Biosynthesis of the cytochalasans. Part III. C-NMR. of cytochalasin B (phomin) and cytochalasin D. Incorporation of [1-13C]- and [2-13C]-sodium acetate.
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Acetates↗
Biomedical subjects
J L Robert
Publications and source records attributed to J L Robert.
[Cicatrization of wounds of the oral mucosa].
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Cicatrix↗
[Preparation for interventions].
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Humans↗
[Lateral diverticula of the pharynx (author's tranl)].
The authors describe two clear-cut cases of hypopharyngeal lateral diverticulum. They have found only 22 published cases. They discuss the nosological limits of the physiological pharyngeal expansions visible under high pressure pharyngography, those of kinetic pharyngoceles which are often forced hernias, finally, the very real but uncommon presence of true lateral diverticula. The passage of barium Therapeutic indications are discussed. The surgical technique is simple.
Adolescent↗
[Postphlebitic disease, stasis microangiopathy].
The terminology of this is incorrect, but hallowed by usage; it is an old thrombosis of the deep veins, and therefore part of the venous zone; it terminates distally in the zone of the terminal circulatory units, that is, at a microangiopathy of interstitial and lymphatic venous stasis, and the interstitium is involved. There is a polyangiopathy, all the vascular systems being involved, and there is a panangiopathy, every coat of the wall being damaged. The hydraulics of the blood, tissular liquids and lymph are progressively and permanently thrown into disorder; losses of head, pressure surges, choking and failure of the pumps, obliteration of the valvular canal all follow one another and tractage occurs. Microangiopathies of stasis are not only situated in the skin, the aponevrotic spaces and the vascular walls, but are situated also in the distribution "networks" which affect the flow-conditions and the interstitial restraint from which the treatment indications derive.
Blood Viscosity↗
The mechanisms of venous stasis in post-phlebitic syndromes.
Venous stasis in post-phlebitic syndromes may be caused by several physiopathological processes. Phlebography and functional investigations (Doppler, occlusive rheoplethysmography) enables us to make a fairly precise analysis of the causal factors: --The obstruction of a large venous collector defines the obstructive syndromes. The size of the stasis depends on the functional value of the substitutional channels; distinction may be made between compensated obstructive syndromes (with efficient substitutional circulation) and poorly or non-compensated obstructive syndromes. --Orthostatic reflux in devalvulated deep veins constitutes another factor of stasis. Distinction to be made between minor reflux, and major reflux with massive reflux in the great trunks and associated insufficiency of the tibial communicators. --Post-phlebitic superficial venous insufficiency is often observed. Its physiopathology is basically no different to that of primary varices, the functioning of the tibial communicators is often perturbed. --The restrictive syndrome, result of functional investigations, corresponds to a reduction of the venous distensibility whose effects are superadded to those of the syndromes described above.
Blood Flow Velocity↗