Phospholipid content of human and guinea pig muscle: Post-mortem changes and variations with muscle composition

Lipids ◽  
1970 ◽  
Vol 5 (5) ◽  
pp. 485-487 ◽  
Author(s):  
Hildegard Hof ◽  
R. Gerald Simon
Keyword(s):  
Guinea Pig ◽  
Phospholipid Content ◽  
Post Mortem ◽  
Muscle Composition ◽  
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 Passive Anaphylaxis following the immediate injection of Antigen after Antiserum

1936 ◽  
Vol 36 (4) ◽  
pp. 570-587 ◽  
Author(s):  
H. R. Dean ◽  
R. Williamson ◽  
G. L. Taylor
Keyword(s):  
Guinea Pig ◽  
Intravenous Injection ◽  
Anaphylactic Shock ◽  
The Body ◽  
Post Mortem ◽  
Abdominal Symptoms ◽  
Respiratory Embarrassment

1. Our experiments show that an intravenous injection of antigen immediately after an intravenous injection of antiserum in the guinea-pig were followed by:(a) Acute shock and death within 5 min. The signs and post-mortem appearances were indistinguishable from acute anaphylactic shock as typically seen in the guinea-pig. Some control animals injected with antiserum only died in a way similar to those which received both antiserum and antigen. These are discussed in detail in the body of the paper.(b) Delayed shock and death some hours later. The post-mortem appearances were those of gastro-intestinal congestion and haemorrhage resembling the changes seen in dogs dying of anaphylactic shock. Such changes were never seen in the control animals.(c) Recovery. Practically all the animals which recovered had symptoms of respiratory embarrassment immediately following the injections of anti-serum and antigen and many had later symptoms of abdominal shock. The animals which were given an injection of antiserum only rarely had any symptoms and never abdominal symptoms.2. It is necessary to test the antisera used by control inoculation since some antisera are toxic.

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

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

scholarly journals Phospholipid synthesis in HeLa cells exposed to immunoglobulin G and complement

1972 ◽  
Vol 128 (4) ◽  
pp. 953-960 ◽  
Author(s):  
Flemming Güttler
Keyword(s):  
Guinea Pig ◽  
Hela Cells ◽  
Immunoglobulin G ◽  
Phospholipid Content ◽  
Phospholipid Synthesis ◽  
Twofold Increase ◽  
And Function ◽  
Phosphate Incorporation ◽  
Pig Serum ◽  
Stimulation Of

1. HeLa cells were cultured in the presence of heterologous immunoglobulin G and guinea-pig serum together with [32P]phosphate. 2. Incorporation of [32P]phosphate was significantly stimulated by anti-HeLa immunoglobulin G and complement-sufficient serum compared with immunoglobulin G from unimmunized rabbits and complement. Within 2.5h heat-inactivated guinea-pig serum and anti-HeLa immunoglobulin G stimulated [32P]phosphate incorporation to the same extent as heat-inactivated complement and immunoglobulin G from unimmunized rabbits. 3. Compared with cells exposed to immunoglobulin G from unimmunized rabbits together with complement, anti-HeLa immunoglobulin G with complement increased the phospholipid content of HeLa cells twofold within 5h of incubation. 4. Exposure of HeLa cells to anti-HeLa immunoglobulin G and complement for 5–22h resulted in a twofold increase in the net accumulation of [32P]phosphate in sphingomyelin and phosphatidylcholine and a 50% increase in the net accumulation of [32P]phosphate in phosphatidylethanolamine, compared with cultures exposed to immunoglobulin G from unimmunized rabbits and complement. 5. A transient accumulation of 32P-labelled lysophosphoglycerides in HeLa cells exposed to antibody and complement was detected, confirming previous findings (Güttler & Clausen, 1969b). 6. The stimulation of [32P]phosphate turnover occurred in cells filling up their cytoplasma with vacuoles. This supports the suggestion that the accumulation of phospholipid in these cells may be concerned with the synthesis and function of cytomembranes.

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.

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