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Resume Le Groupe de pediatrie generale, membre de la Societe francaise de pediatrie, propose des recommandations en direction des familles et des medecins sur l’utilisation des ecrans par les enfants. Plusieurs recommandations ont ete publiees en particulier par l’Academie des Sciences en 2013 et l’Academie Americaine de pediatrie en 2016. Une enquete a precede ces nouvelles recommandations, portant sur l’etat des lieux des consommations d’ecrans par les jeunes enfants en France, le recensement des inquietudes medicales face a leur mesusage, mais aussi de leurs benefices documentes. Le Conseil superieur de l’audiovisuel et l’Union nationale des associations familiales ont ete associes a la redaction. Cinq messages simples sont proposes : comprendre sans diaboliser ; des ecrans dans les espaces de vie collective mais pas dans les chambres ; des temps sans aucun ecran (matin, repas, sommeil, etc.) ; oser et accompagner la parentalite pour les ecrans ; prevenir l’isolement social.

The Groupe de Pediatrie Generale (General Pediatrics Group), a member of the Societe francaise de pediatrie (French Pediatrics Society), has proposed guidelines for families and doctors regarding children's use of digital screens. A number of guidelines have already been published, in particular by the French Academy of Sciences in 2013 and the American Academy of Pediatrics in 2016. These new guidelines were preceded by an investigation into the location of digital screen use by young children in France, a survey of medical concerns on the misuse of digital devices, and a review of their documented benefits. The Conseil Superieur de l'Audiovisuel (Higher Council on Audiovisual Technology) and the Union Nationale de Associations Familiales (National Union of Family Associations) have taken part in the preparation of this document. Five simple messages are proposed: understanding without demonizing; screen use in common living areas, but not in bedrooms; preserve time with no digital devices (morning, meals, sleep, etc.); provide parental guidance for screen use; and prevent social isolation.

International audience; Chloride (Cl-) conductances were studied in primary cultures of the bright part of rabbit distal convoluted tubule (DCTb) by the whole cell patch clamp technique. The bath solution (33 degrees C) contained (in mM): 140 NaCl, 1 CaCl2, 10 N-2-hydroxy-ethylpiperazine-N'-2-ethanesulfonic acid (HEPES), pH 7.4 and the pipette solution 140 N-methyl-D-glucamine (NMDG)-Cl, 5 MgATP, 1 ethylene-glycol-bis(b-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA), 10 HEPES, pH 7.4. We identified a Cl- current activated by 10(-5) M forskolin, 10(-3) M 8-bromo adenosine 3',5'-cyclic monophophosphate (8 Br-cAMP), 10(-6) M phorbol 12-myristate 13-acetate (PMA), 10(-3) M intracellular adenosine 3',5'-cyclic monophophosphate (cAMP) and 10(-7) M calcitonin. The current-voltage relationship was linear and the relative ion selectivity was Br- > Cl- > > I- > glutamate. This current was inhibited by 10(-3) M diphenylamine-2-carboxylate (DPC) and 10(-4) M 5-nitro-2-(3-phenylpropylamino)-benzoate (NPPB) and was insensitive to 10(-3) M 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS). These characteristics are similar to those described for the cystic fibrosis transmembrane conductance regulator (CFTR) Cl- conductance. In a few cases, forskolin and calcitonin induced an outwardly rectifying Cl- current blocked by DIDS. To determine the exact location of the Cl- conductance 6-methoxy-1-(3-sulfonatopropyl) quinolinium (SPQ) fluorescence experiments were carried out. Cultures seeded on collagen-coated permeable filters were loaded overnight with 5 mM SPQ and the emitted fluorescence analyzed by laser-scan cytometry. Cl- removal from the apical solution induced a Cl- efflux which was stimulated by 10(-5) M forskolin, 10(-7) calcitonin and inhibited by 10(-5) M NPPB. In 140 mM NaBr, forskolin stimulated an apical Br- influx through the Cl- pathway. Forskolin and calcitonin had no effect on the basolateral Cl- permeability. Thus in DCTb cultured cells, exposure to calcitonin activates a Cl- conductance in the apical membrane through a cAMP-dependent mechanism.

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.

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.

The prevalence of anti-hepatitis C virus (anti-HCV) antibodies and of hepatitis B markers (HBs antigen, anti-hepatitis B core antigen) was assessed in 63 haemodialysis patients from the Tunisian Sahel. As measured by second generation ELISA assays (Ortho and Organon), the frequency of anti-HCV antibodies was 42% (27/63), while 4 patients (6.3%) were HBs Ag positive and 30 (47.6%) anti-HBc positive. Anti-HCV seropositivity was significantly correlated with duration of dialysis (p = 0.007) and number of blood transfusions (10 units, p = 0.0004). Among 12 subjects with a history of abnormal ALAT levels, 10 were anti-HCV positive (p = 0.0016) and the results suggest hepatitis C viral infection to be the main cause of liver disease in haemodialysis patients in Tunisia.

Changes of intracellular calcium concentrations [Ca2+]i were measured in primary cultured rabbit proximal convoluted tubules (PCT). A dual-excitation, digital-imaging inverted microscope was used to monitor the fura-2 fluorescence. The basal calcium level was 106 +/- 11 nM (n = 36). The stimulatory effects of adenosine triphosphate (ATP), adenosine diphosphate (ADP) and adenosine were studied. ATP and ADP induced transient increases of [Ca2+]i (1059 +/- 115% of the resting level (n = 29), and 659 +/- 134% (n = 10), respectively) by releasing calcium from cytoplasmic stores. Adenosine had less effect (279 +/- 48% of the resting level, n = 3). In the same conditions the ATP antagonist suramin (100 microM) inhibited the action of ATP and ADP to 231 +/- 52% (n = 3), and 308 +/- 29% (n = 4) of the resting level, respectively, but did not modify that of adenosine (281 +/- 72%, n = 3). A pretreatment (500 ng/ml for 2 h at 37 degrees C) of the culture with the toxin of Bordetella pertussis completely blocked the ATP response. Our results are evidence for the presence of a functional suramin-sensitive ATP and ADP puriceptor in cultured renal proximal cells. A pertussis-toxin-sensitive G protein is linked to the transduction mechanism. This receptor is distinct from an adenosine puriceptor also found in the proximal monolayer.

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.

The purpose of this study was to investigate the acute regulation by glucocorticoid of the Na+-H+ exchanger in isolated renal proximal cells of the rabbit. The changes of intracellular pH (pHi) were determined in a bicarbonate-free buffer by the use of a fluorescent pH probe that may be trapped intracellularly, 2,7-biscarboxyethyl-5(6)-carboxyfluorescein (BCECF). The activity of the Na+-H+ exchanger was estimated by measuring the Na+-induced H+ efflux in BCECF-loaded cells acid loaded with nigericin in choline medium. The uptake of 1.5 mM 22Na was also studied in Na+-depleted cells. Acute application of dexamethasone (1 h at 37 degrees C) increased the activity of the Na+-H+ exchanger. Evidence for this was the fact that the hormone enhanced the rate of Na+-dependent H+ efflux in acid-loaded cells and increased the Na entry in normal pH, sodium-depleted cells. These actions were blocked by 0.5 mM amiloride and were specific to glucocorticoids, since mineralocorticoids (aldosterone) did not promote modification either of the H+ efflux or the Na influx. The effect on the kinetics of amiloride-sensitive Na+-H+ exchange indicated that dexamethasone (DEX) increased the activity by increasing the Vmax of the carrier for external sodium (Vmax control = 26.5 +/- 1.7, DEX = 33.0 +/- 2.4 mmol H+.1-1.min-1, n = 5, P less than 0.001) and for external H+ (Vmax control = 20.6, DEX = 25.8 mmol H+.1-1.min-1, n = 2).(ABSTRACT TRUNCATED AT 250 WORDS)

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.

The purpose of this study was to investigate the characteristics of the Na+-H+ exchange in isolated proximal cells from rabbit kidney cortex. The cells were prepared by mechanical dissociation and sequential passages through nylon meshes. The intracellular pH (pHi) was measured in a bicarbonate-free medium [extracellular pH (pHe) = 7.30], using the fluorescent dye 2,7-biscarboxyethyl-5(6)-carboxyfluorescein (BCECF). Resting pHi was 7.13 +/- 0.04 (n = 11) at 20-22 degrees C. Cells were acid loaded with nigericin in choline solution and H+ efflux, induced by extracellular Na+ (Nae), was calculated using a buffering power of 23.6 +/- 0.6 mmol.1-1.pH unit-1 (n = 19) estimated by NH4Cl exposure. In isolated proximal cells, the Na+-H+ antiporter had an apparent Km for Nae of 86.7 +/- 1.5 mM (n = 4) and was competitively inhibited by amiloride with a Ki of 33.3 +/- 6.4 X 10(-6) M (n = 3). Lowering pHe, inhibited the Na+-H+ exchanger. This inhibition was not purely competitive and the Ki was 40.4 +/- 12.7 nM (n = 3). The Na+-H+ exchange was greatly activated when the cytoplasm was acidified. The intracellular H+ concentration dependence did not follow simple Michaelis-Menten kinetics. Of the different cations tested on pHi recovery, such as Li+, choline+, K+, and tetramethylammonium, only Li+ induced an alkalinization of acidified cells similar to that of Na+. 22Na influx measurements indicated that cellular depletion of Na+ stimulated Na+-H+ exchange. The results permit the conclusion that the isolation procedures did not impair the main features of the Na+-H+ antiporter, at least as compared with those previously described in renal brush-border membrane vesicles or in other cellular systems. The integrity of the transporter in isolated proximal cells would permit the direct study of its hormonal and metabolic control.

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.