Biomedical subjects

C Ai

Publications and source records attributed to C Ai.

3 recordsLinked to original sources

PubMed2001

Variation in lipid composition of Chinese mitten-handed crab, Eriocheir sinensis during ovarian maturation.

This experiment was conducted to investigate the variation in lipid composition during the ovarian maturation of the crab Eriocheir sinensis. The Chinese mitten-handed crab broodstock was divided into six different maturation periods according to the size and color of ovary. Ovary, hepatopancreas, muscle, and hemolymph of broodstock in different maturation periods were analyzed for total lipid and fatty acids using gas chromatography, and lipid classes by thin-layer chromatography. The ovarian lipid concentration (expressed as percent wet ovarian weight) increased steadily from stage II (5.4%) to stage IV (19.1%), and decreased to the lowest levels after spawning (stage V, 6.6%). The hepatopancreatic lipid concentration (expressed as percent wet hepatopancreatic weight) increased with maturity of the ovaries, reached a maximum at stage III(2) (29.9%), and decreased during the subsequent period to spawning (16.7%). The muscular and hemolymph lipid concentration did not change markedly during the ovarian development. These results suggest the possible movement of hepatopancreatic lipids to the ovaries during the ovarian maturation. Both triacylglycerol and phosphatidylcholine were responsible for the increase in ovarian lipid concentration during sexual maturation. The fatty acids of total lipid, triacylglycerol, and phosphatidylcholine of the ovaries did not vary systematically during the ovarian maturation, but the ratio between n-3PUFA (polyunsaturated fatty acid) and n-6PUFA did change regularly with the ovarian lipid. These suggest that enough PUFA, especially n-3PUFA, should be supplied to the crab during ovarian maturation.

Animals↗

PubMed2000

Standard errors for the retransformation problem with heteroscedasticity.

Economists often estimate models with a log-transformed dependent variable. The results from the log-transformed model are often retransformed back to the unlogged scale. Other studies have shown how to obtain consistent estimates on the original scale but have not provided variance equations for those estimates. In this paper, we derive the variance for three estimates--the conditional mean of y, the slope of y, and the average slope of y--on the retransformed scale. We then illustrate our proposed procedures with skewed health expenditure data from a sample of Medicaid eligible patients with severe mental illness.

Aged↗

PubMed2000

Heterozygous loss of Six5 in mice is sufficient to cause ocular cataracts.

Myotonic dystrophy (DM) is an autosomal dominant disorder characterized by skeletal muscle wasting, myotonia, cardiac arrhythmia, hyperinsulinaemia, mental retardation and ocular cataracts. The genetic defect in DM is a CTG repeat expansion located in the 3' untranslated region of DMPK and 5' of a homeodomain-encoding gene, SIX5 (formerly DMAHP; refs 2-5). There are three mechanisms by which CTG expansion can result in DM. First, repeat expansion may alter the processing or transport of the mutant DMPK mRNA and consequently reduce DMPK levels. Second, CTG expansion may establish a region of heterochromatin 3' of the repeat sequence and decrease SIX5 transcription. Third, toxic effects of the repeat expansion may be intrinsic to the repeated elements at the level of DNA or RNA (refs 10,11). Previous studies have demonstrated that a dose-dependent loss of Dm15 (the mouse DMPK homologue) in mice produces a partial DM phenotype characterized by decreased development of skeletal muscle force and cardiac conduction disorders. To test the role of Six5 loss in DM, we have analysed a strain of mice in which Six5 was deleted. Our results demonstrate that the rate and severity of cataract formation is inversely related to Six5 dosage and is temporally progressive. Six5+/- and Six5-/- mice show increased steady-state levels of the Na+/K+-ATPase alpha-1 subunit and decreased Dm15 mRNA levels. Thus, altered ion homeostasis within the lens may contribute to cataract formation. As ocular cataracts are a characteristic feature of DM, these results demonstrate that decreased SIX5 transcription is important in the aetiology of DM. Our data support the hypothesis that DM is a contiguous gene syndrome associated with the partial loss of both DMPK and SIX5.

Animals↗