[Dose reduction of radiographs of the pediatric pelvis for diagnosing hip dysplasia using a digital flat-panel detector system]. / Dosisreduktion bei Röntgenaufnahmen des kindlichen Beckenskelettes zur Diagnostik der Hüftgelenksdysplasie unter Verwendung eines digitalen Flachdetektorsystems.

PURPOSE: To evaluate a possible dose reduction in pediatric pelvic radiographs in congenital hip dysplasia using a digital flat-panel system instead of a phosphor-storage system. MATERIALS AND METHODS: During a six-month period, all pediatric patients referred for pelvic radiography for the evaluation of congenital hip dysplasia were randomly assigned to be examined by either a phosphor-storage system or a digital flat-panel system, whereby the latter system was operated with half the radiation dose. Thirty pairs of radiographs were assessed for the visibility of 16 anatomic details and for 5 orthopedic-radiographic measurements (5-point scale with 1 = excellent; three independent observers). The projection indices of Ball and Kommenda and of Tönnis and Brunken were calculated for all radiographs. The Student's t-test was used to compare the flat-panel and the phosphor-storage radiographs for observers' assessments, patients' age and projection indices. RESULTS: In a total of 7560 observations, the scores for the visibility of anatomic details and orthopedic-radiographic measurements were respectively 2.72 and 2.64 for the flat-panel system and 2.93 and 2.79 for the phosphor-storage system. No significant differences were found between both systems (p > 0.05) and between patient age and projection indices (p > 0.05). CONCLUSION: Pediatric pelvic radiographs can be obtained with a digital flat-panel system using half the radiation dose instead of a phosphor-storage system without sacrificing relevant information in the diagnosis of congenital hip dysplasia.

Mouse growth hormone transcription factor Zn-16: unique bipartite structure containing tandemly repeated zinc finger domains not reported in rat Zn-15.

Rat Zn-15 is a transcription factor activating GH gene expression by synergistic interactions with Pit-1, named for 15 DNA-binding zinc fingers, including fingers IX, X, and XI that are responsible for GH promoter binding. In this study, a mouse cDNA for Zn-15 was characterized. The predicted 2192-amino acid mouse protein is 89% identical to rat (r) Zn-15 overall, and is 97% similar in the C-terminal domain necessary for binding the GH promoter. However, the mouse cDNA encodes 16 zinc fingers, and sequences of rZn-15 pituitary cDNAs were the same as the mouse (m) Zn-16; the rat sequence in GenBank has a one nucleotide offset of a 17-bp segment in the finger V region. The mouse and corrected rat sequences contain four tandemly repeated fingers in the N-terminus, each separated by seven amino acids, typical of zinc finger proteins of the transcription factor IIIA-type. Analysis of mZn-16 expression by RT-PCR showed that the mRNA is, produced at similar levels in normal and GH-deficient Ames dwarf (Prop-1 ) mouse pituitaries at postnatal day 1. Mouse Zn-16 mRNA also was detected by ribonuclease protection assay in the pre-somatotrophic mouse cell line GHFT1-5. The Zn-16 protein is bipartite in that the N-terminal half displays tandem spacing typical of most zinc finger proteins, while the C-terminal portion contains long linkers between fingers that cooperatively bind to a DNA response element. Expression in early postnatal pituitary and in pre-somatotrophic cells suggests that Zn-16 could play a role in pituitary development prior to somatotroph differentiation.