984 resultados para Neuronal Death


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Review of Coping with Choices to Die, by C. G. Prado. Cambridge: Cambridge University Press, 2011.

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This paper discusses the question of when pain and distress relief known to hasten death would cross the line between permissible conduct and killing. The issue is discussed in the context of organ donation after cardiac death, and considers the administration of analgesics, sedatives, and the controversial use of paralysing agents in the provision and withdrawal of ventilation.

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The decision of whether a cell should live or die is fundamental for the wellbeing of all organisms. Despite intense investigation into cell growth and proliferation, only recently has the essential and equally important idea that cells control/programme their own demise for proper maintenance of cellular homeostasis gained recognition. Furthermore, even though research into programmed cell death (PCD) has been an extremely active area of research there are significant gaps in our understanding of the process in plants. In this review, we discuss PCD during plant development and pathogenesis, and compare/contrast this with mammalian apoptosis. © 2008 Blackwell Publishing Ltd.

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The prevalence of myths preventing people partial to donation in Australia from consenting is unknown. Respondents (N = 468: 381 donors, 26 non-donors, 61 undecided) were surveyed about their (negative) donation beliefs. Approximately 30% of donors were neutral or supported negative beliefs about organ allocation, especially donation to undesirable organ recipients and a black market organ trade. Confusion about brain death, lack of family and religious support, and discomfort with donation were negative beliefs endorsed by some respondents irrespective of donor preference. Proportionally, donors had greater trust in hospitals/doctors than other groups. Some myths still exist but may vary with donation preference.

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Programmed cell death (PCD) and progenitor cell generation (of glial and in some brain areas also neuronal fate) in the CNS is an active process throughout life and is generally not associated with gliosis which means that PCD can be pathologically silent. The striking discovery that progenitor cell generation (of glial and in some brain areas neuronal fate) is widespread in the adult CNS (especially the hippocampus) suggest a much more dynamic scenario than previously thought and transcends the dichotomy between neurodevelopmental and neurodegenerative models of schizophrenia and related disorders. We suggest that the regulatory processes that control the regulation of PCD and the generation of progenitor cells may be disturbed in the early phase of psychotic disorders underpinning a disconnectivity syndrom at the onset of clinically overt disorders. An ongoing 1H-MRS study of the anterior hippocampus at 3 Tesla in mostly drug-naive first-episode psychosis patients suggests no change in NAA, but significant increases in myo-inositol and lactate. The data suggests that neuronal integrity in the anterior hippocampus is still intact at the early stage of illness or mainly only functionally impaired. However the increase in lactate and myo-inositol may reflect a potential disturbance of generation and PCD of progenitor cells (of glial and in selected brain areas also neuronal fate) at the onset of psychosis. If true the use of neuroprotective agents such as lithium or eicosapentaenoic acid (which inhibit PCD and support cell generation)in the early phase of psychotic disorders may be a potent treatment avenue to explore.

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Addictive drugs can activate systems involved in normal reward-related learning, creating long-lasting memories of the drug's reinforcing effects and the environmental cues surrounding the experience. These memories significantly contribute to the maintenance of compulsive drug use as well as cue-induced relapse which can occur even after long periods of abstinence. Synaptic plasticity is thought to be a prominent molecular mechanism underlying drug-induced learning and memories. Ethanol and nicotine are both widely abused drugs that share a common molecular target in the brain, the neuronal nicotinic acetylcholine receptors (nAChRs). The nAChRs are ligand-gated ion channels that are vastly distributed throughout the brain and play a key role in synaptic neurotransmission. In this review, we will delineate the role of nAChRs in the development of ethanol and nicotine addiction. We will characterize both ethanol and nicotine's effects on nAChR-mediated synaptic transmission and plasticity in several key brain areas that are important for addiction. Finally, we will discuss some of the behavioral outcomes of drug-induced synaptic plasticity in animal models. An understanding of the molecular and cellular changes that occur following administration of ethanol and nicotine will lead to better therapeutic strategies.

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Alcohol use disorders (AUDs) are a major public health problem, and the few treatment options available to those seeking treatment offer only modest success rates. There remains a need to identify novel targets for the treatment of AUDs. The neuronal nicotinic acetylcholine receptors (nAChRs) represent a potential therapeutic target in the brain, as recent human genetic studies have implicated gene variants in the α5 nAChR subunit as high risk factors for developing alcohol dependence. Here, we evaluate the role of 5* nAChR for ethanol-mediated behaviors using α5+/+ and α5-/- mice. We characterized the effect of hypnotic doses of ethanol and investigated drinking behavior using an adapted Drinking-in-the Dark (DID) paradigm that has been shown to induce high ethanol consumption in mice. We found the α5 subunit to be critical in mediating the sedative effects of ethanol. The α5-/- mice showed slower recovery from ethanol-induced sleep, as measured by loss of righting reflex. Additionally the α5-/- mice showed enhanced impairment to ethanol-induced ataxia. We found the initial sensitivity to ethanol and ethanol metabolism to be similar in both α5+/+ and α5-/- mice. Hence the enhanced sedation is likely due to a difference in the acute tolerance of ethanol in mice deficient of the α5 subunit. However the α5 subunit did not play a role in ethanol consumption for ethanol concentrations ranging from 5% to 30% in the DID paradigm. Additionally, varenicline (Chantix®) was effective in reducing ethanol intake in α5-/- mice. Together, our data suggest that the α5 nAChR subunit is important for the sedative hypnotic doses of ethanol but does not play a role in ethanol consumption. Varenicline can be a treatment option even when there is loss of function of the α5 nAChR subunit.

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Dengue is currently the most important arthropod-borne viral disease of humans. Recent work has shown dengue virus displays limited replication in its primary vector, the mosquito Aedes aegypti, when the insect harbors the endosymbiotic bacterium Wolbachia pipientis. Wolbachia-mediated inhibition of virus replication may lead to novel methods of arboviral control, yet the functional and cellular mechanisms that underpin it are unknown.

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There are two predominant theories for lumen formation in tissue morphogenesis: cavitation driven by cell death, and membrane separation driven by epithelial polarity. To define the mechanism of lumen formation in prostate acini, we examined both theories in several cell lines grown in three-dimensional (3D) Matrigel culture. Lumen formation occurred early in culture and preceded the expression of cell death markers for apoptosis (active caspase 3) and autophagy (LC-3). Active caspase 3 was expressed by very few cells and inhibition of apoptosis did not suppress lumen formation. Despite LC-3 expression in all cells within a spheroid, this was not associated with cell death. However, expression of a prostate-secretory protein coincided with lumen formation and subsequent disruption of polarized fluid movement led to significant inhibition of lumen formation. This work indicates that lumen formation is driven by the polarized movement of fluids and proteins in 3D prostate epithelial models and not by cavitation.

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Architecture Post Mortem surveys architecture’s encounter with death, decline, and ruination following late capitalism. As the world moves closer to an economic abyss that many perceive to be the death of capital, contraction and crisis are no longer mere phases of normal market fluctuations, but rather the irruption of the unconscious of ideology itself. Post mortem is that historical moment wherein architecture’s symbolic contract with capital is put on stage, naked to all. Architecture is not irrelevant to fiscal and political contagion as is commonly believed; it is the victim and penetrating analytical agent of the current crisis. As the very apparatus for modernity’s guilt and unfulfilled drives-modernity’s debt-architecture is that ideological element that functions as a master signifier of its own destruction, ordering all other signifiers and modes of signification beneath it. It is under these conditions that architecture theory has retreated to an “Alamo” of history, a final desert outpost where history has been asked to transcend itself. For architecture’s hoped-for utopia always involves an apocalypse. This timely collection of essays reformulates architecture’s relation to modernity via the operational death-drive: architecture is but a passage between life and death. This collection includes essays by Kazi K. Ashraf, David Bertolini, Simone Brott, Peggy Deamer, Didem Ekici, Paul Emmons, Donald Kunze, Todd McGowan, Gevork Hartoonian, Nadir Lahiji, Erika Naginski, and Dennis Maher. Contents: Introduction: ‘the way things are’, Donald Kunze; Driven into the public: the psychic constitution of space, Todd McGowan; Dead or alive in Joburg, Simone Brott; Building in-between the two deaths: a post mortem manifesto, Nadir Lahiji; Kant, Sade, ethics and architecture, David Bertolini; Post mortem: building deconstruction, Kazi K. Ashraf; The slow-fast architecture of love in the ruins, Donald Kunze; Progress: re-building the ruins of architecture, Gevork Hartoonian; Adrian Stokes: surface suicide, Peggy Deamer; A window to the soul: depth in the early modern section drawing, Paul Emmons; Preliminary thoughts on Piranesi and Vico, Erika Naginski; architectural asceticism and austerity, Didem Ekici; 900 miles to Paradise, and other afterlives of architecture, Dennis Maher; Index.

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Many organisations, companies and libraries started to use participatory webs to extend their services and engage more users. However, some librarians are still hesitated to implement participatory webs in their libraries, particularly in developing countries. This paper explores the advantages and disadvantages of participatory webs focusing on collaborative tagging. This paper draws from the literature of published articles discussing topics but not limited to participatory webs, participatory libraries, collaborative tagging, folksonomy and taxonomy. The advantages of implementation of the participatory webs in the library outweigh the disadvantages of it. Participatory webs do not necessarily mean the death of information organisation but it can supplement and improves information organisation in the library. This paper may help to broaden knowledge of LIS professionals in the implementation of participatory webs in the library.

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This series of research vignettes is aimed at sharing current and interesting research findings from our team of international Entrepreneurship researchers. In this vignette, Dr. Mervyn Morris considers the impact on family business operations due to the sudden and unexpected death of a key family member.

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This book describes the mortality for all causes of death and the trend in major causes of death since 1970s in Shandong Province, China.