Changing activities of galactose-metabolizing enzymes during perfusion of suckling-rat liver

The specific activities of the galactose-metabolizing enzymes, galactokinase (EC 2.7.1.6), galactose-1-phosphate uridyltransferase (EC 2.7.7.12), and UDPgalactose 4-epimerase (EC 5.1.3.2), in suckling-rat livers perfused for 90 min with 1 and 4 mM galactose fluctuate significantly with a different pattern of change for each enzyme. Perfusion for 30 min with galactose resulted in a significant increase of transferase specific activity followed by a precipitous decline to about one-fifth of the activity in unperfused liver at 90 min. The increase in transferase activity was also observed when D-glucose was perfused but not when L-glucose, D-fructose, D-xylose, or D-ribose was added to the perfusate. No such changes in transferase activity were observed when adult-rat liver was perfused with galactose. Epimerase activity in the suckling-rat liver was relatively low, and the changes in its activity correlated best with the uptake rate of galactose. The perfused suckling-rat liver may provide a model system for examination of factors that modulate the specific activity of galactose-metabolizing enzymes and effect the metabolism of galactose.     

Analysis of antigen specific T cell helper function in first degree relatives of patients with systemic lupus erythematosus (SLE).

Fourteen families with first degree relatives of patients with systemic lupus erythematosus (SLE) were studied for the ability of their members to respond to the synthetic polypeptide antigen (T,G)-A-L. The family members were also tested for their HLA determinants. All SLE patients tested responded to (T,G)-A-L as measured by the production of (T,G)-A-L specific T cell helper factors by their antigen activated T cells, confirming our previous findings that 100% of SLE donors responded to (T,G)-A-L in contrast to 50% responders in a control population of healthy donors. The general defect in the regulation of immune responses in SLE patients was further indicated by the demonstration that an SLE patient who is a daughter of non-responder parents to (T,G)-A-L, responded to this genetically regulated antigen. In contrast to our observations with SLE patients, the genetic regulation of the ability to respond to (T,G)-A-L was shown not to be impaired in healthy first degree family members of SLE patients and the segregation of the immune response potential in these families was as expected from an inherited dominant trait.     

Evolutionary conservation of brain Thy-1 glycoprotein in vertebrates and invertebrates

The evolutionary conservation of brain Thy-1 glycoprotein in 24 vertebrate and invertebrate species has been investigated by means of a soluble phase radioimmunoassay (RIA) and by the "Western blot" technique. The brain glycoproteins from virtually all the vertebrate species inhibited the precipitation of mouse Thy-1.1 by a rabbit anti-rat Thy-1 antiserum. Most reagents also inhibited the binding of a mouse anti-rat Thy-1 monoclonal antibody to rat Thy-1. Whole tissue glycoproteins from earthworm, snail and oyster and ganglia glycoproteins of a locust species were also found to be inhibitory. Western blotting analysis on NaDod SO4 polyacrylamide gel electrophoresis under reducing conditions revealed a Thy-1 homologous molecule (22-25 KD) in mammals, birds, fish, reptiles and invertebrate species. The snail Thy-1-like molecule was eluted from the gel and was shown to specifically inhibit the serological reaction. The rabbit anti-rat Thy-1 antiserum also detected a doublet molecule of approximately 85,000 KD, which is conserved in all species, including yeast and bacteria. The origin and nature of the presumed glycoproteins is unknown. Our results suggest that the Thy-1 molecule has been conserved throughout metazoan evolution and that the Thy-1 gene is the most conserved among the immune related genes (immunoglobulins, beta 2-microglobulin and major histocompatibility) which share extensive amino acid homology.     

A cognitive-interpersonal case study of a self

This article presents an integrated conception of the self based on cognitive and interpersonal theories. Implications for clinical practice are outlined, which include understanding the therapeutic relationship as a laboratory and change as involving self-expansion. Implications for clinical research are also presented and exemplified by two strategies, which are demonstrated in a single case study of a patient who successfully underwent a brief-term treatment. The first involves the use of Interpersonal Scenarios, which are structured idiographic vignettes scaled on several parameters, to measure change between psychotherapy sessions. The second involves the use of the Structural Analysis of Social Behavior, a measure of interpersonal process, and the Experiencing Scale, a measure of emotional involvement, to measure change within a session.     

A mouse model of galactose-induced cataracts

Galactokinase (GK; EC 2.7.1.6) is the first enzyme in the metabolism of galactose. In humans, GK deficiency results in congenital cataracts due to an accumulation of galactitol within the lens. In an attempt to make a galactosemic animal model, we cloned the mouse GK gene (Glk1) and disrupted it by gene targeting. As expected, galactose was very poorly metabolized in GK-deficient mice. In addition, both galactose and galactitol accumulated in tissues of GK-deficient mice. Surprisingly, the GK-deficient animals did not form cataracts even when fed a high galactose diet. However, the introduction of a human aldose reductase transgene into a GK-deficient background resulted in cataract formation within the first postnatal day. This mouse represents the first mouse model for congenital galactosemic cataract.