Hepatic Expression of Cell Death–inducing DFFA‐like Effector C in Obese Subjects Is Reduced by Marked Weight Loss

The hepatic expression of the cell death–inducing DNA fragmentation factor A–like effector family (CIDEA, CIDEB, and CIDEC) genes is markedly upregulated in mouse models of obesity. We evaluated the expression of CIDE genes in liver of obese human subjects undergoing gastric bypass surgery (GBS), at the time of surgery and again 1 year later when subjects had lost 37.6 ± 1.4% of their initial body weight. At the time of GBS, the expression of CIDEA (r² = 0.20, P = 0.04) and CIDEC (r² = 0.32, P = 0.01) was strongly correlated with BMI, whereas CIDEB was not (r² = 0.01, P = 0.81). One year after surgery, CIDEC expression had declined over 60% (P = 0.02), whereas CIDEA expression did not change (P = 0.20). These data demonstrate that, consistent with previous studies conducted in rodents, hepatic expression of CIDEA and CIDEC, but not CIDEB, is increased in obese humans. Moreover, the hepatic expression of CIDEC is downregulated by marked weight loss.     

Electron Microscopy of an Isometric Caulimo-Like Virus from Sweet Potato (Ipomoea batatas)

A newly recognised virus with isometric particles 50 nm in diameter was detected in Ipomoea batatas (sweet potato) by graft-transmission to I. setosa. Virus particles and intracellular inclusions, although not seen in infected I. batatus, were found in the cytoplasm of most cell types of I. setosa. The caulimo-like particles were most abundant with vesicles immediately adjacent to inclusions. The ovoid or spherical inclusions, which differ markedly from those of caulimovi, ruses, have a large central lacuna and usually several smaller peripheral lacunae. Infected vascular parenchyma cells sometimes protrude into, and occasionally completely occlude, adjacent xylem vessels, observations possibly explaining the sudden wilting and premature senescence of infected leaves.     

The regulation of aerobic polysaccharide synthesis in resting cells of Saccharomyces cerevisiae

Summary An increased polysaccharide synthesis at low external H-ion concentration was found to be associated with an elevated level of glucose-6-phosphate. Differences in the level of glucose-6-phosphate appeared to be due to changes in the activity of phosphofructokinase which in turn appeared to be regulated by the energy status of the cells.     

Biosynthesis of a glycosylated keratin by human keratinocytes

Human keratinocytes, cultured in the presence of D-[1-14C]glucosamine, incorporated radioactivity into a cytoskeleton-associated glycoprotein with Mr 53,000. This glycoprotein co-purified with prekeratin when keratinocyte cytoskeletons were extracted with 0.1 M citric acid/0.1 M sodium citrate and subjected to isoelectric precipitation at pH 4.0. Analysis of the prekeratin polypeptides by two-dimensional gel electrophoresis revealed that the radioactivity was restricted to a single polypeptide with an isoelectric point in the pH range 4.5-5.5. Acid hydrolysis of prekeratin followed by paper chromatography of the hydrolysate showed that the radioactivity was incorporated as glucosamine and not by metabolic conversion to amino acids. Control experiments showed that the radioactivity associated with the glycoprotein of Mr 53,000 was not the result of adsorbed glycolipids or non-enzymatic labelling. In contrast to the incorporation of D-[1-14C]glucosamine and D-[6-3H]glucosamine, no appreciable amounts of L-[6-3H]fucose, D-[2-3H]mannose or 32PO4 were incorporated into this glycoprotein. The immunological relationship of the glycoprotein of Mr 53,000 to the keratins was demonstrated by its reactivity with both polyclonal and monoclonal antisera to keratin.     

Three novel KCNA1 mutations in episodic ataxia type I families

Hereditary paroxysmal ataxia, or episodic ataxia (EA), is a rare, genetically heterogeneous neurological disorder characterized by attacks of generalized ataxia. By direct sequence analysis, a different missense mutation of the potassium channel gene (KCNA1) has been identified in three families with EA. Received: 20 November 1997 / Accepted: 12 January 1998