ライフサイエンスコーパス: Lowry

1 f the valve was demonstrated by performing a Lowry protein assay in the device, wherein fluid flow wa

2 Concentrations of sulfide, ammonia, and Lowry-reactive substances were measured over 48 h.

3 in content of hydrolysates but the Dumas and Lowry methods can also be recommended as alternatives.

4 tly positively correlated with the Dumas and Lowry methods.

5 ordial dwarfism type 1), Roifman (RFMN), and Lowry-Wood (LWS) syndromes.

6 rdial dwarfism type 1, Roifman syndrome, and Lowry-Wood syndrome.

7 classic spectrophotometric methods (Biuret, Lowry, Bradford and Markwell) were applied to evaluate t

8 (GOs) to distinguish Lewis (L) and Bronsted-Lowry (B) adsorption sites at the GO surfaces.

9 ting as hydride donors, but also as Bronsted-Lowry acids.

10 on reactions, and reactions between Bronsted-Lowry acids and bases.

11 -walled carbon nanotubes (SWNTs) in Bronsted-Lowry acids.

12 ch performs a role in the theory of Bronsted-Lowry acids and bases that is similar to the role of the

13 etween intermediate(s) and solvent (Bronsted-Lowry base) is known to drive the reaction, the gas-phas

14 ent (ka) by fluorophotometry, [protein]Ac by Lowry assay, corneal endothelial cell morphology by spec

15 One study, based on Coffin- Lowry cells defective in RSK2, reported that RSK2 was th

16 Coffin-Lowry Syndrome (CLS) is an X-linked mental retardation c

17 Cells from a Coffin-Lowry syndrome patient (deficient in RSK2) or expressing

18 tic disorders such as RASopathies and Coffin-Lowry syndrome.

19 phosphorylation response is normal in Coffin-Lowry cells.

20 s of defective synaptic plasticity in Coffin-Lowry Syndrome (CLS), a cognitive disorder that is cause

21 implicated in the pathophysiology of Coffin-Lowry syndrome.

22 a good animal model for the study of Coffin-Lowry syndrome.

23 Since Coffin-Lowry syndrome and neonatal lactic acidosis are associat

24 l S6 kinase 2 (Rsk2), a model for the Coffin-Lowry syndrome (CLS), exhibit a significant delay in gro

25 ctivating mutations in humans lead to Coffin-Lowry syndrome, our results imply that alterations in GP

26 s of RSK2 activity in humans leads to Coffin-Lowry syndrome, which is manifested by mental retardatio

27 whose diagnosis was later revised to Coffin-Lowry syndrome.

28 ns for distinct RSK isoforms, whereas Coffin-Lowry syndrome has only been associated with mutations i

29 dysmorphic features overlapping with Coffin-Lowry syndrome caused by RPS6KA3 mutations.

30 Differential Lowry protein assay (DLA) of the thiolated Ig reactant a

31 terfaces was also confirmed using a modified Lowry assay that prevents interference from Metrizamide

32 Values for the Lowry and modified Lowry methods varied by 20-50% from control protein valu

33 tho-diphenols; the Lowry assay, the modified Lowry assay, and a new method including a calculation to

34 bound phenols) as determined by the modified Lowry method.

35 gestion, as measured by the disappearance of Lowry-reactive substances and the appearance of ammonia.

36 e-related diseases such as Roifman syndrome, Lowry-Wood syndrome and early-onset cerebellar ataxia.

37 The present study compares the Lowry and BCA protein assays and protein determination b

38 nce of covalently bound ortho-diphenols; the Lowry assay, the modified Lowry assay, and a new method

39 Values for the Lowry and modified Lowry methods varied by 20-50% from c

40 Color development of the Lowry protein assay was tracked over time for bovine ser

41 by increasing working temperature while the Lowry response decreased due to production of smaller-si

42 he differences in response obtained with the Lowry assay in the presence and absence of copper.

43 is assumes that the phenol response with the Lowry assay is not affected by copper.