scholarly journals Toxic encephalopathy in a clinicl case of polycythemia vera

2020 ◽  
Vol 18 (4) ◽  
pp. 249-255
Author(s):  
P. I. Kuznetsova ◽  
M. M. Tanashyan ◽  
A. A. Kornilova
Keyword(s):  
Hepatic Encephalopathy ◽  
Cerebrovascular Disorders ◽  
Toxic Encephalopathy ◽  
Vein Thrombosis ◽  
Toxic Damage ◽  
Myeloproliferative Diseases ◽  
Paramagnetic Substance ◽  
The Relationship ◽  
The Brain

The article deals with a clinical case description of a female patient with toxic encephalopathy against the background of Ph-negative myeloproliferative diseases. The article discusses symptoms and neuroimaging of hepatic encephalopathy developed as a result of a shunt placed after portal vein thrombosis. The issues of etiology and pathogenesis of hepatic encephalopathy, principles of therapy, as well as the unique clinical picture of nervous system damage in this condition are also discussed. Data on the role of manganese in development of toxic encephalopathy, accumulation of paramagnetic substance in the basal ganglia of the brain and development of extrapyramidal symptoms are presented. The pathogenesis of toxic damage to neurons, increase in their sensitivity to hypoxia, and the relationship with the risk of cerebrovascular disorders and development of chronic cerebral ischemia, contributing to reduction of cognitive functions, are described.

The role of tryptophan in hepatic encephalopathy

1993 ◽  
Vol 5 (4) ◽  
pp. 71-75
Author(s):  
C. Aaldijk ◽  
W.W. Van Den Broek ◽  
R.C. Van Der Mast
Keyword(s):  
Hepatic Encephalopathy ◽  
Clinical Picture ◽  
Serotonergic System ◽  
Pathogenetic Mechanisms ◽  
Research Findings ◽  
Glutamine Synthesis ◽  
The Brain ◽  
Tryptophan Uptake

SummaryIn this review the most important hypotheses for the occurrence of the clinical picture of hepatic encephalopathy are discussed. As possible pathogenetic mechanisms are raised: dysfunction of the serotonergic system due to an increased tryptophan uptake in the brain, an elevated intracerebral ammoniac concentration and glutamine synthesis, and a heightened intracerebral GABA-activity.The dysregulation of the serotonergic system as a consequence of the increased intracerebral tryptophan uptake is described as one of the most important pathogenetic mechanisms. The elevated intracerebral ammoniac concentration and the elevated intracerebral glutamine synthesis play in this a facilitating role. The similarity in symptomatology of the clinical picture of HE and the serotonergic syndrome support this hypothesis. Due to contradictory research findings the role of the GABA-ergic system and the occurrence of HE remains unclear.

scholarly journals Kynurenic acid and cancer: facts and controversies

2019 ◽  
Vol 77 (8) ◽  
pp. 1531-1550 ◽  
Author(s):  
Katarzyna Walczak ◽  
Artur Wnorowski ◽  
Waldemar A. Turski ◽  
Tomasz Plech
Keyword(s):  
Kynurenic Acid ◽  
Molecular Mechanisms ◽  
Potential Role ◽  
Cancer Cell Proliferation ◽  
Gastrointestinal Microbiota ◽  
Tryptophan Metabolite ◽  
Peripheral Cells ◽  
The Relationship ◽  
The Brain

Abstract Kynurenic acid (KYNA) is an endogenous tryptophan metabolite exerting neuroprotective and anticonvulsant properties in the brain. However, its importance on the periphery is still not fully elucidated. KYNA is produced endogenously in various types of peripheral cells, tissues and by gastrointestinal microbiota. Furthermore, it was found in several products of daily human diet and its absorption in the digestive tract was evidenced. More recent studies were focused on the potential role of KYNA in carcinogenesis and cancer therapy; however, the results were ambiguous and the biological activity of KYNA in these processes has not been unequivocally established. This review aims to summarize the current views on the relationship between KYNA and cancer. The differences in KYNA concentration between physiological conditions and cancer, as well as KYNA production by both normal and cancer cells, will be discussed. The review also describes the effect of KYNA on cancer cell proliferation and the known potential molecular mechanisms of this activity.

Psychiatric Syndromes Associated with Cerebrovascular Disorders in the African

1958 ◽  
Vol 104 (434) ◽  
pp. 133-143 ◽  
Author(s):  
T. Adeoye Lambo
Keyword(s):  
Environmental Factors ◽  
Cerebrovascular Disorders ◽  
Endogenous Depression ◽  
Personality Factors ◽  
Cerebrovascular Disorder ◽  
Inherited Predisposition ◽  
The Face ◽  
The Subject ◽  
The Relationship

This contribution towards the subject is limited to three of its aspects—namely, the possible aetiological role of inherited predisposition and psychogenic factors (mainly environmental to which the patient is still exposed), the relationship between late endogenous depression and the symptoms of cerebrovascular changes, and prognosis. On the face of it, prognosis of course must ultimately depend on that of the cerebrovascular disorder but apparently hereditary and environmental factors play a more significant role. Inherited predisposition is here assessed in terms of constitutional and personality factors.

Drugs and Drug Policy

2011 ◽  
Author(s):  
Mark A.R. Kleiman ◽  
Jonathan P. Caulkins ◽  
Angela Hawken
Keyword(s):  
Drug Policy ◽  
Illicit Trade ◽  
Beneficial Effects ◽  
Control Drug ◽  
The Subject ◽  
Drugs And Crime ◽  
The Relationship ◽  
Drug Free ◽  
The Brain

While there have always been norms and customs around the use of drugs, explicit public policies--regulations, taxes, and prohibitions--designed to control drug abuse are a more recent phenomenon. Those policies sometimes have terrible side-effects: most prominently the development of criminal enterprises dealing in forbidden (or untaxed) drugs and the use of the profits of drug-dealing to finance insurgency and terrorism. Neither a drug-free world nor a world of free drugs seems to be on offer, leaving citizens and officials to face the age-old problem: What are we going to do about drugs? In Drugs and Drug Policy, three noted authorities survey the subject with exceptional clarity, in this addition to the acclaimed series, What Everyone Needs to Know. They begin by, defining "drugs, " examining how they work in the brain, discussing the nature of addiction, and exploring the damage they do to users. The book moves on to policy, answering questions about legalization, the role of criminal prohibitions, and the relative legal tolerance for alcohol and tobacco. The authors then dissect the illicit trade, from street dealers to the flow of money to the effect of catching kingpins, and show the precise nature of the relationship between drugs and crime. They examine treatment, both its effectiveness and the role of public policy, and discuss the beneficial effects of some abusable substances. Finally they move outward to look at the role of drugs in our foreign policy, their relationship to terrorism, and the ugly politics that surround the issue. Crisp, clear, and comprehensive, this is a handy and up-to-date overview of one of the most pressing topics in today's world.

scholarly journals The Change in William I. Thomas’s View of Biology

Stan Rzeczy ◽  
2018 ◽  
pp. 75-94
Author(s):  
Łukasz Remisiewicz
Keyword(s):  
Social Psychology ◽  
Social Factors ◽  
Social Processes ◽  
Psychological Development ◽  
Departure Point ◽  
The Relationship ◽  
The Brain

In this article the author shows how the exploding role of biology in William Thomas’s sociology and social psychology has changed. Since the beginning of his career, this researcher addressed numerous topics that involved both biological and social factors – he commented on the nature of gender, race, instincts, prejudice and evolution. His departure point was biologism, which proclaimed that innate predispositions are a variable independent of social processes. In the following years, Thomas changed his beliefs, recognising that it was culture and society that left its mark on physiological and psychological development. The changes in Thomas’s reasoning are described by the author against the background of past and present views on the relationship between society and the brain, claiming that his late views could resonate with today’s approaches.

Between Mind and Brain:Final and Efficient Causation in Relation to Neuroplasticity

2012 ◽  
Vol 13 (3) ◽  
pp. 194-208
Author(s):  
Derrick L. Hassert
Keyword(s):  
Mentally Ill ◽  
Behavioral Interventions ◽  
Rational Behavior ◽  
Human Beings ◽  
Efficient Causation ◽  
Final Causes ◽  
The Relationship ◽  
The Brain ◽  
Behavior And Cognition

Reductionism is usually taken for granted in many areas of science, neuroscience and psychology being no exceptions. It is often assumed as scientific orthodoxy that human behavior can be reduced to “what the brain does” without recourse to a consideration of cognition. Although many philosophers and ethicists may seek to reduce or eliminate the concept of mind, other philosophers and ethicists have continually pointed out the logical inconsistencies of such an approach. Via a discussion of efficient and final causes in Aristotelian philosophy, I seek to argue that the understanding of human beings as rational and social creatures has guided and should continue to guide our approach to the care and treatment of the mentally ill. Observations concerning rational behavior and cognition, by necessity, have provided the benchmarks by which clinicians evaluate the effectiveness of somatic/pharmacological or psychological/ behavioral interventions: Eliminative reductionism is inappropriate in this area. In approaching issues pertaining to the relationship between human cognitive functioning and neural functioning, the distinction between capacity and vehicle will be used. However, the fact that mental and behavioral functioning can alter neuronal functioning (and vice versa) necessitates that those working with the mentally ill need to know both the efficient causes—the vehicles of certain capacities—and the role of the capacities themselves and how they relate to possible final causes in giving explanations for behavior. These issues become more significant when considering the ethics of treatment choice for those with mental disorders.

Sex steroids-induced neurogenesis in adult brain: a better look at mechanisms and mediators

2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Hamideh Abotalebi ◽  
Babak Ebrahimi ◽  
Raziyeh Shahriyari ◽  
Reyhaneh Shafieian
Keyword(s):  
Sex Steroids ◽  
Ventricular Zone ◽  
Mammalian Species ◽  
Adult Brain ◽  
Sex Steroid ◽  
Subgranular Zone ◽  
Human Beings ◽  
The Relationship ◽  
The Brain

Abstract Adult neurogenesis is the production of new nerve cells in the adult brain. Neurogenesis is a clear example of the neuroplasticity phenomenon which can be observed in most of mammalian species, including human beings. This phenomenon occurs, at least, in two regions of the brain: the subgranular zone of the dentate gyrus in hippocampus and the ventricular zone of lateral ventricles. Numerous studies have investigated the relationship between sex steroid hormones and neurogenesis of adult brain; of which, mostly concentrated on the role of estradiol. It has been shown that estrogen plays a significant role in this process through both classic and non-classic mechanisms, including a variety of different growth factors. Therefore, the objective of this review is to investigate the role of female sex steroids with an emphasis on estradiol and also its potential implications for regulating the neurogenesis in the adult brain.

L-Dopa metabolism in genetically hypertensive mice: effect of pargyline

1987 ◽  
Vol 65 (12) ◽  
pp. 2390-2395 ◽  
Author(s):  
Nguyen T. Buu ◽  
Johanne Duhaime ◽  
Karoly Racz ◽  
Otto Kuchel ◽  
Gunther Schlager
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Monoamine Oxidase ◽  
Hydroxylase Activity ◽  
Sympathetic Nervous ◽  
The Relationship ◽  
The Brain ◽  
Genetically Hypertensive

This study on the role of the sympathetic nervous system in the development of hypertension involves the measurement of dopamine and norepinephrine accumulation in various tissues of the hypertensive and random-bred normotensive strains of mice at basal levels, and following a pargyline–L-dopa treatment. Under such a treatment, designed to suppress the homeostatic action of monoamine oxidase and to better expose the relationship between dopamine and norepinephrine, the brain and heart of the hypertensive mice accumulated more dopamine than the normotensive mice. There was a significantly lower norepinephrine accumulation in the heart of the hypertensive mice in spite of comparable dopamine-β-hydroxylase activity in this tissue between the two strains of mice. Under the pargyline–L-dopa treatment, the brain and heart of the older mice in both hypertensive and normotensive strains accumulated significantly (p < 0.05) more dopamine than those of their younger counterparts, while their norepinephrine accumulation remained unchanged. The results demonstrated different patterns of response of dopamine and norepinephrine in the development of hypertension.

Allostasis and the developing human brain: Explicit consideration of implicit models

2011 ◽  
Vol 23 (4) ◽  
pp. 955-974 ◽  
Author(s):  
Barbara L. Ganzel ◽  
Pamela A. Morris
Keyword(s):  
Life Sciences ◽  
Developmental Stress ◽  
The Core ◽  
The Social ◽  
Explicit Consideration ◽  
Emotional Systems ◽  
The Relationship ◽  
Stress And Health ◽  
The Brain

AbstractWe previously used the theory of allostasis as the foundation for a model of the current stress process. This work highlighted the core emotional systems of the brain as the central mediator of the relationship between stress and health. In this paper, we extend this theoretical approach to consider the role of developmental timing. In doing so, we note that there are strong implicit models that underlie current developmental stress research in the social and life sciences. We endeavor to illustrate these modelsexplicitlyas we review the evidence behind each one and discuss their implications. We then extend these models to reflect recent findings from research in life span human neuroscience. The result is a new set of developmental allostatic models that provide fodder for future empirical research, as well as novel perspectives on intervention.

scholarly journals The Role of Irisin in Alzheimer’s Disease

2018 ◽  
Vol 7 (11) ◽  
pp. 407 ◽  
Author(s):  
Oh Kim ◽  
Juhyun Song
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Genetic Background ◽  
Senile Plaques ◽  
Metabolic Dysfunction ◽  
Lipid Imbalance ◽  
The Relationship ◽  
The Brain

Alzheimer’s disease (AD) is characterized by progressive memory dysfunction, oxidative stress, and presence of senile plaques formed by amyloid beta (A β ) accumulation in the brain. AD is one of the most important causes of morbidity and mortality worldwide. AD has a variety of risk factors, including environmental factors, metabolic dysfunction, and genetic background. Recent research has highlighted the relationship between AD and systemic metabolic changes such as glucose and lipid imbalance and insulin resistance. Irisin, a myokine closely linked to exercise, has been associated with glucose metabolism, insulin sensitivity, and fat browning. Recent studies have suggested that irisin is involved in the process in central nervous system (CNS) such as neurogenesis and has reported the effects of irisin on AD as one of the neurodegenerative disease. Here, we review the roles of irisin with respect to AD and suggest that irisin highlight therapeutic important roles in AD. Thus, we propose that irisin could be a potential future target for ameliorating AD pathology and preventing AD onset.

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