It is certain that I think. It is highly probable that other people think too. It is highly probable that my thinking occurs only within my own head, but that the processes generating my thinking are distributed within my brain. (It is not even clear how “local” as opposed to distributed the brain processes corresponding to a thought would have to be in order to be “nondistributed”: surely even if a thought were generated by the presence of a single molecule, the molecule itself is distributed in space!) It is highly improbable that anything other than humans and other animals can think today. It is highly probable (for the same reason that it is highly probable that other people think too) that anything that can do anything and everything a person can do (indistinguishably from a person, for a lifetime) can think too. So it is highly probable that a robot that could pass the Turing Test would be able to think. It is possible for the processes generating the thinking in both humans and robots to be distributed more widely than just within their respective heads.
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It is of decisive importance to note that, in so far as I want to know about the experiential and personalistic aspects of what is going on in the capsule, I want (and need) quite essentially to relate the sentient being in the capsule to myself. I need to bring myself into the picture, in a way in which I must not do if I seek a physical description and explanation of what is going on inside the capsule. Suppose the conscious being inside the capsule is an alien. If I want to know what the interior of the capsule looks like to the alien, I want to know what it would be like for me to have occur in my brain processes that are similar in relevant respects to the processes that are going on inside the alien’s brain, associated with perception. And similarly, if I want to know what the alien is experiencing or feeling, I want to know how it would be for me if processes similar in the relevant respects to the processes going on in the alien’s brain were to occur in my own brain. (It may not be possible, of course, for me to know any of this because my brain is too different from the alien’s brain.) If I want to know what the alien asserts, writes or thinks, I want to know what these assertions or thoughts are when translated into my language. All experiential or personalistic aspects of things in the capsule bring me into the picture in an essential way, and involve knowing how things in the capsule relate to my experi- ences and thoughts. Physical descriptions, explanations and under- standing of what is going on inside the capsule, however complete, at no point involve or provide this kind of anthropomorphic, per- sonalistic information: it is this which ensures that the personalistic, the experiential, cannot be reduced to the physical.
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Philosophy, economics and psychology have already analyzed and enriched our conception of decision-making. Neuroeconomics, while still in its infancy, has already started to produce empirical results relevant to philosophy of science, philosophy of mind, moral philosophy and other theoretical approaches of rationality. It can enrich the debate on the relevance of folk-psychological categories such as belief and desire; it challenges the idea that there cannot be a science of rationality; it proposes a causal- mechanistic account of decision-making; it shows that judgments of value are highly affective; and finally, it is a first step toward a naturalistic account of rationality. By breaking down utility-maximization into subspecies (experienced, decision, predicted, remembered), and by identifying the brain processes and circuitry that maximize these types of utilities, neuroeconomics offers a finer description of decision-making than rational-choice theory or psychology alone. Neuroeconomics is a fertile ‘trading zone’ (Thagard) for interdisciplinary exchange between economics, neuroscience, psychology, anthropology, and computer science in the years to come.
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Previous research has suggested that changes in attention con- tribute to high somatic symptom reporting in the absence of a medical cause (Brown et al., 2010; Horvath e al., 1980; Roelofs, 2003). To investigate the neural basis of attentional changes we invited participants who scored high on the SDQ indicating the presence of a number of functional somatic symptoms and, in addi- tion, we invited a control group who scored low on the SDQ indi- cating absence or very weak presence of somatic symptoms to perform a tactile exogenous attention task while their brain activ- ity was recoded. On each trial they were presented with a tactile cue to one of their hands that they were instructed to ignore as it did not inform them about where (same of opposite hand) or what (high or low frequency) the target would be. Overall, partic- ipants were faster to discriminate tactile vibrations at the cued hand showing similar effects of attention on behavioural responses in the two groups. However, electro-cortical recordings revealed group differences in attention effects on somatosensory areas. In particular, we found that the LSN, a correlate of tactile attentional orienting to the body was diminished in people reporting high number of unexplained somatic symptoms. This suggests that the preparatory process for an upcoming tactile event is different in people with high SDQ scores. Further, attentional modulations of target processing were similar for both groups for early laten- cies; however, at mid and later latencies attentional modulations differed. These were present more strongly, in that these were pro- longed, had enhanced amplitude and broader topographic spread in the group scoring high on the SDQ. Taken together, our results show that the brain processes during both orienting of attention and tactile stimulus processing are altered in people with high somatic symptom reporting.
The crucial role of dopaminergic modulation in sev- eral brain processes and its participation in a variety of brain functions including cognitive functions and behav- ioral control indicates that impaired DA signaling can be potentially involved in several major brain disorders. Therefore, the study of clinical features of DA signaling can be a precious tool to reveal the complicated nature of dopaminergic modulation in the brain. Dysfunction of the dopaminergic circuitry can change the normal function of the nervous system, and as a result may cause several neurological and psychiatric disorders. However, along with the clinical applications of dopa- minergic modulation of the nervous system, the role of DA in neuropsychiatric disorders can be simulated by computational models. Computational models may en- hance the treatment techniques of the neuropsychiatric disorders since different agonists or antagonists of DA can be implemented and tested in the computer simula- tions, which do not require a human subject.
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Wakefield makes a compelling case for the virtues of his harm- ful dysfunction concept as a heuristic for clarifying intuitions about the boundaries between disorder and nondisorder. As we illustrate through an examination of Wakefield’s proposal, how- ever, his arguments for adopting the evolutionary-based concept of harmful dysfunction as a standard for conceptualizing and classi- fying mental disorders are based on a faulty assumption of com- parability between mental and biological processes.’ Our critique is organized around a deconstmction of Wakefield’s thesis into its three constituent claims: (a) mental disorder is a straightforward extension to mental processes of the same general concept of disorder used in physical medicine; (b) the harmful dysfunction concept is consistent with, explains, and justifies noncontroversial mental disorder classifications in psychiatry; and (c) harmful dys- function should be adopted as a standard for conceptualizing and classifying mental disorders. We examine each of these claims separately in the service of three related conclusions. In the first section, we argue that Wakefield’s assumption of comparability between biological and mental processes overlooks, and is under- mined by, the unique plasticity of brain design and the special requirements it imposes for conceptualizing the natural functions and dysfunctions of mental and psychological processes. In the second section, we draw on this analysis to show how Wakefield is led by his inadequate consideration of design openness to illusory interpretations of widely accepted mental disorders as harmful evolutionary dysfunctions. In the final section, we elabo- rate on ways in which the functioning designs of genetically closed as well as open brain processes, alone and in combination with striking discontinuities between evolutionary and contemporary social/cultural environments, may impose considerable limits on the coherence and practical viability of a harmful dysfunction concept of mental disorder.
During acute attacks of MS, MMP-9 levels are increased in the CSF, reflecting the changes that are occurring in the brain. Leakage of blood-derived proteins into the extracellular space leads to brain edema, hypoxia, and loss of myelin. While many factors contribute to the initiation of injury in MS, the MMPs play an important role in the final common pathway of tissue damage. Contrast-enhanced MRI shows opening of the BBB at various stages in the relapsing-remitting form of MS. Steroids are used to restore BBB integrity; the injection of high doses of steroids closes the BBB rapidly, but the effect is not long lasting. 42
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programs An analysis of the brain activity while the subject is exposed to a product, for example, it's attractive packaging, or a site that occupies the sales area, a warning sticker for consumer safety and health, or a stimulant-induced by subliminal messages, can produce surprising results. The ability of neuromarketing technic to have a direct insight into the events in the consumer's mind removes any nonspecific and confusion about the observed response of the respondents. Unlike the traditional psychological interpretations of the respondents, by introducing neuromarketing methods and instruments, researchers are able to directly monitor the changes in bioelectric potentials of neurons, without unquestionable m identification of measures of the activities of certain regions of the brain on the stimulus of the environment. So talking about neuromarketing and the application of research techniques in his essay Pushing the buy button Witchalls transmits the explanation of Dr. Kalvert, (Gemma Calvert): "With the help of functional magnetic resonance, you cannot change the behavior of the brain, you cannot force people to get out and buy something. it's a descriptive technique - it describes what the brain does "(Witchalls, 2004). Brain scans identify the activity of specific brain regions, measure the level of impact of the stimulus from the environment, which has led to the understanding that the brain during the automated process makes a number of decisions subconsciously (Camerer, & Thaler, 1995: 209; Camerer, Loewenstein & Prelec, 2005: 9-64).
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A relatively new approach for transient disruption of the BBB involves the systemic administration of various alkylglycerols. There is reversible and concentration- dependant increase in BBB permeability to several anticancer and antibiotic agents. The extent of BBB disruption varied from a 2-fold to a 200 fold increase in methotrexate, depending on the length of the alkyl group and the number of glycerols present in the structure. The effects of alkylglycerols on large-macromolecle permeability in isolated brain capillaries is due to increases in permeability are which result from temporary breakdown of the tight junctions between the cells. The use of alkylglycerol to increase BBB permeability of anticancer agents has been examined in a rat glioma tumour model. 23,24
RESULTS: A closed cephalocele was detected in 9/33 patients (27%) at the level of anterior and middle fossa in 6 and 3 cases, respectively; 6/9 subjects were affected with the attenuated phenotype and 1/9 suffered from epilepsy. Closed cephaloceles did not show a significant association with other brain and spine MR imaging features of Hunter disease, such as enlargement of perivascular spaces, cisterna magna, pituitary sella, ventricles and subarachnoid spaces, craniosynostosis, dens hypoplasia, white matter abnormalities, spinal stenosis due to periodontoid cap, platyspondylia, or intervertebral disk anomalies.
The American National Head Injury Foundation (1 985) defines brain injury as "a traumatic insult to the brain capable of producing physical, intellectual, emotional, social and vocational changes." In New Zealand, as overseas, the numbers of people who have had serious brain injuries has grown considerably. This is largely due to improvements in medical care and surgical techniques which allow people to survive despite severe damage and considerable long-term impairment. As a result, after the acute stage, increasing numbers of people are requiring intensive rehabilitation followed by ongoing support. About 1 70 New Zealanders are hospitalised each week and many more are concussed and have mild head injury. One in every 3 1 5 cases experience ongoing problems (Head Injury Society of New Zealand, 1 994). This has lead to an increasing awareness of brain injury over the last few years and a growing concern about the seriousness and extent of the problem. The estimated cost of public hospital care alone is $25 million, while other costs, buried in the Social Welfare and Accident Rehabilitation Compensation and Insurance CorporationS,s more general funding systems, would considerably outstrip this figure (Head Injury Working Group Document, 1994). Internationally, head trauma is two or three times more common in males, the 1 5 - 29 year old age group being the most at risk (Jennett, 1990:4). More than half of the injuries result from traffic accidents.
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guidance, insight, and mentoring throughout my graduate degree. I am incredibly grateful for the exciting opportunities provided thanks to his immense contribution to obtaining the new fNIRS systems at The University of Western Ontario. Being the first to use this new neuroimaging technique at the Brain and Mind Institute has been a fascinating and challenging experience. I would like to express appreciation towards my lab members at the Language, Reading, and Cognitive Neuroscience Lab for their continuous assistance and for being inspiring leading exemplars. Thank you to my committee members Dr. Ryan Stevenson and Dr. Lisa Archibald for their helpful suggestions regarding this project. Special thanks go to our lab alumna Nicolette for the essential fNIRS help and guidance in the early stages of the project.
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This study shows that quantitative DTI fiber tracking can link the microstructure of an unmyelinated white matter tract to function and behavior during a critical phase of brain devel- opment in preterm neonates. Visual function was assessed with a simple bedside ophthalmologic examination that did not require any specialized equipment. The quantitative fiber- tracking algorithm used a robust, multiple region-of-interest approach to delineate and segment the unmyelinated optic radiations of premature infants. This quantitative technique was capable of detecting spatial and temporal diffusion metric heterogeneities associated with the development and anatomy of the optic radiation.
Studies on this model demonstrated the contribution of hepatic tumor factor, NF-kB/RelA, TNF and interleukin4 in the development of IR [147-149]. Zucker fatty (fa/fa) rat exhibit hyperinsulinemia, glucose intolerance and hyperlipidemia due to deficiency in the leptin receptor and autosomal recessive fa gene . Defect in leptin transportation through the blood brain barrier represented in New Zealand mice strain (NZO), which is a hepatic IR model . The spontaneous deletion mutation in CD36 fatty acid transporter gene developed the OLETF rat as a model to study the IR syndrome in hypertensive, hyper insulinemic glucose intolerant animal  as it resemble the clinical and pathological features of human non-insulin-dependent diabetes mellitus (NIDDM). KK/Ay mouse model with defects in the yellow obese gene represents a condition of severe hyperinsulinaemia, hyperglycaemia, glucose intolerance and obesity due to defective insulin receptor and post-receptor signaling . There are other models of the spontaneously developed IR strains . Although the above-mentioned animal models provided a lot of information about the mechanisms of IR, they did not answer all the questions related to the development of IR in human tissues and relationship between IR and β-cell dysfunction.
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Functional brain imaging reveals a network of areas associated with the acquisition of visuomotor skills. Various tasks have been used in the scanner, such as learning of motor sequences, adaptation to force fields, and bimanual coordination. In general, a reduction in activity in so called “scaffolding” areas (presumably related to controlled processing early in the Fitts progression), including prefrontal cortex, anterior cingulate cortex, and posterior parietal cortex , is often found to precede changes in activity within sensorimotor regions associated with task performance, such as primary motor cortex and the cerebellum 60 . Differences between expert and novice athletes have also been investigated, but the movement requirements of many sports generate serious challenges. Imaging studies have investigated sports-related processing by asking
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PRDM15 orchestrates transcriptional programs governing A/P patterning and brain development in the mouse embryo To examine the impact of PRDM15 depletion on early embryonic processes, namely, A/P patterning, we sequenced the transcriptome of WT versus Prdm15 KO E6.5 embryos. We reasoned this could be the most critical stage for AME specification as AME cells emerge less than 24 hours later. Unbiased clustering of global gene expression separated WT versus Prdm15 KO embryos into distinct groups, in- dicating marked transcriptional differences (Fig. 4A and table S1F). Gene ontology (GO) analysis of the significantly down-regulated genes identified “Pattern specification process,” “Head development,” and “Neural tube development” among the enriched terms. Among these genes, several are important regulators of forebrain development and A/P patterning (Fig. 4B and fig. S4A, and table S1, G to H). We noted a striking reduction in the expression of key components of
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areas of the brain and the edges represent the connections between those areas. Graphs are also used to represent the micro-scale channels of porous media, in which the vertices represent the pores and the edges represent the smaller channels connecting the pores.
The possibility that hysteresis processes are at work in the brain, and can help resolve von Neumann’s puzzle, was pursued in work conducted at the Weizmann Institute of Science in Israel in the 1960s on the physical changes that might account for the memory imprint of a pattern of external stimuli on a chemical system. Katchalsky and Neumann (, p. 178) argued that “the requirements of a sufficiently fast record with low expenditure of energy, and the storage of the record after the stimulus is over, severely limit the choice of possible physical mechanisms... a long retention of the memory imprint is necessary to allow the induction of further consolidation in permanent structures... it seems that this imprint could be based on equilibrium states which are a priori time- independent and stable... but any equilibrium processes are a priori excluded, since equilibrium states are independent of path, and therefore memoryless... the only simple mechanism which seems to answer all biophysical requirements is that of hysteresis”.
Electroencephalography (EEG) is a method used in measuring the electrical activity of the brain. The brain generates rhythmical potentials which originate in the individual neurons of the brain. These potentials get summated as millions of cell discharge synchronously and appear as a surface waveform, the recording of which is known as the electroencephalogram. The neurons, like other cells of the body, are electrically polarized at rest. The interior of the neuron is at a potential of about –70mV relative to the exterior. When a neuron is exposed to a stimulus above a certain threshold, a nerve impulse, seen as a change in membrane potential, is generated which spreads in the cell resulting in the depolarization of the cell. Shortly afterwards, repolarization occurs. The EEG signal can be picked up with electrodes either from scalp or directly from the cerebral cortex. As the neurons in our brain communicate with each other by firing
We have previously reported that carnosine reversed the impairment of mitochondrial permeability transition in primary neurons and astrocytes. Since it is well established that mitochondrial dysfunction contributes to autophagy induction, 16,18 we examined whether carnosine protected against mitochondrial damage and mitophagy. Ischemia resulted in decreased activity of complex I in isolated brain mitochondria suggesting impairment in mitochondrial respiratory function. Ischemic mitochondrial dysfunction was significantly reversed in mitochondria isolated from carnosine-treated rats (Fig. 3A). To determine if there is a link between mitochondrial dysfunction and autophagy, we examined the levels of p-Drp1 and Parkin which play key roles in mitochondrial fragmentation and mitophagy during cell death, respectively. 38-40 The mitochondrial levels of p-Drp1 and Parkin were significantly increased by ischemia, but the increase of p-Drp1 and Parkin were attenuated by carnosine treatment (Fig. 3B).
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