Source:http://linkedlifedata.com/resource/pubmed/id/19870259
Switch to
| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
4
|
| pubmed:dateCreated |
2010-6-23
|
| pubmed:abstractText |
Under uniform diet conditions the normal bile fistula dog will eliminate pretty constant amounts of cholesterol-about 0.5 to 1.0 mg. cholesterol per kilo per 24 hours. Diets rich in cholesterol (egg yolk) will raise the cholesterol output in the bile but compared to the diet intake (1.5 gm. cholesterol) the output increase in the bile is trivial (5-15 mg.). Calves' brains in the diet are inert. Bile salt alone will raise the cholesterol output in the bile as much and often more than a cholesterol rich diet. Bile salt plus egg yolk plus whole bile give maximal output figures for bile cholesterol-60 mg. per 24 hours. Liver injury (chloroform) decreases both bile salt and cholesterol elimination in the bile. Blood destruction (hydrazine) fails to increase the bile cholesterol output and this eliminates the red cell stroma as an important contributing factor. Certain cholagogues (isatin and decholin) will increase the bile flow but cause no change in cholesterol elimination. The ratio of cholesterol to bile salt in the bile normally is about 1 to 100 but the bile salts are more labile in their fluctuations. The ratio is about reversed in the circulating blood plasma where the cholesterol is high (150-300 mg. per cent) and the bile salt concentration very low. Cholesterol runs so closely parallel to bile salt in the bile that one may feel confident of a physical relationship. In addition there is a suspicion that the bile cholesterol is in some obscure fashion linked with the physiological activity of hepatic epithelium.
|
| pubmed:commentsCorrections | |
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:status |
PubMed-not-MEDLINE
|
| pubmed:month |
Mar
|
| pubmed:issn |
0022-1007
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:day |
31
|
| pubmed:volume |
59
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
471-8
|
| pubmed:dateRevised |
2010-9-27
|
| pubmed:year |
1934
|
| pubmed:articleTitle |
STUDIES ON TYPHUS FEVER : XII. THE PASSIVE IMMUNIZATION OF GUINEA PIGS, INFECTED WITH EUROPEAN VIRUS, WITH SERUM OF A HORSE TREATED WITH KILLED RICKETTSIA OF THE MEXICAN TYPE.
|
| pubmed:affiliation |
Department of Bacteriology and Immunology, The Harvard Medical School, Boston.
|
| pubmed:publicationType |
Journal Article
|