ライフサイエンスコーパス: enzyme therapy

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1 ations, and established the effectiveness of enzyme therapy.

2 ant given the advent of specific replacement enzyme therapy.

3 2 years of high-dose (50 U/kg every 2 weeks) enzyme therapy.

4 teoblasts can be corrected by asfotase-alpha enzyme therapy aimed at reducing PPi concentration.

5 g the lowering of adenosine levels using ADA enzyme therapy and also through the use of the adenosine

6 l be useful in examining the efficacy of ADA enzyme therapy and studying the mechanisms underlying th

7 ement has provided impetus for design of new enzyme therapies, and creation of substrate depletion an

8 that included high-calorie diets, pancreatic-enzyme therapy, and fat-soluble vitamin supplements.

9 the toxicity of gliadin and open the way for enzyme therapy as an adjunct to the gluten free diet.

10 st lysosomal storage disease (LSD) for which enzyme therapy became available, and although infusions

11 osine and 2'-deoxyadenosine levels using ADA enzyme therapy decreased the pulmonary eosinophilia and

12 Two patients receiving enzyme therapy developed neutralizing antibodies to acid

13 ADA enzyme therapy diminished the IL-13-induced increase in

14 ld be valuable also in future development of enzyme therapies for other drugs of abuse.

15 g antibodies to acid beta-glucosidase during enzyme therapy for Gaucher disease has significant impli

16 Enzyme therapy for lysosomal storage disorders directed

17 he considerable expense and inconvenience of enzyme therapy for patients, renders the search for alte

18 The advent of efficacious enzyme therapy has emphasized the importance of early di

19 Enzyme therapy has led to improvements in physical and f

20 These studies provide feasibility for LAL enzyme therapy in human WD and CESD.

21 , eliglustat was noninferior to imiglucerase enzyme therapy in maintaining stable platelet counts, he

22 rosis (CF), even with replacement pancreatic enzyme therapy, is often associated with decreased carot

23 ing ADA-deficient mice on low dosages of ADA enzyme therapy led to chronic elevations in lung adenosi

24 n, which was unresponsive to oral pancreatic enzyme therapy or a gluten-free diet.

25 Lowering adenosine by ADA enzyme therapy or genetic deletion of ADORA2B significan

26 herapy-group patients were alive, and 16% of enzyme-therapy patients were alive.

27 A "low-dose" enzyme therapy protocol prevented the pulmonary phenotyp

28 A "high-dose" enzyme therapy protocol resulted in decreased metabolic

29 ADA replacement enzyme therapy resulted in a lowering of adenosine level

30 s that chronic reduction of adenosine by ADA enzyme therapy successfully attenuated penile fibrosis i

31 ADA enzyme therapy successfully corrected the priapic activi

32 e 2 initially showed a favorable response to enzyme therapy that plateaued after 1 year of treatment.

33 The ability to safely and effectively use enzyme therapy to inhibit or reverse visceral-disease pr

34 Moreover, using ADA enzyme therapy to reduce adenosine or a specific antagon

35 ) of lysosomal acid lipase and its use as an enzyme therapy to reduce atherosclerotic lesions in a mo

36 , phase III, controlled trial of proteolytic enzyme therapy versus chemotherapy.

37 Enzyme therapy was discontinued in case 1, with resultan

38 ed donor (URD) BMT as a vehicle for adoptive enzyme therapy was evaluated in this retrospective study

39 The potential for enzyme therapy was tested using mannose terminated human

40 ADA enzyme therapy was used to examine the relative impact o

41 lumbia University, and patients who received enzyme therapy were seen by the participating alternativ

42 GD type 1 (age range, 18-50 years) receiving enzyme therapy who were randomized for this study.

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