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111.
The genetic basis of the effects of ultraviolet B(UVB) radiation on the induction of contact hypersensitivity (CH) to dinitrofluorobenzene (DNFB) has been explored in genetically defined mice. It was found that acute, low-dose UVB radiation produced profound depletion of epidermal Langerhans cells (LC) at UVB-treated sites in all strains of mice tested. However, when DNFB was applied to UVB radiation sites, unresponsiveness developed in some strains of mice, but vigorous contact hypersensitivity was induced in others. The UVB-susceptible phenotype proved dominant or codominant in F1 hybrids derived from parental strains of the susceptible and UVB-resistant phenotypes. Experiments conducted in one set of F1 hybrids derived from two UVB-susceptible parental strains displayed UVB resistance, suggesting gene complementation, and showed that more than one genetic locus was involved. Segregant backcross populations, analyzed for the capacity to develop CH after UVB treatment and skin painting with DNFB, revealed that at least two, and probably three, independent genetic loci participate in determining UVB resistance. Results of experiments with H-2 congenic and recombinant mice derived from the B10 background implicated class I genes of the major histocompatibility complex as relevant genetic factors. These results indicate that there is a dissociation between the effects of UVB radiation on epidermal Langerhans cells and the capacity of a cutaneous surface to support the induction of contact hypersensitivity. The data indicate that the induction of CH to haptens is dependent on normal numbers of functional LC at the skin painting site only in some strains of mice. The data imply that in the so-called UVB-resistant strains of mice, alternative (non-Langerhans cell-dependent) mechanisms allow for the induction of CH. Several independent genetic loci, one of which appears to be H-2, govern this UVB-related effect.  相似文献   
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The effect of theophylline and isoproterenol on bovine tracheal smooth muscle tension and cyclic AMP levels was investigated. Concentrations of isoproterenol (4 × 10?6 M) and theophylline (10 mM) that relaxed carbachol-contracted tracheal muscle by 85–95% did not significantly elevate control levels of cyclic AMP. In the absence of carbachol, several-fold increases in cyclic AMP were caused by isoproterenol although no elevations by theophylline were measurable. However, when isoproterenol and theophylline were administered together, theophylline potentiated the rise in cyclic AMP caused by isoproterenol. Phosphodiesterase studies in tracheal muscle showed the presence of a high and a low Km enzyme which were inhibited by theophylline. Cyclic GMP levels were elevated in muscles contracted by carbachol as well as in carbachol-contracted muscles that had been relaxed by theophylline. In non-tension studies, in which the tracheal muscle was not under isometric tension, carbachol or theophylline alone increased cyclic GMP and together they synergistically elevated cyclic GMP. Atropine blocked the elevation caused by carbachol but not that caused by theophylline. In contrast to theophylline, isoproterenol did not elevate cyclic GMP, and in carbachol-contracted muscles that had been relaxed by isoproterenol, cyclic GMP levels were no different from control. Also, in non-tension studies, isoproterenol decreased basal cyclic GMP and antagonized the increase in cyclic GMP due to carbachol.The results indicate that whole-tissue levels of cyclic AMP and cyclic GMP do not correlate with the state of tracheal smooth muscle tension. Cyclic GMP levels do not clearly correlate with either contraction or relaxation. The inhibition by carbachol of increases in cyclic AMP due to isoproterenol and the inhibition by isoproterenol of increases in cyclic GMP due to carbachol provide evidence for a reciprocal cholinergic-adrenergic antagonism of cyclic AMP and cyclic GMP levels. The antagonism did not appear to be due to either cyclic nucleotide affecting the elevation of the other since the levels of both cyclic nucleotides were depressed.  相似文献   
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Congenic anti-Lyt-3.1 sera have recently been produced by immunizing B6-Lyt-2a mice with thymocytes from either B6-Lyt-2a, Lyt-3a or B6-Lyt-2a, Lyt-3a, H-2k mice (Boos et al. 1978). Surprisingly, mice of the congenic strain B6 failed to produce either anti-Lyt-2.1 or anti-Lyt-3.1 cytotoxic antibodies after identical immunizations. To determine the genetic basis for the difference in response to Lyt-3.1, (B6 × B6-Lyt-2a)Fa mice and progeny of the backcross, (B6 × B6-Lyt-2a)F1 × B6-Lyt-2a, were immunized with B6-Lyt-2a, Lyt-3a, H-2k thymocytes. In addition, thymic biopsies of backcross progeny were performed and thymocytes tested for the Lyt-2.2 antigenic specificity. Results indicate that gene(s) governing the immune response to Lyt-3.1 is (are) linked to theLyt-2 locus, and that the responder allele (linked toLyt-2 a ) shows very poor penetrance in Lyt-2a/Lyt-2b mice.  相似文献   
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Tetrapod biodiversity today is great; over the past 400 Myr since vertebrates moved onto land, global tetrapod diversity has risen exponentially, punctuated by losses during major extinctions. There are links between the total global diversity of tetrapods and the diversity of their ecological roles, yet no one fully understands the interplay of these two aspects of biodiversity and a numerical analysis of this relationship has not so far been undertaken. Here we show that the global taxonomic and ecological diversity of tetrapods are closely linked. Throughout geological time, patterns of global diversity of tetrapod families show 97 per cent correlation with ecological modes. Global taxonomic and ecological diversity of this group correlates closely with the dominant classes of tetrapods (amphibians in the Palaeozoic, reptiles in the Mesozoic, birds and mammals in the Cenozoic). These groups have driven ecological diversity by expansion and contraction of occupied ecospace, rather than by direct competition within existing ecospace and each group has used ecospace at a greater rate than their predecessors.  相似文献   
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Zusammenfassung Es wurde versucht, zwei physiologisch durch die Oxalsäurebildung und die dadurch beeinflußte Richtung der Autolyse verschiedene Rassen von Aspergillus niger ineinander überzuführen. Dies gelang durch Einwirkung von Trocknen bzw. Erhitzen der Sporen und durch Passage über Tannin- und Oxalsäurelösung.Der Übergang der Rasse Göttingen neu (viel Oxalsäure, saure, helle Autolyse) in die Rasse Göttingen alt (wenig Oxalsäure, neutrale bzw. alkalische, dunkle Autolyse) ging bedeutend leichter als umgekehrt.Durch Oxalsäurepassage wird die Rasse Göttingen alt stärker in der Richtung der sauren, die Rasse Göttingen neu stärker in der Richtung der neutralen Autolyse beeinflußt.Die jeweiligen Veränderungen erwiesen sich drei bis acht Generationen, soweit untersucht, konstant.Mit Hilfe ähnlicher Methoden dürften die Veränderungen bei diesem Pilz der experimentellen Analyse zugänglich werden.Kurzer Auszug aus der Dissertation von Paul Hugo Kreutzmann, Untersuchungen über die Variabilität von Aspergillus niger. Göttingen 1935.  相似文献   
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