sputum of cystic fibrosis patients has recently been reported.

88 Human DNase I, an enzyme used to treat cystic fibrosis patients, has been engineered to more ef

89 uclease I (DNase I), an enzyme used to treat cystic fibrosis patients, has been engineered to more ef

90 recognized as a pulmonary pathogen to which cystic fibrosis patients have a particular susceptibilit

91 Among patients with cystic fibrosis patients, highly antibiotic-resistant ba

92 In cystic fibrosis patients, however, LPS-rough strains of

93 hronic bacterial infections commonly seen in cystic fibrosis patients; however, its use during parain

94 line of human airway epithelial cells from a cystic fibrosis patient (IB3-1) or by injection of in vi

95 ed in airway epithelial cells derived from a cystic fibrosis patient (IB3-1).

96 ited States than previously appreciated; 212 cystic fibrosis patients in 24 states were identified as

97 Cystic fibrosis patients in all age groups had higher tr

98 Cystic fibrosis patients in group 1 have improved 5-year

99 n epidemic strain PHDC, known to infect many cystic fibrosis patients in the mid-Atlantic region of t

100 train that is most frequently recovered from cystic fibrosis patients in the mid-Atlantic region of t

101 NFGNB that were recovered from cultures from cystic fibrosis patients in the University of Iowa Healt

102 tant strains of P. aeruginosa (isolated from cystic fibrosis patients) indicating a potential therape

103 pressed in vitro and in vivo by the BCC, and cystic fibrosis patients infected by the BCC species B.

104 s aeruginosa causes significant morbidity in cystic fibrosis patients initiated by the failure of inn

105 kholderia cepacia complex lung infections in cystic fibrosis patients is incomplete.

106 mucoid Pseudomonas aeruginosa isolates from cystic fibrosis patients is under direct control by AlgU

107 and cause chronic infections in the lungs of cystic fibrosis patients is well documented.

108 Interestingly, the fraction of cystic fibrosis patient isolates capable of secreting ty

109 gladioli BCC0238, a clinical isolate from a cystic fibrosis patient, led to the discovery of gladiol

110 ic correction of CFTRDeltaF508 misfolding in cystic fibrosis patients may require repair of defective

111 eptide phage display library with serum from cystic fibrosis patients obtained within the first year

112 osa during chronic respiratory infections in cystic fibrosis patients occurs via mutations that activ

113 agent of cepacia syndrome, primarily affects cystic fibrosis patients, often leading to death.

114 odified HNP-1 was not found in the sputum of cystic fibrosis patients or in leukocyte granules of nor

115 ting all nine genomovars, recovered from 761 cystic fibrosis patients or the natural environment.

116 In the lungs of cystic fibrosis patients, overproduction of mucus leads

117 The majority of cystic fibrosis patients produce a mutant form of CFTR (

118 ains causing chronic pulmonary infections in cystic fibrosis patients produce high levels of alginate

119 is the dominant organism in the majority of cystic fibrosis patients, Pseudomonas constituted the pr

120 s, including patients with anorexia nervosa, cystic fibrosis, patients receiving long-term tube-feedi

121 Eradication of P. aeruginosa in cystic fibrosis patients remains problematic.

122 ucleotide polymorphism scan in one cohort of cystic fibrosis patients, replicating top candidates in

123 in mucopurulent human respiratory mucus from cystic fibrosis patients represses the expression of its

124 isolates collected over time from one of the cystic fibrosis patients revealed independent mutations

125 ve particular relevance to lung infection in cystic fibrosis patients since the altered pulmonary phy

126 ed Burkholderia cenocepacia isolates from 16 cystic fibrosis patients, spanning a period of 2-20 yr a

127 directed approach, we were able to generate cystic fibrosis patient-specific iPSC-derived airway org

128 ate that P. aeruginosa strains isolated from cystic fibrosis patient sputum with increased cif gene e

129 ifferent media, including a medium made from cystic fibrosis patient sputum.

130 heless, azithromycin is successfully used in cystic fibrosis patients, supposedly because of "nonanti

131 seudomonal challenge isolates recovered from cystic fibrosis patients; these isolates are not include

132 The susceptibility of cystic fibrosis patients to bacterial pathogens is assoc

133 s that cause chronic pulmonary infections in cystic fibrosis patients typically undergo mucoid conver

134 ucoid Pseudomonas aeruginosa in the lungs of cystic fibrosis patients, undergoes two different chemic

135 -1, increased pulmonary infection risk among cystic fibrosis patients, upregulated levels of HNP-5 fo

136 ta from early isolates of P. aeruginosa from cystic fibrosis patients was compared with the results f

137 HAE derived from cystic fibrosis patients was not more susceptible to rgP

138 een stable during the previous 3 months, and cystic fibrosis patients were excluded.

139 een stable during the previous 3 months, and cystic fibrosis patients were excluded.

140 Sputum specimens from 240 cystic fibrosis patients were homogenized, serially dilu

141 of Pseudomonas aeruginosa isolates from four cystic fibrosis patients were used to validate the LIGAN

142 e clinical findings and lung pathology of 21 cystic fibrosis patients who had lung transplant.

143 the overall population of nonsense-mutation cystic fibrosis patients who received this treatment, it

144 m cultures or in the exhaled breath of adult cystic fibrosis patients with chronic BCC infection.

145 ed autophagy has previously been reported in cystic fibrosis patients with the common F508del-CFTR mu

146 ility results that may enhance treatment for cystic fibrosis patients with this opportunistic pathoge

147 12/17 A. xylosoxidans strains recovered from cystic fibrosis patients, with P. aeruginosa and with Ar

148 to recombinant A. fumigatus allergens in 55 cystic fibrosis patients without allergic broncho-pulmon