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Viral inactivation is one of the possibilities to reduce the residual risk of blood products. It is now applied to all plasma derived products (PDP). Application of such techniques to labile blood products (LBP) is difficult for two main reasons: any method should inactivate cell-associated viruses and should avoid any injury of the cells constituting the active ingredient. Physical techniques may reduce the viral content of cellular BPL (leucodepletion, washing, gamma irradiation), but none of them is active enough to comply with the present requirements for efficacy. An important work has been dedicated to the development of virus photoinactivation techniques. They consist of the addition of a photoreagent followed by illumination at an appropriate wavelength which results in a photochemical reaction responsible for the viral inactivation. Treatment of platelet concentrates by psoralen derivatives and UV-A illumination significantly inactivate in vitro enveloped and naked viruses, free and cell-associated viruses and also sequences integrated in the viral genome. Recent progresses have led to these results without detectable functional alteration of platelets and mutagenicity. Viral inactivation of red blood cells yet did not reach the same level because hemoglobin does not allow the use of the photoreagent compounds applicable to platelet concentrates. Viral decontamination of fresh frozen plasma by solvent and detergent, active on enveloped viruses, has been used in France since 1992. Other techniques of comparable efficacy, have received an agreement in other countries. The research on viral inactivation of LBP could prove to be of great importance in the near future in bringing additional safety to patients not only for the residual viral risk but maybe also for the residual bacterial risk of LBP.

Skin fibroblasts were isolated from newborn spontaneously hypertensive rats (SHR) and Wistar-Kyoto normotensive rats (WKY) to study their cell growth and reactivity in culture. SHR fibroblasts exhibited an enhanced growth rate in presence of 10 per cent fetal calf serum and a marked increase in 3H thymidine incorporation compared to WKY cells, when confluent quiescent fibroblasts were stimulated by 2, 5, 10 or 15 per cent serum as well as by 10 ng/ml EGF. Inositol phosphate formation determined by exchange chromatography in presence of 20 mM LiC1, was stimulated by serum, 1 microM angiotensin II, I microM bradykinin and 0.1 microM vasopressin in both type of cells labelled with 3H myoinositol. Significantly higher levels were produced in SHR cells by angiotensin II, serum and bradykinin compared to WKY fibroblasts. No difference between the two cell groups was observed with vasopressin. The intracellular pH (pHi) of isolated SHR and WKY fibroblasts was measured in bicarbonate-free medium using the fluorescent dye BCECF. The identical pHi values (7.03 +/- 0.10, n = 5 and 7.04 +/- 0.07, n = 6 for WKY and SHR respectively agree with an absence of Na+/H+ antiport activation in unstimulated cells. This study allows to conclude that skin fibroblasts isolated from newborn SHR, similarly to vascular smooth muscle cells, exhibit an hyperresponsiveness to serum, EGF and angiotensin II. These results demonstrate the presence of an intrinsic cellular developing capacity.

The technical parameters of blood filtration through cotton Imugard IG 500 filters were evaluated. Sixty units of red cell concentrates were filtered. The mean value of the residual leukocytes indicated a leukocyte depletion greater than 98%, disregarding the unit age and the filtration temperature. The number of residual leukocytes was below 1 X 10(8) in 94% of the filtered units and less than 0.3 X 10(8) in 68%. The number of residual platelets was less than 1 X 10(10) in 92% of these units.

An accidental case of delayed haemolytic reaction due to an anti-D allo-immunization in a patient suffering from multiple traumatic injuries allows us to define a procedure of emergency treatment towards non iso-Rhesus transfusions and the problems posed by the detection of acquired allo-antibodies.

Studies concerning the influence of seasons and ultraviolet radiations on the metabolism of 1,25-dihydrocholecalciferol (1,25 (OH)2D), the active form of vitamin D, have given conflicting results. In the present study serum concentrations of the 3 main vitamin D metabolites--25-hydroxyvitamin D, 24,25-dihydroxyvitamin D and 1,25-dihydroxyvitamin D--were measured by radiocompetitive assay (a) monthly during one year in 7 normal subjects, and (b) before, during and after 4 weeks of "whole body" exposure to ultraviolet radiations in 11 other subjects. In study (a) parallel changes in 25-hydroxyvitamin D and 24,25-dihydroxyvitamin D concentrations were observed during the year, with a rise in the summer; there were no significant monthly or quarterly changes in 1,25-dihydroxyvitamin D concentrations. In study (b), 25-hydroxyvitamin D and 24,25-dihydroxyvitamin D concentrations rose by 150% and 200% respectively after 4 weeks' exposure to ultraviolet radiations and again, there were no significant changes in 1,25-dihydroxyvitamin D concentrations. These results confirm that when synthesis of the substrate (25-hydroxyvitamin D) increases, synthesis of 1,25-dihydroxyvitamin D is inhibited by a regulatory process which does not apply to 24,25-dihydroxyvitamin D synthesis.

Several studies have suggested that clonidine, guanfacine and rilmenidine decrease systemic blood pressure by stimulating central alpha 2-adrenergic receptors. However, we have shown that these molecules interact not only with alpha 2-adrenergic but also a new type of "non catecholamine" receptor in rabbit and human renal proximal tubules. This receptor, which we have called the imidazoline-guanidium receptor site (IGRS) seems to be pharmacologically, biochemically and fractionally distinct from alpha 2-adrenergic receptors. In order to determine the relative affinity of rilmenidine for these two types of receptor, we studied its capacity to inhibit the liaison of (H3)-idazoxan, a ligand with a high affinity for the IGRS, and of (H3)-rauwolscine, a ligand selective for alpha 2-adrenergic receptors in the rabbit kidney. The results based on the apparent constants of inhibition (Ki) of the two radioligands [231 +/- 34 nM for (H3)-idazoxan and 2440 +/- 322 nM for (H3)-rauwolscine] showed that the selectivity of rilmenidine was 10 times greater for IGRS than for alpha 2-adrenergic receptors. This preferential activity on IGRS was confirmed by studies of the influx of Na22 into isolated renal proximal tubule cells of the rabbit. They showed that rilmenidine, in contrast to catecholamines, inhibited the transport of Na22 into the renal cells. In conclusion, the data from our studies shows that rilmenidine interacts with renal IGRS and inhibits cellular transport of sodium by a mechanism other than the stimulation of alpha 2-adrenergic receptors.(ABSTRACT TRUNCATED AT 250 WORDS)

Frequent allergic reactions following transfusion are observed. Usually, they are benign but sometimes we observe severe allergic reactions. Adverse reactions may be brought about by least two mechanisms. First, immediate-type hypersensibility reactions due to IgE. Secondly, anaphylactic-type reactions due to interaction between transfused IgA and class specific anti IgA in the recipient's plasma. They are characterized by their severest form (anaphylactic shock). The frequency of severe reactions following the transfusion blood plasma is very low. These transfusion reactions are complement-mediated and kinins-mediated. Prevention of allergic reactions is necessary among blood donors and recipients.

1,25 dihydroxyvitamin D (1,25(OH)2 D) is the active metabolite of vitamin D and has an essential role in bony metabolism on the regulation of the calcium-phosphorus balance. The circulating level of 1,2(OH)2 D is normally between 25 and 45 pg/ml. Isolation of the fraction to be titrated requires sophisticated purification techniques using high performance chromatography (HPLC). In osteomalacia secondary to a deficiency the mean level of 1,25(OH)2 D is low (14.1 +/- 6.9 pg/ml) because of substratum deficiency. Administration of vitamin D supplements is quickly followed by a supraphysiological increase of the level of active metabolite. The role of the parathyroid hormone on the activity of 1-hydroxylase is illustrated by the results of the titration in parathyroid dysfunctions: decrease of the mean level in hypoparathyroidism (18 +/- 6.9 pg/ml), and on the contrary, a significant increase in hyperparathyroidism (56.6 +/- 15.4 pg/ml) despite of a spread of the individual values. In 18 cases of idiopathic hypercalciuria, we have only observed an increase of 1,25(OH)2 D level, in two cases. Titration of 1,25(OH)2 D complements the calcium-phosphorus evaluation to precise the physiopathogenic mechanism of the disorders observed in various diseases. Its interpretation requires the joint measurement of the substratum level, 25-hydroxyvitamin D, and the evaluation of the parathyroid function.