戻る
「早戻しボタン」を押すと検索画面に戻ります。 [閉じる]

コーパス検索結果 (１語後でソート)

通し番号をクリックするとPubMedの該当ページを表示します
1 ham OR Sydenham's OR rheumatic OR minor] AND chorea).
2 provement in dystonia against aggravation of chorea.
3 tem was Streptococcus pyogenes in Sydenham's chorea.
4 oclonal antibody 24.3.1 and sera from active chorea.
5  correlation with Vonsattel score except for chorea.
6 isorder, and therefore similar to Sydenham's chorea.
7 te the dominant loss of striatal neurons and chorea.
8 e patients had rheumatic fever or Sydenham's chorea.
9 nting with dominant parkinsonism and minimal chorea.
10  inhibitory neurons are involved, also their chorea.
11       None had rheumatic fever or Sydenham's chorea.
12 me, as well as rheumatic fever or Sydenham's chorea.
13 manent basal ganglia dysfunction might cause chorea.
14 ndividuals with Huntington's disease-related chorea.
15 ibitor used in the treatment of Huntington's chorea.
16 nt, was associated with faster resolution of chorea.
17 atment guidelines for patients with Sydenham chorea.
18 on and increasing motor impairments, but not chorea.
19 the BG, is characterized by hyperkinesia and chorea.
20 ollowed by dysarthria, dysphagia, ataxia, or chorea.
21 aviors and involuntary movements in Sydenham chorea.
22 nical features of HD, including dystonia and chorea.
23 Most remarkable were the high frequencies of chorea (11%) and cranial neuropathy (17%, including 10%
24 s, including pancreatic insufficiency (67%), chorea (64%), atrial septal defect (24%), microcephaly (
25     It has been hypothesized that Sydenham's chorea, a major manifestation of rheumatic fever, may pr
26 nes result in a variety of diseases, such as chorea acanthocytosis (ChAc), but the cellular functions
27 sociated with the neurodegenerative disorder Chorea Acanthocytosis.
28 tic anemia and resembling the human disorder chorea acanthocytosis.
29 generative hereditary disorders that include chorea-acanthocytosis (ChAc) and McLeod syndrome (MLS).
30                                              Chorea-acanthocytosis (ChAc) and McLeod syndrome are dis
31                                              Chorea-acanthocytosis (ChAc) is a fatal neurodegenerativ
32                                              Chorea-acanthocytosis (ChAc) is a fatal neurological dis
33                                              Chorea-acanthocytosis (ChAc) is a severe, neurodegenerat
34                      The rare human disorder chorea-acanthocytosis (ChAc) is caused by mutations in h
35  of the chorein-encoding gene VPS13A lead to chorea-acanthocytosis (ChAc), a neurodegenerative disord
36 nts result in the neurodegenerative disorder Chorea-Acanthocytosis (ChAc).
37                          The gene mutated in chorea-acanthocytosis (CHAC; approved gene symbol VPS13A
38 axias, dentatorubral-pallidoluysian atrophy, chorea-acanthocytosis and iron-accumulation disorders.
39 nt age-dependent neurodegenerative diseases, chorea-acanthocytosis and Parkinson's disease, respectiv
40 ion of active Lyn and autophagy was found in chorea-acanthocytosis based on Lyn coimmunoprecipitation
41                                           In chorea-acanthocytosis erythrocytes, active Lyn is seques
42 n associated with Atg7 in healthy but not in chorea-acanthocytosis erythrocytes.
43                       Our results uncover in chorea-acanthocytosis erythroid cells an association bet
44                                              Chorea-acanthocytosis is characterized by circulating ac
45                                              Chorea-acanthocytosis is one of the hereditary neurodege
46 ed K+ channel genes, KCNA5 and KCNA6; 6) the chorea-acanthocytosis locus on 9q21; 7) the Huntington-l
47           In addition, reticulocyte-enriched chorea-acanthocytosis red cell fractions exhibited delay
48       We report here for the first time that chorea-acanthocytosis red cells are characterized by imp
49 es and membrane remnants only in circulating chorea-acanthocytosis red cells.
50                                           In chorea-acanthocytosis, we found (1) dyserythropoiesis; (
51 are linked to the neurodegenerative disorder chorea-acanthocytosis.
52 sease is uncontrolled involuntary movements (chorea) accompanied by progressive cognitive and psychia
53 que clinical presentation of childhood-onset chorea and characteristic brain MRI showing symmetrical
54 ar after Charcot's death, Osler published On Chorea and Choreiform Affectations (1894), and in this p
55 sing CB1 levels are strongly correlated with chorea and cognitive deficit.
56 n patients with Parkinson's disease (PD) are chorea and dystonia, and often the two types are intermi
57 isorder with a distinct phenotype, including chorea and dystonia, incoordination, cognitive decline,
58                                              Chorea and dystonia, usually in the legs, occur less com
59  with various diseases, including Huntington chorea and fragile X syndrome.
60 t Charcot had failed to separate, Sydenham's chorea and Huntington's disease.
61 ergic medication had a slower progression in chorea and irritability compared with those not taking s
62 ive neurologic diseases such as Huntington's chorea and late-stage Parkinson disease.
63 ified Neurological Examination (QNE) and its chorea and motor impairment subscales, the Mini-Mental S
64  11 regions containing genes associated with chorea and myokymia: 1) the Huntington disease gene on c
65                                   Sydenham's chorea and other central nervous system illnesses that a
66 mising etiologically targeted treatments for chorea and other hyperkinetic movement disorders.
67 of autoimmune movement disorders [Sydenham's chorea and PANDAS (pediatric autoimmune neuropsychiatric
68 been described in association with dystonia, chorea and parkinsonism.
69 bodies (ABGA) are associated with Sydenham's chorea and pediatric autoimmune neuropsychiatric disorde
70 es are directed at managing symptoms such as chorea and psychiatric disturbances.
71 mAbs 24.3.1, 31.1.1, and 37.2.1 derived from chorea and selected for cross-reactivity with group A st
72 ntervention, especially for the treatment of chorea and some behavioural problems.
73 naling in the immunopathogenesis of Sydenham chorea and will lead to a better understanding of other
74 es resembling those in other mouse models of chorea and/or dystonia and had striatal D2 receptor expr
75 a hyperkinetic score, combining dystonia and chorea, and (2) a hypokinetic score, combining bradykine
76 n with PANDAS, nine children with Sydenham's chorea, and 24 healthy children were evaluated for D8/17
77 isease,movement disorders, ataxia, dystonia, chorea, and Creutzfeldt-Jakob with and Jewish.
78  and early-onset ataxia with a rapid course, chorea, and dementia.
79  including Alzheimer's disease, Huntington's chorea, and glial tumor; however, the precise function o
80 nted with acute-onset confusion, opsoclonus, chorea, and intractable seizures.
81 riable phenotype including ataxia, dystonia, chorea, and parkinsonism, as well as cognitive impairmen
82 s exhibit neuronal dysfunction/degeneration, chorea, and progressive weight loss.
83 t disorders (parkinsonism, dystonia, tremor, chorea, and restless legs syndrome) were included.
84 ed expression in rheumatic fever, Sydenham's chorea, and subgroups of obsessive-compulsive disorder a
85 rs such as Parkinson's disease, Huntington's chorea, and tardive dyskinesia arise from an imbalance b
86 araneoplastic, such as anti-CRMP5-associated chorea, anti-Ma2 hypokinesis and rigidity, anti-Yo cereb
87                                              Chorea antibodies targeted the surface of human neuronal
88 D) is typically made once motor symptoms and chorea are evident.
89 inhibited is consistent with the theory that chorea arises from selective degeneration of striatal pr
90 d movement disorder (opsoclonus, ataxia, and chorea) as well as seizures refractory to treatment.
91 enazine to deutetrabenazine in patients with chorea associated with Huntington disease (HD).
92 er 2 inhibitor approved for the treatment of chorea associated with Huntington disease and tardive dy
93 itor approved in the US for the treatment of chorea associated with Huntington disease and tardive dy
94                          Among patients with chorea associated with Huntington disease, the use of de
95  the treatment of TD and in the treatment of chorea associated with Huntington's Disease.
96 lbenazine was evaluated for the treatment of chorea associated with Huntington's disease.
97 proved deuterated drug, for the treatment of chorea-associated Huntington's disease, and their pharma
98                The clinical features include chorea, ataxia, incoordination, emotional changes and de
99 of hyperkinetic movement disorders including chorea, ballism, athetosis, dystonia, tremor, myoclonus,
100 ) encephalitis, which may cause dyskinesias, chorea, ballismus or dystonia (NMDAR antibodies), the sp
101      These include migraine, encephalopathy, chorea, brain stem dysfunction, myelopathy, mononeuritis
102  the hallmark autoimmune disorder Sydenham's chorea, but PANDAS remains controversial.
103 cal activity correlated with the severity of chorea, but SMR and total energy expenditure did not.
104  Tourette's syndrome, rather than Sydenham's chorea, but who have similar poststreptococcal autoimmun
105 rted at the age of 3 to 4 years and included chorea, cerebellar ataxia, dystonia, and pyramidal tract
106 ade, and symptom scores of motor impairment, chorea, cognition, and mood.
107 ound previously for subjects with Sydenham's chorea compared with normal subjects.
108 ease, valbenazine resulted in improvement in chorea compared with placebo and was well tolerated.
109 NDAS and 89% of the children with Sydenham's chorea, compared with 17% of the healthy children, were
110                                              Chorea control, as measured by the total maximal chorea
111 le safety profile and effectively maintained chorea control.
112 e was titrated on a weekly basis for optimal chorea control.
113             Tetrabenazine is efficacious for chorea control; however, tolerability concerns exist.
114 in Huntington disease (HD), characterized by chorea, dementia and severe weight loss, culminating in
115 ary neurodegenerative disorder that produces chorea, dementia, and death.
116 idlife onset of debilitating and progressive chorea, dementia, and psychological disturbance.
117                                Reactivity of chorea-derived mAb 24.3.1 or SC IgG with D2R was confirm
118 her streptococcal diseases in the absence of chorea did not activate the kinase.
119    Immunotherapy was associated with shorter chorea duration (hazard ratio for chorea resolution, 1.5
120              The planned study outcomes were chorea duration at onset, monophasic course (absence of
121                                   The median chorea duration in patients receiving 1 or more months o
122 ata on clinical characteristics, treatments, chorea duration, relapse, and final outcome were extract
123 icosteroid duration for survival analysis of chorea duration.
124 hypopallesthaesia, upper motor neuron signs, chorea, dystonia, oculomotor signs and cognitive impairm
125 ition, there are recent reports of dystonia, chorea encephalopathy, and dystonic choreoathetosis occu
126      The presence of opsoclonus, ataxia, and chorea expands the clinical phenotype and indicates that
127 tification of PDE10A mutations as a cause of chorea further motivates the study of cAMP signaling in
128                                  In Sydenham chorea, human mAbs derived from disease target the group
129 ptoms comprising various elements, including chorea, hyperactivity, tics, emotional lability, and obs
130 ments and outcomes in patients with Sydenham chorea, immunotherapy, in particular corticosteroid trea
131 ars (SD = 13.3, range 13-63), beginning with chorea in 50%, focal lower limb dystonia in 42.5% and pa
132  the only approved drug for the treatment of chorea in HD, tetrabenazine (TBZ).
133          Citing the use of tetrabenazine for chorea in Huntington disease, adrenocorticotropic hormon
134 ease, with clinical manifestations including chorea, incoordination, ataxia, and dementia.
135 acterized by abnormal involuntary movements (chorea), intellectual impairment and selective neuronal
136                                   Sydenham's chorea is a CNS disorder and sequela of group A streptoc
137                                              Chorea is a hyperkinetic movement disorder resulting fro
138                               Paraneoplastic chorea is described in 16 patients: 11 with limited smal
139                                     Sydenham chorea is the major neurological manifestation of ARF bu
140                                     Sydenham chorea is the most common acquired chorea of childhood w
141 gressive dementia, psychiatric problems, and chorea, is known to be caused by CAG repeat expansions i
142 s on 16p11.2-q11.2; 9) the benign hereditary chorea locus on 14q; 10) the SCA type 5 locus on chromos
143                                 In addition, chorea mAb 24.3.1 and acute chorea sera induced calcium/
144                                              Chorea mAb specificity for purified brain tubulin was co
145          Nucleotide sequence analysis of the chorea mAb V(H) genes revealed that mAb 24.3.1 V(H) gene
146                                          The chorea mAbs labeled both intra- and extracellular Ags of
147    Our novel findings reveal that Sydenham's chorea mAbs target a 55-kDa brain protein with an N-term
148   Lysoganglioside G(M1) inhibited binding of chorea mAbs to tubulin and mAb reactivity with human cau
149 bitory effect for patients with little or no chorea may be due to additional degeneration of projecti
150 ter 27 AIds; the highest SIRs were noted for chorea minor (8.00), lupoid hepatitis (5.75), and Addiso
151                                              Chorea monoclonal antibodies showed specificity for mamm
152  Sydenham chorea is the most common acquired chorea of childhood worldwide; however, treatment is lim
153 s of abnormal movements, typically dystonia, chorea or a combination thereof, without loss of conscio
154 nts, classic antidepressant drugs exacerbate chorea or anxiety.
155 despite the absence of documented Sydenham's chorea or rheumatic fever.
156 ity in diseases such as cancer, Huntington's chorea, or anorexia.
157           Other disorders such as Sydenham's chorea, or chorea related to systemic lupus erythematosu
158                             In patients with chorea, overnight conversion to deutetrabenazine therapy
159  tauopathies, whilst changes in Huntington's chorea, Parkinson's disease, corticobasal degeneration a
160                       Patients had dystonia, chorea, parkinsonism, dysarthria, dysphagia, seizures, c
161 y recurrent and brief attacks of dystonia or chorea precipitated by sudden movements.
162 odified Rankin Scale score 2-6 or persisting chorea, psychiatric, or behavioral symptoms at final fol
163 good: modified Rankin Scale score 0-1 and no chorea, psychiatric, or behavioral symptoms at final fol
164 lies including mental retardation, dystonia, chorea, pyramidal signs and a compulsive and aggressive
165 ther disorders such as Sydenham's chorea, or chorea related to systemic lupus erythematosus and antip
166 th shorter chorea duration (hazard ratio for chorea resolution, 1.51 [95% CI, 1.05-2.19]; P = .03).
167 nged contractions that may contribute to the chorea, rigidity, and dystonia that characterize Hunting
168                                              Chorea, rigidity, dystonia, and muscle weakness are char
169 ead to disease in disorders such as Sydenham chorea (SC) is not known.
170 tington's Disease Rating Scale total maximal chorea score and total motor score were efficacy end poi
171      Primary end point was the total maximal chorea score change from baseline (the average of values
172 tington disease and a baseline total maximal chorea score of 8 or higher (range, 0-28; lower score in
173 ea control, as measured by the total maximal chorea score, was maintained at week 1 and significantly
174 utetrabenazine group, the mean total maximal chorea scores improved from 12.1 (95% CI, 11.2-12.9) to
175 h their sensitivity in diagnosing Sydenham's chorea seems excellent, it is not yet possible to extrap
176 vels of anti-tubulin IgG were found in acute chorea sera and cerebrospinal fluid.
177     In addition, chorea mAb 24.3.1 and acute chorea sera induced calcium/calmodulin-dependent protein
178 rt disease and the neuronal cell in Sydenham chorea share a common streptococcal epitope GlcNAc and t
179  movements, including motor restlessness and chorea, slowing of voluntary movements and cognitive imp
180  individuals, the HDDMS encompasses balance, chorea, speeded tapping and gait.
181 emor, dystonia, Huntington disease and other chorea syndromes, and Tourette syndrome and other chroni
182 hogenic role of autoantibodies in Sydenham's chorea, the prototypic post-streptococcal neuropsychiatr
183                                   Other than chorea, tics and obsessive-compulsive disorder, which co
184 ovement disorders include tremors, dystonia, chorea, tics, myoclonus, stereotypies, restless legs syn
185 s Disease Rating Scale [UHDRS] Total Maximal Chorea [TMC] score of 8 or higher) who were randomly ass
186 netically confirmed Huntington's disease and chorea (Unified Huntington's Disease Rating Scale [UHDRS
187                                   Osler's On Chorea uniquely captures the transition period between t
188        Two had early Parkinsonian tremor and chorea was seen in four, although in two this was attrib
189                                              Chorea was the initial and most prominent symptom in 11
190 tetrabenazine, a novel molecule that reduces chorea, was well tolerated in a double-blind, placebo-co
191 t Huntington's disease patients with greater chorea were disinhibited is consistent with the theory t
192    Human mAbs and autoantibodies in Sydenham chorea were found to signal neuronal cells and activate
193 her (range, 0-28; lower score indicates less chorea) were enrolled from August 2013 to August 2014 an
194                 The mice develop progressive chorea with onset at approximately 9 weeks of age and wi
195 by 3.0 points (95% CI, 2.5-3.4) per year and chorea worsened by 0.3 point per year (95% CI, 0.1-0.5).

 
Page Top