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G A Ellard 《Bulletin of the International Union against Tuberculosis》1976,51(1):144-154
147.
The mutated human gene encoding hepatocyte nuclear factor 1beta inhibits kidney formation in developing Xenopus embryos 总被引:1,自引:0,他引:1 下载免费PDF全文
148.
Clements KM Girard TA Ellard CG Wainwright PE 《Alcoholism, clinical and experimental research》2005,29(6):1049-1059
BACKGROUND: Previous work in our laboratory has shown that exposure to ethanol during the brain growth spurt impairs spatial short-term memory in rats on the delayed matching-to-place (DMP) version of the Morris water maze. The objectives of this study were to ascertain whether this impairment could: 1) be prevented by increasing the length of encoding time and 2) be related to hippocampal c-Fos expression. METHODS: Using an artificial rearing model, male Long-Evans rats were fed 6.5 g/Kg/day of ethanol from postnatal days 6-9, with controls fed an isocaloric amount of maltose dextrin. As adults, rats in each treatment condition were trained and subsequently tested on either the DMP version of the Morris water maze, or on a random platform version (RAN) that incorporated the same performance requirements, but disallowed spatial learning. Brains were processed for c-Fos expression. RESULTS: Ethanol-exposed rats showed longer search trials during training and took longer to learn the DMP task. When the delay between search and recall trials was increased from 60 sec to 120 min, the performance of ethanol-exposed rats was impaired compared with that of controls after a 10 sec, but not after a 45 sec, encoding time. Brain c-Fos expression was increased in hippocampus, prefrontal cortex and visual cortex in rats trained on the DMP compared to the RAN task. Furthermore, in the DMP-trained rats, hippocampal c-Fos expression was lower in ethanol-exposed rats. CONCLUSIONS: These results suggest that the short-term memory impairment of ethanol-exposed rats 1) can be improved slightly by an increase in encoding time and 2) is related to a decrease in c-Fos expression in the hippocampus. 相似文献
149.
Quinlan C Guegan K Offiah A Neill RO Hiorns MP Ellard S Bockenhauer D Hoff WV Waters AM 《Pediatric nephrology (Berlin, Germany)》2012,27(4):581-588
Inactivating mutations in phosphate-regulating endopeptidase (PHEX) cause X-linked hypophosphatemic rickets (XLHR) characterized
by phosphaturia, hypophosphatemia, bony deformities, and growth retardation. We assessed the efficacy of combined calcitriol
and orally administered phosphate (Pi) therapy on longitudinal growth in relation to age at treatment onset in a retrospective,
single-center review of children with XLHR and documented PHEX mutations. Growth was compared in those who started treatment before (G1; N = 10; six boys) and after (G2; N = 13; five boys) 1 year old. Median height standard deviation score (HSDS) at treatment onset was normal in G1: 0.1 [interquartile
range (IR) −1.3 to 0.4) and significantly (p = 0.004) lower in G2 (IR −2.1 (−2.8 to −1.4). Treatment duration was similar [G1 8.5 (4.0–15.2) vs G2 11.9 (6.2–14.3) years; p = 0.56], as were prescribed phosphate and calcitriol doses. Recent HSDS was significantly (p = 0.009) better in G1 [−0.7 (−1.5 to 0.3)] vs G2 [−2.0 (−2.3 to −1.0)]. No effects of gender or genotype on growth could
be identified. Children with PHEX-associated XLHR benefit from early treatment and can achieve normal growth. Minimal catchup
growth was seen in those who started treatment later. Our findings emphasize the importance of early diagnosis to allow treatment
before growth has been compromised. 相似文献
150.
We report a series of patients with transient neonatal diabetes mellitus (TNDM). Paternal uniparental isodisomy of chromosome 6 and heterozygous KCNJ11 and ABC88 mutation were the mutations found. This first reported series of Brazilian patients expands the geographical data on TNDM contributing to better understanding of its pathophysiology. 相似文献