[Bacterial endocarditis with lumbar spondilodiscitis: two new cases (author's transl)].
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Biomedical subjects
Publications and source records attributed to J Lucas.
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The ability of poliovirus virion RNA and double-stranded RNA (replicative form) to replicate in enucleate mouse L cells was investigated. Virion RNA replicated successfully in the absence of the cell nucleus, whereas replicative form infection did not produce any detectable progeny in enucleate cells. The results provide direct evidence of a nuclear requirement early in the infection initiated by replicative form RNA.
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The role of the kidney in hypertension is reviewed in terms of sodium and water homeostasis, of the secretion of renin inappropriate to the state of sodium and water balance and of other renal humoral factors which might be implicated in the hypertensive process. Fundamental to the long-term maintenance of hypertension is an alteration in the relationship between renal perfusion pressure and the excretion of sodium and water. This alteration may be brought about as a result of renal structural damage, sympathetically mediated renal vasoconstriction or the action of renal or extrarenal hormones which modulate sodium and water excretion. When renin is secreted in excess of the prevailing level of sodium and water balance, the generated angiotensin contributes to the hypertension directly through peripheral and renal vasoconstriction. The level of blood pressure in two hypertensive patients with chronic renal failure was found to be highly correlated with the level of plasma renin activity as this was lowered by the administration of a beta-blocking drug. In rats deprived of sodium, renal artery constriction and contralateral nephrectomy was followed by hypertension without any elevation of plasma angiotensin and with a minimal expansion of plasma volume unaccompanied by expansion of extracellular fluid volume. The possible role of this small volume change and of other possible factors in producing hypertension is discussed. Studies in the nephrectomised rat confirmed eariler reports that renal medullayr auto-explants inhibited renoprival hypertension, but neither the identity nor mode of action of the medullary hypotensive factor were further clarified.
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In view of the theory of autoregulation of cell multiplication in a growth organ, we attempted to inhibit renal tubular cell hyperplasia in the remaining kidney 48 hours after controlateral nephrectomy. To do this we drew up a method of measurement of hyperplasia by measuring the rate of uptake of tritiated thymidine in the organ undergoing compensatory growth. We then injected renal cytosol. Whereas the rate of uptake of tritiated thymidine doubles in the growing kidney compared with control animals, the intravenous administration of renal cytosol reduces the renal uptake of the tracer to its basal level. We correlated this observation with the microscopic count of mitotic figures, and noted the existence of parallel fluctuations. Our results seem to support the initial working hypothesis but they do not exclude the possibility of a more complex regulatory mechanism in which serum stimulant factors may also play a role.
In order to demonstrate in the uninephrectomised rat possible circulating serum factors which might induce an increase in the rate of synthesis of DNA in the remaining kidney, we injected intravenously to 125 g rats serum from similar rats uninephrectomised 24 to 48 hours previously. The injections preceded the administration of tritiated thymidine by 13 hours (1.5 ml), 5 hours (1 ml), or 2 hours (1 ml) depending on each group. The parameter studied was the radioactivity of the acid-insoluble fraction of 100 mg of kidney. We observed in uninephrectomised animals receiving no injection of serum that the rate of uptake of the tracer in the remaining kidney doubles 48 hours after nephrectomy but this uptake by the kidneys of unoperated rats is not modified by the injection of serum from similar rats whether uninephrectomised or not. Furthermore the addition of serum from uninephrectomised rats to slices of normal kidney under incubation does not modify the rate of synthesis of DNA. All these results are not in favour of a serum factor regulating compensatory renal hypertrophy.
DNA synthesis by the kidneys was studied in young rats by incorporation of tritiated thymidine. Peak of DNA synthesis was observed as soon as 24 hr after uninephrectomy. No significative difference was observed between control rats and those receiving various doses of serum obtained from uninephrectomized or sham operated rats. Serum of uninephrectomized rats did not increase DNA synthesis in kidney slices in vitro.
Clear supernatant from kidney homogenate injected to an uninephrectomized rat inhibits specifically the incorporation of tritiated thymidine by compensating kidney. This result agrees with the speculation of autoregulation of kidney growth.
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