ライフサイエンスコーパス: oncotic

1 The oncotic agent PS ameliorates lung derangements seen afte

2 clude the oxygen-carrying capacity, superior oncotic and buffering properties, and endogenous antioxi

3 Oncotic and hydrostatic pressure differences control the

4 eas rough Brucella mutants induce macrophage oncotic and necrotic cell death.

5 ith left atrial myxoma and multiple cerebral oncotic aneurysms.

6 Myxomatous cerebral (oncotic) aneurysms following atrial myxoma is a rare neu

7 eases the resistance to cell death following oncotic but not apoptotic stimuli.

8 activating predominantly either apoptotic or oncotic cell death pathway.

9 s highly susceptible to oncotic swelling and oncotic death following ATP depletion.

10 Selective use of potentially proinflammatory oncotic death programs by activated lpr and gld T cells

11 d a strong positive correlation with applied oncotic gradient (Pearson r= 0.59, n= 28, P < 0.001), as

12 me response of glomeruli to a transcapillary oncotic gradient.

13 re extravasated and colocalized with foci of oncotic hepatocytes and chlorotyrosine adducts.

14 rough mutant infection induces necrotic and oncotic macrophage cell death that requires bacterial pr

15 In conclusion, oncotic necrosis and apoptosis can share features and me

16 death typically follows one of two patterns: oncotic necrosis and apoptosis.

17 presents a shared pathway that leads to both oncotic necrosis and apoptosis.

18 g adenosine triphosphate depletion-dependent oncotic necrosis and caspase-dependent apoptosis, with e

19 ed assays, DNA degradation also occurs after oncotic necrosis and leads to pervasive terminal deoxynu

20 Oncotic necrosis appears to be the principal mechanism o

21 During DILI, oncotic necrosis with concomitant release and recognitio

22 In conclusion, liver injury (oncotic necrosis) after BDL correlated with the severity

23 Cell death during APAP toxicity occurs by oncotic necrosis, in which the release of intracellular

24 h shares some features of both apoptotic and oncotic necrosis, might be involved in the pathogenesis

25 Although fusion peptides induced oncotic/necrotic death in cells, treatment with immunoco

26 y by low concentrations of 17beta-E2 induces oncotic/necrotic, but not apoptotic, programmed cell dea

27 ficients to HA and A, there was an effective oncotic pressure (E pi) of between 3.46 and 6.0 cm H2O o

28 cromolecules was assessed from the effective oncotic pressure (omega delta pi) exerted by the perfusa

29 as determined, blood was sampled, and plasma oncotic pressure (pi(A)) was measured.

30 Computation of glomerular intracapillary oncotic pressure (piGC) from knowledge of plasma oncotic

31 icantly faster in groups 2 to 4, and colloid oncotic pressure after resuscitation was greater in grou

32 This suggests that plasma oncotic pressure alone may be a more important determina

33 We tested the hypothesis that plasma oncotic pressure alone, not the plasma-to-lymph oncotic

34 tic pressure (piGC) from knowledge of plasma oncotic pressure and the filtration fraction revealed th

35 vestigate this further, Lp and the effective oncotic pressure difference (f3DeltaPi) acting across th

36 Thus, the effective oncotic pressure difference (sigma black triangle down p

37 hese results support our hypothesis that the oncotic pressure difference across the tumor microvascul

38 otic pressure alone, not the plasma-to-lymph oncotic pressure difference, modulates pulmonary transva

39 ar fluid filtration than the plasma-to-lymph oncotic pressure difference.

40 c pressures were estimated as the sum of the oncotic pressure due to HA alone plus the oncotic pressu

41 ncentration and the decreased transcapillary oncotic pressure gradient.

42 rol animals, even though the plasma-to-lymph oncotic pressure gradients were equal.

43 Starling's equation indicates that reduced oncotic pressure gradients will favor edema formation, a

44 4.5 and 17.7 +/- 2.2 mm Hg; plasma-to-lymph oncotic pressure gradients, respectively, were 4.4 +/- 0

45 Whereas oncotic pressure in blood plasma of various species is k

46 um total protein is the chief determinant of oncotic pressure in humans.

47 ecies is known, no data are available on the oncotic pressure in the interstitial space of tumors.

48 ecause of the leaky nature of tumor vessels, oncotic pressure in tumor interstitium should be close t

49 The high oncotic pressure in tumors is consistent with the elevat

50 Neither the plasma oncotic pressure nor the mean arterial pressure differed

51 he oncotic pressure due to HA alone plus the oncotic pressure of albumin (A) in an HA matrix.

52 ross the endothelial glycocalyx and that the oncotic pressure of interstitial fluid does not directly

53 min (HSA) serves not only as a physiological oncotic pressure regulator and a ligand carrier but also

54 ntial contribution of medullary interstitial oncotic pressure to the net balance of forces influencin

55 ents in serum albumin, immunoglobulin G, and oncotic pressure values were 31, 32, and 26%, respective

56 glomerular filtration during HPP, perfusate oncotic pressure was reduced by lowering the concentrati

57 ack triangle down pi was near 70% of luminal oncotic pressure when the tissue concentration equalled

58 ratio, plasma protein concentration, plasma oncotic pressure, and myocardial contractility.

59 Total solids, colloid oncotic pressure, arterial oxygen content, Hb, lactate,

60 e to hemodilution caused by its high colloid oncotic pressure, but may facilitate diffusive oxygen tr

61 Oncotic pressure, effective at inducing VDAC closure, al

62 effects of (in)Abeta depended on changes in oncotic pressure.

63 aised left atrial pressure elevation, plasma oncotic pressures in dextran and control sheep, respecti

64 We found interstitial oncotic pressures in four human tumor xenografts to be h

65 ic wick method for the direct measurement of oncotic pressures in the interstitial fluid of tumors gr

66 Total interstitial oncotic pressures were estimated as the sum of the oncot

67 ronically increases Lp without affecting the oncotic reflection coefficient.

68 roved with IVIg, we identified apoptotic and oncotic signaling pathways in in vitro and in vivo PV mo

69 the cellular response to either apoptotic or oncotic stimuli.

70 o rendered COS-7 cells highly susceptible to oncotic swelling and oncotic death following ATP depleti