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1 NF-kappaB or NF-kappaB activation inhibitor (NAI).
2 ucleotide Analogue Interference Suppression (NAIS).
3 resistant to neuraminidase (NA) inhibitors (NAIs).
4 susceptibility to neuraminidase inhibitors (NAIs).
5 y prior depletion of intracellular free Na+ (Nai+).
6 malaria model incorporating vaccination and NAI.
7 oid carcinoma after administration of (124)I-NaI.
8 lling of the clonal landscape in response to NAI.
9 inhibited by the presence of the respective NAI.
10 ing influenza A viruses in susceptibility to NAIs.
11 influenza viruses tested were susceptible to NAIs.
12 our study may help to optimize the design of NAIs.
13 ve not been reported to confer resistance to NAIs.
14 spective purified substrates, we showed that NAI-107 forms complexes with bactoprenol-pyrophosphate-c
16 w membrane depolarization was observed after NAI-107 treatment, which could contribute to killing of
18 total of 212 children were studied: 46 with NAIS, 34 with APPIS, 55 with PVI, and 77 controls (male,
19 inhibitory concentrations against all tested NAIs (827-, 25-, 286-, and 702-fold for zanamivir, oselt
21 on of iodine species such as HIO and I2 from NaI aerosolized solutions exposed to 50 ppbv O3 can occu
22 so rapidly determining the effectiveness of NAIs against new viral strains is vital for deciding how
23 associated with contact ion-pair binding of NaI (alpha = 1300, DeltaGalpha = -18 kJ mol(-1)) and NaC
24 of (125)I-DCIBzL, 111 MBq (3 mCi) of (125)I-NaI, an equivalent amount of nonradiolabeled DCIBzL, or
27 ) exhibited reduced inhibition by all of the NAIs and two variants (E119D and E119D-H274Y) retained t
28 za antivirals, the neuraminidase inhibitors (NAIs) and the adamantanes, are well characterized, as ar
30 Analyses suggested an independent role for NAI antibody in protection, which was similar in the IIV
32 re we demonstrate the effective induction of NAi antibody titers after H5N1 vaccination in humans.
34 The conserved residues that interact with NAIs are under selective pressure, but only a few have b
37 Currently, neuraminidase (NA) inhibitors (NAIs) are the first choice for influenza prevention and
42 lassified neonatal arterial ischemic stroke (NAIS), arterial presumed perinatal ischemic stroke (APPI
44 olyzes ATP to export three intracellular Na (Nai) as it imports two extracellular K (Ko) across anima
45 ility of vaccines, neuraminidase inhibitors (NAIs), as the only available class of drugs for AIVs in
50 6, and D151) that directly interact with the NAIs but have not been reported to confer resistance to
51 a signal from the intracellular compartment (Nai) compared with an external standard (monitored by Na
52 owever, analysis of this model revealed that NAI, compounded by a subpopulation with only partial pro
53 using pairs of spherical ions (NaCl > NaBr > NaI) correlates to experimental observations (NaI > NaCl
54 were examined in the presence of 3 and 25 mM NaI, corresponding to I(-)-activated and I(-)-inhibited
59 ion to explore the possibility of extracting NAI drug efficacy using only the observed viral titer de
61 tified 156 genes that strongly differentiate NAI, EFFE, and MEM CD8(+) T cells; these genes provide p
62 ed ex vivo from cervical lymph node cells of NaI-fed or control mice, suggesting that the iodide-rich
64 ifluorocarbene (generated from PhHgCF(3) and NaI) gave diastereomeric mixtures of the 2,2-difluorospi
65 difluorocarbene [generated from (CF3)2Hg and NaI] gave a diastereomeric mixture of the 3',4'-difluoro
67 ced in the following order: NaSCN > NaClO4 > NaI > NaNO3 approximately NaBr > NaCl > pure water appro
71 e less effort in vaccination as the level of NAI in a population, and as disease prevalence, increase
72 rin pairs per volume of MOF that bind PC and NAI in such a way that they are primed to form the requi
73 bulin autoantibodies when they receive 0.05% NaI in their drinking water beginning at 8 wk of age.
75 utoimmune thyroiditis (SAT) when given 0.05% NaI in their drinking water, whereas B cell-deficient NO
76 IFN-gamma(-/-)NOD.H-2h4 mice given 0.05% NaI in their water develop severe thyroid epithelial cel
77 e effectiveness of neuraminidase inhibitors (NAIs) in humans infected with influenza A(H7N9) viruses
78 e effectiveness of neuraminidase inhibitors (NAIs) in reducing mortality when given to hospitalized p
79 ically relevant nicotine aerosol inhalation (NAI) induced transient reduction and irregular fluctuati
80 rehensive understanding of the mechanisms of NAI-induced inhibition of influenza virus and help lead
82 y acquired immunity (NAI) to severe malaria; NAI is caused by repeated exposure to infectious bites a
85 ) mice develop severe TEC H/P, and 2-3 wk of NaI is sufficient for optimal development of severe TEC
87 ation is eliminated using the sodium iodide (NaI) isolation method and that the level of oxo8dG in nu
88 cation of the recently introduced chaotropic NaI method, reducing our estimate of the level of steady
89 ance and continued surveillance of potential NAI multidrug-resistant influenza virus variants, as wel
90 cells are treated with the icSHAPE chemical NAI-N3 followed by selective chemical enrichment of NAI-
91 followed by selective chemical enrichment of NAI-N3-modified RNA, which provides an improved signal-t
95 e extracted from the Paracoccus membranes by NaI or alkaline treatment, unlike the peripheral subunit
96 e extracted from the Paracoccus membranes by NaI or alkaline treatment, which is consistent with the
98 Treatments with chaotropic reagents (urea, NaI, or NaBr) or with alkaline buffer (pH 10-12) resulte
100 utation (H274Y) conferring resistance to the NAI oseltamivir emerged worldwide in the A/H1N1 virus su
101 ed resistant variants in the presence of the NAIs oseltamivir carboxylate and zanamivir in MDCK cells
102 ltidrug resistance to the currently approved NAIs oseltamivir, zanamivir, and peramivir by assessing
103 in N6, and 4 in N8) conferred resistance to NAIs (oseltamivir carboxylate, zanamivir, or peramivir)
104 utions associated with reduced inhibition by NAIs (oseltamivir, zanamivir, and peramivir): (i) novel
105 al planar gamma-camera images and whole-body NaI probe counts were obtained to estimate (131)I-antibo
106 aotropic technique of DNA isolation by using NaI produced the lowest and least variable oxo8dG values
107 lving Rh-catalyzed aziridination followed by NaI-promoted rearrangement to an isomeric cyclic sulfami
108 I compare to different alkali metal iodides: NaI, RbI, CsI; also investigation of different potassium
109 rse effects were not increased overall among NAI recipients (RR, 1.01 [CI, 0.94 to 1.08]; RD, 0.1 per
110 ention for AIV-infected patients, studies on NAI resistance among AIVs have been limited, and markers
111 NA amino acid substitutions associated with NAI resistance among influenza viruses of N3, N7, and N9
112 sential to identify the molecular markers of NAI resistance among specific NA subtypes of avian influ
113 by a S31N mutation in the matrix gene, while NAI resistance can result from a number of mutations in
114 Although various mutations associated with NAI resistance have been identified, the amino acid subs
116 ort profiles of NA substitutions that confer NAI resistance in AIVs of the N4, N5, N6, and N8 NA subt
117 ating antiviral susceptibility monitoring of NAI resistance in AIVs.IMPORTANCE The frequency of human
118 he molecular changes in NA that could confer NAI resistance in avian viruses grown in immortalized mo
119 gence of a single NA mutation conferring pan-NAI resistance in the clinical setting reinforces the pr
120 We identified 16 NA substitutions conferring NAI resistance in the tested AIV subtypes; some are nove
121 strate that each NA subtype possesses unique NAI resistance markers, and knowledge of these substitut
135 nd B virus infections, so the development of NAI-resistant viruses with superior fitness is a public
136 ss of the risk assessment for the fitness of NAIs-resistant seasonal H1N1 and H3N2, pandemic 2009 H1N
137 d HA, a single vaccine dose induced a strong NAi response that was not significantly boosted by a sec
138 %, whereas the inhibition of NF-kappaB using NAI resulted in a decrease in females from 45 to 20%.
139 complexes with a different concentration of NaI showed that the mutations decreased affinity between
140 seltamivir, an oral neuraminidase inhibitor (NAI), so rapidly determining the effectiveness of NAIs a
142 mma(-/-) NOD.H-2h4 mice given sodium iodide (NaI)-supplemented water develop a slow onset autoimmune
143 oseltamivir-treated patient were tested for NAI susceptibility in vitro; their replicative fitness w
150 nominal counting rates were obtained for the NaI systems, and the bismuth germanate (BGO) systems wer
153 l basis underlying differentiation of naive (NAI) T cells into effector (EFFE) and memory (MEM) cells
154 emonstrated reduced inhibition by all of the NAIs tested in both the backbone of the 2009 H1N1 pandem
156 Using difluorocarbene, generated from TMSCF3/NaI, these spirocycles were produced in yields up to 97%
157 also showed reduced inhibition by all of the NAIs, though their overall viral fitness was impaired in
158 hibition (HAI) and neuraminidase inhibition (NAI) titer decline in the absence of infection were esti
160 and 9 wk after injection using spectrometric NaI(Tl) and HPGe detectors, and imaging between 5 and 10
164 ty for acyl transfer from N-acetylimidazole (NAI) to different pyridylcarbinol (PC) regioisomers (2-P
165 high levels of naturally acquired immunity (NAI) to severe malaria; NAI is caused by repeated exposu
169 er research is needed about whether starting NAI treatment >5 days after symptom onset may also conve
170 ed odds of hospital admission compared to no NAI treatment (adjusted odds ratio, 0.24; 95% confidence
171 d a nonsignificant reduction associated with NAI treatment (at any time) versus none (OR, 0.72 [95% C
176 We investigated the impact of outpatient NAI treatment on subsequent hospitalization in patients
178 adjustment for preadmission antibiotics and NAI treatment propensity, preadmission NAI treatment was
179 luenza A(H1N1) pandemic, early initiation of NAI treatment reduced the likelihood of severe outcomes
180 spitalization, outpatient or community-based NAI treatment significantly reduced the likelihood of re
182 s and NAI treatment propensity, preadmission NAI treatment was associated with decreased odds of hosp
184 5.8%) received outpatient or community-based NAI treatment, 928 of 2395 (38.8%) with available data h
191 ent also confirms that the loss of a neutral NaI unit, instead of an Na(+) ion, occurs during the dis
192 the dissolution processes, loss of a neutral NaI unit, occurs when six or more water molecules have b
194 To illustrate its utility, we calculate NAI values for the entire coding sequence and across a s
197 te in Drosophila that Clock misexpression in nai;ve brain regions induces circadian gene expression.
201 residues in framework stabilization, we used nai;ve phage-displayed libraries, combinatorial alanine-
203 sented by mature dendritic cells in the DLN, nai;ve T cells can respond to self antigens or tumor ant
206 sectional study, three different age sets of nai;ve TgCRND8 and non-Tg mice were tested: 10-12, 12-14
207 ant preconcentration and alignment of PC and NAI via coordination to framework porphyrin sites (orien
208 and ATP-induced processing were blocked when NaI was substituted for NaCl within the medium; substitu
213 AT), all TGF-beta transgenic (Tg) mice given NaI water for 2-7 mo developed thyroid lesions character
216 ccines will perform in regions with existing NAI, we developed a simple malaria model incorporating v
217 the labeling of arylstannanes using [(125)I]NaI, where products were isolated in high specific activ
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