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 sitive individuals with the exception of the Cystic Fibrosis patient.

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

4 as of a nonresistance strain isolated from a cystic fibrosis patient.

5 and BCC1622, both isolated from the lungs of cystic fibrosis patients.

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

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

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

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

10 also a risk factor for lung exacerbations in cystic fibrosis patients.

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

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

13 pathogen that infects immunocompromised and cystic fibrosis patients.

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

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

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

17 the pulmonary tracts of chronically infected cystic fibrosis patients.

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

19 us associated with respiratory infections in cystic fibrosis patients.

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

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

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

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

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

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

26 es significant morbidity and mortality among cystic fibrosis patients.

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

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

29 ains causing chronic pulmonary infections in cystic fibrosis patients.

30 enotype associated with lethal infections in cystic fibrosis patients.

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

32 pathogen that infects immunocompromised and cystic fibrosis patients.

33 s in immunocompromised individuals including cystic fibrosis patients.

34 e commonly associated with lung infection in cystic fibrosis patients.

35 chronic Pseudomonas aeruginosa infections in cystic fibrosis patients.

36 ections in the antibiotic-treated airways of cystic fibrosis patients.

37 -associated bacterial burden in the lungs of cystic fibrosis patients.

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

39 within the extracellular DNA of sputum from cystic fibrosis patients.

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

41 ctions and are the leading cause of death in cystic fibrosis patients.

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

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

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

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

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

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

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

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

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

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

52 uces progressive respiratory inflammation in cystic fibrosis patients.

53 um abscessus are increasing in prevalence in cystic fibrosis patients.

54 ommunities chronically colonize the lungs of cystic fibrosis patients.

55 pportunistic pathogen infecting the lungs of cystic fibrosis patients.

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

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

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

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

60 inflammation and progressive lung damage in cystic fibrosis patients.

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

62 ections in immunocompromised individuals and cystic fibrosis patients.

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

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

65 eatment to reduce pulmonary exacerbations in cystic fibrosis patients: (1) inverse probability weight

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

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

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

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

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

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

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

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

74 piratory isolates from two recently infected cystic fibrosis patients and an epidemiologically-linked

75 evaluated on respiratory specimens from non-cystic fibrosis patients and compared to the mycobacteri

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

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

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

79 re infections mainly in immunocompromised or cystic fibrosis patients and is able to resist antimicro

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

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

82 t biofilms in immunocompromised individuals, cystic fibrosis patients, and in chronic wounds.

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

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

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

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

87 Cystic fibrosis patients are recommended complex, time-i

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

89 ude exhaled breath condensate collected from cystic fibrosis patients as well as in vitro-cultured hu

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

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

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

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

94 uginosa, a predominant bacterial pathogen in cystic fibrosis patients, can metabolize multiple drugs

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

96 2a clinical trial, which included nine adult cystic fibrosis patients chronically infected with P. ae

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

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

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

100 Cystic fibrosis patients depend on their caregiver's abi

101 d in this way to measure CFTR function using cystic fibrosis patient-derived iPSC lines before and af

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

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

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

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

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

107 mportant component of the lung microbiome in cystic fibrosis patients, from samples dominated by huma

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

109 Approximately 10% of cystic fibrosis patients harbor nonsense mutations in th

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

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

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

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

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

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

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

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

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

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

120 Cystic fibrosis patients in all age groups had higher tr

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

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

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

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

125 corales, and fungal respiratory cultures for cystic fibrosis patients; inadequate capacity for fungal

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

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

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

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

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

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

132 CFTR, the anion channel mutated in cystic fibrosis patients, is a model ABC protein whose A

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

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

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

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

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

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

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

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

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

142 Preexisting antibodies in PA-colonized cystic fibrosis patients primarily target the CbpD AA10

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

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

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

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

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

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

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

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

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

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

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

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

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

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

157 model, and in sputum samples recovered from cystic fibrosis patients that contain multiple mixed bac

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

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

160 workflow was applied to sputum samples from cystic fibrosis patients to map O-glycosylation features

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

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

163 -1, increased pulmonary infection risk among cystic fibrosis patients, upregulated levels of HNP-5 fo

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

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

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

167 gladioli strains isolated from the lungs of cystic fibrosis patients were found to produce unusual l

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

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

170 eudomonas aeruginosa is of major concern for cystic fibrosis patients where this infection can be fat

171 s of the chronic P. aeruginosa infections in cystic fibrosis patients which display recalcitrance to

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

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

174 Eight cystic fibrosis patients with A. xylosoxidans were treat

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

176 Long-term infection of the airways of cystic fibrosis patients with Pseudomonas aeruginosa is

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

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

179 12/17 A. xylosoxidans strains recovered from cystic fibrosis patients, with P. aeruginosa and with Ar

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