A preference-based semantics for CTD reasoning

In [8] the authors developed a logical system based on the definition of a new non-classical connective ⊗ capturing the notion of reparative obligation. The system proved to be appropriate for handling well-known contrary-to-duty paradoxes but no model-theoretic semantics was presented. In this paper we fill the gap and define a suitable possible-world semantics for the system for which we can prove soundness and completeness. The semantics is a preference-based non-normal one extending and generalizing semantics for classical modal logics.

Sapientia, 1982, Vol. XXXVII, nº 145 (número completo)

Contenido: La participación del ser III : la participación del acto de ser o existencia / Octavio N. Derisi – La metafísica cristiana en el desarrollo del pensamiento occidental / Alberto Caturelli – El “principium essendi” del hombre y su conocimiento / Julio R. Méndez – El intelecto en el De Anima de Aristóteles : comentario a los capítulos cuarto y quinto del libro III / Ciro Schmidt Andrade – La formación metafísica cristiana en la universidad / Octavio N. Derisi – Rasgos actuales del pensamiento político de Aristóteles / Alberto Buela – Notas y comentarios -- Bibliografía

Nutrient Enhanced Coastal Ocean Productivity (NECOP). Data report: CTD and hydrographic data, R/V Pelican cruise, April 3-11, 1993

The Nutrient Enhanced Coastal Ocean Productivity (NECOP) Program is a component of NOAA's Coastal Ocean Program. The central hypothesis of this research is: Anthropogenic nutrient inputs have enhanced coastal ocean productivity with subsequent impacts on coastal ocean water quality, living resource yields, and the global marine carbon cycle. The initial study area for this program is the Mississippi/Atchafalaya River Outflow and adjacent Louisiana shelf region.

原子核~(145)Tb的多准粒子激发态

利用能量为165 MeV的32S束流, 通过反应118Sn(32S, 1p4n)布居了145Tb的高自旋态. 基于标准在束核谱学实验测量结果, 首次建立了激发能高达 7.4 MeV的145Tb能级纲图. 145Tb的能级结构具有球形原子核的特征, 其高自旋态是由单粒子激发形成的. 根据邻近N = 80同中子素核结构的系统性, 采用一个11/2h价质子与偶偶核芯144Gd的弱耦合很好地解释了145Tb激发能在2 MeV以下的能级结构. 利用多准粒子壳模型组态解释了激发能在2 MeV以上的晕态和部分近晕态能级.

~(145)Tb的高自旋态能级纲图

利用能量为 1 61— 1 75MeV的32 S束流 ,通过反应118Sn( 32 S ,1p4n)产生了145 　Tb的高自旋态 .进行了γ射线的激发函数、γ γ t符合测量 .首先建议了由 2 4条能级和 4 2条γ跃迁组成的145 Tb核的能级纲图 ,并指定了各条能级的自旋值及部分低位能级的宇称 .用一个πh11/ 2 价质子与144 Gd核芯激发态的耦合定性地解释了145 Tb的一些低位激发态

Experimental study of the beta-delayed proton decays of Er-145,Er-147

The beta-delayed proton decays of Er-145,Er-147 have been studied experimentally using the Ni-58 + Mo-92 reaction at beam energy of 383 MeV. On the basis of a He-jet apparatus coupled with a tape transport system, the beta-delayed proton radioactivities both from the nu s(1/2) ground state and the nu h(11/2) isomer in Er-145,Er-147 were observed by proton-gamma coincidence measurements. By analyzing the time distributions of the 4(+) -> 2(gamma)(+) transitions in the granddaughter nuclei Dy-144,Dy-146, the half-lives of 1.0 +/- 0.3 s and 1.6 +/- 0.2 s have been deduced for the nu h(11/2) isomers in Er-145,Er-147, respectively.

~(145)Er的β延发质子衰变性质研究；Properties of β-delayed Proton Decay of ~(145)Er

通过92Mo(58Ni,2p3n)熔合蒸发反应生成了非常缺中子核145Er。利用氦喷嘴带传输系统把研究目标核传输到低本底测量站,进行了质子-γ符合测量,得到了不受同量异位素干扰的145Er的β延发质子谱。经过仔细分析与延发质子符合的γ谱,发现了145Er的11/2-同核异能态具有β延发质子衰变性质。经拟合退激144Dy不同激发态γ跃迁的衰变曲线,得出145Er的1/2+基态和11/2-同核异能态的半衰期分别为(1.6±0.6)和(0.6±0.1)s。最后,简单介绍了中重质量区缺中子新核素的合成及衰变研究计划。

Yeast screens identify the RNA polymerase II CTD and SPT5 as relevant targets of BRCA1 interaction.

BRCA1 has been implicated in numerous DNA repair pathways that maintain genome integrity, however the function responsible for its tumor suppressor activity in breast cancer remains obscure. To identify the most highly conserved of the many BRCA1 functions, we screened the evolutionarily distant eukaryote Saccharomyces cerevisiae for mutants that suppressed the G1 checkpoint arrest and lethality induced following heterologous BRCA1 expression. A genome-wide screen in the diploid deletion collection combined with a screen of ionizing radiation sensitive gene deletions identified mutants that permit growth in the presence of BRCA1. These genes delineate a metabolic mRNA pathway that temporally links transcription elongation (SPT4, SPT5, CTK1, DEF1) to nucleopore-mediated mRNA export (ASM4, MLP1, MLP2, NUP2, NUP53, NUP120, NUP133, NUP170, NUP188, POM34) and cytoplasmic mRNA decay at P-bodies (CCR4, DHH1). Strikingly, BRCA1 interacted with the phosphorylated RNA polymerase II (RNAPII) carboxy terminal domain (P-CTD), phosphorylated in the pattern specified by the CTDK-I kinase, to induce DEF1-dependent cleavage and accumulation of a RNAPII fragment containing the P-CTD. Significantly, breast cancer associated BRCT domain defects in BRCA1 that suppressed P-CTD cleavage and lethality in yeast also suppressed the physical interaction of BRCA1 with human SPT5 in breast epithelial cells, thus confirming SPT5 as a relevant target of BRCA1 interaction. Furthermore, enhanced P-CTD cleavage was observed in both yeast and human breast cells following UV-irradiation indicating a conserved eukaryotic damage response. Moreover, P-CTD cleavage in breast epithelial cells was BRCA1-dependent since damage-induced P-CTD cleavage was only observed in the mutant BRCA1 cell line HCC1937 following ectopic expression of wild type BRCA1. Finally, BRCA1, SPT5 and hyperphosphorylated RPB1 form a complex that was rapidly degraded following MMS treatment in wild type but not BRCA1 mutant breast cells. These results extend the mechanistic links between BRCA1 and transcriptional consequences in response to DNA damage and suggest an important role for RNAPII P-CTD cleavage in BRCA1-mediated cancer suppression.

Permanent draft genomes of four new coccolithoviruses: EhV-18, EhV-145, EhV-156 and EhV-164

Coccolithoviruses infect the marine coccolithophorid microalga Emiliania huxleyi. Here, we describe the genomes of four new coccolithoviruses isolated from UK coastal locations. Of particular interest, EhV-18 and EhV-145 encode serine palmitoyltransferase function via two distinct genes, whereas all other coccolithoviruses have SPT as a gene fusion of LCB1/LCB2 domains.