ライフサイエンスコーパス: may explain why

1 Spontaneous fluctuations of neural activity may explain why sensory responses vary across repeated presen

2 hese data uncover a direct role for RANK in lung cancer and may explain why female sex hormones accelerate lung cancer de

3 the pathophysiology differs between males and females, and may explain why symptoms appear after adolescence when the ex

4 nt for why an insulin granule is selected for secretion and may explain why newly synthesized insulin is preferentially s

5 eutic strategies for patients with various cancer types and may explain why some patients respond better to WEE1 inhibito

6 he brain should be considered with regards to human use and may explain why fatigue, headaches and nervousness have been

7 rvations from the thermodynamic analysis of the PagP barrel may explain why cysteine, despite possessing a polar sulfhydr

8 In combination, these parasite-induced changes in behaviour may explain why parasitized gobies are poor competitors for r

9 olism of glutamine and related analogs by GDH in the L cell may explain why GLP-1 secretion, but not that of insulin, is

10 diomyocytes to oxygen deprivation in humans and chimpanzees may explain why humans are more prone to certain heart diseas

11 Taken together, our data may explain why colonization of superantigen-producing S. aur

12 This difference in nucleosome destabilization may explain why Nhp6A and Hmo1 function at different genomic

13 These differences may explain why pediatric cancer patients have a higher risk

14 Our findings may explain why osteogenesis imperfecta-causing mutations in

15 ns at distinct levels of the perceptual-inference hierarchy may explain why hallucinations and delusions tend to cluster

16 Such selection acting over human evolutionary history may explain why we cooperate readily with unrelated and unfam

17 These insights may explain why modeled viral fusion occurs preferentially ne

18 the existence of mutually exclusive competing interactions, may explain why some proteins are dynamic while others are ri

19 The insensitivity of cells to ISRIB during acute ISR may explain why ISRIB does not cause overt toxic side effects

20 y low estimated inhibition levels at median exposure levels may explain why no relationship between exposure to TTR-bindi

21 This mechanism may explain why the Hox code is maintained throughout the lif

22 tal determinants combined with larval connectivity patterns may explain why the northern Galapagos Islands (Darwin, Wolf)

23 The indole-mediated reduction in cytoplasmic pH may explain why indole provides E. coli with a degree of prot

24 These countervailing selective pressures may explain why a breadth of sizes exist and even coexist whe

25 These processes may explain why uncontaminated primordial mantle is so diffic

26 een high-temperature tolerance and increased N requirements may explain why N limitation inhibited adaptation.

27 Results may explain why many CNVs affect a similar range of neuropsyc

28 previously reported, and, together with the other results, may explain why clinical effect is lost if SLIT is discontinu

29 on-induced alternative translation initiation (fsATI), that may explain why only TRESK-MT is associated with migraine.

30 abilities and suggest a potential underlying mechanism that may explain why variability quenching occurs.

31 We formulate six processes that may explain why the largest losses are observed specifically

32 Here we propose that Gestalt theory may explain why rodent islet architecture has historically be

33 This may explain why DCs respond faster and more vigorously to TLR

34 This may explain why defects in a single component often produce c

35 This may explain why eliminating HIV susceptibility in circulating

36 This may explain why Giardia trophozoites adhere to the small inte

37 This may explain why N-Ph and N-Bu imines are not hydrogenated.

38 This may explain why naturally occurring allergen-specific IgG ant

39 This may explain why TBI patients are more vulnerable to cognitive

40 This may explain why the net effect of mTOR inhibitors is paradoxi

41 This may explain why we do not observe shared mutations among clin

42 ess and aid in stress adaptation, and this stress tolerance may explain why many cancers aberrantly express MAGEs Here, w

43 This versatility may explain why a variety of organisms have extensively explo

44 mechanism of killing for cationic, amphipathic AMPs, which may explain why most AMPs require micromolar concentrations f

45 s of the P-TEFb subunit cyclin T1 than primary cells, which may explain why many LRAs are functional in model systems but

46 areas with comparable ice-bathymetry configurations, which may explain why changes in the density structure of the water

47 dimer with BMP2 or BMP4 during mammalian development, which may explain why mutations in either Bmp4 or Bmp7 lead to a si

48 he last process is the rods' competition for glucose, which may explain why rods also provide the RdCVF signal to compens

49 al an important species difference in OCN regulation, which may explain why serum concentrations of OCN are higher in mou

50 t express high levels of TLR9 and low levels of TLR7, which may explain why TLR9 dysregulation is particularly consequent