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J Müller

Publications and source records attributed to J Müller.

At least 847 records · Page 47Linked to original sources

[Metabolism of 15N-14C-acetylurea in the sheep].

3 male sheep (phi 48.3 kg) were fed a semisynthetic diet containing acetyl urea as sole protein source and 15N-14C labelled acetyl urea (urea-C labelled) by intraruminal tube. A half life period of 4 hrs was established for the removal of labelled acetyl urea from the TCE-soluble portion of the ruminal fluid. The degree of 14C labelling in ruminal proteins was very low whereas the extent of 15N labelled protein synthesis was quite marked reaching a maximum between the 18th and 24th hour of experiment. The steepest rise of 15N incorporation into ruminal proteins was found to occur between 8 to 12 hrs after start of the experiment, i.e. at the time of peak level of 15N returned from 15N urea via the rumino-hepatic circulation. 23.3% of the amount of 14C activity administered (mean of all 3 experimental animals) was excreted through respiration. The curve patterns of both isotopes in the TCE soluble portion of the ruminal fluid were similar to that of the degasified TCE soluble portion of the blood blasma. At the peak time (8 hrs) a concentration of the nitrogen isotope of about 4 atom% excess of 15N was observed. The level of 14C labeling in blood plasma proteins was insignificant when compared with that of 15N labelling. The ratio at the peak time was 1:10; the same ratio was found for ruminal proteins. From this it can be concluded that the process of labelling of blood plasma proteins proceeds mainly through microbial protein synthesis. Sheep I and III excreted an average of 60.6% of 14C activity and 57.0% of the administered excess of 15N in the urine. 6 hrs after the beginning of the experiment 81% of the amount of urinary 14C activity was found to occur as acetyl urea; after 48 hrs this amount had decreased to 50%. All experimental sheep excreted a urinary sediment consisting mainly of acetyl urea. The level of faecal 14C excretion (1.4%-2.9% of the amount administered) was considerably lower than that of 15N excretion (9.1%--15.6% of the administered dose). The TCE soluble fraction of the faeces contained up to 2% of the 14C dose and 3% of the 15N dose. The true digestibility data of 15N from 15N acetyl urea varied between 96.4% and 98.2%. An average of 40.9% was obtained for the 15N balance over the 7-day trial period.

Animals↗

Changes in blood hormone levels during the immune response.

Injection of three different antigens into rats or mice led in the course of several days to about a threefold increase in serum corticosterone levels and concommitantly to a decrease in thyroxine (rats). In view of the known immuno-suppressive effect of the glucocorticoids the possibility is considered that the endocrine changes induced during the immune response could significantly modulate the subsequent character of the immune response, e.i. magnitude, duration and lymphoid cell proliferation, however, a more complete pattern of hormonal variations and their cause needs to be established. These findings while admittedly preliminary, suffice to provide an indication of a temporal pattern of hormonal change during the immune response which could be important in immunoregulation.

Animals↗

[Free fatty acids and hydrocarbons in cerebrospinal fluid (author's transl)].

Initial experiments on the constant appearance of unesterified fatty acids and hydrocarbons in cereborspinal fluid are presented. With the present method of analysis, these two groups of substances can always be detected in cerebrospinal fluid. The constitution of the unesterified fatty acids as well as the hydrocarbons was determined using gaschromatography linked to mass spectrometry. There is no evidence that the unesterified fatty acids are derived from the blood, or that they are breakdown products of other lipid classes of the cerebrospinal fluid. The origin and significance of the hydrocarbons are not yet known, and remain the subject of further investigations.

Fatty Acids, Nonesterified↗

[Differential diagnostic difficulties in myoclonic-astatic petit mal status].

Myoclonic-astatic attack syndromes tend more than other attack forms to produce states. Their clinical picture can be various and therefore cause differential-diagnostic difficulties. On four own examples they are referred to. Most frequently it will be necessary to differentiate the hardly adjustable attack syndrome from on overdose of anticonvulsives. Also the state of absences, the state of psychomotoric attacks, and the impulsive-petit-mal state can make differential-diagnostic difficulties. Furthermore, additional encephalitic processes with cerebral decompensation in anyway injured children, and the myoclonic variants of familial amaurotic idiocy are to be to consider. An EEG examination is indispensable; consideration of the total situtation, observation of the course, and recording of the actual findings are necessary.

Anticonvulsants↗