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1                                              POMA disease antisera (6/6) recognize the third KH domai
2                                              POMA was examined in a randomized controlled trial under
3 e associations with POMA balance (P = 0.02), POMA gait scores (P < 0.01), and IADL (P < 0.01).
4 t (2.96 points), DGI (2.29), BBS (1.97), and POMA (0.83).
5 suggest that the Mini-BESTest, DGI, BBS, and POMA are responsive outcome measures for PD.
6 nsiveness of the Mini-BESTest, DGI, BBS, and POMA in PwPD.
7 8 points for the Mini-BESTest, DGI, BBS, and POMA, respectively.
8 sments using the Mini-BESTest, DGI, BBS, and POMA.
9 nd Performance-Oriented Mobility Assessment (POMA) are essential for assessing balance impairments in
10  paraneoplastic opsoclonus-myoclonus ataxia (POMA) antigen.
11  Paraneoplastic opsoclonus myoclonus ataxia (POMA) is a neurologic disorder thought to be mediated by
12  paraneoplastic opsoclonus myoclonus ataxia (POMA) patients with latent cancer, reduced inhibitory co
13  paraneoplastic opsoclonus myoclonus ataxia (POMA), a disorder associated with breast cancer and moto
14  paraneoplastic opsoclonus myoclonus ataxia (POMA), an autoimmune neurologic disease characterized by
15  paraneoplastic opsoclonus myoclonus ataxia (POMA), Nova-1 and Nova-2 proteins are present as auto-an
16  paraneoplastic opsoclonus-myoclonus ataxia (POMA).
17  paraneoplastic opsoclonus-myoclonus ataxia (POMA).
18 [paraneoplastic opsoclonus-myoclonus ataxia (POMA)].
19  paraneoplastic opsoclonus-myoclonus-ataxia (POMA).
20 in vitro, and this binding can be blocked by POMA antisera.
21 tions for 10-days at doses of 80 or 320 mg/d POMA versus placebo (1:1:1 ratio).
22                                    High-dose POMA exerted significant effects on clinical symptoms, b
23                                    High-dose POMA significantly reduced ketamine-induced BPRS total s
24                                     However, POMA antisera recognize antigens that are widely express
25 l for understanding the motor dysfunction in POMA.
26 to the cause of abnormal motor inhibition in POMA.
27 m for the loss of motor function observed in POMA patients.
28 ults demonstrate that the immune response in POMA targets a family of highly related sequence-specifi
29 A may underlie the motor dysfunction seen in POMA.
30 ate with the predominantly motor symptoms in POMA.
31  0.04, d = -0.44, respectively), but neither POMA dose significantly suppressed ketamine-induced dACC
32                  Thus, a cardinal feature of POMA is the production of antibodies that inhibit Nova-1
33                                          One POMA disease antigen, termed Nova-1, has been identified
34 eptor 2/3 (mGluR2/3) agonists (pomaglumetad [POMA] and TS-134) were assessed in two Phase Ib proof of
35 d a folate-caged pomalidomide prodrug, FA-S2-POMA, by incorporating a folate group as a caging and gu
36 A antisera to clone a cDNA encoding a second POMA disease antigen termed Nova-2.
37 he development of cognitive deficits in some POMA patients.
38     95 healthy volunteers were randomized to POMA and 63 to TS-134.
39                                 We have used POMA antisera to clone a cDNA encoding a second POMA dis
40 howed significant negative associations with POMA balance (P = 0.02), POMA gait scores (P < 0.01), an
41 a significant positive association only with POMA balance scores (P < 0.045).