ライフサイエンスコーパス: bulbar

1 ing efficiency (3.6% +/- 0.9%) than superior bulbar (1.1% +/- 0.3%; P < 0.05) and inferior bulbar cel

2 h with respect to explant size than superior bulbar (13.4 +/- 1.9-fold growth; P < 0.05 and P < 0.01,

3 < 0.05 and P < 0.01, respectively), inferior bulbar (13.6 +/- 1.6-fold growth; P = 0.01 and P < 0.01,

4 ory bulb lesions that disrupt the pattern of bulbar activation produced by these enantiomers degraded

5 rant are based on differences in patterns of bulbar activation revealed in such maps.

6 erties are not systematically represented in bulbar activity and encourage further searches for bette

7 te again the functional relationship between bulbar activity patterns and odor perception.

8 e better predicted by normalized than by raw bulbar activity profiles; and (iii) a recurrent excitato

9 predictions based on 2-deoxyglucose maps of bulbar activity that enantiomers of terpinen-4-ol should

10 , these results show that GABABRs on cortico-bulbar afferents gate excitatory transmission in a targe

11 While these ensembles are driven by primary bulbar afferents, and shaped by intracortical recurrent

12 The index case of Family A had bulbar ALS and frontemporal dementia (FTD) at 43.

13 The bulbar ALSFRS-R subscore of the positive LMN damage grou

14 Notably, the bulbar ALSFRS-R subscore was correlated with cortical th

15 The results show that bulbar and facial muscle weakness and wasting are associ

16 o, duration of disease and degree of ocular, bulbar and facial weakness.

17 Goblet cells from rat bulbar and forniceal conjunctiva were grown in organ cul

18 A multivariable model that included lower bulbar and gross motor subscores, female gender, younger

19 ory memory, but also significantly decreases bulbar and hippocampal neurogenesis.

20 All 8 tumors were bulbar and in the exposure zone.

21 y, tear production, ocular surface staining, bulbar and limbal redness, tear volume, anterior blephar

22 Both bulbar and mucosal cell preparations prolong the surviva

23 fore, provides a bioassay that discriminates bulbar and mucosal cell preparations, and a useful tool

24 e and chronic stimulation when compared with bulbar and palpebral epithelia.

25 ing to involve truncal, neck-flexor, facial, bulbar and respiratory muscles.

26 1b and GalNAc-GD1a, and between the cranial, bulbar and sensory variants of GBS and antibodies to the

27 These associations were similar for bulbar and spinal ALS but stronger for those with a dela

28 e central and peripheral corneal epithelium, bulbar and tarsal conjunctival epithelia, tarsal conjunc

29 cale-Revised (ALSFRS-R total, upper limb and bulbar) and upper motor neuron burden assessments in a l

30 on in ALS was derived from focal initiation, bulbar- and cervical-onset may date from head-face and u

31 The results indicate that input to bulbar areas that are activated by a series of homologou

32 lesions destroyed the dorsal and dorsomedial bulbar areas that have been identified in optical and el

33 hat GABAB receptors are expressed in cortico-bulbar axons that synapse on granule cells and receptor

34 and by their axon trajectory, show that the bulbar cell preparations have around twice the potency o

35 ulbar (1.1% +/- 0.3%; P < 0.05) and inferior bulbar cells (1.6% +/- 0.8%; P < 0.05).

36 t human tau hyperphosphorylation in anterior bulbar cells is spatiotemporally correlated with a highl

37 of human tau in identified neurons (anterior bulbar cells) in the lamprey central nervous system.

38 Compared with the previous findings with bulbar cells, the mucosal cell cultures contained only 5

39 Finally, bulbar cholinergic enhancement of mitral/tufted cell odo

40 y stages of their integration into the mouse bulbar circuitry and highlight a critical period during

41 mary odor representations are transformed by bulbar circuitry into secondary representations based on

42 d integration of adult-born neurons into the bulbar circuitry of lactating mothers.

43 There were also high rates of predictable bulbar complications (86% had dribbling, 60% had glue ea

44 >=70 years old (56%), with carcinomas of the bulbar conjunctiva (83.0%).

45 s compared with non-SCD controls, giving the bulbar conjunctiva a "blanched" avascular appearance in

46 +)CD11b(+) conventional DCs was noted in the bulbar conjunctiva and near the limbal area of corneas f

47 trephine was used to produce lesions of the bulbar conjunctiva down to the level of the bare sclera.

48 um, or in the context of preserving superior bulbar conjunctiva for future glaucoma surgeries.

49 ornea in 11 cases (34%), limbus in 23 (72%), bulbar conjunctiva in 31 (97%), fornix in 9 (28%), tarsu

50 d superior (SB) versus exposed temporal (TB) bulbar conjunctiva in control versus aqueous tear defici

51 ed limbus, ciliary vascular endothelium, and bulbar conjunctiva in rabbits injected with S. aureus.

52 Epithelial cells of the bulbar conjunctiva near the limbus are mitotically activ

53 ng the movement of GFP-positive cells in the bulbar conjunctiva near the limbus.

54 All 4 tumors occurred in the bulbar conjunctiva of patients between 41 to 53 years of

55 Impression cytology (IC) was taken from the bulbar conjunctiva of the right eye for periodic acid-Sc

56 w Zealand White rabbits were killed, and the bulbar conjunctiva was isolated.

57 The inferior bulbar conjunctiva was sampled using calcium alginate sw

58 ivochalasis affecting the temporal and nasal bulbar conjunctiva was strongly correlated with age (eta

59 3L in the palpebral epidermis, palpebral and bulbar conjunctiva, corneal epithelium and meibomian gla

60 usly along the upper and lower palpebral and bulbar conjunctiva, throughout the epithelium and substa

61 ted from the inferior conjunctival fornix or bulbar conjunctiva.

62 nction of the eyelid, through the fornix and bulbar conjunctiva.

63 P may cause inflammation and scarring of the bulbar conjunctiva.

64 eby a needle is used to inject dye under the bulbar conjunctiva.

65 reviously reported cases had occurred in the bulbar conjunctiva; and its occurrence in association wi

66 < 0.0014), peripheral corneal (P < 0.0001), bulbar conjunctival (P < 0.0021), and tarsal conjunctiva

67 observed during whole-cell patch clamping of bulbar conjunctival epithelium are a Ba(2+)- and Cs(+)-s

68 MCA velocities correlated significantly with bulbar conjunctival flow velocities (P < or =.008, Fishe

69 , without corneal or eyelid changes and mild bulbar conjunctival hyperaemia in a third of cases.

70 Bulbar conjunctival hyperemia and ocular symptoms decrea

71 xtaforniceal (3/4, 75%), or nasal (1/4, 25%) bulbar conjunctival nodules, which were asymptomatic (3/

72 the central corneal, peripheral corneal, or bulbar conjunctival stroma; meibomian glands; skin; reti

73 ed intravital microscopy (CAIM) to determine bulbar conjunctival vessel velocity during the same visi

74 experiments aimed at unraveling the cortico-bulbar connectivity.

75 Between these, bulbar dermoids are common and represent a significant c

76 gion of the left motor cortex in relation to bulbar disability, and in Broca's area and its homologue

77 who developed progression of orbital (retro-bulbar) disease at 4 months.

78 ained relatively unchanged in terms of their bulbar distribution during the first 3 postnatal weeks.

79 Bulbar dopamine release may serve a gain control functio

80 of rat and mouse OB to show that a subset of bulbar dopaminergic neurons possess an AIS and that thes

81 y was a prominent manifestation, followed by bulbar dysfunction and fatigue.

82 The bulbar dysfunction was resulted from the mixed UMN and L

83 tenance genes, key clinical features such as bulbar dysfunction, hearing loss and gastrointestinal di

84 amyotrophic lateral sclerosis without severe bulbar dysfunction, NIV improves survival with maintenan

85 weakness, 3 = moderate generalized weakness, bulbar dysfunction, or both, and 4 = severe generalized

86 severity, based around the common feature of bulbar dysfunction.

87 y in patients with facial muscle weakness or bulbar dysfunction.

88 Some axons had bulbar endings within the basal epithelium, but most pro

89 ster of highly branched fibers with multiple bulbar endings.

90 s of spinal and bulbar motor neurons causing bulbar, facial and limb weakness.

91 The study also suggests more prominent bulbar, facial and respiratory involvement in individual

92 ment histories, and established a new ocular-bulbar-facial-respiratory (OBFR) score.

93 The CL on the orbital side and the reflected bulbar fascia on the global side of the muscle constitut

94 We also show that tunable cortico-bulbar feedback is critical for generating beta, but not

95 tic inputs from nasal airflow alone, cortico-bulbar feedback, or intrinsic membrane properties of the

96 t onset, rostrocaudal gradient and prominent bulbar findings are present.

97 nism, a rostrocaudal gradient, and prominent bulbar findings.

98 all patients and in the subgroup with better bulbar function (n=20).

99 cantly increased in patients who worsened in bulbar function (n=6, p<0.0001).

100 e quality-of-life indices in those with poor bulbar function, including microsym (p=0.018), but confe

101 oups classified by the rate of upper limb or bulbar functional decline.

102 urgical lesions that removed the majority of bulbar glomeruli activated by these odorants (as demonst

103 and that deafferentation of the majority of bulbar glomeruli may be primarily without effect on odor

104 In all participants, both inferior bulbar (IB) and temporal bulbar (TB) cytology specimens

105 In patients with severe bulbar impairment, NIV improves sleep-related symptoms,

106 The region of onset was bulbar in 17 patients, lower limb in 31 patients and upp

107 Using the same tasks paired with local bulbar infusions of noradrenergic and cholinergic drugs,

108 anism for encoding information by modulating bulbar inhibition.

109 is recurrent network can enhance or suppress bulbar input, depending on whether the input arrives bef

110 rge excitatory network that can dominate the bulbar input.

111 contribution to activity driven by afferent bulbar inputs.

112 occurs is not well understood, but the local bulbar interneurons appear to be centrally involved in t

113 Bulbar interneurons such as periglomerular and granule c

114 This second, proximal pathway allows bulbar interneurons to assay divergent versions of the s

115 gic synaptic connections on several types of bulbar interneurons.

116 vs 42.3%), milder disease severity with less bulbar involvement (25.0% vs 46.2%), and absence of resp

117 MuSK-MG) is often associated with persistent bulbar involvement, including marked facial weakness and

118 eptor (AChR-MG) patients who have persistent bulbar involvement, is not clear.

119 In ALS patients without significant bulbar involvement, novel tests of RMS have greater pred

120 For patients without significant bulbar involvement, sniff P(di) had greatest predictive

121 In patients with significant bulbar involvement, tests of respiratory muscle strength

122 fied according to the presence or absence of bulbar involvement.

123 Three had early bulbar involvement.

124 d trends to greater reductions in those with bulbar involvement.

125 ups of patients with and without significant bulbar involvement.

126 for NODDI parameter differences relating to bulbar involvement.

127 affected melanocytes compared to surrounding bulbar keratinocytes.

128 y bulb (OB), turn to migrate radially to the bulbar layers, where they differentiate into interneuron

129 Bulbar lesions destroyed the dorsal and dorsomedial bulb

130 Rats with bulbar lesions had good to near perfect retention on the

131 Subgroups with bulbar, lower and upper limb onset showed different decl

132 nd depression at excitatory synapses between bulbar M/T cells and cortical neurons in slices of mouse

133 yngeal neuropathy or weakness, macroglossia, bulbar manifestations, or low lung volumes, predispose p

134 and GP-1 were also detected within isolated bulbar melanocytes, although this change was not clearly

135 tor neurons") in cerebral cortex, and spinal/bulbar motor neurons (SMN; "lower motor neurons") in spi

136 e is defined by selective loss of spinal and bulbar motor neurons causing bulbar, facial and limb wea

137 uropathy with sensory ataxia, ocular, and/or bulbar motor weakness in the presence of a monoclonal Ig

138 have predominantly localised, in many cases bulbar, muscle weaknesses (face, tongue, pharynx, etc) a

139 had motor weakness affecting oculomotor and bulbar muscles as fixed or as relapsing-remitting featur

140 longer poly-Q AR in the X-linked spinal and bulbar muscular atrophied AR could contribute to the wea

141 en identified in patients with distal spinal bulbar muscular atrophy (dSBMA) and Perry's syndrome.

142 neurodegenerative disease distal spinal and bulbar muscular atrophy (dSBMA).

143 been linked to the development of spinal and bulbar muscular atrophy (SBMA or Kennedy disease).

144 the androgen receptor (AR) causes spinal and bulbar muscular atrophy (SBMA) and is associated with mi

145 Spinal and bulbar muscular atrophy (SBMA) impairs motor function in

146 Spinal and bulbar muscular atrophy (SBMA) is a hereditary neuromusc

147 Spinal and bulbar muscular atrophy (SBMA) is a heritable neurodegen

148 Spinal and bulbar muscular atrophy (SBMA) is a motor neuron disease

149 Spinal and bulbar muscular atrophy (SBMA) is a motor neuron disease

150 Spinal and bulbar muscular atrophy (SBMA) is a neurodegenerative di

151 Spinal and bulbar muscular atrophy (SBMA) is a neuromuscular diseas

152 Spinal and bulbar muscular atrophy (SBMA) is a neuromuscular diseas

153 Spinal and bulbar muscular atrophy (SBMA) is a progressive neurodeg

154 Spinal and bulbar muscular atrophy (SBMA) is a progressive neuromus

155 Spinal bulbar muscular atrophy (SBMA) is a progressive, late on

156 Spinal and bulbar muscular atrophy (SBMA) is an inherited neuromusc

157 X-linked spinal and bulbar muscular atrophy (SBMA) is an inherited neuromusc

158 Spinal and bulbar muscular atrophy (SBMA) is an X-linked motoneuron

159 Spinal and bulbar muscular atrophy (SBMA) is caused by polyglutamin

160 X-linked spinal and bulbar muscular atrophy (SBMA) is characterized by adult

161 Spinal and bulbar muscular atrophy (SBMA) is characterized by loss

162 Spinal and bulbar muscular atrophy (SBMA) is one of a growing numbe

163 Spinal and bulbar muscular atrophy (SBMA) is one of eight inherited

164 Spinal and bulbar muscular atrophy (SBMA) results from a CAG repeat

165 en receptor (AR) protein leads to spinal and bulbar muscular atrophy (SBMA), a neurodegenerative dise

166 eating a mouse model for X-linked spinal and bulbar muscular atrophy (SBMA), a neuromuscular disorder

167 els is a therapeutic approach for spinal and bulbar muscular atrophy (SBMA), a polyglutamine disorder

168 Here we consider X-linked spinal and bulbar muscular atrophy (SBMA), a repeat disorder caused

169 Spinal and bulbar muscular atrophy (SBMA), an adult-onset neurodege

170 odel of the polyglutamine disease spinal and bulbar muscular atrophy (SBMA), an adult-onset, slowly p

171 the androgen receptor (AR) causes spinal and bulbar muscular atrophy (SBMA), an X-linked neuromuscula

172 muscular atrophy (SMA), X-linked spinal and bulbar muscular atrophy (SBMA), and amyotrophic lateral

173 amyotrophic lateral sclerosis (ALS), spinal-bulbar muscular atrophy (SBMA), and spinal muscular atro

174 r (AR), a protein associated with spinal and bulbar muscular atrophy (SBMA), and the nuclear protein

175 polyglutamine diseases, including Spinal and Bulbar Muscular Atrophy (SBMA), Huntington's disease (HD

176 Spinal and bulbar muscular atrophy (SBMA), or Kennedy's disease, is

177 yQ)-expanded AR proteotoxicity in spinal and bulbar muscular atrophy (SBMA).

178 the androgen receptor (AR) causes spinal and bulbar muscular atrophy (SBMA).

179 Spinal and bulbar muscular atrophy (SBMA, also known as Kennedy's d

180 Spinal and bulbar muscular atrophy (SBMA, Kennedy's disease) is one

181 X-linked spinal and bulbar muscular atrophy (SBMA; Kennedy's disease) is a p

182 tic potential in the treatment of spinal and bulbar muscular atrophy and may also be a possible appro

183 ially be a therapeutic target for spinal and bulbar muscular atrophy and related polyglutamine diseas

184 X-linked spinal and bulbar muscular atrophy is a degenerative disease affect

185 Spinal bulbar muscular atrophy is a neurodegenerative disorder

186 Spinal and bulbar muscular atrophy is an X-linked degenerative moto

187 Spinal and bulbar muscular atrophy is an X-linked motor neuron dise

188 Spinal and bulbar muscular atrophy mice that carry 100 pathogenic p

189 ured embryonic motor neurons from spinal and bulbar muscular atrophy mice, which was accompanied by i

190 The neurodegenerative disorder spinal and bulbar muscular atrophy or Kennedy disease is caused by

191 ing the role of AR proteolysis in spinal and bulbar muscular atrophy pathogenesis.

192 tive effect on muscle function in spinal and bulbar muscular atrophy patients, in addition to the tox

193 Using a mouse model of spinal and bulbar muscular atrophy that exhibits many of the charac

194 Kennedy disease (KD, or spinal and bulbar muscular atrophy) is caused by a CAG/polyglutamin

195 R) to Kennedy's disease (X-linked spinal and bulbar muscular atrophy) was a major step forward, the d

196 Spinal and bulbar muscular atrophy, also known as Kennedy's disease

197 atorubral pallidoluysian atrophy, spinal and bulbar muscular atrophy, and the spinocerebellar ataxias

198 drogen receptor, causing X-linked spinal and bulbar muscular atrophy, impairs its function as a trans

199 hat, in the polyglutamine disease spinal and bulbar muscular atrophy, proteolysis of the mutant andro

200 ntial of arimoclomol in mice with spinal and bulbar muscular atrophy.

201 models of the neuromuscular disorder spinal bulbar muscular atrophy.

202 eptor, an Hsp90 client mutated in spinal and bulbar muscular atrophy.

203 and in a knock-in mouse model of spinal and bulbar muscular atrophy.

204 , Charcot-Marie-Tooth disease and spinal and bulbar muscular atrophy.

205 o involved in the pathogenesis of spinal and bulbar muscular atrophy.

206 Equally important is the bulbar musculature maintaining the architecture of a pat

207 t not exclusively, young adult females, with bulbar, neck, or respiratory muscle weakness.

208 d makes specific predictions for the cortico-bulbar network connectivity that is learned by odor expo

209 It remains unknown how the bulbar network functions when rapid and persistent chang

210 ng of the top-down projections and the intra-bulbar network via adult neurogenesis.

211 n between neural and perceptual effects of a bulbar neuromodulator.

212 Further, locations of ERK activation in bulbar neurons after exposure to single odorants corresp

213 t only replenishes the population of DAergic bulbar neurons but that it also restores olfactory senso

214 togenetic activation of raphe axons affected bulbar neurons through dual release of serotonin and glu

215 The sensitivity of bulbar neurons to iGluR agonists and odorants was establ

216 d) stimulated activity-dependent labeling of bulbar neurons, which was blocked with a mixture of the

217 hat cholinergic input is primarily acting on bulbar neurons.

218 tion of tonic inhibitory synaptic input onto bulbar neurons.

219 luR subtypes function heterogeneously in the bulbar neurons.

220 s: daily activities (by history), behaviour, bulbar, ocular motor, limb motor and gait/midline.

221 We found that, as in the case of bulbar OEC preparations, the mucosal cells also restored

222 those with C9ORF72 expansion had commonly a bulbar onset (42.2% compared with 25.0% among non-C9ORF7

223 5.6, and C/C 65.5; p < 0.001), more frequent bulbar onset (A/A 29.6%, A/C 31.8%, and C/C 43.1%; p < 0

224 to diagnosis was 1.01 years (IQR 0.67-1.67), bulbar onset 28.7%, cervical onset 33.5% and lumbar onse

225 PBA was associated with bulbar onset and dysfunction, upper motor neuron dysfunc

226 C9ORF72 cases included both limb and bulbar onset disease and all cases showed combined upper

227 t diagnosis had a median survival similar to bulbar onset patients.

228 t, and had a median survival time similar to bulbar onset patients.

229 plasma (n=62) may be higher in patients with bulbar onset than in patients with spinal onset.

230 f young-onset amyotrophic lateral sclerosis, bulbar onset was found to be significantly under-represe

231 Three cases had a bulbar onset, significantly more than expected (P = 0.00

232 idation levels) in a subset of patients with bulbar onset.

233 ng female cases in general, and among female bulbar-onset cases in particular, was the most striking

234 nknown mutations, namely a high incidence of bulbar-onset disease and comorbidity with frontotemporal

235 rogressors had shorter diagnosis delay, more bulbar-onset disease, and a lower ALS Functional Rating

236 diagnosis delay, lower body mass index, more bulbar-onset disease, lower ALSFRS-R total score, and we

237 In head-face area, the cortical thickness of bulbar-onset group was significantly lower than that of

238 hibited earlier age of onset than those with bulbar-onset.

239 factors are known, including site of onset (bulbar or limb), age at symptom onset, delay from onset

240 rant experience can provide insight into how bulbar organization gives rise to efficient processing.

241 gressive dystonia with predominant cervical, bulbar, orofacial, and upper limb involvement.

242 However, a comprehensive projection map of bulbar output neurons at single-axon resolution is lacki

243 cortical feedback can shape the activity of bulbar output neurons by enabling precisely timed spikes

244 both spontaneous and odour-evoked firing of bulbar output neurons.

245 descending flaccid paralysis with prominent bulbar palsies such as diplopia, dysarthria, dysphonia,

246 ildren with a congenital upper motor neurone bulbar palsy (excluding pure speech dyspraxia) to clarif

247 pical ALS (HR, 1.0 [reference]), progressive bulbar palsy (HR, 1.48; 95% CI, 0.58-3.75; P = .41), and

248 The key features are progressive ponto-bulbar palsy and bilateral sensorineural deafness.

249 9 days, flaccid areflexic quadriparesis and bulbar palsy developed.

250 e most recent childhood forms of progressive bulbar palsy to be genetically defined.

251 progressive muscular atrophy and progressive bulbar palsy together as part of the same syndrome, the

252 ess and recurrent attacks of respiratory and bulbar paralysis since birth, nerve stimulation at physi

253 severe weight loss and an outcome similar to bulbar patients.

254 isynaptic inhibitory control specifically of bulbar principal cells that respond to that odor.

255 aled that the study children had significant bulbar problems (with 80% still needing a modified diet

256 months, at least in patients without severe bulbar problems.

257 rons interact with principal cells to affect bulbar processing is not known, but the mechanism is lik

258 y serve to "tune" the principal responses of bulbar projection neurons by way of inhibitory interneur

259 nimals showed marked expansions of 2A4(+)ORN bulbar projections, with 2-15-fold increases in numbers

260 or neurons in the olfactory mucosa and their bulbar projections.

261 The bulbar recurrent projections are coarsely topographic.

262 bjective scales, the Efron and the Validated Bulbar Redness (VBR) grading scales.

263 improvements in tear breakup time and ocular bulbar redness, compared with placebo, for both forms of

264 psular cataract extraction from the superior bulbar region.

265 milarly interconnected glomeruli in the same bulbar region.

266 so as to reduce the correlations between the bulbar representations of similar stimuli.

267 s at birth, who displayed mildly progressive bulbar, respiratory and generalized limb weakness with p

268 generated by patterned activation within the bulbar response has not been explored.

269 the distribution patterns of epithelial and bulbar responses previously characterized using single-u

270 ons receive a prominent innervation from the bulbar serotonergic nuclear complex.

271 Patients with sub-acute bulbar, shoulder, and neck weakness pose unique challeng

272 de of the fornix; others were present on the bulbar side.

273 or adult forms typically experience ataxia, bulbar signs and spasticity, and a more slowly progressi

274 Bulbar signs and symptoms, including dysarthria in 10 an

275 onset (100.0% vs 62.7%; P = .03), had fewer bulbar signs at maximal worsening (0% vs 41.3%; P = .01)

276 conal condition and the derived, monovalvar, bulbar state of the outflow tract in modern actinopteryg

277 In those patients with bulbar strictures who fail or are not suitable for these

278 he sub-basal nerves and ended with a single, bulbar swelling.

279 el to the surface and terminated with single bulbar swellings.

280 on, gait disturbance, split leg syndrome and bulbar symptomatology related to vocalisation and breath

281 18, 40%), ophthalmoplegia (n = 20, 45%), and bulbar symptoms (n = 6, 13%).

282 including wasting, fasciculations and severe bulbar symptoms, occurred over the following 6-12 months

283 patients, who are often females with marked bulbar symptoms.

284 ansmission in broadly tuned neurons, whereas bulbar synapses dominate excitatory synaptic responses i

285 on disease, our knowledge of the progressive bulbar syndromes has significantly increased in recent y

286 enetic diagnosis may allow treatment in some bulbar syndromes.

287 anisms and genetic causes of the progressive bulbar syndromes.

288 timulation-induced plasticity in the cortico-bulbar system.

289 ants, both inferior bulbar (IB) and temporal bulbar (TB) cytology specimens stained for MUC5AC reveal

290 cted from C57Bl/6 mice by the standard retro-bulbar technique were much higher than those obtained wh

291 obtained by filter paper-stripping from the bulbar temporal region for mRNA isolation.

292 one central nervous system region defined as bulbar, upper limb, lower limb or diaphragmatic), diagno

293 we discuss a case of a safety pin within the bulbar urethra inserted by a young boy for sexual gratif

294 of CD4(+) T cells showed unique pathological bulbar vacuolation in the brain parenchyma of infected m

295 showed changes in neurofilaments and ApoE in bulbar versus limb onset fast progressing ALS.

296 tified by trial site, area of disease onset (bulbar vs other areas), and previous use of riluzole.

297 sing the possibility that site of ALS onset (bulbar vs spinal) may influence pNF-H levels in peripher

298 laccid limb weakness (n=10; asymmetric n=7), bulbar weakness (n=6), and cranial nerve VI (n=3) and VI

299 Three patients also had myasthenia gravis, bulbar weakness, or symptoms that initially suggested mo

300 S in a subgroup of patients with significant bulbar weakness.