On the Stability of BHJ and BFJ Adducts with BF, CO and N2

Ab-initio SCF MO calculations have been carried out on the adducts of borane and boron trifluoride with carbon monoxide, dinitrogen, and boron fluoride. The calculations correctly predict that BH3 forms stronger complexes than BF3 and that CO forms · stronger complexes than N2. It is predicted that the complexes of BF should be even stronger. These trends ca\u27n be understood from the energies and wave functions of the HOMO and LUMO orbitals of the components

On the Stability of BHJ and BFJ Adducts with BF, CO and N2

Ab-initio SCF MO calculations have been carried out on the adducts of borane and boron trifluoride with carbon monoxide, dinitrogen, and boron fluoride. The calculations correctly predict that BH3 forms stronger complexes than BF3 and that CO forms · stronger complexes than N2. It is predicted that the complexes of BF should be even stronger. These trends ca\u27n be understood from the energies and wave functions of the HOMO and LUMO orbitals of the components

The Melting Points of the Inert Gas Solids

The melting points of the heavy inert gases and of some other simple molecules show an excellent linear correlation with the depths of their diatomic potential wells, and the slope of the correlation line is in accord with Lindemann’s theory of melting

Low levels of ATM in breast cancer patients with clinical radiosensitivity

BACKGROUND AND PURPOSE Adjuvant radiotherapy for cancer can result in severe adverse side effects for normal tissues. In this respect, individuals with anomalies of the ATM (ataxia telangiectasia) protein/gene are of particular interest as they may be at risk of both breast cancer and clinical radiosensitivity. The association of specific ATM gene mutations with these pathologies has been well documented, however, there is uncertainty regarding pathological thresholds for the ATM protein. RESULTS Semi-quantitative immuno-blotting provided a reliable and reproducible method to compare levels of the ATM protein for a rare cohort of 20 cancer patients selected on the basis of their severe adverse normal tissue reactions to radiotherapy. We found that 4/12 (33%) of the breast cancer patients with severe adverse normal tissue reactions following radiotherapy had ATM protein levels < 55% compared to the mean for non-reactor controls. CONCLUSIONS ATM mutations are generally considered low risk alleles for breast cancer and clinical radiosensitivity. From results reported here we propose a tentative ATM protein threshold of ~55% for high-risk of clinical radiosensitivity for breast cancer patients.The authors acknowledge grant support from the Royal Australian and New Zealand College of Radiologists

Carbon Dynamics On The Louisiana Continental Shelf And Cross-Shelf Feeding Of Hypoxia

Large-scale hypoxia regularly develops during the summer on the Louisiana continental shelf. Traditionally, hypoxia has been linked to the vast winter and spring nutrient inputs from the Mississippi River and its distributary, the Atchafalaya River. However, recent studies indicate that much of the shelf ecosystem is heterotrophic. We used data from five late July shelfwide cruises from 2006 to 2010 to examine carbon and oxygen production and identify net autotrophic areas of phytoplankton growth on the Louisiana shelf. During these summer times of moderate river flows, shelfwide pH and particulate organic carbon (POC) consistently showed strong signals for net autotrophy in low salinity (\u3c25) waters near the river mouths. There was substantial POC removal via grazing and sedimentation in near-river regions, with 66–85 % of POC lost from surface waters in the low and mid-salinity ranges without producing strong respiration signals in surface waters. This POC removal in nearshore environments indicates highly efficient algal retention by the shelf ecosystem. Updated carbon export calculations for local estuaries and a preliminary shelfwide carbon budget agree with older concepts that offshore hypoxia is linked strongly to nutrient loading from the Mississippi River, but a new emphasis on cross-shelf dynamics emerged in this research. Cross-shelf transects indicated that river-influenced nearshore waters \u3c15 m deep are strong sources of net carbon production, with currents and wave-induced resuspension likely transporting this POC offshore to fuel hypoxia in adjacent mid-shelf bottom waters

A diverse view of science to catalyse change

Valuing diversity leads to scientific excellence, the progress of science and, most importantly, it is simply the right thing to do. We must value diversity not only in words, but also in actions

TMEM106B is a genetic modifier of frontotemporal lobar degeneration with C9orf72 hexanucleotide repeat expansions

Hexanucleotide repeat expansions in chromosome 9 open reading frame 72 (C9orf72) have recently been linked to frontotemporal lobar degeneration (FTLD) and amyotrophic lateral sclerosis, and may be the most common genetic cause of both neurodegenerative diseases. Genetic variants at TMEM106B influence risk for the most common neuropathological subtype of FTLD, characterized by inclusions of TAR DNA-binding protein of 43 kDa (FTLD-TDP). Previous reports have shown that TMEM106B is a genetic modifier of FTLD-TDP caused by progranulin (GRN) mutations, with the major (risk) allele of rs1990622 associating with earlier age at onset of disease. Here, we report that rs1990622 genotype affects age at death in a single-site discovery cohort of FTLD patients with C9orf72 expansions (n = 14), with the major allele correlated with later age at death (p = 0.024). We replicate this modifier effect in a 30-site international neuropathological cohort of FTLD-TDP patients with C9orf72 expansions (n = 75), again finding that the major allele associates with later age at death (p = 0.016), as well as later age at onset (p = 0.019). In contrast, TMEM106B genotype does not affect age at onset or death in 241 FTLD-TDP cases negative for GRN mutations or C9orf72 expansions. Thus, TMEM106B is a genetic modifier of FTLD with C9orf72 expansions. Intriguingly, the genotype that confers increased risk for developing FTLD-TDP (major, or T, allele of rs1990622) is associated with later age at onset and death in C9orf72 expansion carriers, providing an example of sign epistasis in human neurodegenerative disease