Is canine hepatocerebellar degeneration syndrome an animal model for carbohydrate-deficient glycoprotein syndrome in humans? An example of sequencing glycoprotein glycans with mass spectrometry.

The clinical symptoms and morphologic features of canine hepatocerebellar degeneration syndrome (CHD) bear striking resemblance to those of human carbohydrate-deficient glycoprotein syndrome (CDGS). The characteristic biochemical and molecular features of human CDGS lie in the truncated carbohydrate side chains of serum transferrin and numerous other glycoproteins of affected persons. Therefore, to explore the biochemical similarities between CHD and CDGS, we compared the structures of the carbohydrate side chains of canine serum transferrin isolated from a normal and a CHD-affected dog. Because of the very small quantity of serum transferrin available from the CHD-affected dog, we used analytical procedures that minimize sample consumption. In this scheme, we used microbore liquid chromatography interfaced to electrospray tandem mass spectrometry to identify and purify the glycopeptides from the tryptic digest of canine serum transferrin. This was followed by a series of exoglycosidase digestions coupled with mass spectrometric detection to sequence the carbohydrate side chains of the glycopeptides. With these procedures we completely characterized the carbohydrate chains attached to serum transferrin isolated from both a normal and a CHD-affected dog. However, we found no discernible differences in glycosylation of the carbohydrate side chains of serum transferrin from these two animals, suggesting that the biochemical defect in puppies with CHD differs from that in children with CDGS.

The role of plasma thyroid hormones in the regulation of body weight of single comb White Leghorn and broiler embryos.

Studies were conducted to determine if sex differences in embryo weights existed in a light-weight breed of chickens (the Single Comb White Leghorn, SCWL) and in a heavy broiler strain of chickens. Plasma thyroid hormone concentration was measured to determine its relationship to embryo weight. Male SCWL embryos were heavier than females at 15 and 17 days of incubation, but not at 13 days. Male broiler embryos were heavier than females at 13 and 15 days of incubation, but not at 17 days. There was no sex difference in the levels of plasma triiodothyronine (T3) or of tetraiodothyronine (T4) of SCWL embryos at those respective ages. The plasma T4 in male broiler embryos was significantly lower than that in the females at 15 and 17 days of incubation, but not at 13 days. There was no relationship between plasma T3, and the weight of SCWL embryos. There were significant linear regressions of embryo weight on the plasma T4 levels for SCWL males at 13 and 15 days of incubation and for SCWL females at 13 and 17 days of incubation, respectively. A significant regression of embryo weight on plasma T4 was found in female broiler embryos at 13 days of age, but not in females at other ages or in males at any of the ages studied.

Neuraminidase induces capacitation and acrosome reaction in mammalian spermatozoa.

The treatment of epididymal spermatozoa of guinea pig and ejaculated spermatozoa of rabbit with neuraminidase from Arthrobacter ureafaciens induced significant acrosome reaction while the neuraminidase from Cl. perfringens failed to do so. The addition of the neuraminidase inhibitors kept the enzyme induced acrosome reaction to the control level. The zona-free hamster ova test showed that the treatment of spermatozoa with Arthrobacter neuraminidase rendered 82% of the guinea pig and 69% of the rabbit spermatozoa capable of fertilization. Thus, neuraminidase seems to enhance the rate of acrosome reaction by first capacitating spermatozoa in vitro.