Mitochondrial changes in the guinea-pig muscle after envenomation withVespa orientalis venom

1971 ◽  
Vol 27 (3) ◽  
pp. 303-304 ◽  
Author(s):  
U. Sandbank ◽  
J. Ishay ◽  
S. Gitter
Keyword(s):  
Guinea Pig ◽  
Pig Muscle

Adenosine triphosphate concentration in guinea pig muscle after denervation

1957 ◽  
Vol 13 (3) ◽  
pp. 117-118 ◽  
Author(s):  
L. Michelazzi ◽  
M. A. Mor ◽  
M. U. Dianzani
Keyword(s):  
Guinea Pig ◽  
Adenosine Triphosphate ◽  
Pig Muscle

scholarly journals Interstitial fluid from guinea-pig muscle

1962 ◽  
Vol 162 (1) ◽  
pp. 44-53 ◽  
Author(s):  
R. Creese ◽  
J. L. D'Silva ◽  
D. M. Shaw
Keyword(s):  
Guinea Pig ◽  
Interstitial Fluid ◽  
Pig Muscle

The fine structure of the guinea-pig muscle spindle

1973 ◽  
Vol 140 (3) ◽  
pp. 357-368 ◽  
Author(s):  
R. W. Banks ◽  
N. T. James
Keyword(s):  
Fine Structure ◽  
Guinea Pig ◽  
Muscle Spindle ◽  
Pig Muscle

RICKETS AND OSTEOPOROSIS IN XENOPUS LAEVIS

1950 ◽  
Vol 7 (1) ◽  
pp. 64-81 ◽  
Author(s):  
H. M. BRUCE ◽  
A. S. PARKES
Keyword(s):  
Vitamin D ◽  
Bone Formation ◽  
Guinea Pig ◽  
Xenopus Laevis ◽  
Calcium Deficiency ◽  
Cod Liver Oil ◽  
Normal Bone ◽  
Horse Liver ◽  
Different Types ◽  
Pig Muscle

Gross deformities appeared in Xenopus laevis maintained for about 2 yr. under laboratory conditions on a diet containing no live food. Radiographs of the affected animals revealed defective calcification of the skeleton. All animals bred in the colony were defective, and only the original adults taken from the wild had normal bones. A description of the different types of skeleton found, and later produced experimentally, is given. An analysis of the conditions under which the defects became manifest showed X. laevis to be very susceptible to lack of vitamin D. Calcification in this species is greatly affected by the nature of the basal food. Normal bones are formed when the toads are fed on a diet of rabbit liver (or ox liver) supplemented with cod-liver oil and calcium. Horse liver is toxic, causing a depression of growth and a failure of calcification even with the supplements. With guinea-pig muscle a far larger supplement of vitamin D is required to prevent the development of general calcium deficiency and to permit normal bone formation. The failure of calcification is identified as rickets with osteoporosis and its relation to these diseases in other species is discussed.

HISTOCHEMISTRY AND CYTOCHEMISTRY OF EXPERIMENTALLY DENERVATED GUINEA PIG MUSCLE. I.

1965 ◽  
Vol 60 (1) ◽  
pp. 39-65 ◽  
Author(s):  
Leon A.H. Hogenhuis ◽  
W. King Engel
Keyword(s):  
Guinea Pig ◽  
Pig Muscle

scholarly journals Studies on synthesis and degradation rates and some molecular properties of guinea-pig muscle acylphosphatase

1984 ◽  
Vol 217 (2) ◽  
pp. 499-505 ◽  
Author(s):  
G Liguri ◽  
P Nassi ◽  
G Camici ◽  
G Manao ◽  
G Cappugi ◽  
...  
Keyword(s):  
Guinea Pig ◽  
Group Analysis ◽  
Exchange Chromatography ◽  
Molecular Forms ◽  
Stoichiometric Ratio ◽  
Main Form ◽  
Purification Technique ◽  
Degradation Rates ◽  
Pig Muscle ◽  
Synthesis And Degradation

Acylphosphatase (acylphosphate phosphohydrolase, EC 3.6.1.7) was purified from guinea-pig muscle by a procedure involving immuno-affinity chromatography and a subsequent ion-exchange chromatography. This purification technique gave an overall yield of about 60% and permitted the isolation of three molecular forms with acylphosphatase activity, with a distribution greatly resembling those found in horse and turkey muscle. The main form appears to be very similar to the corresponding form in horse and turkey muscle, as indicated by amino acid composition, end-group analysis, the presence of glutathione as a mixed disulphide in almost the same stoichiometric ratio and kinetic analysis. From turnover data, the main form of acylphosphatase in guinea-pig muscle exhibits a degradation constant of 0.10 day-1, corresponding to a half-life of 6.8 days. These values are very close to those found for muscle total soluble proteins.

scholarly journals Telomerase inhibition causes premature senescence of fetal guinea pig muscle cells

2020 ◽  
Author(s):  
Stephanie E. Hallows ◽  
Timothy R.H. Regnault ◽  
Dean H. Betts
Keyword(s):  
Oxidative Stress ◽  
Guinea Pig ◽  
Muscle Cells ◽  
Telomerase Activity ◽  
In Utero ◽  
Premature Senescence ◽  
Telomerase Inhibition ◽  
Pig Muscle ◽  
Cells Cultured ◽  
Oxygen Concentrations

AbstractPremature senescence in low birth weight rodents is associated with later life metabolic disease, including the development of insulin resistance. Telomerase, a reverse transcriptase enzyme with telomeric and non-telomeric functions, is present at high levels during development to maintain and repair long telomere lengths and to protect cells from oxidative stress-induced growth arrest. Adverse In utero environments are often associated with increased reactive oxygen species (ROS), and ROS have been documented to impair/alter telomerase function. We postulate that telomerase protects cells against oxidative stress-induced damage, and its inhibition could lead to premature senescence. A primary cell line of fetal guinea pig muscle cells was differentiated under high (20%) and low (1-2%) oxygen concentrations and telomerase activity was pharmacologically inhibited using a synthetic tea catechin. Following 48 hours, ROS detection was conducted with MitoSOX, Mitotracker and 6-carboxy-2’,7’-dichlorodihydrofluorescein diacetate staining. Cells cultured at 20% O2 and treated with a telomerase activity inhibitor displayed reduced cell growth rates and increased levels of senescence markers, including p21 and p53. Telomeric DNA damage, measured by phosphorylated-γH2A.X staining at telomeres, was significantly increased in cells cultured at all oxygen concentrations with telomerase inhibition. Telomerase inhibition altered metabolic signaling (e.g. mTOR, p66Shc) and increased mitochondrial ROS levels. Telomerase may protect cells during development from adverse in utero environments that cause premature senescence.

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