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Retarded Growth (retarded + growth)

Distribution by Scientific Domains

Medical Sciences	50%

Selected Abstracts

Growth defect in Grg5 null mice is associated with reduced Ihh signaling in growth plates

DEVELOPMENTAL DYNAMICS, Issue 1 2002
Wen-Fang Wang
Abstract Gene-targeted disruption of Grg5, a mouse homologue of Drosophila groucho (gro), results in postnatal growth retardation in mice. The growth defect, most striking in approximately half of the Grg5 null mice, occurs during the first 4,5 weeks of age, but most mice recover retarded growth later. We used the nonlinear mixed-effects model to fit the growth data of wild-type, heterozygous, and Grg5 null mice. On the basis of preliminary evidence suggesting an interaction between Grg5 and the transcription factor Cbfa1/Runx2, critical for skeletal development, we further investigated the skeleton in the mice. A long bone growth plate defect was identified, which included shorter zones of proliferative and hypertrophic chondrocytes and decreased trabecular bone formation. This decreased trabecular bone formation is likely caused by a reduced recruitment of osteoblasts into the growth plate region of Grg5 null mice. Like the growth defect, the growth plate and trabecular bone abnormality improved as the mice grew older. The growth plate defect was associated with reduced Indian hedgehog expression and signaling. We suggest that Grg5, a transcriptional coregulator, modulates the activities of transcription factors, such as Cbfa1/Runx2 in vivo to affect Ihh expression and the function of long bone growth plates. © 2002 Wiley-Liss, Inc. [source]

Chromosome 18 suppresses tumorigenic properties of human prostate cancer cells

GENES, CHROMOSOMES AND CANCER, Issue 3 2006
Audrey Gagnon
Although prostate cancer is still the most diagnosed cancer in men, most genes implicated in its progression are yet to be identified. Chromosome abnormalities have been detected in human prostate tumors, many of them associated with prostate cancer progression. Indeed, alterations (including deletions or amplifications) of more than 15 human chromosomes have been reported in prostate cancer. We hypothesized that transferring normal human chromosomes into human prostate cancer cells would interfere with their tumorigenic and/or metastatic properties. We used microcell-mediated chromosome transfer to introduce human chromosomes 10, 12, 17, and 18 into highly tumorigenic (PC-3M-Pro4) and highly metastatic (PC-3M-LN4) PC-3-derived cell lines. We tested the in vitro and in vivo properties of these hybrids. Introducing chromosome 18 into the PC-3M-LN4 prostate cancer cell line greatly reduced its tumorigenic phenotype. We observed retarded growth in soft agar, decreased invasiveness through Matrigel, and delayed tumor growth into nude mice, both subcutaneously and orthotopically. This phenotype is associated with a marker in the 18q21 region. Combined with the loss of human chromosome 18 regions often seen in patients with advanced prostate cancer, our results show that chromosome 18 encodes one or more tumor-suppressor genes whose inactivation contributes to prostate cancer progression. © 2005 Wiley-Liss, Inc. [source]

Acute and Chronic Effects of Nitrite on White Shrimp, Litopenaeus vannamei, Cultured in Low-Salinity Brackish Water

JOURNAL OF THE WORLD AQUACULTURE SOCIETY, Issue 3 2004
Amit Gross
The marine white shrimp Litopenaeus vannamei is widely cultured. Recently, farmers have begun to culture this shrimp in low-salinity brackish water (< 6 g/L). The intensification of shrimp culture often results in occurrences of elevated nitrite concentration during the growing season. Nitrite is toxic to shrimp and exposure to high concentrations may cause retarded growth and mortalities. The current study was aimed at investigating the acute and chronic toxicity of nitrite to L. vannamei grown in low-salinity (2 g/L) brackish water. Studies of the 96-h EC50 and LC50 values of nitrite were performed to determine the acute toxicity, and an aquarium growth study (2 d post exposure to elevated nitrite concentrations) was conducted to evaluate the chronic effects of nitrite on shrimp production. The 96-h EC50 and LC50 values for juvenile L. vannamei grown in water of 2 g/L salinity was about 9 mg/L NO2 -N, suggesting a safe concentration for shrimp production in ponds to be less than 0.45 mgIL NO2 -N. Exposing shrimp to nitrite concentration of 4 mg/L for 2 d reduced their growth but did not affect their survival. [source]

ESE-3, an Ets family transcription factor, is up-regulated in cellular senescence

CANCER SCIENCE, Issue 9 2007
Makoto Fujikawa
Normal cells irreversibly stop dividing after being exposed to a variety of stresses. This state, called cellular senescence, has recently been demonstrated to act as a tumor-suppressing mechanism in vivo. A common set of features are exhibited by senescent cells, but the molecular mechanism leading to the state is poorly understood. It has been shown that p38, a stress-induced mitogen-activated protein kinase (MAPK), plays a pivotal role in inducing cellular senescence in diverse settings. To better understand the senescence-inducing pathway, microarray analyses of normal human fibroblasts that ectopically activated p38 were performed. It was found that five genes encoding ESE-3, inhibin ,A, RGS5, SSAT and DIO2 were up-regulated in senescent cells induced by RasV12, H2O2 and telomere shortening, but not in quiescent or actively growing cells, suggesting that these genes serve as molecular markers for various types of cellular senescence. The ectopic expression of ESE-3 resulted in retarded growth, up-regulation of p16INK4a but not of p21, and increased levels of SA-,-gal activity. In contrast, RGS5, SSAT and the constitutive active form of the inhibin ,A receptor gene did not induce such senescence phenotypes when ectopically expressed. ESE-3 expression increased the activity of the p16INK4a promoter in a reporter assay, and recombinant ESE-3 protein bound to the Ets-binding sequences present in the promoter. These results suggest that ESE-3 plays a role in the induction of cellular senescence as a downstream molecule of p38. (Cancer Sci 2007; 98: 1468,1475) [source]