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Notes: —The effect of 1-hydroxy-3-aminopyrrolidone-2(HA-966), a CNS depressant, was studied on the metabolism of [14C]glucose and [3H]acetate in the brain in mice. HA-966 had a marked effect on glucose metabolism. The conversion of glucose carbon into amino acids associated with the tricarboxylic acid cycle (‘cycle’) was severely reduced, while the concentration of brain glucose was approximately doubled. Relative to the specific radioactivity of glucose in the brain, the specific radioactivity of alanine was 60–70 per cent of the control, indicating a reduction in the rate of glycolysis, and those of the‘cycle’amino acids were also lowered. A reduction in‘cycle’flux of 30–35 per cent was estimated. It was established that the depressed glucose utilization flux was not due to either impaired uptake of glucose from blood to brain or to hypothermia. In contrast to [14C]glucose, there was no change in the labelling of the amino acid fraction from [3H]acetate, which is preferentially metabolized in the 'small’compartment believed to be associated with glia. Thus it seems that CNS depression caused by HA-966 resulted in a selective decrease in energy production in the‘large’metabolic compartment where glucose is oxidized preferentially and which is believed to be associated with neuronal structures.The results also suggested that communication between the metabolic compartments mediated via glutamine and GABA was reduced, since the labelling from [3H]acetate of glutamine was increased and that of GABA decreased by HA-966.

Notes: Abstract— Thiamine deficiency produced by administration of pyrithiamine to rats maintained on a thiamine-deficient diet resulted in a marked disturbance in amino acid and glucose levels of the brain.In the two pyrithiamine-treated groups of rats (Expt. A and Expt. B) there was a significant decrease in the levels of glutamate (23%, 9%) and aspartate (42%, 57%), and an increase in the levels of glycine (26%, 27%) in the brain, irrespective of whether the animals showed signs of paralysis (Expt. A) or not (Expt. B). as a result of thiamine deficiency. A significant decrease in the levels of γ-aminobutyrate (22%) and serine (28%) in the brain was also observed in those pyrithiamine-treated rats which showed signs of paralysis (Expt. A). Threonine content increased by 57% in Expt. A and 40% in Expt. B in the brain of pyrithiamine-treated rats, but these changes were not statistically significant.The utilization of [U-14C]glucose into amino acids decreased and accumulation of glucose and [U-14C]glucose increased significantly in the brain after injection of [U-14C]glucose to pyrithiamine-treated rats which showed abnormal neurological symptoms (Expt. A). The decrease in 14C-content of amino acids was due to decreased conversion of [U-14C]glucose into alanine, glutamate, glutamine, aspartate and γ-aminobutyrate. The flux of [14C]glutamate into glutamine and γ-aminobutyrate also decreased significantly only in the brain of animals paralysed on treatment with pyrithiamine.The decrease in the labelling of, amino acids was attributed to a decrease in the activities of pyruvate dehydrogenase and α-oxoglutarate dehydrogenase in the brain of pyrithiamine-treated rats. The measurement of specific radioactivity of glucose, glucose-6-phosphate and lactate also indicated a decrease in the activities of glycolytic enzymes in the brain of pyrithiamine-treated animals in Expt. A only. It was suggested that an alteration in the rate of oxidation in vivo of pyruvate in the brain of thiamine-deficient rats is controlled by the glycolytic enzymes, probably at the hexokinase level.The lack of neurotoxic effect and absence of significant decrease in the metabolism of [U-14C]glucose in the brain of pyrithiamine-treated animals in Expt. B were probably due to the fact that animals in Expt. B were older and weighed more than those in Expt. A, both at the start and the termination of the experiments.

Notes: Stimulated emission at 5.1 μm was demonstrated from a broad area In1−xAlxSb/InSb heterostructure diode laser grown by molecular beam epitaxy. For a 5 μs pulse and a 500 Hz repetition rate the threshold current density was 1480 A cm−2 at 77 K and the maximum operating temperature was 90 K at a current density of 2680 A cm−2. Maximum peak power output was estimated to be 28 mW per facet at 77 K and 4500 A cm−2.

Notes: Contradictory reports regarding the ability of complement receptor type 2 (CR2,CD21) on normal B cells to activate complement (C′) via the alternative pathway (AP), prompted us to compare the performance of human peripheral blood B cells and the Epstein–Barr virus-positive Burkitt's lymphoma cell line, Raji (a well characterized AP activator) by using flow cytometry. Measured in terms of the membrane deposition of C3 fragments per cell, Raji cells were significantly (6- to 26-fold) more effective as complement activators than were normal B cells. Raji cells were also found to express approximately four to five times as many CR2 as normal B cells. In addition, they distinguished themselves by displaying a greater Ca2+-dependent activation, with pooled normal human sera (NHS) as the complement source, and by degrading unprotected C3b fragments from iC3b to C3dg/C3d at a significantly lower rate than the B cells. The Ca2+ dependency of Raji cell activation was found to be partially a result of classical pathway (CP) triggering by specific antibodies in the NHS, although other triggering mechanisms may also be involved. If the influence of these variations between Raji cells and normal B cells was excluded, by relating deposition of anti-C3d-reactive fragments, during AP activation, to the number of CR2 expressed, the difference in performance between the two cell types was found to be insignificant.

Notes: Seventy B-cell alloantisera were tested by microcytotoxicity against a panel of B-cell-enriched and T-cell-enriched lymphocytes. Six groups were discerned and have tentatively been designated DIg 1–7 (for Duke immunoglobulin-positive cell groups). These alloantisera were used to type an HLA-A/B recombinant family. Two groups were observed to segregate in this family, DIg 7 with the HLA-B locus and DIg 2 with the HLA-A locus.

Notes: In vitro exposure of mouse thymocytes to complexes of polyadenylic:polyuridylic acid (poly A:U) effected, within 6 h, the release of soluble factor(s) capable of nonspecifically enhancing IgM and IgG plaque-forming cells (PFCs) in in vitro primary and secondary spleen cell responses to burro erythrocytes. Poly A:U stimulation was, most likely, polyclonal, since production of soluble factor(s) occurred in the absence of antigen and in serum-free culture media. Poly A:U-induced soluble factor(s) were not capable of substituting for T cells but were dependent on T cells for the expression of PFC enhancement. These data support the hypothesis that the mechanism of poly A:U's adjuvant action is polyclonal stimulation of T cells, causing early induction and release of nonspecific, soluble PFC-enhancing factor(s).