Compton profiles of Si: Pseudopotential calculation and reconstruction effects

Using an ab initio pseudopotential calculation, we compute Compton profiles of silicon along the (100), (110), and (111) directions, and then reconstruct the pseudo-wave-functions to regain the oscillatory behavior of the all-electron valence wave functions near the atomic cores. We study the effect that this reconstruction has on the Compton profiles and their anisotropies. We find a decrease in the magnitude of the profiles at small wave vectors and in their anisotropies. These changes bring the theoretical predictions closer to experimental results.

Increased repair and cell survival in cells treated with DIR1 antisense oligonucleotides: implications for induced radioresistance

Purpose: To determine whether repression of a recently isolated, X-ray-responsive gene, DIR1, using antisense oligonucleotides could affect clonogenic cell survival and repair of DNA strand breaks and have a possible role in the mechanism underlying the phenomenon of 'induced radioresistance' (IRR).

Identification of a BRCA1-mRNA Splicing Complex Required for Efficient DNA Repair and Maintenance of Genomic Stability

Mutations within BRCA1 predispose carriers to a high risk of breast and ovarian cancers. BRCA1 functions to maintain genomic stability through the assembly of multiple protein complexes involved in DNA repair, cell-cycle arrest, and transcriptional regulation. Here, we report the identification of a DNA damage-induced BRCA1 protein complex containing BCLAF1 and other key components of the mRNA-splicing machinery. In response to DNA damage, this complex regulates pre-mRNA splicing of a number of genes involved in DNA damage signaling and repair, thereby promoting the stability of these transcripts/proteins. Further, we show that abrogation of this complex results in sensitivity to DNA damage, defective DNA repair, and genomic instability. Interestingly, mutations in a number of proteins found within this complex have been identified in numerous cancer types. These data suggest that regulation of splicing by the BRCA1-mRNA splicing complex plays an important role in the cellular response to DNA damage.

The Economics of Total War and Reconstruction, 1914-1922

This chapter features a discussion of the economy and mobilization for the First World War. The authors analyse the implications and cost of total war, concluding with an examination of its contradictory legacies. In studying the war’s impact on Germany in particular, the chapter provides an in-depth look at the consequences of war on Europe’s strongest pre-war economy, without the complications of separating out the issues of a developing country, which can mimic those faced in wartime. The economic challenges that warring parties faced during the war included mobilization, warfare, labour shortage, impaired domestic economic activity, restricted international trade, a systematic redistribution of resources towards the war economy, food rationing, the predictable emergence of black markets, and a drop in living standards. The authors also discuss strategies to meet the significant financial demands associated with the war, and its tumultuous economic and political aftermath.

Marine organisms for bone repair and regeneration

Bioprospecting has led to increased interest in potential applications for marine organisms and their by-products. As a rich source of mineralising porous organisms, our seas and oceans could provide new directions for bone tissue engineering particularly in the supply of biomimetic templates that may enhance in vivo and ex vivo bone formation. In this chapter we examine the history of marine organism use in this field; exploring how these organisms could be utilised, given the problems of sustainability, and reviewing the current evidence to support their use for bone repair and regeneration.

DNA mismatch repair and the DNA damage response to ionizing radiation:making sense of apparently conflicting data

The DNA mismatch repair (MMR) pathway detects and repairs DNA replication errors. While DNA MMR-proficiency is known to play a key role in the sensitivity to a number of DNA damaging agents, its role in the cytotoxicity of ionizing radiation (IR) is less well characterized. Available literature to date is conflicting regarding the influence of MMR status on radiosensitivity, and this has arisen as a subject of controversy in the field. The aim of this paper is to provide the first comprehensive overview of the experimental data linking MMR proteins and the DNA damage response to IR. A PubMed search was conducted using the key words "DNA mismatch repair" and "ionizing radiation". Relevant articles and their references were reviewed for their association between DNA MMR and IR. Recent data suggest that radiation dose and the type of DNA damage induced may dictate the involvement of the MMR system in the cellular response to IR. In particular, the literature supports a role for the MMR system in DNA damage recognition, cell cycle arrest, DNA repair and apoptosis. In this review we discuss our current understanding of the impact of MMR status on the cellular response to radiation in mammalian cells gained from past and present studies and attempt to provide an explanation for how MMR may determine the response to radiation.

DNA mismatch repair and the transition to hormone independence in breast and prostate cancer

The molecular basis for the progression of breast and prostate cancer from hormone dependent to hormone independent disease remains a critical issue in the management of these two cancers. The DNA mismatch repair system is integral to the maintenance of genomic stability and suppression of tumorigenesis. No firm consensus exists regarding the implications of mismatch repair (MMR) deficiencies in the development of breast or prostate cancer. However, recent studies have reported an association between mismatch repair deficiency and loss of specific hormone receptors, inferring a potential role for mismatch repair deficiency in this transition. An updated review of the experimental data supporting or contradicting the involvement of MMR defects in the development and progression of breast and prostate cancer will be provided with particular emphasis on their implications in the transition to hormone independence.