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1 e phosphatase (PTPase) assays, we found that sodium stibogluconate, a drug used in treatment of leish
3 o, approximately 58-fold more effective than sodium stibogluconate, and increased mouse splenic-pLck-
5 ly, pharmacological inhibition of SHP-1 with sodium stibogluconate augmented the function of all engi
6 B/c mice with imipramine in combination with sodium stibogluconate cleared organ Sb(R)LD parasites an
7 ably, pharmacologic inhibition of SHP-1 with sodium stibogluconate counteracted CD20 mAb-induced NK h
8 f SHP-2 and PTP1B required 100 micrograms/ml sodium stibogluconate, demonstrating differential sensit
9 term treatment with the antileishmanial drug sodium stibogluconate failed to significantly alter the
11 sages, isolated parasites were refractory to sodium stibogluconate in in-vitro drug sensitivity assay
12 fective as the standard antileishmanial drug sodium stibogluconate in treatment of cutaneous leishman
13 , the cure rate of antimonial compounds (eg, sodium stibogluconate) in the treatment of visceral leis
15 These data represent the first evidence that sodium stibogluconate inhibits PTPases and augments cyto
16 d when treated with the antileishmanial drug sodium stibogluconate, <10% of mice were cured when the
17 ted IL-13(-/-) mice also responded poorly to sodium stibogluconate-mediated chemotherapy compared wit
18 tavalent state as a complex in drugs such as sodium stibogluconate (Pentostam) and meglumine antimona
19 SHP-1 enzymatic activity via the cancer drug sodium stibogluconate potently augmented Treg suppressor
22 ent antimony-carbohydrate complexes, such as sodium stibogluconate (SSG), has been reported to prolon
23 tion and the activity of the SHP-1 inhibitor sodium stibogluconate that induced IFN-gamma(+) cells fo
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