Brain, decade

Bassiony MM and Lyketsos CG (2003) Delusions and hallucinations in Alzheimer s disease review of the brain decade. Psychosomatics 44 (5) 388M01... 

Problems involving routine calculations are solved much faster and more reliably by computers than by humans. Nevertheless, there are tasks in which humans perform better, such as those in which the procedure is not strictly determined and problems which are not strictly algorithmic. One of these tasks is the recognition of patterns such as feces. For several decades people have been trying to develop methods which enable computers to achieve better results in these fields. One approach, artificial neural networks, which model the functionality of the brain, is explained in this section. 

Maximizing Human Potential Decade of the Brain 1990—2000, Report of the Subcommittee on Brain and Behavioral Sciences, Office of Science and Technology Pohcy, Washington, D.C., 1991, p. 76 A. M. Chutorian, C. P. LaScala, C. N. Ores, and R. Nass, PediatNeurol 1, 335 (1985) C. S. Wing, Lang. Speech, Hear. Sere. Schools 21, 22 (1990). 

Importantly, over the past decade it has been demonstrated that chemokines and chemokine receptors are not restricted to leukocytes. In the brain, chemokine receptors are not only found in microglia and astrocytes but also in oligodendrocytes, neurons, and along the brain microvasculature. In this chapter, we will focus on the functions of chemokine receptors expressed by resident CNS cells during physiologic and inflammatory conditions. 

Iproniazid and imipramine seemed to work as antidepressants, but how did they achieve their effects It would be another decade before the chemical-imbalance theory was launched. In 1965, Joseph Schildkraut at the National Institute of Mental Health in Washington, DC, published a groundbreaking paper in which he argued that depression was caused by a deficiency of the neurotransmitter norepinephrine in the gaps between neurons in the brain.8 Two years later Alec Coppen, a physician at West Park Hospital in Surrey, published another version of the chemical-imbalance theory. His version differed from Schildkraut s in that it put most of the blame on a different neurotransmitter, emphasizing serotonin rather than norepinephrine as the neurotransmitter that was lacking.9... 

TRPV4 was identified a decade ago as an osmotransducer that is expressed in lung, heart, kidney, airway muscle cells, sensory neurons, brain, skin, gut, sympathetic nerves, inner ear, endothelium, and fat tissue [58-61]. TRPV4 is activated by heat (27-34°C), endogenous substances such as anandamide (59, AA) and the arachi-donic acid metabolite 5,6-epoxyeicosatrienoic acid (60, 5,6-EET), a plant dimeric diterpenoid bisandrographolide A (61, BAA), and the semisynthetic phorbol ester 4a-phorbol-12,13-didecanoate (62, 4a-PDD) [62],... 

In the last decade, the roles of stem and progenitor cells in the differentiation of the embryonic nervous system have become illuminated, leading to fundamental advances in our knowledge of the regulation of cell fates in the brain. Much is still needed for us to understand the interplay between genetic and cell communication events that leads to normal generation of the complex nervous system. These issues are important to resolve if we are to learn how disease or trauma affect the growing brain. 

Cerebral metabolic rate declines from developmental levels and plateaus after maturation. Reliable quantitative data on the changes in cerebral circulation and metabolism in humans from the middle of the first decade of life to old age have been reported [2,39,44]. By 6 years of age, cerebral blood flow and oxygen consumption already have attained high rates, and they decline thereafter to the rates of normal young adulthood [45]. Oxygen is utilized in the brain almost entirely for the oxidation of carbohydrates [46]. The equation for the complete oxidation of glucose is ... 

Motor neuron disease is characterized clinically by weakness, muscle atrophy and spasticity. This illness, often termed Lou Gehrig s disease in the United States, is the most common adult-onset form of MND with a prevalence of approximately 2-3 per 100,000 people [1-3,10, 25, 28]. Each year in the United States, in excess of 5,000 people are diagnosed with ALS. In parts of the United Kingdom, 1 in =500 deaths are attributed to some form of MND. The principal clinical signs of ALS include progressive limb weakness, which may be symmetrical or asymmetrical atrophy of appendicular, bulbar and respiratory muscles and spasticity [1,2,26,28]. The paralysis/muscle atrophy and spasticity are the result of degeneration of motor neurons in the spinal cord/brain stem and motor cortex respectively. The onset of this illness is typically in the fifth or sixth decade of life affected individuals usually... 

The rapid progress in proteomics and peptidomics during the last decade offers us new possibilities to study clinical aspects of disorders and diseases related to the brain [1], These strategies also offer new tools to follow chemical modifications and altered metabolic disturbances that may be indicative of pathophysiological adaptations related to environmental and psychosocial prolonged stress. These techniques can contribute to developments in the diagnostic and therapeutic fields of psychiatric... 

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