Response to IGF-1 Generation Test in Short Prepubertal Children Born Very Preterm or at Term

2015 ◽  
Vol 84 (5) ◽  
pp. 298-304 ◽  
Author(s):  
Harriet L. Miles ◽  
José G.B. Derraik ◽  
Valentina Chiavaroli ◽  
Paul L. Hofman ◽  
Wayne S. Cutfield
HORMONES ◽  
2013 ◽  
Vol 12 (1) ◽  
pp. 86-92 ◽  
Author(s):  
Silvano Bertelloni ◽  
Giampiero I. Baroncelli ◽  
Eleonora Dati ◽  
Silvia Ghione ◽  
Fulvia Baldinotti ◽  
...  

2003 ◽  
Vol 92 (5) ◽  
pp. 1-1 ◽  
Author(s):  
GMSJ Stoelhorst ◽  
SE Martens ◽  
M Rijken ◽  
van Zwieten PHT ◽  
AH Zwinderman ◽  
...  

2015 ◽  
Vol 46 (S 01) ◽  
Author(s):  
M. Cremer ◽  
K. Jost ◽  
S. Schulzke ◽  
P. Weber ◽  
A. Datta

1973 ◽  
Vol 12 (01) ◽  
pp. 26-34
Author(s):  
D. Liakakos ◽  
D. Ikkos ◽  
P. Vlachos ◽  
S. Gonticas ◽  
P. Matsioulas ◽  
...  

La fixation thyroïdienne du 131I a été mesurée en 50 enfants non-goitreux agés de 2 à 12 ans (17 masculins, 33 féminins). Les valeurs de fixation des enfants grèques (l’erreur standard ± pour les deux sexes était 38,8 ± 1,81; 59,1 ± 2,17; 60,2 ± 2,16 à 3, 24 et 48 heures) sont les plus élevées rapportées jusqu’à maintenant das la litérature donnant preuve à la pénurie de l’iode dans notre pays. Une autre manifestation de la pénurie de l’iode était l’observation, que dans 41% des enfants prépubertaires les valeurs PB 131I à 48 heures étaient plus élevées que la limite supérieure normale de 0,4% par litre.Les enfants féminines montraient des valeurs de fixation significativement (P < 0,05) plus élevées que les masculins avec un taux de différence des valeurs moyennes de 1,34; 1,19; et 1,15 à 3, 24 et 48 heures.


1991 ◽  
Vol 65 (04) ◽  
pp. 355-359 ◽  
Author(s):  
E Gray ◽  
J Watton ◽  
S Cesmeli ◽  
T W Barrowcliffe ◽  
D P Thomas

SummaryThe in vitro anticoagulant activities of recombinant desulphatohirudin (r-hirudin) were studied in the activated partial thromboplastin time (APTT) and the thrombin generation test : systems. In the APTT at concentrations below 5 μg/ml, r-hirudin showed a dose-response curye. At concentrations above 5 μg/ml, the plasma became unclottable, but in the thrombin generation test , at least 10 μg/ml of r-hirudin was required for full inhibition of thrombin generation. The antithrombotic effect was assessed using a rabbit venous stasis model; 150 μg/ml r-hirudin completely prevented thrombus formation at 10 and 20 min stasis. At antithrombotic dose, the mean bleeding time ratio measured in a rabbit ear template model, was not prolonged over control values. At higher doses, the bleeding time ratios were higher than those observed for the same dosage of heparin. These data indicate that while r-hirudin is an effective antithrombotic agent, antithrombotic doses have to be carefully titrated to avoid excessive bleeding.


1966 ◽  
Vol 15 (03/04) ◽  
pp. 349-364 ◽  
Author(s):  
A.H Özge ◽  
H.C Rowsell ◽  
H.G Downie ◽  
J.F Mustard

SummaryThe addition of trace amounts of adrenaline to whole blood in plasma in vitro increased factor VIII, factor IX and whole plasma activity in the thromboplastin generation test. This was dose dependent.Adrenaline infusions less than 22 (μg/kg body weight in normal dogs accelerated clotting, increased factor IX, factor VIII and whole plasma activity in the thromboplastin generation test and caused a fall in blood pH. In a factor IX deficient dog, there was no increase in factor IX activity. After adrenaline infusions, however, the other changes occurred and were of the same order of magnitude as in the normal. Adrenaline in doses greater than 22 μg/kg body weight did not produce as great an effect on clotting in normal or factor IX deficient dogs. The platelet count in the peripheral blood was increased following the infusion of all doses of adrenaline. These observations suggest that the accelerating effect of adrenaline on clotting is not mediated through increase in activity of a specific clotting factor.


1960 ◽  
Vol 04 (03) ◽  
pp. 369-375 ◽  
Author(s):  
E. H Braun ◽  
David B. Stollar

SummaryA case of haemophilia in a young white girl is described. There was a history of bleeding from birth. The thromboplastin generation test was grossly abnormal and A. H. G. levels were below 1%. Bleeding time and capillary morphology was within normal limits. Dental extraction after transfusion caused almost uncontrollable haemorrhage.A complete family history was obtained for four generations. There was no case of a “bleeder” amongst these.The girl’s apparent sex was confirmed by sex chromatin studies.


1967 ◽  
Vol 18 (01/02) ◽  
pp. 040-056 ◽  
Author(s):  
E. J Walter Bowie ◽  
P Didisheim ◽  
J. H Thompson ◽  
C. A Owen

SummaryPatients (from 5 kindreds) with variants of von Willebrand’s disease are described. In one kindred the depression of factor VIII was moderate (20 to 40% of normal) and transfusion of 500 ml of normal plasma led to an increase higher than anticipated and to an almost normal level of factor VIII 17 to 24 hrs later. This represents the usual type of von Willebrand’s disease.In the second kindred the concentration of factor VIII was less than 2 % of normal in the son and daughter, who had severe bleeding and hemarthroses.The third kindred was characterized by reduction of factor VIII and a long bleeding time as well as by a serum defect in the thromboplastin-generation test comparable to that seen in patients with hemophilia B, yet with normal levels of factors IX, X, and VII. The severity of the serum defect, the positive result with the Rumpel-Leede test, and the reduced platelet activity in the thromboplastin-generation test are all compatible with the diagnosis of thrombopathy or ‘‘thrombopathic hemophilia.” In two other kindreds, one patient had a long bleeding time and normal levels of factor VIII and another had a normal bleeding time and decrease of factor VIII. The last patient had the type of response to transfusion usually seen in von Willebrand’s disease.In four kindreds, platelet adhesiveness in vivo was found to be strikingly abnormal (virtually absent).It would appear, therefore, that von Willebrand’s disease forms a spectrum, and whether the kindreds reported simply reflect variations of a single genetic disease state or represent separate entities will be answered only by clarification of the underlying etiology of that disease.


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