[Indications and results of intrahypophyseal implantation of radioactive isotopes in cases of diabetic retinopathy].
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Biomedical subjects
Publications and source records attributed to P Guillot.
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Ten 5-6 year-old unshorn ewes were dipped in a 0.025% lindane solution. Lindane residues in fat and plasma were analysed by gas liquid chromatography with an electron capture detector. The sensitivity of the method was 0.02 microgram/g for fat and 0.005 microgram/ml for plasma. Blood samples of 5 sheep were collected up to 84 days. The highest concentration of lindane detected in plasma was 107 +/- 37 ng/ml, 48 h after treatment. The disposition of lindane in plasma was studied by linear regression. Omental fat samples were removed by biopsies at 7 or 14 day intervals for 154 days. Fat concentrations of lindane were very high, respectively 30.46 +/- 14.6 ug/g, 8.09 +/- 4.57 micrograms/g, and 1.72 +/- 0.81 micrograms/g, 7, 28 and 70 days after dipping. In plasma and fat, the coefficients of elimination calculated by linear regression were similar (0.00190 +/- 0.00053 h-1 for plasma, 0.00196 +/- 0.00031 h-1 for fat). The tolerance recommended in France (2 micrograms/g in fat) was obtained 59.7 +/- 9.7 days after this treatment.
A commercial formulation of chloramphenicol and oxytetracycline was administered to dairy cows and bullocks by the intramuscular route. Concentrations of drugs were determined in milk and edible tissues by high-performance liquid chromatographic and microbiological methods. The data allowed the calculation of withdrawal times for milk (4 and 17 milkings for chloramphenicol and oxytetracycline, respectively) and for tissues (35 days for chloramphenicol, more than 35 days for oxytetracycline, depending on the levels at the injection sites). Hence oxytetracycline residues were the most persistent in these types of foods, according to our dosage scheme.
The Th1/Th2 paradigm has stimulated extensive research into the mechanisms underlying T-cell polarization; alternative activation of antigen-presenting cells (APCs) has turned out to be the corresponding concept APC polarization. Macrophages (M phi) as well as dendritic cells (DCs) can undergo Th1- or Th2-like polarization; APC1 and APC2 thus acquire the capacity to drive the development of naive T cells and the reactivation of resting T cells towards either a Th1 or a Th2 phenotype, respectively. Among polarized APC, effector macrophages are classically activated by mediators such as IFN-gamma, TNF-alpha or LPS (M phi 1), while M phi 2 are alternatively activated by IL-4, IL-10 or PGE(2). M phi 2 exhibit a unique molecular repertoire including receptors of innate immunity with broad specificity for foreign antigen and anti-inflammatory cytokines such as IL-1 receptor antagonist and alternative macrophage activation-associated CC-chemokine (AMAC)-1. While DC1 are well characterized, contradictory results have been obtained for DC2 that may either represent immature myeloid DCs or lymphoid DCs. Altogether, APC2 have come to age; they mediate Th2 differentiation, tolerance induction, downregulation of inflammation and healing. Thus, APC2 represent a hitherto neglected, but indispensable major pathway of APC activation and function.
A liquid chromatographic method has been developed for the measurement of chloramphenicol (CAP) in muscle, liver, and kidney. The mean recovery levels were 82.6, 75.3, and 79.2% in muscle, liver, and kidney, respectively. The method was repeatable and reproducible for CAP measurement in muscle, with a detection limit of 1 microgram/kg. Investigation of CAP stability in muscle, liver, and kidney showed that CAP stability in muscle was good at -20 degrees C; for spiked liver and kidney, degradation of CAP was observed, and the use of piperonyl butoxide (PB) for metabolism inhibition was recommended for recovery and linearity studies. However, PB was unnecessary for preservation of treated animal tissues if samples were cut into cubes and cooled at -20 degrees C, just after slaughter, pending analysis. With these limitations, CAP can be measured in liver and kidney.
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Concepts regarding the nosology, pathophysiology and pathogenesis of reflex sympathetic dystrophy syndrome are currently in a state of flux. Causalgia and reflex sympathetic dystrophy syndrome are now generally felt to be on the same continuum and as a result interest for defining criteria for the latter condition has waned. The pathogenic role of adrenergic sympathetic activity has been so successfully challenged that the last international consensus conference judged inappropriate any reference to the sympathetic system in the terms used to designate these conditions, thus confirming the position long defended by most French authors. The vasomotor abnormalities may be due to antidromic release of neuromediators by the endings of polymodal C fibers. These fibers do not belong to the sympathetic system but often travel with sympathetic nerves, a characteristic that may explain the efficacy of sympathetic nerve blocks, although other possibilities exist including a placebo effect. Also, efferent sympathetic fibers may undergo activation by nonadrenergic mediators. The mechanisms capable of initiating and perseverating activation of polymodal C afferents are being actively investigated and have been found to exhibit similarities with the mechanisms underlying peripheral and central sensitization of pain-producing afferents. Growth factors, such as nerve growth factor, may play an important role in causalgia. In "reflex sympathetic dystrophy syndrome", microcirculatory stasis may contribute to the initiation or perpetuatation of the disorders. Further work on the nerve supply to the venular network and on the venoarterial reflex is needed.