Role of the microsomal mixed-function amine oxidase in the oxidation of N,N-disubstituted hydroxylamines

S-Adenosylhomocysteine inhibits betaine-homocysteine methyltransferase. The inhibition is nonlinear, competitive in relation to homocysteine, and noncompetitive in relation to betaine. S-Adenosylhomocysteine activates cystathionine synthase at all concentrations of the substrates, serine and homocysteine. By altering the distribution of homocysteine between these competing pathways, S-adenosylhomocysteine may be significant in the regulation of methionine metabolism in the intact animal.     

Type III hyperlipoproteinemia in a patient with idiopathic hemochromatosis

Summary A 60-year-old man is reported with idiopathic hemochromatosis and type III hyperlipoproteinemia. Regular phlebotomy therapy and fenofibrate treatment favorably influenced the disorder of iron metabolism and the lipid disease. Evidence is given that both errors of metabolism are independently inherited diseases, although the symptoms of the first (idiopathic hemochromatosis) may aggravate the expression of the second (type III hyperlipoproteinemia).     

Immunological Studies in Kaposi's Sarcoma in Uganda

An evaluation of humoral and cellular immune mechanisms was performed on patients with Kaposi''s sarcoma in Uganda. Antibody responses and immunoglobulin levels were normal in all patients studied. Nevertheless, a striking impairment in the delayed hypersensitivity response to dinitrochlorobenzene was noted in patients with the “malignant” type of tumour.     

The influence of protein malnutrition on T cell, natural killer cell, and lymphokine-activated killer cell function, and on biological responsiveness to high-dose interleukin-2

Protein malnutrition is prevalent in cancer patients, however the influence of protein-calorie malnutrition on anti-tumor immune effector mechanisms is unclear. In addition, the effect of malnutrition on host immunological and biological responsiveness to recombinant interleukin-2 (rIL-2) is unknown. In Swiss mice (n = 100), we observed that T cell activation, T cell response to rIL-2, T suppressor cell generation, cytotoxic T lymphocyte development, and the cytolytic activity of LAK cells were not significantly impaired by two or three weeks of feeding with a 2.5% protein diet compared with mice fed an isocaloric diet in which protein calories constituted 24% of the total. In CBA/J mice (n = 100), we observed a significant (P less than 0.05) impairment of poly(I:C)-inducible natural killer cell function in mice ingesting the 2.5% diet. In both A/J (n = 40) and Swiss mice (n = 40), cytotoxic responses after 3 days treatment with rIL-2 (5 X 10(6) U/kg body wt. three times daily) were comparable in both dietary groups. These studies demonstrate that protein depletion is associated with impaired poly (I:C)-induced natural killer cell function in CBA/J mice. However, T cell function and biological responsiveness to high-dose rIL-2 were not significantly impaired.     

Pathway analysis of NAD+ metabolism

NAD(+) is well known as a crucial cofactor in the redox balance of metabolism. Moreover, NAD(+) is degraded in ADP-ribosyl transfer reactions, which are important components of multitudinous signalling reactions. These include reactions linked to DNA repair and aging. In the present study, using the concept of EFMs (elementary flux modes), we established all of the potential routes in a network describing NAD(+) biosynthesis and degradation. All known biosynthetic pathways, which include de novo synthesis starting from tryptophan as well as the classical Preiss-Handler pathway and NAD(+) synthesis from other vitamin precursors, were detected as EFMs. Moreover, several EFMs were found that degrade NAD(+), represent futile cycles or have other functionalities. The systematic analysis and comparison of the networks specific for yeast and humans document significant differences between species with regard to the use of precursors, biosynthetic routes and NAD(+)-dependent signalling.     

17β-Estradiol-mediated increase in Cu/Zn superoxide dismutase expression in the brain: a mechanism to protect neurons from ischemia

A number of studies have demonstrated that 17β-estradiol (E(2)) protects the brain from ischemia and yet the mechanism by which this hormone brings about its protective effect is unclear. Interestingly, like E(2), overexpression of the oxidative stress response protein Cu/Zn superoxide dismutase (SOD1), which plays a critical role in regulating reactive oxygen species, also protects the brain from ischemia. Because we previously showed that E(2) treatment of cultured mammary cells increases SOD1 expression, we hypothesized that E(2) might increase SOD1 expression in the brain and that this E(2)-mediated increase in SOD1 expression might help to protect the brain from ischemia. We now show that SOD1 is expressed in cortical neurons, that SOD1 expression is increased by exposure of brain slice cultures to E(2), and that the E(2)-mediated increase in SOD1 expression is further augmented by exposure of brain slice cultures to increased superoxide levels or oxygen and glucose deprivation. Importantly, when cortical neurons are exposed to increased superoxide levels and markers of protein and DNA damage, nitrotyrosine and 8-oxoguanine, respectively, are measured, both protein and DNA damage are reduced. In fact, E(2) reduces nitrotyrosine and 8-oxoguanine levels in brain slice cultures regardless of whether they have or have not been exposed to increased superoxide levels. Likewise, when brain slice cultures are treated with E(2) and deprived of oxygen and glucose, 8-oxoguanine levels are reduced. Taken together, these studies provide a critical link between E(2) treatment, SOD1 expression, and neuroprotection and help to define a mechanism through which E(2)-mediated neuroprotection may be conferred.     

Heat of reaction measurements for hydrothermal carbonization of biomass

This paper presents a set of calorimetric measurements with the aim of better understanding the calorific nature of hydrothermal carbonization. Presented values so far show an inadequately high scatter to do so, preventing a well funded assessment of the energetic feasibility of this process.The heat released during hydrothermal carbonization at 240 °C measured with the applied differential calorimetry setup is −1.06 MJ/kg_glucose,daf with a standard deviation of 14%, −1.07 MJ/kg_{cellulose,daf} with a standard deviation of 9%, and −0.76 MJ/kg_wood,daf with a standard deviation of 32%. These results are in good agreement with the theoretically derived maximum heat release. Despite the comparably high experimental standard deviation of these results, their accuracy is considerably higher than previously published results.