475 research outputs found

    The Bar in America: The Role of Elitism in a Liberal Democracy

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    Part I of this Note argues that liberal democracy, the free market, and science have contributed to the increasing atomization of American society. When each person and her views are glorified, universal standards of good become undermined, values become relative, and a sense of community becomes evanescent. Part II argues that individualism is incapable of accounting for the commonweal and therefore is inherently amoral because morality is concerned largely with determining when an individual\u27s will should be subservient to the will of others. Part III considers the nature of elitism and equality and attributes the demise of elitist institutions in America to the rise of individualism and egalitarianism. When liberal democracy, bolstered by the free market and science, overturned discriminatory institutions of the past, it rightfully eliminated the immoral excesses of institutional elitism. Unfortunately, liberal democracy did so without discretion, discrediting not only the immoral aspects of elitism but its desirable aspects as well. The ethic of service to others that is the most sacred quality of the legal profession, therefore, is threatened. Moreover, the destruction of elitist institutions has left a vacuum that has not been filled. The country, therefore, needs a force that promotes a sense of community and embodies an ethos of service to others. Finally, Part IV argues that the Bar is a distinctive public calling which engenders special access to, and control over, the instruments of government and a unique ability to affect private rights. By virtue of this elite position, the Bar has a moral responsibility to serve the public. The Bar should fulfill its duties by countering the atomizing influences of liberal democracy, the free market, and science through the example of service to others

    Introduction of Hypermatrix and Operator Notation into a Discrete Mathematics Simulation Model of Malignant Tumour Response to Therapeutic Schemes In Vivo. Some Operator Properties

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    The tremendous rate of accumulation of experimental and clinical knowledge pertaining to cancer dictates the development of a theoretical framework for the meaningful integration of such knowledge at all levels of biocomplexity. In this context our research group has developed and partly validated a number of spatiotemporal simulation models of in vivo tumour growth and in particular tumour response to several therapeutic schemes. Most of the modeling modules have been based on discrete mathematics and therefore have been formulated in terms of rather complex algorithms (e.g. in pseudocode and actual computer code). However, such lengthy algorithmic descriptions, although sufficient from the mathematical point of view, may render it difficult for an interested reader to readily identify the sequence of the very basic simulation operations that lie at the heart of the entire model. In order to both alleviate this problem and at the same time provide a bridge to symbolic mathematics, we propose the introduction of the notion of hypermatrix in conjunction with that of a discrete operator into the already developed models. Using a radiotherapy response simulation example we demonstrate how the entire model can be considered as the sequential application of a number of discrete operators to a hypermatrix corresponding to the dynamics of the anatomic area of interest. Subsequently, we investigate the operators’ commutativity and outline the “summarize and jump” strategy aiming at efficiently and realistically address multilevel biological problems such as cancer. In order to clarify the actual effect of the composite discrete operator we present further simulation results which are in agreement with the outcome of the clinical study RTOG 83–02, thus strengthening the reliability of the model developed

    Applying a 4D multiscale in vivo tumor growth model to the exploration of radiotherapy scheduling: The effects of weekend treatment gaps and p53 gene status on the response of fast growing solid tumors

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    The present paper aims at demonstrating clinically oriented applications of the multiscale four dimensional in vivo tumor growth simulation model previously developed by our research group. To this end the effect of weekend radiotherapy treatment gaps and p53 gene status on two virtual glioblastoma tumors differing only in p53 gene status is investigated in silico. Tumor response predictions concerning two rather extreme dose fractionation schedules (daily dose of 4.5 Gy administered in 3 equal fractions) namely HART (Hyperfractionated Accelerated Radiotherapy weekend less) 54 Gy and CHART (Continuous HART) 54 Gy are presented and compared. The model predictions suggest that, for the same p53 status, HART 54 Gy and CHART 54 Gy have almost the same long term effects on locoregional tumor control. However, no data have been located in the literature concerning a comparison of HART and CHART radiotherapy schedules for glioblastoma. As non small cell lung carcinoma (NSCLC) may also be a fast growing and radiosensitive tumor, a comparison of the model predictions with the outcome of clinical studies concerning the response of NSCLC to HART 54 Gy and CHART 54 Gy is made. The model predictions are in accordance with corresponding clinical observations, thus strengthening the potential of the model

    Acute abdomen due to primary omentitis: a case report

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    This is an Open Access article distributed under the terms of the Creative Commons Attribution Licens

    Interplay between the endogenous opioid system and proteasome complex: Beyond signaling

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    Intracellular signaling mechanisms underlying the opioid system regulation of nociception, neurotransmitters release, stress responses, depression, and the modulation of reward circuitry have been investigated from different points of view. The presence of the ubiquitin proteasome system (UPS) in the synaptic terminations suggest a potential role of ubiquitin-dependent mechanisms in the control of the membrane occupancy by G protein-coupled receptors (GPCRs), including those belonging to the opioid family. In this review, we focused our attention on the role played by the ubiquitination processes and by UPS in the modulation of opioid receptor signaling and in pathological conditions involving the endogenous opioid system. The collective evidence here reported highlights the potential usefulness of proteasome inhibitors in neuropathic pain, addictive behavior, and analgesia since these molecules can reduce pain behavioral signs, heroin self-administration, and the development of morphine analgesic tolerance. Moreover, the complex mechanisms involved in the effects induced by opioid agonists binding to their receptors include the ubiquitination process as a post-translational modification which plays a relevant role in receptor trafficking and degradation. Hence, UPS modulation may offer novel opportunities to control the balance between therapeutic versus adverse effects evoked by opioid receptor activation, thus, representing a promising druggable target
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