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 cute hemorrhagic enteritis, myocarditis, and cerebellar disease.
2 nd offer a possible model of immune-mediated cerebellar disease.
3 cute hemorrhagic enteritis, myocarditis, and cerebellar disease.
4 hen this system is impaired in patients with cerebellar disease.
5 h cerebellar disease and 36 controls without cerebellar disease.
6 ad range of cognitive and motor phenomena in cerebellar disease.
7 tric morbidity of patients with degenerative cerebellar diseases.
8 tures promote the behavioral presentation of cerebellar diseases.
9           Despite the absence of symptomatic cerebellar disease, a decrease in the number of Purkinje
10 ysed cross-sectional data from 72 cases with cerebellar disease and 36 controls without cerebellar di
11 probe the integrity of specific functions in cerebellar disease, and new imaging methods to quantitat
12 ion of VZ progenitors in the pathogenesis of cerebellar diseases associated with deregulated Shh sign
13                                              Cerebellar disease burden and cerebro-cerebellar connect
14 ntention tremor plus other clinical signs of cerebellar disease (cerebellar tremor).
15 ed a series of 31 patients with degenerative cerebellar diseases, compared with 21 patients with Hunt
16 g the CaV2.1 subunit are associated with the cerebellar disease episodic ataxia type 2 (EA2).
17                  We identified enrichment of cerebellar disease genes in distinct cell populations in
18  all mood disorders in both the degenerative cerebellar diseases group (68%) and the Huntington's dis
19 se group (43%); the rate in the degenerative cerebellar diseases group was significantly higher than
20 will be suitable for investigating causes of cerebellar diseases in vivo from the molecular to the be
21 any, if not most, patients with degenerative cerebellar diseases may benefit from psychiatric interve
22 rs was 77% in the patients with degenerative cerebellar diseases, nearly identical to that in the pat
23 ent and would aid in better understanding of cerebellar disease pathogenesis caused due to deregulati
24 hange was present in 26% of the degenerative cerebellar diseases patients, 48% of the Huntington's di
25           A total of 19% of the degenerative cerebellar diseases subjects and 71% of the Huntington's
26  disorders in the patients with degenerative cerebellar diseases suggests that many, if not most, pat
27 stress-associated proteins in the context of cerebellar disease, we have profiled the expression of E