Inhibitory effect of norepinephrine on immunoreactive corticotropin-releasing factor release from the rat hypothalamus in vitro

Effects of catecholamines on immunoreactive corticotropin-releasing factor (I-CRF) release from the rat hypothalamus were examined using a rat hypothalamic perifusion system and a rat CRF RIA in vitro. Norepinephrine had a potent inhibitory effect on I-CRF release in a dose-dependent manner at 0.1 nM-1 microM concentrations, but dopamine did not. This inhibitory effect of norepinephrine was completely blocked by propranolol, but only partially blocked by phentolamine. Isoproterenol also had a potent inhibitory effect at 0.01-100 nM concentrations, and a high dose of phenylephrine (10 nM) inhibited I-CRF release. Clonidine did not influence I-CRF release. These results suggest that norepinephrine inhibits I-CRF release mainly through the beta-adrenergic receptor and partially through the alpha 1-receptor.     

Cloning and DNA homology of 3-isopropylmalate dehydrogenase genes from thermophilic bacilli

Abstract Clostridium thermoaceticum was cultivated heterotrophically under CO₂, carbon monoxide (CO), and H₂ gas phases. Formate dehydrogenase (FDH) levels increased 4-fold in CO cultures; formyltetrahydrofolate synthetase (FTS) levels were not influenced by the cultivation gas phases tested. While CO dehydrogenase (CODH) was slightly stimulated in CO cultures, CO-dependent acetyl phosphate-synthesizing system (APSS) activity increased sharply in both CO and H₂ cultures. Y _glucose values increased, whereas doubling times and acetate to biomass ratios decreased significantly in CO cultures, suggesting that CO cultures were energetically dissimilar to non-CO cultures. This finding, together with the absence of CO-dependent ATP-independent synthesis of formyltetrahydrofolate (formyl-THF), supports the hypothesis that conservation of CO-derived energy involves electron transport phosphorylation.     

IL-22-Producing RORγt-Dependent Innate Lymphoid Cells Play a Novel Protective Role in Murine Acute Hepatitis

Retinoid-related orphan receptor (ROR) γt is known to be related to the development and function of various immunological compartments in the liver, such as Th17 cells, natural killer T (NKT) cells, and innate lymphoid cells (ILCs). We evaluated the roles of RORγt-expressing cells in mouse acute hepatitis model using RORγt deficient (RORγt^−/−) mice and RAG-2 and RORγt double deficient (RAG-2^−/− × RORγt^−/−) mice. Acute hepatitis was induced in mice by injection with carbon tetrachloride (CCl₄), to investigate the regulation of liver inflammation by RORγt-expressing cells. We detected RORC expression in three compartments, CD4⁺ T cells, NKT cells, and lineage marker-negative SCA-1⁺Thy1^high ILCs, of the liver of wild type (WT) mice. CCl₄-treated RORγt^−/− mice developed liver damage in spite of lack of RORγt-dependent cells, but with reduced infiltration of macrophages compared with WT mice. In this regard, ILCs were significantly decreased in RAG-2^−/− × RORγt^−/− mice that lacked T and NKT cells. Surprisingly, RAG-2^−/− × RORγt^−/− mice developed significantly severer CCl₄-induced hepatitis compared with RAG-2^−/− mice, in accordance with the fact that hepatic ILCs failed to produce IL-22. Lastly, anti-Thy1 monoclonal antibody (mAb), but not anti-NK1.1 mAb or anti-asialo GM1 Ab administration exacerbated liver damage in RAG-2^−/− mice with the depletion of liver ILCs. Collectively, hepatic RORγt-dependent ILCs play a part of protective roles in hepatic immune response in mice.     

Change in the H2 photoproduction capability in a synchronously grown aerobic nitrogen-fixing cyanobacterium,Synechococcus sp. Miami BG 043511

Synchronously growing cells of nitrogen-fixing Synechococcus sp. Miami BG 043511 were harvested periodically and the capability for hydrogen photoproduction in closed vessels was measured under hydrogen production conditions. The capability for hydrogen photoproduction in cells was correlated with that of cellular carbohydrate content. Cells with a high carbohydrate content exhibited a high capacity for hydrogen production and those with low carbohydrate content exhibited low capacity for hydrogen production. Nitrogenase activity at the onset of incubation did not coincide with a capability for the cells to produce hydrogen during the subsequent incubation period. Interestingly, when cells with a high capacity for hydrogen photoaccumulation were incubated, alternate periods of hydrogen and oxygen accumulation were observed at 12 hour intervals. About 0.5 ml of hydrogen per ml of cell suspension was accumulated in flasks during the initial 12-h incubation period. These observations indicate that the use of synchronous culture can be one of the ways of provide materials suitable not only for basic studies but also for applied aspects of hydrogen photoproduction.     

Spermidine-dependent proteins are involved in the fusion of mouse alveolar macrophages induced by 1 alpha,25-dihydroxyvitamin D3 and interleukin 4

We have reported that 1 alpha,25-dihydroxyvitamin D3 [1 alpha,25(OH)2D3] directly induces fusion of mouse alveolar macrophages by a mechanism involving protein synthesis (H. Tanaka et al., 1984, FEBS Lett. 174, 61). While examining further the mechanism of the fusion, we found that polyamines, most likely spermidine, are involved as an important intracellular mediator of the 1 alpha,25(OH)2D3 action in inducing protein synthesis, which in turn induces fusion of macrophages (T. Hayashi et al., 1986, J. Bone Miner. Res. 1, 235). In this study, spermidine-dependent proteins responsible for inducing fusion were examined by electrophoresis of [35S]methionine-labeled proteins. 1 alpha,25(OH)2D3 increased synthesis of 14 proteins at 24 h after the addition, before it initiated fusion at 36 h. When spermidine synthesis was inhibited by adding methylglyoxal bis(guanylhydrazone) (MGBG), the enhanced synthesis in 9 of the 14 proteins induced by 1 alpha,25(OH)2D3 was greatly diminished with a concomitant inhibition of fusion. Further addition of spermidine restored the synthesis of these 9 proteins and the fusion as well. The synthesis of 3 of the 9 proteins was similarly induced by interferon-gamma, retinoic acid, or lipopolysaccharides, which induced activation but not fusion of macrophages. The apparent molecular weights of the remaining 6 proteins were 142K, 98K, 78K, 60K, 50K, and 42K. Recombinant mouse interleukin 4 (IL-4) also induced fusion of alveolar macrophages by a spermidine-dependent mechanism, and it increased the synthesis of 5 proteins (172K, 98K, 78K, 53K, and 50K). These results suggest that 3 spermidine-dependent proteins (98K, 78K, and 50K) are involved in the fusion of mouse alveolar macrophages induced by 1 alpha,25(OH)2D3 and IL-4.