ライフサイエンスコーパス: we determined

1 We determined 1,200 mg to be the recommended single-agent dos

2 We determined a crystal structure of CaM bound to a peptide e

3 Also, using principal component and cluster analyses, we determined a strong negative relationship between total ph

4 amine receptor structure, function, and ligand recognition, we determined crystal structures of the D4 dopamine receptor

5 Here, we determined disease stage-dependent changes in myocardial e

6 We determined Fic in multiple cellular assays and cell types

7 antagonistic efficacy of endothelial-derived prostacyclin, we determined how Iloprost reverses ADP-mediated signaling ev

8 Using prion permissive cells, we determined how impairment of endocytosis affects productiv

9 We determined how the chemical composition of primary ambient

10 nvestigate the involvement of PLAG1 in testicular function, we determined (i) the spatial distribution of PLAG1 in the te

11 We determined IOL power calculations with the Sanders-Retzlaf

12 oped for the assessment of tissue sodium content in humans, we determined skin sodium content at the level of the calf in

13 fic strain variants (<5% inter-subject strain sharing), and we determined that a single strain typically dominated each s

14 We determined that chrysophanol inhibited the functional and

15 Here we determined that increased expression of XRN2 induced EMT a

16 Through transcriptomic profiling, we determined that low expression of the ergothioneine transp

17 We determined that MyBP-HL protein was myofilament associated

18 We determined that selinexor causes thrombocytopenia by block

19 We determined that SNPs with low LLD have significantly large

20 Using rationally designed short peptide sequences, we determined that the charge type and identity of amino acid

21 atrix-assisted laser desorption/ionization (MALDI) imaging, we determined that the drug penetrates the entire MCTS.

22 In this study we determined that the in planta heterologous expressed OeGLU

23 From the results of the kinetics experiments, we determined that the reversion of the quadricyclanes occurs

24 By combining our measurements with biophysical modeling, we determined that the ribosomal footprint extends 13 nucleot

25 We determined that the xRRM of LARP7 binds to the 3 stem loop

26 We determined that these defects are caused by hyperphosphory

27 Using receptor-blocking antibodies and activation peptides, we determined that thrombin-mediated injury depended upon int

28 Using gadolinium-enhanced T1-weighted MRI, we determined that vascular permeability is not homogeneous b

29 We determined the age- and sex-adjusted risk of death for eac

30 We determined the circulating levels of 7 selected candidate

31 We determined the clinical significance of minimal residual d

32 Here, using sulfur-SAD phasing, we determined the crystal structure of m4-1BB to 2.2-A resolu

33 Here, we determined the crystal structure of the N-terminal half of

34 physical basis of enhanced protein solubility and function, we determined the crystallographic structure of one such LGK

35 We determined the effect of three enhanced strategies for ter

36 To evaluate SGE-516 in Scn1a (+/-) mice, we determined the effect of treatment on hyperthermia-induced

37 We determined the frequency, risk factors, and mortality risk

38 sthma in a birth cohort using administrative databases, and we determined the impact of adjusting for potential confounde

39 From these free-energy calculations, we determined the kinetics and pathways for major products (e

40 We determined the kinetics of growth and turnover of nitric o

41 We determined the number of OHCAs that occurred within 100 m

42 Using receiver operating characteristic (ROC) curves, we determined the optimal cut-off values for each score for t

43 Using Cox methods, we determined the relationship between in-hospital AKI and ri

44 We determined the spectrum of SNVs in a single human cell aft

45 Using cryo-electron tomography and subtomogram averaging, we determined the structure of the COPI coat assembled on mem

46 We determined the structures of the CL40 and CL59 complexes w

47 We determined the subcellular distribution of individual mach

48 Here, we determined the X-ray crystallographic structures of two ca

49 ify the association between LC n-3 PUFA intake and CVD risk.We determined whether a PCSK9 variant (rs11206510), which has

50 Here, we determined whether dysregulated expression of the gap junc