Absolute single photoionization cross-sections of Br3+: Experiment and theory

Absolute single photoionization cross section measurements for Br3+ ions are reported in the photon energy range 44.79-59.54 eV at a photon energy resolution of 21 ±3 meV. Measurements were performed at the Advanced Light Source at Lawrence Berkeley National Laboratory using the merged-beams technique. Numerous resonance features in the experimental spectrum are assigned and their energies and quantum defect values are tabulated. The cross-section measurements are also compared with Breit-Pauli R-matrix calculations with suitable agreement over the photon energy range investigated. Analysis of the measured spectrum including Rydberg resonance series identifications produced a new emperical determination of the ionizational potential of Br3+ of 46.977 ± 0.050 eV, which is 805 meV lower than the most recently published value of 47.782 eV. This disparity between our determination and the earlier published value is similar to an 843 meV shift in the accepted ionization potential published for iso-electronic Se2+ as part of this same research program

Can a falling tree make a noise in two forests at the same time?

It is a commonplace to claim that quantum mechanics supports the old idea that a tree falling in a forest makes no sound unless there is a listener present. In fact, this conclusion is far from obvious. Furthermore, if a tunnelling particle is observed in the barrier region, it collapses to a state in which it is no longer tunnelling. Does this imply that while tunnelling, the particle can not have any physical effects? I argue that this is not the case, and moreover, speculate that it may be possible for a particle to have effects on two spacelike separate apparatuses simultaneously. I discuss the measurable consequences of such a feat, and speculate about possible statistical tests which could distinguish this view of quantum mechanics from a ``corpuscular'' one. Brief remarks are made about an experiment underway at Toronto to investigate these issues.Comment: 9 pp, Latex, 3 figs, to appear in Proc. Obsc. Unr. Conf.; Fig 2 postscript repaired on 26.10.9

RANTing about C9orf72

A noncoding repeat expansion in the C9orf72 gene is the most common genetic cause of frontotemporal dementia and amyotrophic lateral sclerosis. In this issue of Neuron, Ash et al. (2013) show that despite being noncoding the repeats are translated, leading to widespread neuronal aggregates of the translated proteins

Polygenic Risk Scoring is an Effective Approach to Predict Those Individuals Most Likely to Decline Cognitively Due to Alzheimer’s Disease

BACKGROUND: There is a clear need for simple and effective tests to identify individuals who are most likely to develop Alzheimer’s Disease (AD) both for the purposes of clinical trial recruitment but also for improved management of patients who may be experiencing early pre-clinical symptoms or who have clinical concerns. OBJECTIVES: To predict individuals at greatest risk of progression of cognitive impairment due to Alzheimer’s Disease in individuals from the Alzheimer’s Disease Neuroimaging Initiative (ADNI) using a polygenic risk scoring algorithm. To compare the performance of a PRS algorithm in predicting cognitive decline against that of using the pTau/Aß1-42 ratio CSF biomarker profile. DESIGN: A longitudinal analysis of data from the Alzheimer’s Disease Neuroimaging Initiative study conducted across over 50 sites in the US and Canada. SETTING: Multi-center genetics study. PARTICPANTS: 515 subjects who upon entry to the study were diagnosed as cognitively normal or with mild cognitive impairment. MEASUREMENTS: Use of genotyping and/or whole genome sequencing data to calculate polygenic risk scores and assess ability to predict subsequent cognitive decline as measured by CDR-SB and ADAS-Cog13 over 4 years RESULTS: The overall performance for predicting those individuals who would decline by at least 15 ADAS-Cog13 points from a baseline mild cognitive impairment in 4 years was 72.8% (CI:67.9-77.7) AUC increasing to 79.1% (CI: 75.6-82.6) when also including cognitively normal participants. Assessing mild cognitive impaired subjects only and using a threshold of greater than 0.6, the high genetic risk participant group declined, on average, by 1.4 points (CDR-SB) more than the low risk group over 4 years. The performance of the PRS algorithm tested was similar to that of the pTau/Aß1-42 ratio CSF biomarker profile in predicting cognitive decline. CONCLUSION: Calculating polygenic risk scores offers a simple and effective way, using DNA extracted from a simple mouth swab, to select mild cognitively impaired patients who are most likely to decline cognitively over the next four years

A rare presentation of atypical demyelination: tumefactive multiple sclerosis causing Gerstmann's syndrome

r. KS has been supported by a Higher Education Funding Council for England (HEFCE) Clinical Senior Lectureshi

Improved ventricular function during inhalation of PGI(2) aerosol partly relies on enhanced myocardial contractility

Inhaled prostacyclin (PGI(2)) aerosol induces selective pulmonary vasodilation. Further, it improves right ventricular ( RV) function, which may largely rely on pulmonary vasodilation, but also on enhanced myocardial contractility. We investigated the effects of the inhaled PGI(2) analogs epoprostenol (EPO) and iloprost (ILO) on RV function and myocardial contractility in 9 anesthetized pigs receiving aerosolized EPO (25 and 50 ng center dot kg(-1) center dot min(-1)) and, consecutively, ILO (60 ng center dot kg(-1) center dot min(-1)) for 20 min each. We measured pulmonary artery pressure ( PAP), RV ejection fraction (RVEF) and RV end-diastolic-volume (RV-EDV), and left ventricular end-systolic pressure-volume-relation (end-systolic elastance, E-es). EPO and ILO reduced PAP, increased RVEF and reduced RVEDV. E-es was enhanced during all doses tested, which reached statistical significance during EPO25ng and ILO, but not during EPO50ng. PGI(2) aerosol enhances myocardial contractility in healthy pigs, contributing to improve RV function. Copyright (C) 2005 S. Karger AG, Basel

Exome sequencing in a consanguineous family clinically diagnosed with early-onset Alzheimer's disease identifies a homozygous CTSF mutation

We have previously reported the whole genome genotyping analysis of 2 consanguineous siblings clinically diagnosed with early onset Alzheimer's disease (AD). In this analysis, we identified several large regions of homozygosity shared between both affected siblings, which we suggested could be candidate loci for a recessive genetic lesion underlying the early onset AD in these cases. We have now performed exome sequencing in one of these siblings and identified the potential cause of disease: the CTSF c.1243G>A:p.Gly415Arg mutation in homozygosity. Biallelic mutations in this gene have been shown to cause Type B Kufs disease, an adult-onset neuronal ceroid lipofuscinosis with some cases resembling the impairment seen in AD

Lack of correlation between Ki-67 labelling index and tumor size of anterior pituitary adenomas

AIMS AND BACKGROUND: The Ki-67 is a nuclear antigen detected by the monoclonal antibody MIB-1 and its Labeling Index (LI) is considered a marker of normal and abnormal cell proliferation. Pituitary adenomas are generally well differentiated neoplasms, even if in about one third of cases they are invasive of surrounding tissues. The aim of this study is to evaluate the correlation between Ki-67 labelling index and tumor size of pituitary adenomas extimated by means CT and MRI and confirmed at operation. METHODS: Using the monoclonal antibody MIB-1, we evaluated the expression of Ki-67 in 121 anterior pituitary adenomas consecutively operated on in a 48-month period. RESULTS: In relation to neuroradiological (CT and MRI) and surgically verified tumor size, we identified 24 microadenomas, 27 intrasellar macroadenomas, 34 intra-suprasellar macroadenomas, and 36 intra-supra-parasellar macroadenomas. The adenomas were non-infiltrating (76 cases) and infiltrating (45 cases) adenomas. The wall of the cavernous sinus (CS) was infiltrated in 18 cases. Forty-eight adenomas were non-functioning and 73 functioning. The overall mean ± SD Ki-67 LI was 2.72 ± 2.49% (median 1.6). It was 2.59 ± 1.81 in microadenomas, 2.63 ± 3.45 in intrasellar macroadenomas, 1.91 ± 2.11 in intra-suprasellar macroadenomas, and 3.29 ± 5.45 in intra-supra-parasellar macroadenomas (p = 0.27). It was 3.73 ± 5.13% in infiltrating and 2.03 ± 2.41% in non-infiltrating adenomas (p = 0.02), and 5.61 ± 7.19% in CS-infiltrating versus 2.09 ± 2.37% in CS-non-infiltrating adenomas (p = 0.0005). CONCLUSIONS: Our preliminary results seem to exclude significative correlations between Ki-67 LI and tumor size of anterior pituitary adenomas, even if this index can be considered a useful marker in the determination of the infiltrative behaviour of these tumors