crista

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crista

 [kris´tah] (pl. cris´tae) (L.)
cris´tae cu´tis dermal ridges.
crista gal´li a thick, triangular process projecting upward from the cribriform plate of the ethmoid bone.
Miller-Keane Encyclopedia and Dictionary of Medicine, Nursing, and Allied Health, Seventh Edition. © 2003 by Saunders, an imprint of Elsevier, Inc. All rights reserved.

CREST

(krest),
[TA] Acronym for calcinosis, Raynaud phenomenon, esophageal motility disorders, sclerodactyly, and telangiectasia. See: CREST syndrome.

crest

(krest), [TA]
1. A ridge, especially a bony ridge.
See also: crista.
2. The ridge of the neck of a male animal, especially of a stallion or bull.
3. Feathers on the top of a bird's head, or fin rays on the top of a fish's head.
Synonym(s): crista [TA]
[L. crista]
Farlex Partner Medical Dictionary © Farlex 2012

crista

(krĭs′tə)
n. pl. cris·tae (-tē)
1. Anatomy A crest or ridge, as on the top of a bone.
2. Biology One of the inward projections or folds of the inner membrane of a mitochondrion.
The American Heritage® Medical Dictionary Copyright © 2007, 2004 by Houghton Mifflin Company. Published by Houghton Mifflin Company. All rights reserved.

crest

(krest) [TA]
A ridge, especially a bony ridge.
Synonym(s): crista [TA] .
[L. crista]
Medical Dictionary for the Health Professions and Nursing © Farlex 2012

crista

A crest or ridge.
Collins Dictionary of Medicine © Robert M. Youngson 2004, 2005

crista

(pl. cristae) a fold in the inner membrane of a MITOCHONDRION enclosing a cisterna-like space inside the fold, on which the electron-transport reactions of AEROBIC RESPIRATION take place.
Collins Dictionary of Biology, 3rd ed. © W. G. Hale, V. A. Saunders, J. P. Margham 2005

crest

(krest) [TA]
A ridge, especially a bony ridge.
Synonym(s): crista [TA] .
[L. crista]
Medical Dictionary for the Dental Professions © Farlex 2012
References in periodicals archive ?
Schafer, "Supramolecular organization of protein complexes in the mitochondrial inner membrane," Biochimica et Biophysica Acta (BBA)--Molecular Cell Research, vol.
Mitochondria play a fundamental role in energy metabolism, apoptosis, and oxidative stress [67] in the myocardium, and the mitochondrial inner membrane maintains a transmembrane gradient of ions and integrity of the mitochondrion itself.
Xu et al., "The mitochondrial inner membrane GTPase, optic atrophy 1 (Opa1), restores mitochondrial morphology and promotes neuronal survival following excitotoxicity," Journal of Biological Chemistry, vol.
(8) Damage to mitochondrial membranes occurs in various diseases, mainly by oxidation, and this can result in loss of mitochondrial inner membrane potential and impairment in the ability of mitochondria to produce high-energy molecules.
This influx of protons results in collapse of the mitochondrial inner membrane potential ([PSI]m), uncoupling of oxidative phosphorylation, and rapid depletion of adenosine triphosphate (ATP) stores.
For mitochondrial [beta]-oxidation, long-chain FA are activated to their CoA esters by Acyl-CoA synthase in the cytosol and on the mitochondrial outer membrane; the mitochondrial inner membrane is impermeable to acyl-CoA esters.
The release of cytochrome c from the mitochondrial inner membrane, an event which is believed to be secondary to the onset of MPT (Zhang et al.
MDDSs cause a reduction in cellular mtDNA content (2).At the present time, mutations in at least 9 genes [POLG, [4] polymerase (DNA directed), gamma; DGUOK, deoxyguanosine kinase; TK2, thymidine kinase, mitochondrial; TYMP, thymidine phosphorylase; MPV17, MpV17 mitochondrial inner membrane protein; SUCLA2, succinate-CoA ligase, ADP-forming, beta subunit; SUCLG1, succinate-CoA ligase, alpha sub unit; RRM2B, ribonucleotide reductase M2 B (TP53 inducible); C10orf2, chromosome 10 open reading frame 2 (also known as TWINKLE)] have been found to cause mtDNA depletion (3-17).
CoQ10 supports ATP synthesis in the mitochondrial inner membrane and stabilizes cell membranes, thus preserving cellular integrity and function.
From there, the energy is transferred to the electron transport system associated with the mitochondrial inner membrane. Although several studies have suggested that propofol has a direct effect on oxidative phosphorylation, (2,21,22) it remains unclear whether propofol exerts this effect by uncoupling the mitochondrial electron flow (20) or by a protonophoric effect, increasing the proton influx across the inner mitochondrial membrane.
The complex is comprised of 4 subunits that are imported into the mitochondrion and as a complex is anchored to the mitochondrial inner membrane by the Fe-S center of one of its subunits.[3,4] Fe-S centers represent a common denominator in several respiratory-chain complexes; hence, defects in these centers can lead to decreased assembly and combined deficiency of several complexes.[3] Therefore, a deficiency of SDH together with deficiencies in other complexes is not uncommon among patients with respiratory-chain defects.[4] The first reported nuclear encoded gene mutation that caused a respiratory-chain defect was a point mutation in the gene encoding the [F.sub.p] subunit of SDH (MIM 255125).[5]
Of course, CO can suppress the activity of succinate dehydrogenase which combined with mitochondrial inner membrane to partly affect the results of OD in MTT assay.

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