EXPERIMENTAL RICKETS IN RATS Sherman, H. C.; Pappenheimer, A. M.
The Journal of experimental medicine,
08/1921, Letnik:
34, Številka:
2
Journal Article
Recenzirano
Odprti dostop
1. A simple diet is presented which regularly induced rickets in young rats.
2. The substitution of 0.4 per cent secondary potassium phosphate for a small part of calcium lactate in this diet ...completely inhibited the development of rickets.
3. Quantitative determinations of calcium in the bodies of parallel rats showed a marked increase of calcium content in the rats receiving the added phosphate over those which developed rickets.
4. While it is thus shown by x-rays and by histological examinations and by quantitative chemical analysis that added potassium phosphate increased the assimilation and normal deposition of calcium, it may be the quantitative relationship between the inorganic ions rather than actual deficiency of any one of them which was here the determining factor in the cause or prevention of rickets. Our experiments and conclusions do not exclude the possibility of other causes of rickets than those here discussed.
1. Inoculation of suspensions of brain, cord, ganglia or nerves of chickens with neurolymphomatous lesions, into newly hatched chicks, is followed by the development of typical lesions in ...approximately 25 per cent of cases. 2. In control chickens kept under laboratory conditions the incidence of the disease is about 7 per cent. 3. The disease does not become manifest until at least 2 months after inoculation; symptoms may not appear until after 4 months. 4. The active agent is not destroyed by 50 per cent glycerol in 9 days at ice box temperature.
Summary
The molecular weight of the type-specific M-protein isolated from group A hemolytic streptococcus is 41,000. The molecule is an extremely elongated one with an axial ratio close to 25 to 1. ...As expected from the large axial ratio, solutions of M-protein show high viscosity.
1. Fowl paralysis (neurolymphomatosis gallinarum) is a disease entity, with characteristic clinical and pathological features.
2. The disease occurs in all parts of the United States, Holland, ...Austria and probably South America.
3. The disease appears to be endemic in certain foci. Having once appeared, the disease tends to persist through successive years.
4. It occurs with about equal frequency in both sexes; all common breeds may be affected.
5. Symptoms appear between the 3rd and 18th months. Typical clinical cases have not been observed outside of these limits.
6. The conspicuous symptoms are (a) asymmetrical, partial and progressive paralysis of the wings and both legs, and rarely of neck muscles; (b) occasional grey discoloration of iris, with blindness. Nutrition is usually preserved.
7. The duration is variable; the outcome is usually fatal, but spontaneous recovery may rarely occur.
8. The principal pathological changes are found in the nervous system. In the peripheral nerves, the essential feature is an intense infiltration of lymphoid, plasma cells, and large mononuclears. This is accompanied by a myelin degeneration in the more advanced lesions, but the cellular infiltrations appear to precede the degenerative changes. In brain, cord and meninges, there are similar infiltrations predominantly perivascular.
Infiltrations of the iris with lymphoid and plasma cells are found in the cases showing gross discoloration of the iris.
Visceral lymphomata, originating usually in the ovary, are associated in a certain percentage of the cases. Evidence is presented in favor of the view that this association is not accidental, and that the lymphomata are a manifestation of the disease.
9. Infiltrations of the spinal cord and brain, rarely of the peripheral nerves, are frequently present in birds showing no clinical symptoms. These are interpreted as mild cases of the same disease.
10. No microorganisms of etiological significance have been demonstrated in the tissues or by cultural methods.
1. Inoculation of suspensions of brain, cord, ganglia or nerves of chickens with neurolymphomatous lesions, into newly hatched chicks, is followed by the development of typical lesions in ...approximately 25 per cent of cases.
2. In control chickens kept under laboratory conditions the incidence of the disease is about 7 per cent.
3. The disease does not become manifest until at least 2 months after inoculation; symptoms may not appear until after 4 months.
4. The active agent is not destroyed by 50 per cent glycerol in 9 days at ice box temperature.
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