Mechanism of growth retardation of the adenocarcinoma EO 771

1987 ◽  
Vol 26 (2) ◽  
pp. 125-141 ◽  
Author(s):  
I. D. Bassukas ◽  
B. Maurer-Schultze
1998 ◽  
pp. 59-62 ◽  
Author(s):  
L Even ◽  
V Bronstein ◽  
Z Hochberg

The mechanism of growth retardation in Turner's syndrome has not been resolved. It is often referred to as a bone dysplasia, although endocrine derangement has not been ruled out. The present study was undertaken to evaluate the maturation of individual bones of the hand and wrist in girls with Turner's syndrome and thereby obtain information which may aid in elaborating the possible mechanism of the growth retardation in girls with Turner's syndrome. Hand and wrist films of 24 girls with Turner's syndrome, 11 normal girls with short stature and 23 normal controls were evaluated, using the references of Greulich and Pyle. Each bone or epiphysis was given an individual 'age'. During childhood the Turner patients showed the greatest delay in bone age of the phalangeal bones while the least delayed were the radius and ulna (long bones) and metacarpals. The carpal bones showed intermediate retardation. This pattern and extent of maturational retardation was clearly different from that of the short stature normal group, who showed uniform retardation of all bones. During adolescence, the phalangeal bones were further retarded and the carpal bones showed a moderate retardation. The unique profile of bone maturation in Turner's syndrome suggests an insult to chondroplasia, which may be related to estrogen deficiency or to an as yet undetermined endocrine or paracrine derangement.


1991 ◽  
Vol 19 (4) ◽  
pp. 296-304
Author(s):  
J.A. Paraskevopoulos ◽  
P.E. Karayannacos ◽  
I. Dontas ◽  
D. Kotsarelis ◽  
S. Drouva ◽  
...  

1989 ◽  
Vol 61 (02) ◽  
pp. 243-245 ◽  
Author(s):  
J G Thornton ◽  
B J Molloy ◽  
P S Vinall ◽  
P R Philips ◽  
R Hughes ◽  
...  

SummaryA panel of haemostatic tests was perfomed on 400 primiparous women at 28 weeks to test whether one or more could predict the development of pregnancy complications. Fifteen women subsequently developed pre-eclampsia with significant proteinuria and 13 delivered growth retarded infants. There were no significant differences between mothers in the pre-eclampsia group and 22 randomly selected controls. A stepwise logistic discriminant analysis of the data did not produce a significant model. In the growth retarded group only beta thromboglobulin levels were significantly lower than in the controls (p <0.05), although in the logistic discriminant analysis the inclusion of both beta thromboglobulin and fibrin degradation products led to a borderline significant improvement in fit of the model. We conclude that the haemostatic variables studied are not significantly changed at 28 weeks nor clinically useful predictors of either pre-eclampsia or fetal growth retardation.


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