Search results for 'pathophysiology' (try it on Scholar)

41 found
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  1.  20
    A. H. Louie (2013). Explications of Functional Entailment in Relational Pathophysiology. Axiomathes 23 (1):81-107.
    I explicate how various relational interactions between (M,R)-systems may have realizations in pathophysiology, and how the possible reversals of the effects of these interactions then become therapeutic models. Functional entailment receives a rigorous category-theoretic treatment, and plays a crucial role in this continuing saga of relational biology.
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  2.  15
    Yue Chen (2003). Spatial Integration in Perception and Cognition: An Empirical Approach to the Pathophysiology of Schizophrenia. Behavioral and Brain Sciences 26 (1):86-87.
    Evidence for a dysfunction in cognitive coordination in schizophrenia is emerging, but it is not specific enough to prove (or disprove) this long-standing hypothesis. Many aspects of the external world are spatially mapped in the brain. A comprehensive internal representation relies on integration of information across space. Focus on spatial integration in the perceptual and cognitive processes will generate empirical data that shed light on the pathophysiology of schizophrenia.
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  3. Björn Albrecht, Henrik Uebel-von Sandersleben, Holger Gevensleben & Aribert Rothenberger (2015). Pathophysiology of ADHD and Associated Problems—Starting Points for NF Interventions? Frontiers in Human Neuroscience 9.
  4.  16
    Joseph L. Price & Wayne C. Drevets (2012). Neural Circuits Underlying the Pathophysiology of Mood Disorders. Trends in Cognitive Sciences 16 (1):61-71.
  5. Alexander Bürkle (2001). Physiology and Pathophysiology of Poly(ADP‐Ribosyl)Ation. Bioessays 23 (9):795-806.
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  6. Klaus Poeck (1969). Pathophysiology of Emotional Disorders Associated with Brain Damage. In P. Vinken & G. Bruyn (eds.), Handbook of Clinical Neurology. North Holland 3--343.
     
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  7.  4
    Christophe Antczak, Ingrid De Meester & Brigitte Bauvois (2001). Ectopeptidases in pathophysiology. Bioessays 23 (3):251-260.
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  8. Kingsley M. Stevens (1981). The Pathophysiology of Influenzal Pneumonia in 1918. Perspectives in Biology and Medicine 25 (1):115-125.
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  9.  1
    E. G. Lakatta (1988). Chaotic Behavior of Myocardial Cells: Possible Implications Regarding the Pathophysiology of Heart Failure. Perspectives in Biology and Medicine 32 (3):421-433.
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  10.  2
    Srinivasa N. Raja & Ursula Wesselmann (1997). Sympathetically Maintained Pain: Confusing Classification, Ill-Defined Diagnostic Criteria, and Puzzling Pathophysiology. Behavioral and Brain Sciences 20 (3):462-462.
    Recent studies indicate a role of the sympathetic nervous system in acute and chronic pain. However, the terminology of the clinical sympathetically maintained pain (SMP) syndromes continues to be confusing and the criteria for diagnosis of SMP are being refined. (blumberg et al.) Despite significant progress in recent years, the mechanisms of the interaction between the sympathetic and sensory systems in SMP remain puzzling.
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  11. M. Corbetta, M. J. Kincade & G. L. Shulman (2002). Two Neural Systems for Visual Orienting and the Pathophysiology of Unilateral Spatial Neglect. In Hans-Otto Karnath, David Milner & Giuseppe Vallar (eds.), The Cognitive and Neural Bases of Spatial Neglect. Oxford University Press 259--273.
     
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  12. Sheng Li & Gerard E. Francisco (2015). New Insights Into the Pathophysiology of Post-Stroke Spasticity. Frontiers in Human Neuroscience 9.
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  13. Marian A. Packham (1984). Platelets: Pathophysiology and Antiplatelet Drug Therapy By Harvey J. Weiss. Perspectives in Biology and Medicine 27 (2):314-316.
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  14. Joseph C. Wu, Benjamin V. Siegel, Richard J. Haier & Monte S. Buchsbaum (1990). Testing the Swerdlow/Koob Model of Schizophrena Pathophysiology Using Positron Emission Tomography. Behavioral and Brain Sciences 13 (1):168-170.
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  15.  24
    Laurence Foss (1998). The Biomedical Paradigm and the Nobel Prize: Is It Time for a Change? Theoretical Medicine and Bioethics 19 (6):621-644.
    An examination of the early history of Nobel Committee deliberations, coupled with a survey of discoveries for which prizes have been awarded to date – and, equally revealing, discoveries for which prizes have not been awarded – reveals a pattern. This pattern suggests that Committee members may have internalized the received, biomedical model and conferred awards in accord with the physicalistic premises that ground this model. I consider the prospect of a paradigm change in medical science and the possible repercussions (...)
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  16. Joseph T. Giacino & J. T. Whyte (2005). The Vegetative and Minimally Conscious States: Current Knowledge and Remaining Questions. Journal of Head Trauma Rehabilation 20 (1):30-50.
  17.  6
    Sergio Bagnato, Cristina Boccagni, A. Sant'Angelo, Alexander A. Fingelkurts, Andrew A. Fingelkurts, C. Gagliardo & G. Galardi (2014). Long-Lasting Coma. Functional Neurology 29 (3):201-205.
    In this report, we describe the case of a patient who has remained in a comatose state for more than one year after a traumatic and hypoxic brain injury. This state, which we refer to as long-lasting coma (LLC), may be a disorder of consciousness with significantly different features from those of conventional coma, the vegetative state, or brain death. On the basis of clinical, neurophysiological and neuroimaging data, we hypothesize that a multilevel involvement of the ascending reticular activating system (...)
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  18.  10
    Niall Shanks, Ray Greek & Jean Greek (2009). Are Animal Models Predictive for Humans? Philosophy, Ethics, and Humanities in Medicine 4 (1):2.
    It is one of the central aims of the philosophy of science to elucidate the meanings of scientific terms and also to think critically about their application. The focus of this essay is the scientific term predict and whether there is credible evidence that animal models, especially in toxicology and pathophysiology, can be used to predict human outcomes. Whether animals can be used to predict human response to drugs and other chemicals is apparently a contentious issue. However, when one (...)
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  19. Rajendra D. Badgaiyan (2009). Theory of Mind and Schizophrenia☆. Consciousness and Cognition 18 (1):320-322.
    A number of cognitive and behavioral variables influence the performance in tasks of theory of mind (ToM). Since two of the most important variables, memory and explicit expression, are impaired in schizophrenic patients, the ToM appears inconsistent in these patients. An ideal instrument of ToM should therefore account for deficient memory and impaired ability of these patients to explicitly express intentions. If such an instrument is developed, it should provide information that can be used not only to understand the (...) but also to monitor patients. (shrink)
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  20.  51
    Kai Vogeley, M. Moskopp Kurthen, P. Falkai & W. Maier (1999). Essential Functions of the Human Self Model Are Implemented in the Prefrontal Cortex. Consciousness and Cognition 8 (3):343-363.
    The human self model comprises essential features such as the experiences of ownership, of body-centered spatial perspectivity, and of a long-term unity of beliefs and attitudes. In the pathophysiology of schizophrenia, it is suggested that clinical subsyndromes like cognitive disorganization and derealization syndromes reflect disorders of this self model. These features are neurobiologically instantiated as an episodically active complex neural activation pattern and can be mapped to the brain, given adequate operationalizations of self model features. In its unique capability (...)
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  21. Anand Kumar & Barry Smith (2003). The Unified Medical Language System and the Gene Ontology: Some Critical Reflections. In KI 2003: Advances in Artificial Intelligence.
    The Unified Medical Language System and the Gene Ontology are among the most widely used terminology resources in the biomedical domain. However, when we evaluate them in the light of simple principles for wellconstructed ontologies we find a number of characteristic inadequacies. Employing the theory of granular partitions, a new approach to the understanding of ontologies and of the relationships ontologies bear to instances in reality, we provide an application of this theory in relation to an example drawn from the (...)
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  22.  41
    Helena Sunvisson, Barbara Habermann, Sara Weiss & Patricia Benner (2009). Augmenting the Cartesian Medical Discourse with an Understanding of the Person's Lifeworld, Lived Body, Life Story and Social Identity. Nursing Philosophy 10 (4):241-252.
    Using three paradigm cases of persons living with Parkinson's Disease (PD) the authors make a case for augmenting and enriching a Cartesian medical account of the pathophysiology of PD with an enriched understanding of the lived body experience of PD, the lived implications of PD for a particular person's concerns and coping with the illness. Linking and adding a thick description of the lived experience of PD can enrich caregiving imagination and attunement to the patient's possibilities, concerns and constraints. (...)
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  23.  4
    A. R. Singh & S. A. Singh (2009). Notes on a Few Issues in the Philosophy of Psychiatry. Mens Sana Monographs 7 (1):128.
    _The first part called the Preamble tackles: (a) the issues of silence and speech, and life and disease; (b) whether we need to know some or all of the truth, and how are exact science and philosophical reason related; (c) the phenomenon of Why, How, and What; (d) how are mind and brain related; (e) what is robust eclecticism, empirical/scientific enquiry, replicability/refutability, and the role of diagnosis and medical model in psychiatry; (f) bioethics and the four principles of beneficence, non-malfeasance, (...)
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  24.  10
    William T. Carpenter Jr (2012). The Future of Schizophrenia Pharmacotherapeutics: Not so Bleak. Mens Sana Monographs 10 (1):13.
    Chlorpromazine efficacy in schizophrenia was observed 60 years ago. Advances in pharmacotherapy of this disorder have been modest with effectiveness still limited to the psychosis psychopathology and mechanism still dependent on dopamine antagonism. While a look backward may generate pessimism, future discovery may be far more robust. The near future will see significant changes in paradigms applied in discovery. Rather than viewing schizophrenia as a disease entity represented by psychosis, the construct will be deconstructed into component psychopathology domains. Each domain (...)
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  25.  11
    S. Goldman, Regional Cerebral Glucose Metabolism in Akinetic Catatonia and After Remission.
    K L Kahlbaum published in 1874 the first recorded description of catatonia. Akinetic catatonia is now defined as a neuropsychiatric syndrome principally characterised by akinesia, mutism, stupor, and catalepsy. 1 Even if some advances have been made in the recognition of catatonia, in particular by the development of different rating scales, 1 the pathophysiology of this syndrome is not clearly established. A right handed 14 year old girl presented with akinetic catatonia during an episode of depression in the context (...)
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  26.  4
    Geoffrey Burnstock (2012). Purinergic Signalling: Its Unpopular Beginning, its Acceptance and its Exciting Future. Bioessays 34 (3):218-225.
    Adenosine 5′-triphosphate (ATP) was identified in 1970 as the transmitter responsible for non-adrenergic, non-cholinergic neurotransmission in the gut and bladder and the term ‘purinergic’ was coined. Purinergic cotransmission was proposed in 1976 and ATP is now recognized as a cotransmitter in all nerves in the peripheral and central nervous systems. P1 (adenosine) and P2 (ATP) receptors were distinguished in 1978. Cloning of these receptors in the early 1990s was a turning point in the acceptance of the purinergic signalling hypothesis. There (...)
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  27.  26
    Andrew J. E. Seely (2013). Embracing the Certainty of Uncertainty: Implications for Health Care and Research. Perspectives in Biology and Medicine 56 (1):65-77.
    Centuries of scientific progress have been devoted to reducing uncertainty. Newtonian physics, introduced over 300 years ago, allowed for precise prediction of planetary and tidal motion, falling bodies and infinitely more, in addition to allowing the construction of the material world. The 20th century witnessed a revolution in our understanding of organ and cellular function and dysfunction, elucidation of pathways, mediators, receptors, and molecular interactions, and breakthroughs in the characterization of replication, transcription, and translation, all of which has been integral (...)
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  28.  8
    Sean A. Spence & Chris D. Frith (1999). Towards a Functional Anatomy of Volition. Journal of Consciousness Studies 6 (8-9):8-9.
    In this paper we examine the functional anatomy of volition, as revealed by modern brain imaging techniques, in conjunction with neuropsychological data derived from human and non-human primates using other methodologies. A number of brain regions contribute to the performance of consciously chosen, or ‘willed', actions. Of particular importance is dorsolateral prefrontal cortex , together with those brain regions with which it is connected, via cortico-subcortical and cortico-cortical circuits. That aspect of free will which is concerned with the voluntary selection (...)
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  29.  6
    Debra Titone & J. Bruno Debruille (2003). Guarding Against Over-Inclusive Notions of “Context”: Psycholinguistic and Electrophysiological Studies of Specific Context Functions in Schizophrenia. Behavioral and Brain Sciences 26 (1):108-109.
    Phillips & Silverstein offer an exciting synthesis of ongoing efforts to link the clinical and cognitive manifestations of schizophrenia with cellular accounts of its pathophysiology. We applaud their efforts but wonder whether the highly inclusive notion of “context” adequately captures some important details regarding schizophrenia and NMDA/glutamate function that are suggested by work on language processing and cognitive electrophysiology.
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  30.  16
    Mohamed Y. Rady & Joseph L. Verheijde (2010). Retraction: End-of-Life Discontinuation of Destination Therapy with Cardiac and Ventilatory Support Medical Devices: Physician-Assisted Death or Allowing the Patient to Die? BMC Medical Ethics 11 (1):20-.
    BackgroundBioethics and law distinguish between the practices of "physician-assisted death" and "allowing the patient to die."DiscussionAdvances in biotechnology have allowed medical devices to be used as destination therapy that are designed for the permanent support of cardiac function and/or respiration after irreversible loss of these spontaneous vital functions. For permanent support of cardiac function, single ventricle or biventricular mechanical assist devices and total artificial hearts are implanted in the body. Mechanical ventilators extrinsic to the body are used for permanent support (...)
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  31.  16
    John C. Marshall, Jennifer M. Gurd & Gereon R. Fink (2002). Catatonia, Motor Neglect, and Hysterical Paralysis: Some Similarities and Differences. Behavioral and Brain Sciences 25 (5):587-588.
    We outline some ways in which motor neglect (the underutilization of a limb despite adequate strength) and hysterical paralysis (failure to move a limb despite no relevant structural damage or disease) may throw light on the pathophysiology of catatonia. We also comment on the manifold inadequacies of distinguishing too firmly between symptoms of “neurologic origin” and of “psychiatric origin.”.
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  32.  12
    Jürgen Zielasek & Wolfgang Gaebel (2008). Modularity in Philosophy, the Neurosciences, and Psychiatry. Poiesis and Praxis 6 (1-2):93-108.
    The neurosciences are generating new findings regarding genetic and neurobiological aspects of the pathophysiology of mental disorders. Especially, certain genetic risk factors like neuregulin-1 seem to predispose individuals to a psychotic phenotype beyond the limits of traditional classificatory boundaries between organic psychoses in Alzheimer’s disease, bipolar affective disorder and schizophrenia. Little, however, is known about how such genetic risk factors actually confer an increased risk for psychosis in an individual patient. A gap between neuroscientific findings and psychopathological phenomena exists. (...)
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  33.  12
    Else Daniel Kondziella, Klaus Hansen R. Danielsen, Erik Carsten Thomsen & Peter Arlien-Soeborg C. Jansen (2009). 1 H Mr Spectroscopy of Gray and White Matter in Carbon Monoxide Poisoning. Journal of Neurology 256 (6).
    Carbon monoxide intoxication leads to acute and chronic neurological deficits, but little is known about the specific noxious mechanisms. 1 H magnetic resonance spectroscopy may allow insight into the pathophysiology of CO poisoning by monitoring neurochemical disturbances, yet only limited information is available to date on the use of this protocol in determining the neurological effects of CO poisoning. To further examine the short-term and long-term effects of CO on the central nervous system, we have studied seven patients with (...)
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  34.  14
    Alfonso Troisi & Francesca R. D'Amato (2005). Deficits in Affiliative Reward: An Endophenotype for Psychiatric Disorders? Behavioral and Brain Sciences 28 (3):365-366.
    Depue & Morrone-Strupinsky's (D&M-S's) model of affiliation meets the criteria advanced for the definition of behavior systems and endophenotypes. We argue that its application in psychiatry could be useful for identifying a biological pathophysiology common to a variety of conditions that are currently classified in very different categories of psychiatric nosography, including autism, schizoid personality, primary psychopathy, and dismissing attachment.
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  35.  13
    Gregory Fricchione (2002). Catatonia: A Disorder of Motivation and Movement. Behavioral and Brain Sciences 25 (5):584-585.
    Georg Northoff employs a comparison with Parkinson's disease in an effort to tease apart the underlying pathophysiology of psychogenic catatonia. Northoff's extensive treatment of the subject is abetted by his own research as well as the research of others. Nevertheless, a number of points concerning basal ganglia/thalamocortical processing need to be raised, some adding support to his hypothesis and others detracting from it.
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  36.  9
    Raffaele Manni, Michele Terzaghi, Pietro-Luca Ratti, Alessandra Repetto, Roberta Zangaglia & Claudio Pacchetti (2011). Hallucinations and REM Sleep Behaviour Disorder in Parkinson's Disease: Dream Imagery Intrusions and Other Hypotheses. Consciousness and Cognition 20 (4):1021-1026.
    REM sleep behaviour disorder is a REM sleep-related parasomnia which may be considered a “dissociated state of wakefulness and sleep”, given that conflicting elements of REM sleep and of wakefulness coexist during the episodes, leading to motor and behavioural manifestations reminiscent of an enacted dream. RBD has been reported in association with α-synucleinopathies: around a third of patients with Parkinson’s disease have full-blown RBD.Recent data indicate that PD patients with RBD are more prone to hallucinations than PD patients without this (...)
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  37.  3
    Carrie E. Bearden & John R. Monterosso (2002). Catatonia Isn't Ready for a Unified Theory. Behavioral and Brain Sciences 25 (5):579-580.
    Northoff's target article presents a unifying theory of the pathophysiology of catatonia, as compared to Parkinson's disease. We address two arguments in particular that do not appear justified by available evidence: (1) The physiological basis of catatonia is the breakdown of right hemisphere prefrontal-parietal cortical connectivity, and (2) Dysfunction in this system results in specific deficits in termination of action.
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  38.  10
    Bernhard Bogerts (2002). Does Catatonia Have a Specific Brain Biology? Behavioral and Brain Sciences 25 (5):580-581.
    Dr. Northoff's comprehensive comparison of clinical symptoms and neurobiological findings in catatonia with that of Parkinson's disease through integration of various levels of investigation, from neurochemistry up to the subjective experience, is a good example of the new strategies we need to improve our understanding of psychiatric disorders. His multimodal approach, leading to the hypothesis that different pathophysiologies of transcortical “horizontal modulation” and “bottom-up/top-down” – orbitofrontal/basal ganglia – “vertical modulations,” may explain many clinical aspects of catatonia and Parkinson's disease, and (...)
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  39.  3
    William A. Phillips & Steven M. Silverstein (2004). Unity and Diversity in Disorders of Cognitive Coordination. Behavioral and Brain Sciences 27 (4):594-599.
    Studies of aging and autism as outlined by Bertone, Mottron, & Faubert (Bertone et al.) and by Faubert & Bertone suggest that disorders of cognitive coordination involving impairments of dynamic gestalt grouping and context-sensitivity may be common to several different disorders. We agree that such studies may shed light on these processes and their neuronal bases. However, we also emphasize that dynamic grouping and context-sensitivity can fail in various ways, and that, although the underlying pathophysiology may often involve NMDA-receptor (...)
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  40. Inga Griskova & Sidse M. Arnfred (2008). An Electrophysiological Approach to Investigations of Sensory Dysfunction in Schizophrenia. Poiesis and Praxis 6 (3-4):175-189.
    Sensory dysfunction has been shown to be a part of the pathophysiology of schizophrenia. Nowadays we have an objective, non-invasive tool with which to measure neural manifestations of sensory dysfunction. Defined as time-locked changes to external stimuli in the EEG, event-related potentials (ERPs) provide an objective index of information processing in the human brain. Importantly, ERPs may be analyzed through a variety of approaches such as conventional ERP analysis, analysis in the time-frequency domain, microstate segmentation and topographical analysis, as (...)
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  41. K. Omote (1997). Are Intrinsic Inhibitory Systems Activated or Inhibited in Pathological Pain States? Behavioral and Brain Sciences 20 (3):461-462.
    Neuroplastic changes in the inhibitory systems contribute to pathological pains such as hyperalgesia. Activation or inhibition of the intrinsic inhibitory systems may depend on the pathophysiology which induces a sustained pain state. The mechanisms of hyperalgesia, opioid insensitivity following nerve injury, and opioid tolerance may be related to common neuroplastic changes. [wiesenfeld-hallin et al.].
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