ライフサイエンスコーパス: mitochondrial swelling

1 ated to experimental parameters (Ca(2+) flux/mitochondrial swelling).

2 embranes during renal ischemia and prevented mitochondrial swelling.

3 lcium into the mitochondria, thus leading to mitochondrial swelling.

4 roblasts were also resistant to H2O2-induced mitochondrial swelling.

5 ning of the permeability transition pore and mitochondrial swelling.

6 ly resolved light scattering consistent with mitochondrial swelling.

7 er mitochondrial membrane and did not induce mitochondrial swelling.

8 condensation, margination of chromatin, and mitochondrial swelling.

9 in a significant inhibition of Ca2+-induced mitochondrial swelling, an index of pore opening.

10 Treatment with antioxidants rescued mitochondrial swelling and cell death in Drp1KO Purkinje

11 ter inhibitor ruthenium red showed increased mitochondrial swelling and cytochrome c release and decr

12 iabetic mice, which was further confirmed by mitochondrial swelling and cytochrome c release induced

13 pening of the PTP with consequent persistent mitochondrial swelling and deenergization (the MPT).

14 However, granzyme C did cause rapid mitochondrial swelling and depolarization in intact cell

15 Both the extent and rate of calcium-induced mitochondrial swelling and depolarization varied greatly

16 nously added Ca(2+), promoted Ca(2+)-induced mitochondrial swelling and depolarization, and accelerat

17 y also undergo structural alterations during mitochondrial swelling and disruption.

18 It is characterized by somal and mitochondrial swelling and formation of DNA single-stran

19 Diazoxide induced moderate mitochondrial swelling and increase in the cytosolic fra

20 tochondrial membrane permeability and causes mitochondrial swelling and intrinsic apoptosis.

21 CDDO-Me rapidly induced caspase-independent mitochondrial swelling and loss of inner membrane struct

22 Early mitochondrial swelling and loss of the mitochondrial mem

23 tochondrial toxins (e.g. MPP(+)) resulted in mitochondrial swelling and lysosome reduction.

24 FRD produced mitochondrial swelling and membrane depolarization in FR

25 philin inhibitor Debio-025 similarly reduced mitochondrial swelling and necrotic disease manifestatio

26 otic and necrotic stimuli induce progressive mitochondrial swelling and outer mitochondrial membrane

27 nd brains of Ppif null mice are resistant to mitochondrial swelling and permeability transition in vi

28 on-induced oxygen radicals and inhibition of mitochondrial swelling and permeability transition.

29 a are resistant to Abeta- and Ca(2+)-induced mitochondrial swelling and permeability transition.

30 (3) Fragmentation: Along with massive mitochondrial swelling and release of cytochrome c into

31 brane permeability, permitted MPTP-dependent mitochondrial swelling and restored necrotic cell death.

32 ereas cyclophilin D-overexpressing mice show mitochondrial swelling and spontaneous cell death.

33 icularly vulnerable to oxidative stress, and mitochondrial swelling and vacuolization are among the e

34 Mitochondrial swelling and vacuolization are early signs

35 eduction of glycinergic innervation preceded mitochondrial swelling and vacuolization.

36 etaminophen reduced tissue damage, degree of mitochondrial swelling, and loss of mitochondrial membra

37 opening of the permeability transition pore, mitochondrial swelling, and rapid release of the peptide

38 mproved mitochondrial ATP synthesis, reduced mitochondrial swelling, and retention of normal morpholo

39 chrome c-releasing factors caused detectable mitochondrial swelling, arguing that matrix swelling is

40 l desquamation, with toxic vacuolization and mitochondrial swelling as hallmarks of the cellular dama

41 ene and protein expression measurements, and mitochondrial swelling assays.

42 honium ions in the mitochondrial suspension, mitochondrial swelling by observing absorbance changes,

43 ure produced rod-selective apoptosis without mitochondrial swelling by translocating cytosolic Bax to

44 MI and CPG resulted in significant mitochondrial swelling compared with baseline volume.

45 om controls subjected to rapid pacing showed mitochondrial swelling consistent with calcium overload.

46 er membrane permeabilization, which leads to mitochondrial swelling, cytochrome c release to the cyto

47 Mitochondrial swelling, cytochrome c release, and decrea

48 ndria, replacement of KCl by LiCl suppressed mitochondrial swelling, depolarization, and a release of

49 drial permeability transition (MPT), such as mitochondrial swelling, depolarization, and membrane per

50 pase-3 immunoreactivity were associated with mitochondrial swelling-disruption in sites of TAI.

51 ransient K(+) influx into the matrix causing mitochondrial swelling followed by activation of the K(+

52 In addition, we detected mitochondrial swelling in human OS xenografts in mice an

53 mitochondria shutdown in infected cells and mitochondrial swelling in pure neural leprosy nerves.

54 Bcl-xL expression also prevents mitochondrial swelling in response to agents that inhibi

55 reen (HTS), using an assay of Ca(2+)-induced mitochondrial swelling in the cryopreserved mitochondria

56 In addition, ryanodine inhibited mitochondrial swelling induced by Ca(2+) overload.

57 tide microinjection into cells abolished the mitochondrial swelling induced by overexpression of alph

58 ly and completely released in the absence of mitochondrial swelling is uncertain.

59 l permeability transition (MPT) and leads to mitochondrial swelling, membrane depolarization, and rel

60 d cytoplasmic changes with vacuolization and mitochondrial swelling, nuclear condensation, and sustai

61 plasmic vesicles, nuclear membrane blebbing, mitochondrial swelling, nuclear inclusions, and absence

62 Ultrastructurally, mitochondrial swelling occurs initially, followed by dis

63 sition pore, because IGF-I failed to inhibit mitochondrial swelling or depolarization.

64 oncentration of Bax, there was no detectable mitochondrial swelling or depolarization.

65 activation elicits cell protection (without mitochondrial swelling or durable memory) by inhibiting

66 potential was detected in vivo, although no mitochondrial swelling or loss of transmembrane potentia

67 Similarly, CsA failed to prevent mitochondrial swelling or PEG-induced shrinkage after sw

68 late kinase release, was not associated with mitochondrial swelling or substantial loss of electrical

69 drial permeability transition (mPT) leads to mitochondrial swelling, outer membrane rupture and the r

70 DZX resulted in significant mitochondrial swelling (P<0.0001 versus Tyrode).

71 to MI + DZX or CPG+DZX significantly reduced mitochondrial swelling (P<0.003 MI+DZX versus MI + DZX +

72 cated astrocytes exposed to t-bOOH exhibited mitochondrial swelling prior to cell death (lactate dehy

73 nm, and 2), permeability transition-related mitochondrial swelling results in breaching and disrupti

74 ory (preconditioning) results from triggered mitochondrial swelling that causes enhanced substrate ox

75 t but resembles mammalian apoptosis, causing mitochondrial swelling, transmembrane potential dissipat

76 of tetraphenylphosphonium, and by monitoring mitochondrial swelling, using light absorbance measureme

77 Mitochondrial swelling was observed by electron microsco

78 c release occurred with only a 20% change in mitochondrial swelling, was an early event in the PTP, a

79 Additional increases in mitochondrial swelling were seen when the astrocytes wer

80 to control cells, the probands' cells showed mitochondrial swelling, which was exacerbated upon treat

81 of Zn(2+) (with Ca(2+)) to cause pronounced mitochondrial swelling, which was far greater than that

82 Electron microscopy showed mitochondrial swelling with abnormalities in shapes and