代贖代toreplacetotaketheplaceoftoactfortodosomethingonbehalfofforinplaceoftoactastobetheactingpresidentetcgenerationagegrouphistoricalperioderadateagedynastylineofrulersgeologyerageochronologicunitgrammarShortfor代名詞代名词dàimíngcíshortfor代詞代词dàicípronounhistoricalgeographyShortfor代國代国DàiguóstateofDaiasurnameSouthernMinaffairmatterarchaicsubstitutionarchaicpricecostchargehistoricalshiroaunitoflandpricegenerationofafamilyreignofaroyaldecadeeragenerationofaroyalfamilyeraagedecadechargefareratefeepricerentindicatingyearsspanningaspecificperiod-ies-hundreds贖toredeemtoransomatonementwashingawayyoursin속죄하다clearingyourdebtbyofferingmoneywealthoreffort속바치다TorecoverownershipofsomethingbybuyingitbackToliberatebypaymentofaransomTosetfreebyforceTosaverescueToclearreleasefromdebtorblameToexpiateatoneforToconvertsomebondorsecurityintocashTosavefromastateofsinandfromitsconsequencesTorepairrestoreToreformchangeforthebetterTorestorethehonourworthorreputationofoneselforsomethingToreclaimbuybackrepurchaseabandonMoneypaidforthefreeingofahostageTheywereheldfortwomilliondollarsransomTheywereheldtoransomThereleaseofacaptiveorofcapturedpropertybypaymentofaconsiderationprisonershopelessofransomhistoricallawUKAsumpaidforthepardonofsomegreatoffenceandthedischargeoftheoffenderalsoafinepaidinlieuofcorporalpunishmentobsoleteTodeliverespeciallyincontextofsinorrelevantpenalties14thcenturyTopayapricetosetsomeonefreefromcaptivityorpunishment.toransomprisonersfromanenemyToexactaransompaymentinexchangeforthefreedomofbuyredeemransomatonefor

 代贖代toreplacetotaketheplaceoftoactfortodosomethingonbehalfofforinplaceoftoactastobetheactingpresidentetcgenerationagegrouphistoricalperioderadateagedynastylineofrulersgeologyerageochronologicunitgrammarShortfor代名詞代名词dàimíngcíshortfor代詞代词dàicípronounhistoricalgeographyShortfor代國代国DàiguóstateofDaiasurnameSouthernMinaffairmatterarchaicsubstitutionarchaicpricecostchargehistoricalshiroaunitoflandpricegenerationofafamilyreignofaroyaldecadeeragenerationofaroyalfamilyeraagedecadechargefareratefeepricerentindicatingyearsspanningaspecificperiod-ies-hundreds贖toredeemtoransomatonementwashingawayyoursin속죄하다clearingyourdebtbyofferingmoneywealthoreffort속바치다TorecoverownershipofsomethingbybuyingitbackToliberatebypaymentofaransomTosetfreebyforceTosaverescueToclearreleasefromdebtorblameToexpiateatoneforToconvertsomebondorsecurityintocashTosavefromastateofsinandfromitsconsequencesTorepairrestoreToreformchangeforthebetterTorestorethehonourworthorreputationofoneselforsomethingToreclaimbuybackrepurchaseabandonMoneypaidforthefreeingofahostageTheywereheldfortwomilliondollarsransomTheywereheldtoransomThereleaseofacaptiveorofcapturedpropertybypaymentofaconsiderationprisonershopelessofransomhistoricallawUKAsumpaidforthepardonofsomegreatoffenceandthedischargeoftheoffenderalsoafinepaidinlieuofcorporalpunishmentobsoleteTodeliverespeciallyincontextofsinorrelevantpenalties14thcenturyTopayapricetosetsomeonefreefromcaptivityorpunishment.toransomprisonersfromanenemyToexactaransompaymentinexchangeforthefreedomofbuyredeemransomatonefor































댓글

댓글 쓰기

이 블로그의 인기 게시물

Major depressive disorder (MDD), also known as clinical depression, is a mental disorder[10] characterized by at least two weeks of pervasive low mood, low self-esteem, and loss of interest or pleasure in normally enjoyable activities. Introduced by a group of US clinicians in the mid-1970s,[11] the term was adopted by the American Psychiatric Association for this symptom cluster under mood disorders in the 1980 version of the Diagnostic and Statistical Manual of Mental Disorders (DSM-III), and has become widely used since. The disorder causes the second-most years lived with disability, after lower back pain.[12] The diagnosis of major depressive disorder is based on the person's reported experiences, behavior reported by family or friends, and a mental status examination.[13] There is no laboratory test for the disorder, but testing may be done to rule out physical conditions that can cause similar symptoms.[13] The most common time of onset is in a person's 20s,[3][4] with females affected about three times as often as males.[14] The course of the disorder varies widely, from one episode lasting months to a lifelong disorder with recurrent major depressive episodes. Those with major depressive disorder are typically treated with psychotherapy and antidepressant medication.[1] While a mainstay of treatment, the clinical efficacy of antidepressants is controversial.[15][16][17][18] Hospitalization (which may be involuntary) may be necessary in cases with associated self-neglect or a significant risk of harm to self or others. Electroconvulsive therapy (ECT) may be considered if other measures are not effective.[1] Major depressive disorder is believed to be caused by a combination of genetic, environmental, and psychological factors,[1] with about 40% of the risk being genetic.[5] Risk factors include a family history of the condition, major life changes, childhood traumas, environmental lead exposure,[19] certain medications, chronic health problems, and substance use disorders.[1][5] It can negatively affect a person's personal life, work life, or education, and cause issues with a person's sleeping habits, eating habits, and general health.[1][5] Signs and symptoms See also: Digital media use and mental health § Depression An 1892 lithograph of a woman diagnosed with melancholia A person having a major depressive episode usually exhibits a low mood, which pervades all aspects of life, and an inability to experience pleasure in previously enjoyable activities.[20] Depressed people may be preoccupied with or ruminate over thoughts and feelings of worthlessness, inappropriate guilt or regret, helplessness or hopelessness.[21] Other symptoms of depression include poor concentration and memory,[22] withdrawal from social situations and activities, reduced sex drive, irritability, and thoughts of death or suicide. Insomnia is common; in the typical pattern, a person wakes very early and cannot get back to sleep. Hypersomnia, or oversleeping, can also happen,[23] as well as day-night rhythm disturbances, such as diurnal mood variation.[24] Some antidepressants may also cause insomnia due to their stimulating effect.[25] In severe cases, depressed people may have psychotic symptoms. These symptoms include delusions or, less commonly, hallucinations, usually unpleasant.[26] People who have had previous episodes with psychotic symptoms are more likely to have them with future episodes.[27] A depressed person may report multiple physical symptoms such as fatigue, headaches, or digestive problems; physical complaints are the most common presenting problem in developing countries, according to the World Health Organization's criteria for depression.[28] Appetite often decreases, resulting in weight loss, although increased appetite and weight gain occasionally occur.[29] Major depression significantly affects a person's family and personal relationships, work or school life, sleeping and eating habits, and general health.[30] Family and friends may notice agitation or lethargy.[23] Older depressed people may have cognitive symptoms of recent onset, such as forgetfulness,[31] and a more noticeable slowing of movements.[32] Depressed children may often display an irritable rather than a depressed mood;[23] most lose interest in school and show a steep decline in academic performance.[33] Diagnosis may be delayed or missed when symptoms are interpreted as "normal moodiness".[34] Elderly people may not present with classical depressive symptoms.[35] Diagnosis and treatment is further complicated in that the elderly are often simultaneously treated with a number of other drugs, and often have other concurrent diseases.[35] Cause Further information: Biology of depression and Epigenetics of depression A cup analogy demonstrating the diathesis–stress model that under the same amount of stressors, person 2 is more vulnerable than person 1, because of their predisposition[36] The etiology of depression is not yet fully understood.[37][38][39] The biopsychosocial model proposes that biological, psychological, and social factors all play a role in causing depression.[5][40] The diathesis–stress model specifies that depression results when a preexisting vulnerability, or diathesis, is activated by stressful life events. The preexisting vulnerability can be either genetic,[41][42] implying an interaction between nature and nurture, or schematic, resulting from views of the world learned in childhood.[43] American psychiatrist Aaron Beck suggested that a triad of automatic and spontaneous negative thoughts about the self, the world or environment, and the future may lead to other depressive signs and symptoms.[44][45] Genetics Genes play a major role in the development of depression.[46] Family and twin studies suggest that genetic factors account for nearly 40% of the variation in risk for major depressive disorder. Like most psychiatric disorders, major depression is likely shaped by a combination of many individual genetic influences.[47] In 2018, a genome-wide association study discovered 44 genetic variants linked to risk for major depression;[48] a 2019 study found 102 variants in the genome linked to depression.[49] However, it appears that major depression is less heritable compared to bipolar disorder and schizophrenia.[50][51] Research focusing on specific candidate genes has been criticized for its tendency to generate false positive findings.[52] There are also other efforts to examine interactions between life stress and polygenic risk for depression.[53] Other health problems Depression can also arise after a chronic or terminal medical condition, such as HIV/AIDS or asthma, and may be labeled "secondary depression".[54][55] It is unknown whether the underlying diseases induce depression through effect on quality of life, or through shared etiologies (such as degeneration of the basal ganglia in Parkinson's disease or immune dysregulation in asthma).[56] Depression may also be iatrogenic (the result of healthcare), such as drug-induced depression. Therapies associated with depression include interferons, beta blockers,[57] isotretinoin,[58] contraceptives,[57] cardiac agents,[59] anticonvulsants,[60] and hormonal agents.[61] Celiac disease is another possible contributing factor.[62] Substance use in early age is associated with increased risk of developing depression later in life.[63] Depression occurring after giving birth is called postpartum depression and is thought to be the result of hormonal changes associated with pregnancy.[64] Seasonal affective disorder, a type of depression associated with seasonal changes in sunlight, is thought to be triggered by decreased sunlight.[65] Vitamin B2, B6 and B12 deficiency may cause depression in females.[66] A 2025 study found that, among more than 172,500 adults in the UK aged 39 and older, those with a history of depression experienced the onset of chronic illnesses approximately 30% earlier than those without depression.[67] Environmental Adverse childhood experiences (incorporating childhood abuse, neglect and family dysfunction) markedly increase the risk of major depression, especially if more than one type.[68] Childhood trauma also correlates with severity of depression, poor responsiveness to treatment and length of illness.[69] Some are more susceptible than others to developing mental illness such as depression after trauma, and various genes have been suggested to control susceptibility.[70] Couples in unhappy marriages have a higher risk of developing clinical depression.[71] There appears to be a link between air pollution and depression and suicide. There may be an association between long-term PM2.5 exposure and depression, and a possible association between short-term PM10 exposure and suicide.[72] Living alone has been found to increase the risk of depression by 42%.[6] Pathophysiology Further information: Biology of depression and Epigenetics of depression The pathophysiology of depression is not completely understood, but current theories center around monoaminergic systems, the circadian rhythm, immunological dysfunction, HPA-axis dysfunction, and structural or functional abnormalities of emotional circuits. Derived from the effectiveness of monoaminergic drugs in treating depression, the monoamine theory posits that insufficient activity of monoamine neurotransmitters is the primary cause of depression. Evidence for the monoamine theory comes from multiple areas. First, acute depletion of tryptophan—a necessary precursor of serotonin and a monoamine—can cause depression in those in remission or relatives of people who are depressed, suggesting that decreased serotonergic neurotransmission is important in depression.[73] Second, the correlation between depression risk and polymorphisms in the 5-HTTLPR gene, which codes for serotonin receptors, suggests a link.[74] Third, decreased size of the locus coeruleus, reduced activity of tyrosine hydroxylase, increased density of alpha-2 adrenergic receptor, and evidence from rat models suggest decreased adrenergic neurotransmission in depression.[75] Furthermore, decreased levels of homovanillic acid, altered response to dextroamphetamine, responses of depressive symptoms to dopamine receptor agonists, decreased dopamine receptor D1 binding in the striatum,[76] and polymorphism of dopamine receptor genes implicate dopamine, another monoamine, in depression.[77][78] Lastly, increased activity of monoamine oxidase, which degrades monoamines, has been associated with depression.[79] However, the monoamine theory is inconsistent with observations that serotonin depletion does not cause depression in healthy persons, that antidepressants instantly increase levels of monoamines but take weeks to work, and the existence of atypical antidepressants which can be effective despite not targeting this pathway.[80] One proposed explanation for the therapeutic lag, and further support for the deficiency of monoamines, is a desensitization of self-inhibition in raphe nuclei by the increased serotonin mediated by antidepressants.[81] However, disinhibition of the dorsal raphe has been proposed to occur as a result of decreased serotonergic activity in tryptophan depletion, resulting in a depressed state mediated by increased serotonin. Further countering the monoamine hypothesis is the fact that rats with lesions of the dorsal raphe are not more depressive than controls; the finding of increased jugular 5-HIAA in people who are depressed that normalized with selective serotonin reuptake inhibitor (SSRI) treatment, and the preference for carbohydrates in people who are depressed.[82] Already limited, the monoamine hypothesis has been further oversimplified when presented to the general public.[83] A 2022 review found no consistent evidence supporting the serotonin hypothesis linking serotonin levels and depression.[84] HPA-axis abnormalities have been suggested in depression given the association of CRHR1 with depression and the increased frequency of dexamethasone test non-suppression in people who are depressed. However, this abnormality is not adequate as a diagnosis tool because its sensitivity is only 44%.[85] These stress-related abnormalities are thought to be the cause of hippocampal volume reductions seen in people who are depressed.[86] Furthermore, a meta-analysis yielded decreased dexamethasone suppression, and increased response to psychological stressors.[87] Further abnormal results have been obscured with the cortisol awakening response, with increased response being associated with depression.[88] There is also a connection between the gut microbiome and the central nervous system, otherwise known as the Gut-Brain axis, which is a two-way communication system between the brain and the gut. Experiments have shown that microbiota in the gut can play an important role in depression, as people with MDD often have gut-brain dysfunction. One analysis showed that those with MDD have different bacteria in their guts. Bacteria Bacteroidetes and Firmicutes were most affected in people with MDD, and they are also impacted in people with irritable bowel syndrome.[89] Another study showed that people with IBS have a higher chance of developing depression, which shows the two are connected.[90] There is even evidence suggesting that altering the microbes in the gut can have regulatory effects on developing depression.[89] Theories unifying neuroimaging findings have been proposed. The first model proposed is the limbic-cortical model, which involves hyperactivity of the ventral paralimbic regions and hypoactivity of frontal regulatory regions in emotional processing.[91] Another model, the cortico-striatal model, suggests that abnormalities of the prefrontal cortex in regulating striatal and subcortical structures result in depression.[92] Another model proposes hyperactivity of salience structures in identifying negative stimuli and hypoactivity of cortical regulatory structures resulting in a negative emotional bias and depression, consistent with emotional bias studies.[93] Immune pathogenesis theories on depression The newer field of psychoneuroimmunology, the study between the immune system and the nervous system and emotional state, suggests that cytokines may impact depression. Immune system abnormalities have been observed, including increased levels of cytokines -cells produced by immune cells that affect inflammation- involved in generating sickness behavior, creating a pro-inflammatory profile in MDD.[94][95][96] Some people with depression have increased levels of pro-inflammatory cytokines and some have decreased levels of anti-inflammatory cytokines.[97] Research suggests that treatments can reduce pro-inflammatory cell production, like the experimental treatment of ketamine with treatment-resistant depression.[98] With this, in MDD, people will more likely have a Th-1 dominant immune profile, which is a pro-inflammatory profile. This suggests that there are components of the immune system affecting the pathology of MDD.[99] Another way cytokines can affect depression is in the kynurenine pathway, and when this is overactivated, it can cause depression. This can be due to too much microglial activation and too little astrocytic activity. When microglia get activated, they release pro-inflammatory cytokines that cause an increase in the production of COX2. This, in turn, causes the production of PGE2, which is a prostaglandin, and this catalyzes the production of indolamine, IDO. IDO causes tryptophan to get converted into kynurenine, and kynurenine becomes quinolinic acid.[100] Quinolinic acid is an agonist for NMDA receptors, so it activates the pathway. Studies have shown that the post-mortem brains of patients with MDD have higher levels of quinolinic acid than people who did not have MDD. With this, researchers have also seen that the concentration of quinolinic acid correlates to the severity of depressive symptoms.[101] Diagnosis Assessment Further information: Rating scales for depression Caricature of a man with depression A diagnostic assessment may be conducted by a suitably trained general practitioner, or by a psychiatrist or psychologist,[30] who records the person's current circumstances, biographical history, current symptoms, family history, and alcohol and drug use. The assessment also includes a mental state examination, which is an assessment of the person's current mood and thought content, in particular the presence of themes of hopelessness or pessimism, self-harm or suicide, and an absence of positive thoughts or plans.[30] Specialist mental health services are rare in rural areas, and thus diagnosis and management is left largely to primary-care clinicians.[102] This issue is even more marked in developing countries.[103] Rating scales are not used to diagnose depression, but they provide an indication of the severity of symptoms for a time period, so a person who scores above a given cut-off point can be more thoroughly evaluated for a depressive disorder diagnosis. Several rating scales are used for this purpose;[104] these include the Hamilton Rating Scale for Depression,[105] the Beck Depression Inventory[106] or the Suicide Behaviors Questionnaire-Revised.[107] Primary-care physicians have more difficulty with underrecognition and undertreatment of depression compared to psychiatrists. These cases may be missed because for some people with depression, physical symptoms often accompany depression. In addition, there may also be barriers related to the person, provider, and/or the medical system. Non-psychiatrist physicians have been shown to miss about two-thirds of cases, although there is some evidence of improvement in th

이미지
  Major depressive disorder   ( MDD ), also known as   clinical depression , is a   mental disorder [ 10 ]   characterized by at least two weeks of pervasive   low mood , low   self-esteem , and   loss of interest or pleasure   in normally enjoyable activities. Introduced by a group of US clinicians in the mid-1970s, [ 11 ]   the term was adopted by the   American Psychiatric Association   for this   symptom cluster   under   mood disorders   in the 1980 version of the   Diagnostic and Statistical Manual of Mental Disorders   (DSM-III), and has become widely used since. The disorder causes the second-most   years lived with disability , after   lower back pain . [ 12 ] The diagnosis of major depressive disorder is based on the person's reported experiences, behavior reported by family or friends, and a  mental status examination . [ 13 ]  There is no laboratory test for the diso...
자세한 내용 보기

In philosophy, the self is an individual's own being, knowledge, and values, and the relationship between these attributes. The first-person perspective distinguishes selfhood from personal identity. Whereas "identity" is (literally) sameness[1] and may involve categorization and labeling,[2] selfhood implies a first-person perspective and suggests potential uniqueness. Conversely, "person" is used as a third-person reference. Personal identity can be impaired in late-stage Alzheimer's disease and in other neurodegenerative diseases. Finally, the self is distinguishable from "others". Including the distinction between sameness and otherness, the self versus other is a research topic in contemporary philosophy[3] and contemporary phenomenology (see also psychological phenomenology), psychology, psychiatry, neurology, and neuroscience. Although subjective experience is central to selfhood, the privacy of this experience is only one of many problems in the philosophy of self and the scientific study of consciousness. Psychology Main article: Psychology of self The psychology of self is the study of either the cognitive and affective representation of one's identity or the subject of experience. The earliest formulation of the self in modern psychology forms the distinction between two elements I and me. The self as I, is the subjective knower. While, the self as Me, is the subject that is known.[4] Current views of the self in psychology positions the self as playing an integral part in human motivation, cognition, affect, and social identity.[5] Self, following the ideas of John Locke, has been seen as a product of episodic memory[6] but research on people with amnesia reveals that they have a coherent sense of self based on preserved conceptual autobiographical knowledge.[7] Hence, it is possible to correlate cognitive and affective experiences of self with neural processes. A goal of this ongoing research is to provide grounding insight into the elements of which the complex multiple situated selves of human identity are composed. What the Freudian tradition has subjectively called, "sense of self" is for Jungian analytic psychology, where one's identity is lodged in the persona or ego and is subject to change in maturation. Carl Jung distinguished, "The self is not only the center but also the whole circumference which embraces both conscious and unconscious; it is the center of this totality...".[8] The Self in Jungian psychology is "the archetype of wholeness and the regulating center of the psyche ... a transpersonal power that transcends the ego."[9][10] As a Jungian archetype, it cannot be seen directly, but by ongoing individuating maturation and analytic observation, can be experienced objectively by its cohesive wholeness-making factor.[11] Meanwhile, self psychology is a set of psychotherapeutic principles and techniques established by the Austrian-born American psychoanalyst Heinz Kohut upon the foundation of the psychoanalytic method developed by Freud, and is specifically focused on the subjectivity of experience, which, according to self psychology, is mediated by a psychological structure called the self.[12] Examples of psychiatric conditions where such "sameness" may become broken include depersonalization, which sometimes occurs in schizophrenia, where the self appears different from the subject. Psychiatry See also: Self-disorder and Depersonalization The 'Disorders of the Self' have also been extensively studied by psychiatrists.[13] For example, facial and pattern recognition take large amounts of brain processing capacity but pareidolia cannot explain many constructs of self for cases of disorder, such as schizophrenia or schizoaffective disorder. One's sense of self can also be changed upon becoming part of a stigmatized group. According to Cox, Abramson, Devine, and Hollon (2012), if an individual has prejudice against a certain group, like the elderly and then later becomes part of this group. This prejudice can be turned inward causing depression.[14] The philosophy of a disordered self, such as in schizophrenia, is described in terms of what the psychiatrist understands are actual events in terms of neuron excitation but are delusions nonetheless, and the schizo-affective or a schizophrenic person also believes are actual events in terms of essential being. PET scans have shown that auditory stimulation is processed in certain areas of the brain, and imagined similar events are processed in adjacent areas, but hallucinations are processed in the same areas as actual stimulation. In such cases, external influences may be the source of consciousness and the person may or may not be responsible for "sharing" in the mind's process, or the events which occur, such as visions and auditory stimuli, may persist and be repeated often over hours, days, months or years—and the afflicted person may believe themselves to be in a state of rapture or possession. Neuroscience Main article: Neural basis of self Two areas of the brain that are important in retrieving self-knowledge are the medial prefrontal cortex and the medial posterior parietal cortex.[15] The posterior cingulate cortex, the anterior cingulate cortex, and medial prefrontal cortex are thought to combine to provide humans with the ability to self-reflect. The insular cortex is also thought to be involved in the process of self-reference.[16] Sociology Culture consists of explicit and implicit patterns of historically derived and selected ideas and their embodiment in institutions, cognitive and social practices, and artifacts. Cultural systems may, on the one hand, be considered as products of action, and on the other, as conditioning elements of further action.[17] The way individuals construct themselves may be different due to their culture.[18] Hazel Rose Markus and Shinobu Kitayama's theory of the interdependent self hypothesizes that representations of the self in human cultures fall on a continuum from independent to interdependent. The independent self is supposed to be egoistic, unique, separated from the various contexts, critical in judgment, and prone to self-expression. The interdependent self is supposed to be altruistic, similar with the others, flexible according to contexts, conformist, and unlikely to express opinions that would disturb the harmony of his or her group of belonging.[19] However, this theory has been criticized by other sociologists, including David Matsumoto[20] for being based on popular stereotypes and myths about different cultures rather than on rigorous scientific research. A 2016 study[21] of 10,203 participants from 55 cultural groups also failed to find a correlation between the postulating series of causal links between culture and self-construals, finding instead that correlations between traits varied both across cultures did not correlate with Markus & Kitayama's identifications of "independent" or "interdependent" self.[22] Philosophy Main article: Philosophy of self The philosophy of self seeks to describe essential qualities that constitute a person's uniqueness or a person's essential being. There have been various approaches to defining these qualities. The self can be considered as the source of consciousness, the agent responsible for an individual's thoughts and actions, or the substantial nature of a person which endures and unifies consciousness over time. The self has a particular prominence in the thought of René Descartes (1596-1650).[23] In addition to the writings of Emmanuel Levinas (1906-1995) on "otherness", the distinction between "you" and "me" has been further elaborated in Martin Buber's 1923 philosophical work Ich und Du. In philosophy, the problem of personal identity[24] is concerned with how one is able to identify a single person over a time interval, dealing with such questions as, "What makes it true that a person at one time is the same thing as a person at another time?" or "What kinds of things are we persons?" A question related to the problem of personal identity is Benj Hellie's vertiginous question. The vertiginous question asks why, of all the subjects of experience out there, this one—the one corresponding to the human being referred to as Benj Hellie—is the one whose experiences are live? (The reader is supposed to substitute their own case for Hellie's.)[25] Hellie's argument is closely related to Caspar Hare's theories of egocentric presentism and perspectival realism, of which several other philosophers have written reviews.[26] Similar questions are also asked repeatedly by J. J. Valberg in justifying his horizonal view of the self,[27] and by Thomas Nagel in The View from Nowhere.[28][29] Tim S. Roberts refers to the question of why a particular organism out of all the organisms that happen to exist happens to be you as the "Even Harder Problem of Consciousness".[30] Open individualism is a view in the philosophy of self, according to which there exists only one numerically identical subject, who is everyone at all times, in the past, present and future.[31]: 617  It is a theoretical solution to the question of personal identity, being contrasted with "Empty individualism", the view that personal identities correspond to a fixed pattern that instantaneously disappears with the passage of time, and "Closed individualism", the common view that personal identities are particular to subjects and yet survive over time.[31]: xxii  Open individualism is related to the concept of anattā in Buddhist philosophy where the term anattā (Pali: 𑀅𑀦𑀢𑁆𑀢𑀸) or anātman (Sanskrit: अनात्मन्) is the doctrine of "non-self" – that no unchanging, permanent self or essence can be found in any phenomenon. While often interpreted as a doctrine denying the existence of a self, anatman is more accurately described as a strategy to attain non-attachment by recognizing everything as impermanent, while staying silent on the ultimate existence of an unchanging essence.[32][33] In contrast, dominant schools of Hinduism assert the existence of Ātman as pure awareness or witness-consciousness,[34][35][36] "reify[ing] consciousness as an eternal self."[37] One thought experiment in the philosophy of personal identity is the teletransportation paradox. It deals with whether the concept of one's future self is a coherent concept. The thought experiment was formulated by Derek Parfit in his 1984 book Reasons and Persons.[38] Derek Parfit and others consider a hypothetical "teletransporter", a machine that puts you to sleep, records your molecular composition, breaking you down into atoms, and relaying its recording to Mars at the speed of light. On Mars, another machine re-creates you (from local stores of carbon, hydrogen, and so on), each atom in exactly the same relative position. Parfit poses the question of whether or not the teletransporter is actually a method of travel, or if it simply kills and makes an exact replica of the user.[39] Then the teleporter is upgraded. The teletransporter on Earth is modified to not destroy the person who enters it, but instead it can simply make infinite replicas, all of whom would claim to remember entering the teletransporter on Earth in the first place. Using thought experiments such as these, Parfit argues that any criteria we attempt to use to determine sameness of person will be lacking, because there is no further fact. What matters, to Parfit, is simply "Relation R", psychological connectedness, including memory, personality, and so on.[40] Religion Main article: Religious views on the self Religious views on the Self vary widely. The Self is a complex and core subject in many forms of spirituality. Two types of Self are commonly considered—the Self that is the ego, also called the learned, superficial Self of mind and body, egoic creation, and the Self which is sometimes called the "True Self", the "Observing Self", or the "Witness".[41] In Hinduism, the Ātman (Self), despite being experienced as an individual, is actually a representation of the unified transcendent reality, Brahman.[42] Our experience of reality doesn't match the nature of Brahman due to māyā. One description of spirituality is the Self's search for "ultimate meaning" through an independent comprehension of the sacred. Another definition of spiritual identity is: "A persistent sense of Self that addresses ultimate questions about the nature, purpose, and meaning of life, resulting in behaviors that are consonant with the individual’s core values. Spiritual identity appears when the symbolic religious and spiritual value of a culture is found by individuals in the setting of their own life. There can be different types of spiritual Self because it is determined by one's life and experiences."[43] Human beings have a Self—that is, they are able to look back on themselves as both subjects and objects in the universe. Ultimately, this brings questions about who we are and the nature of our own importance.[44] Traditions such as in Buddhism see the attachment to Self is an illusion that serves as the main cause of suffering and unhappiness.[

이미지
  In   philosophy , the   self   is an   individual 's own   being ,   knowledge , and   values , and the relationship between these attributes. The first-person perspective distinguishes selfhood from  personal identity . Whereas "identity" is (literally) sameness [ 1 ]  and may involve  categorization  and  labeling , [ 2 ]  selfhood implies a first-person perspective and suggests potential uniqueness. Conversely, "person" is used as a third-person reference. Personal identity can be impaired in late-stage  Alzheimer's disease  and in other  neurodegenerative diseases . Finally, the self is distinguishable from "others". Including the distinction between sameness and  otherness , the self versus other is a research topic in contemporary  philosophy [ 3 ]  and contemporary  phenomenology  (see also  psychological phenomenology ),  psychology ,  psychiatry , ...
자세한 내용 보기

Psychology is the scientific study of the mind and behavior.[1][2] Its subject matter includes the behavior of humans and nonhumans, both conscious and unconscious phenomena, and mental processes such as thoughts, feelings, and motives. Psychology is an academic discipline of immense scope, crossing the boundaries between the natural and social sciences. Biological psychologists seek an understanding of the emergent properties of brains, linking the discipline to neuroscience. As social scientists, psychologists aim to understand the behavior of individuals and groups.[3][4] A professional practitioner or researcher involved in the discipline is called a psychologist. Some psychologists can also be classified as behavioral or cognitive scientists. Some psychologists attempt to understand the role of mental functions in individual and social behavior. Others explore the physiological and neurobiological processes that underlie cognitive functions and behaviors. As part of an interdisciplinary field, psychologists are involved in research on perception, cognition, attention, emotion, intelligence, subjective experiences, motivation, brain functioning, and personality. Psychologists' interests extend to interpersonal relationships, psychological resilience, family resilience, and other areas within social psychology. They also consider the unconscious mind.[5] Research psychologists employ empirical methods to infer causal and correlational relationships between psychosocial variables. Some, but not all, clinical and counseling psychologists rely on symbolic interpretation. While psychological knowledge is often applied to the assessment and treatment of mental health problems, it is also directed towards understanding and solving problems in several spheres of human activity. By many accounts, psychology ultimately aims to benefit society.[6][7][8] Many psychologists are involved in some kind of therapeutic role, practicing psychotherapy in clinical, counseling, or school settings. Other psychologists conduct scientific research on a wide range of topics related to mental processes and behavior. Typically the latter group of psychologists work in academic settings (e.g., universities, medical schools, or hospitals). Another group of psychologists is employed in industrial and organizational settings.[9] Yet others are involved in work on human development, aging, sports, health, forensic science, education, and the media.

이미지
 Psychology is the scientific study of the mind and behavior.[1][2] Its subject matter includes the behavior of humans and nonhumans, both conscious and unconscious phenomena, and mental processes such as thoughts, feelings, and motives. Psychology is an academic discipline of immense scope, crossing the boundaries between the natural and social sciences. Biological psychologists seek an understanding of the emergent properties of brains, linking the discipline to neuroscience. As social scientists, psychologists aim to understand the behavior of individuals and groups.[3][4] A professional practitioner or researcher involved in the discipline is called a psychologist. Some psychologists can also be classified as behavioral or cognitive scientists. Some psychologists attempt to understand the role of mental functions in individual and social behavior. Others explore the physiological and neurobiological processes that underlie cognitive functions and behaviors. As part of an interd...
자세한 내용 보기