Cascade-Exciton Model Analysis of Proton Spallation from 10 MeV to 5 GeV

We have used an extended version of the Cascade-Exciton Model (CEM) to analyze more than 600 excitation functions for proton induced reactions on 19 targets ranging from C-12 to Au-197, for incident energies ranging from 10 MeV to 5 GeV. We have compared the calculations to available data, to calculations using approximately two dozen other models, and to predictions of several phenomenological systematics. We present here our conclusions concerning the relative roles of different reaction mechanisms in the production of specific final nuclides. We comment on the strengths and weaknesses of the CEM and suggest possible further improvements to the CEM and to other models.Comment: 9 pages, to be published in Nuclear Instruments and Methods

Antiplatelet therapy and the vascular tree

While treatment with aspirin plus clopidogrel may be valid as an adjunct to percutaneous coronary intervention, other issues remain to be addressed before routine combination therapy is recommended for any level of atherosclerosi

Empathy at Work in a Social Service Agency: Individual Experiences and Systems Theory

This thesis explores empathy within interpersonal relationships at a social service organization. I conducted a research study to explore theoretical concepts and individuals’ experiences of these concepts in their work setting at a social service agency in New York City. I conducted observations and interviews through a lens of ecological systems theory and the relationalcultural approach. In this paper I review guiding concepts of empathy, attunement, and compassion fatigue, as well as the Sanctuary model. I share first-person accounts from interviews conducted during the research study to explicate individuals’ experiences related to the above concepts in their own words. I then provide concluding notes and ideas for change based on the data and my experience as a researcher

Expectations of fragment decay from highly excited nuclei

The statistical model is used to illustrate the consequences of a successive binary decay mechanism as the initial nuclear excitation is pushed towards the limits of stability. The partition of the excitation energy between light and heavy fragments is explicitly calculated, as are the consequences of the decay of the primary light fragments to particle-bound residual nuclei which would be observed experimentally. The test nucleus 100 44 Ru is considered at initial excitations of 100, 200, 400, and 800 MeV. Exit channels of n, p, and α; and 100 clusters of 3 ≤ Z ≤ 20 ≤ 4, 6 ≤ A ≤ 48 are considered from all nuclides in the deexcitation cascade. The total primary and final cluster yields are shown versus Z and initial excitation. The primary versus final yields are also shown individually for 12C, 26Mg, and 48Ca. We show how multifragmentation yields will change with the excitation energy due to a successive binary decay mechanism. Measurements that may be prone to misinterpretation are discussed, as are those that should be representative of initial nucleus excitation

Dynamical treatment of Fermi motion in a microscopic description of heavy ion collisions

A quasiclassical Pauli potential is used to simulate the Fermi motion of nucleons in a molecular dynamical simulation of heavy ion collisions. The thermostatic properties of a Fermi gas with and without interactions are presented. The inclusion of this Pauli potential into the quantum molecular dynamics (QMD) approach yields a model with well defined fermionic ground states, which is therefore also able to give the excitation energies of the emitted fragments. The deexcitation mechanisms (particle evaporation and multifragmentation) of the new model are investigated. The dynamics of the QMD with Pauli potential is tested by a wide range of comparisons of calculated and experimental double-differential cross sections for inclusive p-induced reactions at incident energies of 80 to 160 MeV. Results at 256 and 800 MeV incident proton energy are presented as predictions for completed experiments which are as yet unpublished

Arterial and Venous Thrombosis in Cancer Patients

The most frequent ultimate cause of death is myocardial arrest. In many cases this is due to myocardial hypoxia, generally arising from failure of the coronary macro- and microcirculation to deliver enough oxygenated red cells to the cardiomyocytes. The principle reason for this is occlusive thrombosis, either by isolated circulating thrombi, or by rupture of upstream plaque. However, an additionally serious pathology causing potentially fatal stress to the heart is extra-cardiac disease, such as pulmonary hypertension. A primary cause of the latter is pulmonary embolus, considered to be a venous thromboembolism. Whilst the thrombotic scenario has for decades been the dominating paradigm in cardiovascular disease, these issues have, until recently, been infrequently considered in cancer. However, there is now a developing view that cancer is also a thrombotic disease, and notably a disease predominantly of the venous circulation, manifesting as deep vein thrombosis and pulmonary embolism. Indeed, for many, a venous thromboembolism is one of the first symptoms of a developing cancer. Furthermore, many of the standard chemotherapies in cancer are prothrombotic. Accordingly, thromboprophylaxis in cancer with heparins or oral anticoagulation (such as Warfarin), especially in high risk groups (such as those who are immobile and on high dose chemotherapy), may be an important therapy. The objective of this communication is to summarise current views on the epidemiology and pathophysiology of arterial and venous thrombosis in cancer

The prevention and treatment of venous thromboembolism with LMWHs and new anticoagulants

As the risk factors for thrombosis are becoming better understood, so is the need for anticoagulation. The inherent difficulties with warfarin are such that a low-molecular-weight heparin (LMWH) is often the key therapeutic. However, there are several different species of LMWH available to the practitioner, which leads to the need for an objective guide. New agents are coming onto the marketplace, and these may supersede both warfarin and the heparins. The current report will review the biochemistry and pharmacology of different LWMHs and identify which are more suitable for the different presentations of venous thromboembolism. It will conclude with a brief synopsis of new agents which may supersede warfarin and heparin