ライフサイエンスコーパス: nasal epithelia

1 based lentivirus vector (GP64-FIV) to murine nasal epithelia.

2 ut the airways, while CNT2 was restricted to nasal epithelia.

3 s through the cribriform plate, and into the nasal epithelia.

4 d NO-dependent chloride transport across the nasal epithelia.

5 anion secretory currents in wild-type and CF nasal epithelia.

6 ve cells or fibers in the olfactory nerve or nasal epithelia.

7 y in the olfactory bulb, olfactory nerve, or nasal epithelia.

8 ion of human cells, including those of human nasal epithelia.

9 critical for efficient virus replication in nasal epithelia.

10 though they were far lower than those in the nasal epithelia.

11 In nasal epithelia 1-EBIO produced only a small transient e

12 experiments using cultures of primary human nasal epithelia and human bronchial epithelia have estab

13 It is also expressed by nasal epithelia and neural crest-derived facial structur

14 munity, but also to its superior invasion of nasal epithelia and resistance to the cell-intrinsic bar

15 function in cell systems and patient-derived nasal epithelia and restored airway volume homeostasis.

16 diversity among tuft cells that extends from nasal epithelia and type II taste cells to ex-Aire-expre

17 fate of the ectoderm from which the lens and nasal epithelia are derived.

18 Furthermore, Myhre syndrome nasal epithelia are impaired in bacterial killing.

19 n, spinal cord, sensory ganglia, retina, and nasal epithelia, as well as in the pituitary, and is ref

20 The presence of increased CCL5 levels in nasal epithelia at the time of bronchiolitis or the deve

21 ype 1 (HSV-1) primarily targets the oral and nasal epithelia before establishing latency in the trige

22 (apical, basolateral, paracellular) in human nasal epithelia cultures using experimental (Ussing Cham

23 1.2-43.3; P = .028), and CCL5 expression in nasal epithelia during acute RSV infection (OR, 3.8; 95%

24 ted across the various regions of the bovine nasal epithelia following conjugation with deslorelin an

25 analysis documented persistent expression in nasal epithelia for approximately 1 year without signifi

26 We conclude that: (1) normal, but not CF, nasal epithelia have a constitutively active DPC-sensiti

27 f HCO3- via CFTR; and (2) both normal and CF nasal epithelia have Na+-independent, H2DIDS-sensitive A

28 es and persistently expresses a transgene in nasal epithelia in the absence of agents that disrupt th

29 ant asthma-associated methylation changes in nasal epithelia of adult white asthmatic patients.

30 al hCFTR expression was also observed in the nasal epithelia of CF mutant mice.

31 t) measurements are routinely carried out on nasal epithelia of CF patients in the clinic.

32 h 4PBA therapy inducing CFTR function in the nasal epithelia of deltaF508-homozygous CF patients.

33 uction of influenza virus replication in the nasal epithelia of HA vector-immunized mice suggested an

34 lture and of the Cl- transport defect in the nasal epithelia of mice homozygous for the deltaF508 mut

35 ced in primary nasal epithelial cultures and nasal epithelia of patients with CRSwNP.

36 reased colonization in mouse nasopharynx and nasal epithelia, resulting in decreased transmission.

37 In vivo studies of CF mouse nasal epithelia revealed an increase in goblet cell numb

38 In CF nasal epithelia the activation of calcium-activated chlo

39 d that ELX/TEZ/IVA improved CFTR function in nasal epithelia to a level of 46.5% (interquartile range

40 tro, many S. epidermidis isolates stimulated nasal epithelia to produce antimicrobial peptides, killi

41 both CF mouse models, Cl(-) permeability of nasal epithelia was restored in a sustained manner by zi

42 ensive insights into metabolic activities in nasal epithelia, which contribute to achieve a full unde

43 f IB3-1 cells with 0.1-1 mM 4PBA and primary nasal epithelia with 5 mM 4PBA also resulted in the appe

44 ulose-formulated AcGP64-FIV transduced mouse nasal epithelia with much greater efficiency than simila