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1 d delayed development of the ossicles in the middle ear.
2 phological stage of the definitive mammalian middle ear.
3 n of pneumococci from the nasopharynx to the middle ear.
4 headphones that bypass the ear canal and the middle ear.
5 f frogs to communicate effectively without a middle ear.
6 pact on responses to hypoxia in the inflamed middle ear.
7 earing loss as sound waves fail to reach the middle ear.
8 e presence of a bacterial biofilm within the middle ear.
9 g/mL of methylprednisolone injected into the middle ear.
10 iofilms within the excised material from the middle ear.
11 tympanic bone, which forms the floor of the middle ear.
12 ulates the transmission of sound through the middle ear.
13 e when it invades the bloodstream, lungs, or middle ear.
14 chinchilla nasopharynx and infection of the middle ear.
15 edia, due primarily to the small size of its middle ear.
16 dge, the earliest known definitive mammalian middle ear.
17 ocated in the region of the jugular bulb and middle ear.
18 inoculated OFF and remained OFF, within the middle ear.
19 transmigration to and persistence within the middle ear.
20 r selection for ON switching of modA2 in the middle ear.
22 g blood (4 of 15), conjunctiva (1 of 14), or middle ear (2 of 21) isolates than among carriage isolat
23 tary trough for mandibular attachment of the middle ear-a transitional condition of the predecessors
24 rlier developing, cartilaginous incus of the middle ear, abutting the cranial base to form a cranio-m
27 ring, through inertial forces exerted by the middle ear and cochlear fluid, and that this can be test
29 may increase bacterial transmigration to the middle ear and could thus increase the risk of clinicall
30 impaired clearance of S. pneumoniae from the middle ear and dissemination to the bloodstream during A
31 o test the hypothesis that GAS colonizes the middle ear and establishes itself in localized, three-di
33 respiratory and reproductive tracts and the middle ear and generate fluid flow in these organs via s
34 on through airborne sound that displaces the middle ear and induces a pressure difference across the
36 hindering the clearance of bacteria from the middle ear and leading to sepsis and a high mortality ra
38 that evolution of such key characters as the middle ear and the tribosphenic teeth is far more labile
39 ther areas also stimulated by intense noise (middle ear and vestibule) as it was absent in CD1 mice w
41 troducing the sensing optical fiber into the middle-ear and its aiming at the incus was investigated
43 or controlling infections in the airways and middle ear, and for maintaining immune homeostasis in mo
44 terized by effusion and tissue damage in the middle ear, and in the TLR2(-/-) mice, the outcome of in
45 lacement, ossified Meckel's cartilage of the middle ear, and specialized xenarthrous articulations of
46 been previously identified in any mammalian middle ear, and the morphology of each auditory bone dif
47 dent element into part of the malleus of the middle ear, and the presence of a restricted contact bet
49 l to clearing pathogenic infections from the middle ear are distributed according to developmental de
51 illness and are isolated from up to half of middle ear aspirates from children with acute otitis med
52 imulation of the umbo, as well as within the middle ear at the round window and otic capsule, induced
55 and neuraminidase genes among 342 carriage, middle ear, blood, and cerebrospinal fluid (CSF) pneumoc
57 hat clearly illustrates this transition: the middle ear bones are connected to the mandible via an os
58 signaling in patterning the stapes and incus middle ear bones derived from the equivalent pharyngeal
61 rvived to adulthood and had normal outer and middle ears but had the same inner ear defects as the Tb
62 lm formation, growth, and eradication in the middle ear, but also may provide much-needed quantifiabl
65 the RWM niche through a bullaostomy into the middle ear cavity allowing directed delivery of compound
68 vides the first mouse model for the study of middle ear cavity defects, while also being of direct re
69 s that line the posterior dorsal pole of the middle ear cavity which was previously thought to contai
70 an tube orifice at the ventral region of the middle ear cavity, consisting mostly of a lumen layer of
71 ic deposition of cholesterol crystals in the middle ear cavity, enlarged Eustachian tube, and chronic
72 raniofacial abnormalities, including a small middle ear cavity, short nasal bone, and malformed inter
74 racterized by the occurrence of fluid in the middle-ear cavity in the absence of any signs of acute e
79 expression and biofilm formation within the middle-ear chamber and an inverse relationship between P
81 stablish computed tomography (CT) staging of middle ear cholesteatoma and assess its impact on the se
87 cell-derived structure that encapsulates all middle ear components, and that defects in these process
88 he lack of certainty regarding diagnosis for middle ear conditions, resulting in many patients being
93 raniosynostosis, other craniofacial defects, middle-ear defects, cleft palate, cleft lip, limb defect
95 e the cause of the hearing impairment to the middle ear, demonstrating over-ossification at the round
96 eviews our studies of the effect of monaural middle ear destruction on midbrain auditory response pro
101 transgenic mice, we show that the mammalian middle ear develops through cavitation of a neural crest
108 h planktonic and adherent populations in the middle ear, disruption of mucosal biofilms already resid
109 l mammaliaforms and the definitive mammalian middle ear (DMME) of extant mammals; it reveals complex
110 These include surgical approaches to the middle ear, documentation of the murine middle ear respo
112 f antimicrobial treatment on the duration of middle ear effusion (MEE) and concomitant hearing impair
113 composition (microbiota) present in matched middle ear effusion (MEE) samples, external ear canal (E
115 of MGAS5005 Deltasrv were isolated from the middle ear effusion, and MGAS5005 Deltasrv was found ran
117 e years of age, 429 children with persistent middle-ear effusion were randomly assigned to have tympa
118 e healthy young children who have persistent middle-ear effusion, as defined in our study, prompt ins
119 younger than 3 years of age with persistent middle-ear effusion, prompt as compared with delayed ins
121 from the nasopharynx of healthy children or middle ear effusions from patients with otitis media, re
122 low-passage NTHi clinical isolates from the middle ear effusions of patients with chronic otitis med
123 in the chinchilla, inducing culture-positive middle ear effusions, whereas pgm and siaB mutants were
126 bacteria exist in culture-negative pediatric middle-ear effusions and that experimental infection wit
127 to explain the failure to culture NTHi from middle-ear effusions, recalcitrance to antibiotics and i
129 downstream effects on TGFbeta signalling in middle ear epithelia at the time of development of chron
130 ic S. aureus has the ability to invade human middle ear epithelial cells (HMEECs) in a dose and time
131 nduced mucin MUC5AC upregulation in cultured middle ear epithelial cells and in the middle ear of mic
137 f the most common infectious diseases of the middle ear especially affecting children, leading to del
140 surveillance, all OM episodes submitted for middle ear fluid culture in children <3 years from 2004
141 on pneumococcal and overall OM necessitating middle ear fluid culture in children aged <2 years in so
142 le pneumococci from nasopharyngeal swabs and middle ear fluid of Finnish children and demonstrate tha
144 e investigate the potential for detection of middle ear fluid, which has significant implications for
150 xo11 is expressed in epithelial cells of the middle ears from late embryonic stages through to day 13
153 ctural features that are likely critical for middle ear functions and related to OM susceptibility.
158 lar to the stapes superstructure, increasing middle ear impedance and attenuating the intensity of so
159 ges: (i) an eardrum collecting sound, (ii) a middle ear impedance converter, and (iii) a cochlear fre
160 e reduction of this air volume increases the middle ear impedance, resulting in an up to 20 dB gain i
162 sis, acquisition of the definitive mammalian middle ear in allotherians such as this specimen was ind
163 the morphological gap between the mandibular middle ear in basal mammaliaforms and the definitive mam
165 is very low or absent in normal or diseased middle ear in mouse and human, and salivary expression a
166 lations that shift from OFF to ON within the middle ear induce significantly greater disease severity
170 fluenza A virus exacerbation of experimental middle ear infection is independent of the pneumococcal
171 ed a significant attenuation in a chinchilla middle ear infection model and a minor attenuation in a
172 te immunity, this disease is prolonged after middle ear infection with nontypeable Haemophilus influe
173 Haemophilus influenzae, a major pathogen of middle ear infection, and upregulate a monocyte-attracti
174 r infection is highly prevalent in children, middle ear infection-induced inner ear inflammation can
175 to understand the molecular pathogenesis of middle ear infection-induced inner ear inflammation.
180 ing loss that is not explained by concurrent middle ear infections is another characteristic of CMV-r
182 tes is different to the distribution seen in middle ear infections, suggesting different modA alleles
185 ostinfection inhibited MUC5AC expression and middle ear inflammation induced by S. pneumoniae and red
187 uppurative otitis media (CSOM) refers to the middle ear inflammation which is clinically characterize
188 tant in the transition from acute to chronic middle ear inflammation, and a potential molecular targe
190 m response (ABR) thresholds during and after middle ear infusion of salicylate in artificial perilymp
191 OM pathogen components or cytokines from the middle ear into the inner ear, the underlying mechanisms
192 demonstrate that effective cavitation of the middle ear is intimately linked to growth of the auditor
195 Otitis media (OM), the inflammation of the middle ear, is the most common disease and cause for sur
196 us agalactiae protein, was present in 31% of middle ear isolates and occurred 3.6 (95% CI, 1.2 to 11.
197 (95% CI, 1.2 to 5.5) times more often among middle ear isolates than carriage, blood, or meningitis
198 both S. pneumoniae serotype 6A and 14 in the middle ear lavage fluid samples from Bf/C2(-/)(-), Bf(-)
202 arynx and to elicit severe infections of the middle ears, lungs, and blood that are associated with h
203 ecreased significantly (P = .0006) among the middle ear/mastoid isolates (2011, 50% [74/149]; 2012, 4
204 protein to the round window membrane in the middle ear may be able to reverse sensorineural hearing
205 lus influenzae (NTHi) bacteria in an ex vivo middle ear (ME) aspirate from the chinchilla model of ex
207 lineate the role of CCL3 in OM, we evaluated middle ear (ME) responses of ccl3(-/-)mice to nontypeabl
208 increases during long-term infection in the middle ear (ME), but the host cellular immune response t
209 d as a chronic low-grade inflammation of the middle ear (ME), without any signs of infection and with
211 elson interferometer, designed to serve as a middle-ear microphone for totally implantable cochlear-
213 companied by a significant thickening of the middle ear mucosa lining, expansion of mucin-secreting g
214 ms of pathogenic bacteria are present on the middle ear mucosa of children with chronic otitis media
216 that phosphorylation of JNK isoforms in the middle ear mucosa preceded but paralleled mucosal hyperp
220 se (JNK) mitogen-activated protein kinase in middle ear mucosal hyperplasia in animal models of bacte
225 function was characterized by the absence of middle ear muscle reflexes, distortion product otoacoust
226 ure, the temporal sensitivity threshold, the middle-ear muscle reflex, and the auditory-brainstem res
229 e acoustic thresholds for contraction of the middle ear muscles, which may be a reflection of underly
231 y trajectories, functional properties of the middle ear of AMHs and Neandertals are largely similar.
233 nt within the biofilms formed by NTHI in the middle ear of the chinchilla in an experimental otitis m
234 uced bacterial infection was observed in the middle ear of the Junbo mouse model when NTHi was devoid
235 nactivated Streptococcus pneumoniae into the middle ears of BALB/c mice resulted in a significant inf
236 h NT H. influenzae strains isolated from the middle ears of children with otitis media but that are n
238 Biofilms were macroscopically visible in the middle ears of euthanized animals infected with NTHi 86-
239 of large, macroscopic structures within the middle ears of MGAS5005- and MGAS5005 Deltasrv-infected
241 ctively collected pneumococcal isolates from middle ear or mastoid cultures from children from 2011 t
244 scle contractions restrain the motion of the middle ear ossicles, attenuating the transmission of low
248 uncharacterized combination of interrelated middle ear pathologies and suggest Rpl38 deficiency as a
251 phy (HRCT) and MRI are helpful in evaluating middle ear pathologies, usage being indication specific.
254 ed include patients undergoing intracranial, middle ear, posterior eye, intramedullary spine, and pos
255 nfection administration of rolipram into the middle ear potently inhibited S. pneumoniae-induced MUC5
258 s of transfer of sound through the outer and middle ear prior to the calculation of an excitation pat
259 of mucosal biofilms already resident within middle ears prior to immunization and rapid resolution o
262 us silica coating was established on ceramic middle ear prostheses, which then served as a base for f
263 the middle ear, documentation of the murine middle ear response to various pathogens and inflammator
264 ger sequencing, RNA-sequencing of saliva and middle ear samples, 16S rRNA sequencing, molecular model
265 ired bacterial persistence in the chinchilla middle ear, similar to our previous results with luxS mu
266 d after direct electrical stimulation in the middle ear space, indicating that non-specific stimulati
269 Subsequently, the relative prevalence of the middle ear-specific gene regions among a large panel of
272 mR) were significantly more prevalent in the middle ear strains (96%, 100%, 100%, and 97%, respective
273 hxuA, hxuB, hxuC, hemR, and hup) between 514 middle ear strains from children with AOM and 235 throat
276 and must have evolved independently from the middle ear structures of monotremes and therian mammals.
277 of SWIR light allows better visualization of middle ear structures through the tympanic membrane, inc
278 ofilms in vitro as well as in the chinchilla middle ear, suggesting that biofilm formation in vivo mi
281 sease-causing NTHI strains isolated from the middle ear than in colonizing NTHI strains and H. haemol
283 tremely common pediatric inflammation of the middle ear that often causes pain and diminishes hearing
286 of cilia in the epithelium of the mammalian middle ear, thus illustrating novel structural features
287 The mouse homologue, Fndc1, is expressed in middle ear tissue and its expression is upregulated upon
288 te this proliferative lesion from uninvolved middle ear tissue based on the characteristic autofluore
291 nging techniques to noninvasively assess the middle ear to detect and quantify biofilm microstructure
292 modifications were introduced to the assumed middle-ear transfer function and to the way that specifi
294 pharyngeal pouch (PPI) in forming outer and middle ears, we tissue-specifically inactivated the gene
295 ay alter bacterial transmigration toward the middle ear, where it could have clinically relevant impl
296 ctor in bacterial growth and survival in the middle ear, where nutrients such as histidine may be fou
297 st Streptococcus pneumoniae infection in the middle ear, wild-type (WT; C57BL/6) and TLR2-deficient (
298 terpreted to be for gliding and a mandibular middle ear with a unique character combination previousl
299 clinical findings as the gold standard, all middle ears with chronic OM showed evidence of biofilms,