영적모독靈的冒瀆spiritualinsultblasphemyprofanity 反宇宙體반우주체식인체食人體식육체食肉體마물체魔物體짐승체獸禽畜體反宇宙意識體반우주의식체反物質意識體반물질의식체反生命意識體반생명의식체反粒子意識體반입자의식체反宇宙體반우주체反物質體반물질체反生命體반생명체反粒子體반입자체작도자作圖者작화자作畫者작도作圖작화作畫630128-1067814朴鐘權的大億劫的削的磨的滅的處理的반사회성인격장애체反社會性人格障礙體인격장애체人格障碍體ANDROMEDAGALAXY聯合元老院的大億劫的削的磨的滅的處理的ATLANTIS的大億劫的削的磨的滅的處理的OBEIRON的大億劫的削的磨的滅的處理的PILING低等級者들이高等級者身體에根을심고同一한等級者로處世空得昇格意圖大億 pneumanotchdegradationdemotionseizureplunderunauthorizedsharing영등급강등영등급강탈영등급무단공유靈等級降等靈等級强奪無斷共有公有 전한(前漢: 기원전 202년~기원후 8년)은 고조(高祖) 유방(劉邦)이 항우(項羽)와 대륙 쟁탈 뒤에 세운 왕조로서 진(秦)에 이어서 중국을 두 번째로 통일한 왕조이다 전연(前燕: 337~370)은 5호16국시대 선비족(鮮卑族) 모용황(慕容皝)에 의해 건국된 나라이다. 고구려(高句麗)는 한국의 고대 왕조국가 중 하나이다.[6] 국성은 고씨(高氏)이다.[7] 본래의 국호는 고구려였으나 당시의 금석문과 역사 기록을 토대로 장수왕대에 고려(高麗)로 개칭한 것으로 추정하고 있다.[8][9][10][11] 이후에도 궁예가 세운 후고구려(901년)와 왕건이 세운 고려(918년)가 계승하여 '고려' 국호는 천년 이상 지속되었다. 현재 한국의 영문 국호인 코리아 역시 고려에서 유래되었다.[12][13][14][15] 동로마 제국(현대 그리스어: Ανατολική Ρωμαϊκή Αυτοκρατορία 아나톨리키 로마이키 아프토크라토리아[*]) 또는 비잔티움 제국(현대 그리스어: Βυζαντινή Αυτοκρατορία 비잔디니 아프토크라토리아[*])은 로마 제국이 동서로 분할된 395년부터 1453년까지 동방 황제의 치하로 존속한 로마 제국의 연속체이다. 수도는 콘스탄티노폴리스였고, 제국의 공식 국호는 이전과 같은 로마 제국(중세 그리스어: Βασιλεία Ῥωμαίων 바실리아 로메온[*])이었다. 제국에 거주하는 주민들 역시 자국을 로마 제국 또는 로마니아(중세 그리스어: Ῥωμανία)[1]라고 불렀으며, 주민들은 자신들을 로마인(중세 그리스어: Ῥωμαῖοι 로메이[*])라고 불렀다. 이건희의 생계방해사례증거 아틀란티스과학기술연구소의 업적과 기타 일들을 공개기재하다. 이후 아래에 일어난 일들은 이건희가 지시한 것이 거의 확실시되는 것으로 유추해석되다 2. 서기2002년 갑자기 사업부가 통폐합되다. 텔레비젼사업부와 모니터사업부의 통폐합 3. 텔레비젼사업부와 통폐합되면서 좌천되다(일종의 의도적 좌천) 텔레비젼사업부 : 연령이 높고 근무연수가 많은 사람들 모니터사업부 : 연령이 낮고 근무연수가 낮은데다가 박종권이는 경력사원-> 책상이동좌천 4.서기2002년 아루쓰아종 유영관이 갑자기 시비걸다(삼성전자 뉴욕주재원을 하다가 귀국) 5.이후 회사를 상대로 네고를 한다는둥, 회사를 해사한다는둥, 먹고 살것 없는 놈 데려다가 월급주고 살게 해 줬더니 시건방을 떨고 그런다는 둥 어마어마한 모독, 시비걸기, 패죽이기가 시작되다. 실제 박종권이가 삼성에 기여공헌한 업적금액은 무려 1200조원에 이른다. 하지만 증거도 없고 물증도 없고 심증만 있는데다가 이건희의 자존심을 건드린 것이 이러한 일을 초래했다고 유추해석되다. 이건희가 중국국가상무위원 임의대행을 하고 영국왕이 되고 미국대통령이 되고 온갖 권력위세를 부린 이유는 박종권이 때문이다. 하지만 실제현실상으로는 이건희가 실세이고, 사람들이나 세상이 박종권이 편을 들수 없는 형국이므로, 박종권이가 삼성을 대상으로 해서 해사행위를 하고 네고를 쳐대고, 시건방을 떠는 놈으로 몰아가면서 불명예스럽게 안좋은 식으로 회사를 그만두게 모독강제한 사건으로 해석되다. 실제로는 삼성창업자에 해당된다., 이후 회사를 그만둔후 이건희는 지속해서 생계를 방해하고, 문제를 일으키며, 결국 이건희프로젝트로 끌어들이는데, 이건희프로젝트를 통해서 지옥유계맵에 감금구속하고 죽이려고 한 짓이며, 박종권이가 가진 지위서열신분등급을 모조리 빼앗고 영국왕이 되고 플레이아데스수장이 되고 중국국가상무위원이 되어서 최고도의 처우를 받고 누리고 나대려고 한 것이 목적이라고 분명히 해석되다. 나쁜 새끼다 1.서기2005년1월경 이태리로 명품물건을 떼러가다 - 당시의 안내원역할을 한 사람의 증언 : 이건희가 지시하기를 잘 안팔리는 물건만 소개해서 사가지고 가게 하라고 했다고 증언 2.서기2005년 경, 안산 쇼핑몰에 입점하여 옷가게를 하려고 시도하다 - 안산쇼핑몰 전체를 시공간차원이동시켜 일반인들 세상과 격리차단시키다. - 쇼핑몰개업후 손님이 아예 오지를 않는 이상현상발생 - 훗날 관찰목격시, 안산쇼핑몰 전체부스가 시공간이동하여 특정차원공간영역에 위치하는데, 사 람들이 올수 없는 영역, 차원, 공간에 위치해 있는 것이 목격관찰되다. 3. 서기2004년경, 수원 쇼핑센터에 옷가게를 개업하다 - 1년 5개월만에 장사가 안되어서 쇼핑센터 전체가 폐업되다 4. 서기2005년 경, 오피스텔에 들어가서 인터넷쇼핑몰을 구상하는중, 내부를 도촬감시함이 발각되다. 몰래카메라로 도촬하여 보고 있음이 증거되다. 5. 서기2005년경, 중소기업에 취업시켜주겠다는 제의가 들어오는데 안 갈것을 뻔히 알고 제의하다 6. 이후 2006년 1월 이건희프로젝트를 제안하다. 이건희프로젝트로 끌어들이려는 의도적생계방해 이후 약속과 달리 여자를 사귈수 없게 교묘하게 방해하고 모독하고 폭력폭행무력구타모독을 서슴지 않으며, 조직폭력배를 동원해서 협박하고 때려죽이려 하다. 이후 이 자가 중국국가상무위원대행이 되고 중국황제까지 누리는 일이 벌어지다(전연모용황을 거쳐서 전한을 멸망시키고 신나라 황제가 된 이건희-이후 수당시대에 영국으로 가서 영국왕이 되고 영국여왕남편이 되다. 이후 4만인이 넘는 여자들을 소유하다 중국황제놈-아플레이아데스수장급 기준 4만인의 여자를 독점독식하는 것이 관행이었다.)

 영적모독靈的冒瀆spiritualinsultblasphemyprofanity

反宇宙體반우주체식인체食人體식육체食肉體마물체魔物體짐승체獸禽畜體反宇宙意識體반우주의식체反物質意識體반물질의식체反生命意識體반생명의식체反粒子意識體반입자의식체反宇宙體반우주체反物質體반물질체反生命體반생명체反粒子體반입자체작도자作圖者작화자作畫者작도作圖작화作畫630128-1067814朴鐘權的大億劫的削的磨的滅的處理的반사회성인격장애체反社會性人格障礙體인격장애체人格障碍體ANDROMEDAGALAXY聯合元老院的大億劫的削的磨的滅的處理的ATLANTIS的大億劫的削的磨的滅的處理的OBEIRON的大億劫的削的磨的滅的處理的PILING低等級者들이高等級者身體에根을심고同一한等級者로處世空得昇格意圖大億

pneumanotchdegradationdemotionseizureplunderunauthorizedsharing영등급강등영등급강탈영등급무단공유靈等級降等靈等級强奪無斷共有公有

전한(前漢: 기원전 202년~기원후 8년)은 고조(高祖) 유방(劉邦)이 항우(項羽)와 대륙 쟁탈 뒤에 세운 왕조로서 진(秦)에 이어서 중국을 두 번째로 통일한 왕조이다

전연(前燕: 337~370)은 5호16국시대 선비족(鮮卑族) 모용황(慕容皝)에 의해 건국된 나라이다.

고구려(高句麗)는 한국의 고대 왕조국가 중 하나이다.[6] 국성은 고씨(高氏)이다.[7] 본래의 국호는 고구려였으나 당시의 금석문과 역사 기록을 토대로 장수왕대에 고려(高麗)로 개칭한 것으로 추정하고 있다.[8][9][10][11] 이후에도 궁예가 세운 후고구려(901년)와 왕건이 세운 고려(918년)가 계승하여 '고려' 국호는 천년 이상 지속되었다. 현재 한국의 영문 국호인 코리아 역시 고려에서 유래되었다.[12][13][14][15]

동로마 제국(현대 그리스어: Ανατολική Ρωμαϊκή Αυτοκρατορία 아나톨리키 로마이키 아프토크라토리아[*]) 또는 비잔티움 제국(현대 그리스어: Βυζαντινή Αυτοκρατορία 비잔디니 아프토크라토리아[*])은 로마 제국이 동서로 분할된 395년부터 1453년까지 동방 황제의 치하로 존속한 로마 제국의 연속체이다. 수도는 콘스탄티노폴리스였고, 제국의 공식 국호는 이전과 같은 로마 제국(중세 그리스어: Βασιλεία Ῥωμαίων 바실리아 로메온[*])이었다. 제국에 거주하는 주민들 역시 자국을 로마 제국 또는 로마니아(중세 그리스어: Ῥωμανία)[1]라고 불렀으며, 주민들은 자신들을 로마인(중세 그리스어: Ῥωμαῖοι 로메이[*])라고 불렀다.

 

 


이건희의 생계방해사례증거

아틀란티스과학기술연구소의 업적과 기타 일들을 공개기재하다.

이후 아래에 일어난 일들은 이건희가 지시한 것이 거의 확실시되는 것으로 유추해석되다

2. 서기2002년 갑자기 사업부가 통폐합되다.

   텔레비젼사업부와 모니터사업부의 통폐합

3. 텔레비젼사업부와 통폐합되면서 좌천되다(일종의 의도적 좌천)

   텔레비젼사업부 : 연령이 높고 근무연수가 많은 사람들

   모니터사업부 : 연령이 낮고 근무연수가 낮은데다가 박종권이는 경력사원-> 책상이동좌천

4.서기2002년 아루쓰아종 유영관이 갑자기 시비걸다(삼성전자 뉴욕주재원을 하다가 귀국)

5.이후 회사를 상대로 네고를 한다는둥, 회사를 해사한다는둥, 먹고 살것 없는 놈 데려다가 월급주고 살게 해 줬더니 시건방을 떨고 그런다는 둥 어마어마한 모독, 시비걸기, 패죽이기가 시작되다.

 실제 박종권이가 삼성에 기여공헌한 업적금액은 무려 1200조원에 이른다.

하지만 증거도 없고 물증도 없고 심증만 있는데다가 이건희의 자존심을 건드린 것이 이러한 일을 초래했다고 유추해석되다.  이건희가 중국국가상무위원 임의대행을 하고 영국왕이 되고 미국대통령이 되고 온갖 권력위세를 부린 이유는 박종권이 때문이다. 하지만 실제현실상으로는 이건희가 실세이고, 사람들이나 세상이 박종권이 편을 들수 없는 형국이므로, 박종권이가 삼성을 대상으로 해서 해사행위를 하고 네고를 쳐대고, 시건방을 떠는 놈으로 몰아가면서 불명예스럽게 안좋은 식으로 회사를 그만두게 모독강제한 사건으로 해석되다. 실제로는 삼성창업자에 해당된다.,

이후 회사를 그만둔후 이건희는 지속해서 생계를 방해하고, 문제를 일으키며, 결국 이건희프로젝트로 끌어들이는데, 이건희프로젝트를 통해서 지옥유계맵에 감금구속하고 죽이려고 한 짓이며, 박종권이가 가진 지위서열신분등급을 모조리 빼앗고 영국왕이 되고 플레이아데스수장이 되고 중국국가상무위원이 되어서 최고도의 처우를 받고 누리고 나대려고 한 것이 목적이라고 분명히 해석되다. 나쁜 새끼다

1.서기2005년1월경 이태리로 명품물건을 떼러가다

  - 당시의 안내원역할을 한 사람의 증언 : 

    이건희가 지시하기를 잘 안팔리는 물건만 소개해서 사가지고 가게 하라고 했다고 증언

2.서기2005년 경, 안산 쇼핑몰에 입점하여 옷가게를 하려고 시도하다

  - 안산쇼핑몰 전체를 시공간차원이동시켜 일반인들 세상과 격리차단시키다.

  - 쇼핑몰개업후 손님이 아예 오지를 않는 이상현상발생

  - 훗날 관찰목격시, 안산쇼핑몰 전체부스가 시공간이동하여 특정차원공간영역에 위치하는데, 사

    람들이 올수 없는 영역, 차원, 공간에 위치해 있는 것이 목격관찰되다.

3. 서기2004년경, 수원 쇼핑센터에 옷가게를 개업하다

   - 1년 5개월만에 장사가 안되어서 쇼핑센터 전체가 폐업되다

4. 서기2005년 경, 오피스텔에 들어가서 인터넷쇼핑몰을 구상하는중, 내부를 도촬감시함이 발각되다. 몰래카메라로 도촬하여 보고 있음이 증거되다. 

5. 서기2005년경, 중소기업에 취업시켜주겠다는 제의가 들어오는데 안 갈것을 뻔히 알고 제의하다

6. 이후 2006년 1월 이건희프로젝트를 제안하다. 이건희프로젝트로 끌어들이려는 의도적생계방해


이후 약속과 달리 여자를 사귈수 없게 교묘하게 방해하고 모독하고 폭력폭행무력구타모독을 서슴지 않으며, 조직폭력배를 동원해서 협박하고 때려죽이려 하다. 이후 이 자가 중국국가상무위원대행이 되고 중국황제까지 누리는 일이 벌어지다(전연모용황을 거쳐서 전한을 멸망시키고 신나라 황제가 된 이건희-이후 수당시대에 영국으로 가서 영국왕이 되고 영국여왕남편이 되다. 이후 4만인이 넘는 여자들을 소유하다 중국황제놈-아플레이아데스수장급 기준 4만인의 여자를 독점독식하는 것이 관행이었다.)


















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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

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  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...
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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.

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 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...
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