The Myelin-DeficientRat Mutant: Partial Recovery of Oligodendrocyte Maturation in vitro

1990 ◽  
Vol 12 (4-5) ◽  
pp. 326-339 ◽  
Author(s):  
A. Espinosa de los Monteros ◽  
M. Zhang ◽  
M.N. Gordon ◽  
S. Kumar ◽  
S.A. Scully ◽  
...  
Keyword(s):  
Partial Recovery ◽  
Maturation In Vitro ◽  
Myelin Deficient

Abnormalities in Oligodendrocyte Subpopulations in the md Rat Partial Recovery of Maturation in Vitro

1990 ◽  
Vol 605 (1 Myelination a) ◽  
pp. 386-387
Author(s):  
A. ESPINOSA DE LOS MONTEROS ◽  
M. ZHANG ◽  
M. N. GORDON ◽  
S. KUMAR ◽  
S. SCULLY ◽  
...  
Keyword(s):  
Partial Recovery ◽  
Maturation In Vitro

scholarly journals Glycine ameliorates mitochondrial dysfunction caused by ABT-199 in porcine oocytes

2021 ◽  
Author(s):  
Sicong Yu ◽  
Lepeng Gao ◽  
Yang Song ◽  
Xin Ma ◽  
Shuang Liang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Dysfunction ◽  
Oocyte Maturation ◽  
Mitochondrial Function ◽  
Protective Action ◽  
Damage Model ◽  
Developmental Competence ◽  
Free Calcium ◽  
Maturation In Vitro

Abstract Mitochondria play an important role in controlling oocyte developmental competence. Our previous studies showed that glycine can regulate mitochondrial function and improve oocyte maturation in vitro. However, the mechanisms by which glycine affects mitochondrial function during oocyte maturation in vitro have not been fully investigated. In this study, we induced a mitochondrial damage model in oocytes with the Bcl-2-specific antagonist ABT-199. We investigated whether glycine could reverse the mitochondrial dysfunction induced by ABT-199 exposure and whether it is related to calcium regulation. Our results showed that ABT-199 inhibited cumulus expansion, decreased the oocyte maturation rate and the intracellular glutathione (GSH) level, caused mitochondrial dysfunction, induced oxidative stress, which was confirmed by decreased mitochondrial membrane potential (Δ⍦m) and the expression of mitochondrial function-related genes (PGC-1α), and increased reactive oxygen species (ROS) levels and the expression of apoptosis-associated genes (Bax, caspase-3, CytC). More importantly, ABT-199-treated oocytes showed an increase in the intracellular free calcium concentration ([Ca 2+]i) and had impaired cortical type 1 inositol 1,4,5-trisphosphate receptors (IP3R1) distribution. Nevertheless, treatment with glycine significantly ameliorated mitochondrial dysfunction, oxidative stress and apoptosis, glycine also regulated [Ca 2+]i levels and IP3R1 cellular distribution, which further protects oocyte maturation in ABT-199-induced porcine oocytes. Taken together, our results indicate that glycine has a protective action against ABT-199-induced mitochondrial dysfunction in porcine oocytes.

scholarly journals Chronological Changes of Bovine Follicular Oocyte Maturation in Vitro

1986 ◽  
Vol 27 (4) ◽  
pp. 505-519 ◽  
Author(s):  
K. P. Xu ◽  
T. Greve ◽  
S. Smith ◽  
P. Hyttel
Keyword(s):  
Oocyte Maturation ◽  
Maturation In Vitro

Weightlessness affects cytoskeleton of rat utricular hair cells during maturation in vitro

Neuroreport ◽  
2002 ◽  
Vol 13 (16) ◽  
pp. 2139-2142 ◽  
Author(s):  
Sophie Gaboyard ◽  
Marie-Pierre Blanchard ◽  
C??cile Travo ◽  
Michel Viso ◽  
Alain Sans ◽  
...  
Keyword(s):  
Hair Cells ◽  
Maturation In Vitro

Drug activity against Onchocerca gutturosa males in vitro: a model for chemotherapeutic research on onchocerciasis

1987 ◽  
Vol 61 (4) ◽  
pp. 271-281 ◽  
Author(s):  
Simon Townson ◽  
C. Connelly ◽  
A. Dobinson ◽  
R. Muller
Keyword(s):  
Culture System ◽  
Serum Proteins ◽  
Good Condition ◽  
Calf Serum ◽  
New Drugs ◽  
Foetal Calf Serum ◽  
Partial Recovery ◽  
Feeder Cells ◽  
Compound Identification

ABSTRACTAn in vitro system for chemotherapeutic research using adult male Onchocerca gutturosa has been developed as a model for O. volvulus. Using a culture system consisting of medium MEM+10% heat inactivated foetal calf serum (IFCS)+LLCMK2 (monkey kidney) feeder cells in an atmosphere of 5% CO2 in air, we examined the effects of a range of antiparasitic drugs on worm motility. Ivermectin, levamisole, furapyrimidone, Mel W, chloroquine, metrifonate, flubendazole, amoscanate and the Ciba-Geigy compounds CGP 6140, CGP 20′376 and CGI 17658 either immobilized or significantly reduced motility levels at a concentration of 5x10−5M or less within a 7-day period. Worms were affected at very low concentrations by ivermectin (effective conc. to reduce motility levels to 50% of controls, 3.14x10−8M), levamisole (7.95x10−8M), CGP 6140 (8.87x10−9M) and CGP 20′376 (2.78x10−8M). Difficulties were experienced in accurately repeating the immotile endpoint for levamisole due to an inconsistent partial recovery of motility. Over a 7-day period diethylcarbamazine had little effect on motility levels, while suramin caused a slight increase in activity compared to controls at some timepoints. Subsequent experiments demonstrated some differences in drug efficacy depending on the presence or absence of serum and feeder cells in the culture system probably because of drug avidly binding to serum proteins. However, serum and cells were found to be essential ingredients of the culture system to maintain worms in good condition, indicating that new drugs should be evaluated both in the presence and absence of serum and cells. Comparisons were made between the responses of O. gutturosa and Brugia pahangi to certain drugs and these species were found to significantly differ in their sensitivities to ivermectin and a novel compound (Wellcome), indicating that Onchocerca parasites should be used wherever possible for compound identification and development intended for the treatment of onchocerciasis. The in vitro system described here, using male O. gutturosa, provides a basis for further research and a practical alternative to O. volvulus.

Intrinsic Myelin Proteins Are Normally Synthesized in vitro in the Myelin-Deficient (mld)Mutant Mouse

1983 ◽  
Vol 6 (4-5) ◽  
pp. 246-250 ◽  
Author(s):  
Jean-Marie Matthieu ◽  
Guillermina Almazan ◽  
Thomas V. Waehneldt
Keyword(s):  
Mutant Mouse ◽  
Myelin Proteins ◽  
Myelin Deficient
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