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1 which lacks auditory responses and has hair-cell degeneration.
2 s characterized by progressive photoreceptor cell degeneration.
3 xpression leads to photoreceptor and bipolar cell degeneration.
4 ssion of normal opsin leads to photoreceptor cell degeneration.
5 pture could be a direct trigger for the hair cell degeneration.
6 , atypical nuclei, perinuclear clearing, and cell degeneration.
7 of Bmp8b causes male infertility due to germ cell degeneration.
8 lear inclusion (NI) formation and late-onset cell degeneration.
9 ds gene mutations resulting in photoreceptor cell degeneration.
10 ed by ibogaine mediates excitotoxic Purkinje cell degeneration.
11 -onset, and relentless form of photoreceptor cell degeneration.
12 ormer being associated with evidence of beta-cell degeneration.
13 bogaine displayed clear evidence of Purkinje cell degeneration.
14 eless sufficient to induce bilateral granule cell degeneration.
15 be controlled with small molecules to reduce cell degeneration.
16 gical symptom onset and more severe Purkinje cell degeneration.
17 ted males demonstrated RPE and photoreceptor cell degeneration.
18 otoxic stress response, contributing to hair cell degeneration.
19 Iron-containing microglia showed signs of cell degeneration.
20 t contributes to aminoglycoside-induced hair cell degeneration.
21 mossy-fiber sprouting 5-6 weeks after mossy cell degeneration.
22 chromophore showed accelerated photoreceptor cell degeneration.
23 s of CCP1 in mice causes cerebellar Purkinje cell degeneration.
24 With time this causes cone cell degeneration.
25 ults from retinal pigmented epithelium (RPE) cell degeneration.
26 m of SCA17 transgenic mice prior to Purkinje cell degeneration.
27 F3A loss results in very rapid photoreceptor cell degeneration.
28 dysmorphic stereocilia and progressive hair cell degeneration.
29 response to MPP+ treatment, which led to the cell degeneration.
30 VH infusion did not induce dopaminergic cell degeneration.
31 el abolished the RD-associated photoreceptor cell degeneration.
32 asilar papilla at the earliest signs of hair cell degeneration.
33 ve a therapeutic role in human photoreceptor cell degenerations.
34 -) mice lose hearing and manifest outer hair cell degeneration after systemic cisplatin treatment.
35 y is characterized by vascular smooth muscle cell degeneration and accumulation of diagnostic granula
37 entiviral knockdown of EZH2 rescued Purkinje cell degeneration and behavioral abnormalities in Atm(-/
38 etes mellitus at 30+ weeks of age, when beta-cell degeneration and both amorphous and amyloid deposit
40 1 in mice causes severe ataxia with Purkinje cell degeneration and cerebellar atrophy, partially rese
41 e mutant channels, leading over time to hair-cell degeneration and contributing to their deafness.
42 ysiological potentials likely underlies hair cell degeneration and deafness in Va and Va(J) mice.
43 echanism for the terminal phases of neuronal cell degeneration and death in human neurodegenerative d
44 activation of this receptor induces neuronal cell degeneration and death via stimulation of caspases.
45 -finger transcription factors, leads to germ cell degeneration and defective sperm production in adul
46 retinas against light-induced photoreceptor cell degeneration and inhibited photoreceptor apoptosis.
48 Histopathological findings revealed beta-cell degeneration and loss consistent with the drop in t
51 ounding the SG neurons, leading to satellite cell degeneration and subsequent SG degeneration with a
52 gene expression is synchronal with nucellar cell degeneration and thus, nucellin may be involved wit
54 which disruptions in NMNAT1 lead to retinal cell degeneration and would provide a resource for testi
60 ity that glial dysfunction leads to Purkinje cell degeneration, and generated mice that express ataxi
62 as knocked out leading to postnatal Purkinje cell degeneration, and standard delay eyeblink condition
63 GSIS, suggest a molecular mechanism for beta-cell degeneration as a consequence of Ide deficiency, an
65 overlapping phenotypes arising from Purkinje cell degeneration, cerebellar atrophy and varying degree
66 of Purkinje cells revealed findings of dark cell degeneration consistent with excitotoxic injury.
67 tion of sodium influx to development of dark cell degeneration (DCD) in Purkinje neurons (PNs) follow
68 -induced delayed neurotoxicity known as dark cell degeneration (DCD) that is expressed as cytoplasmic
69 days old), AMPA produced in addition to dark cell degeneration (DCD), an edematous type of toxicity (
70 erker, a recessive mutation that causes hair cell degeneration, deafness, and vestibular dysfunction.
71 bal Npc1 null mice, suggesting that Purkinje cell degeneration does not underlie these phenotypes.
73 mild fatty degeneration and inflammation to cell degeneration, fibrosis, and cirrhosis with or witho
74 wever, their involvement in cochlear sensory cell degeneration following acoustic trauma is unknown.
76 ial activation may be involved in the nigral cell degeneration in 6-OHDA induced parkinsonian mice.
80 or comparable transneuronal retinal ganglion cell degeneration in both primate species and show that
82 ivatives (13n and 36a) caused adrenocortical cell degeneration in guinea pigs treated with these inhi
88 ms of PNH that include toxins, anterior horn cell degeneration in motor neurone disease and genetic d
89 e non-cell-autonomous nature of the Purkinje cell degeneration in our SCA7 mouse model indicates that
93 immune/inflammatory factors in dopaminergic cell degeneration in parkinsonian substantia nigra, we a
94 fied as a candidate gene to explain Purkinje cell degeneration in pcd mice, but its function remains
95 n, but unlike Nna1, neither rescues Purkinje cell degeneration in pcd mice, indicating that they do n
97 unctional changes that characterize ganglion cell degeneration in the glaucomatous eye, and following
98 to 4.2mm posterior to the bregma to examine cell degeneration in the retrosplenial and piriform regi
102 t a novel signaling pathway for dopaminergic cell degeneration, in which MPP+ induces the up-regulati
103 due primarily to a late-onset photoreceptor cell degeneration involving initially the rods but event
108 ze that the slowly progressive photoreceptor cell degeneration is secondary to abnormal function of t
110 Atg7(Deltapan) mice exhibit severe acinar cell degeneration, leading to pancreatic inflammation an
111 a (SNpc), a brain region where dopamine (DA) cell degeneration leads to Parkinson's disease (PD), exp
112 iably exhibit embryonic or larval lethality, cell degenerations, malformation of the posterior body,
115 ion mutants, and light-induced photoreceptor cell degeneration models), the use of Tb(3+) or Eu(3+) d
116 re implanted into the cerebellum of Purkinje cell degeneration mutant mice (pcd/pcd), a model of adul
121 nerve transection (ONTx) to induce ganglion cell degeneration, or in combination with an ionotropic
122 protected from glaucomatous retinal ganglion cell degeneration out to 14 months of age (oldest assess
131 ne have been shown to be related to Purkinje cell degeneration (pcd) phenotypes including ataxia in m
132 e classical recessive mouse mutant, Purkinje cell degeneration (pcd), exhibits adult-onset degenerati
133 autosomal recessive mouse mutation, Purkinje cell degeneration (pcd), was first identified through it
134 s have previously demonstrated that Purkinje cell-degeneration (pcd) mutant mice are impaired in eyeb
135 neurons, causes the same pattern of Purkinje cell degeneration, providing a clue to the mechanism of
138 to its decreased expression following nigral cell degeneration suggests that it may play an important
139 ermine whether sustained waking causes brain cell degeneration, three parallel strategies were used.
140 rapid, marked by type I alveolar epithelial cell degeneration, type II alveolar epithelial cell hype
141 ANF ameliorates mutant TBP-mediated Purkinje cell degeneration via protein kinase C (PKC)-dependent s
143 after intense-light treatment, photoreceptor cell degeneration was estimated by determining the level
146 scopic observations demonstrated morphologic cell degeneration well before lactate dehydrogenase rele
148 lastoma cells resulted in vacuologenesis and cell degeneration, whereas ES treatment after FIG4-small
149 s exhibiting cerebellar atrophy and Purkinje cell degeneration whose subtypes arise from 31 distinct
150 ession and aggregation of hA might link beta-cell degeneration with diabetes onset and progression, b
151 llar autopsy material showed severe Purkinje cell degeneration, with abnormal intracellular accumulat
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