Anna Clark (2008) History’s Children: History Wars in the Classroom. UNSW Press, Sydney, 178 pages

“History’s Children” stems from Anna Clark’s 2004 postdoctoral research into the ways in which Australian students connect with the past, and aims at bringing some classroom perspectives into the public debates about Australian history education. Although the title makes reference to the “History Wars”, there is little evidence of contestation, engagement, passion or intellectual excitement in Clark’s conclusions about what happens in history classrooms. Rather, Clark’s small focus groups with 182 high school students in 34 high schools around Australia indicate that “it got a bit dismal hearing student after student being so dismissive of Australian history” (p. 143). Apart from some enthusiasm for the study of Australians at war, a sort of resigned boredom seems to characterise what students have to say about learning Australian history, despite their acknowledgement that it is important to “know about” it.

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.

Effect of amino acid substitutions at the subunit interface on the stabiity and aggregation properties of a dimeric protein: role of Arg 178 and Arg 218 at the dimer interface of thymidylate synthase

The significance of two interface arginine residues on the structural integrity of an obligatory dimeric enzyme thymidylate synthase (TS) from Lactobacillus casei was investigated by thermal and chemical denaturation. While the R178F mutant showed apparent stability to thermal denaturation by its decreased tendency to aggregate, the Tm of the R218K mutant was lowered by 5 degrees C. Equilibrium denaturation studies in guanidinium chloride (GdmCl) and urea indicate that in both the mutants, replacement of Arg residues results in more labile quaternary and tertiary interactions. Circular dichroism studies in aqueous buffer suggest that the protein interior in R218K may be less well-packed as compared to the wild type protein. The results emphasize that quaternary interactions may influence the stability of the tertiary fold of TS. The amino acid replacements also lead to notable alteration in the ability of the unfolding intermediate of TS to aggregate. The aggregated state of partially unfolded intermediate in the R178F mutant is stable over a narrower range of denaturant concentrations. In contrast, there is an exaggerated tendency on the part of R218K to aggregate in intermediate concentrations of the denaturant. The 3 A crystal structure of the R178F mutant reveals no major structural change as a consequence of amino acid substitution. The results may be rationalized in terms of mutational effects on both the folded and unfolded state of the protein. Site specific amino acid substitutions are useful in identifying specific regions of TS involved in association of non-native protein structures.

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.

~(176,178)Os新低位激发态的识别

利用在束实验产生具有β+/EC衰变性质核素176,178Ir,分析了在束实验条件下获得的γ-γ符合数据,识别出了176Os的4条新能级和13条新γ跃迁、178Os的5条新能级和14条新γ跃迁。籍助氦喷嘴快速带传输系统,进一步对176Ir的β+/EC衰变进行了测量,在确认在束测量新γ射线的同时建议了176Ir的一个低自旋同核异能态。通过两准粒子耦合的半经验计算,建议了176,178Ir基态及同核异能态的组态。

形变双奇核~(178)Ir转动带能级的旋称反转

利用１５２Ｓｍ（３１Ｐ，５ｎγ）１７８Ｉｒ反应产生并研究了双奇核１７８Ｉｒ的高自旋态．实验中进行了１７８Ｉｒ核的在束 γ测量，包括γ射线的激发函数测量、Ｘ－γ和γ－γ符合测量．首次建立了双奇核１７８Ｉｒ基于πｈ９／２νｉ１３／２和πｈ１１／２νｉ１３／２准粒子组态上的转动带能级纲图．发现在低自旋区，两个转动带能级均出现旋称反转．对此核区半退耦带的旋称反转作了简要的分析和讨论．

beta(+)/EC decay and systematic analysis of Ir-176,Ir-178

The gamma rays following the beta(+)/EC decay of Ir-176,Ir-178 nuclei have been investigated using in-beam gamma-ray experiment. In addition, with the aid of a helium-jet recoil fast tape transport system, the beta(+)/EC decay of Ir-176 was further studied, the new gamma rays were proved and a low-spin isomer was proposed in Ir-176. The isomeric state was analysized according to the systematics in neighboring nuclei.

C 178 INST-D 2013. 359 Presentación selectiva de detalles de diseño de piezas de tejido.

10 fotografías a color.

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.