document_title: History of mental disorders

question_text: where did the term mental illness come from

text: History of mental disorders

text: Historical conceptions of abnormal behavior[edit]

text: For thousands of years, humans have tried to explain and control problematic behavior. But our efforts always derive from theories or models of behavior popular at the time, and the purpose is to explain 'why someone is like that'. Three major models, namely, supernatural model, biological model and psychological model.[1]

text: Supernatural tradition[edit]

text: For much of our recorded history, deviant behavior has been considered a reflection of the battle between good and evil. When confronted with unexplainable, irrational behavior and by suffering and upheaval, people have perceived evil. In fact, in the Great Persian Empire from 900 to 600 B.C., all physical and mental disorders were considered the work of the devil.[2]

text: Biological tradition[edit]

text: Physical causes of mental disorders have been sought in history. Important to this tradition are a man, Hippocrates; a disease, syphilis; and the early consequences of believing that psychological disorders are biologically caused.[3]

text: Psychological tradition[edit]

text: This was a precursor to modern psychosocial treatment approaches to the causation of psychopathology, with the focus on psychological, social and cultural factors. Well known philosophers like Aristotle, Plato, etc., wrote about the importance of fantasies, dreams, cognitions, and thus anticipated, to some extent, later developments in psychoanalytic thought and cognitive science. They also advocated humane and responsible care for individuals with psychological disturbances.[4]

text: Ancient period[edit]

text: Mesopotamia[edit]

text: Mental illnesses were well known in ancient Mesopotamia,[5] where diseases and mental disorders were believed to be caused by specific deities.[6] Because hands symbolized control over a person, mental illnesses were known as "hands" of certain deities.[6] One psychological illness was known as Qāt Ištar, meaning "Hand of Ishtar".[6] Others were known as "Hand of Shamash", "Hand of the Ghost", and "Hand of the God".[6] Descriptions of these illnesses, however, are so vague that it is usually impossible to determine which illnesses they correspond to in modern terminology.[6] Mesopotamian doctors kept detailed record of their patients' hallucinations and assigned spiritual meanings to them.[5] A patient who hallucinated that he was seeing a dog was predicted to die;[5] whereas, if he saw a gazelle, he would recover.[5] The royal family of Elam was notorious for its members frequently suffering from insanity.[5] Erectile dysfunction was recognized as being rooted in psychological problems.[5]

text: Egypt[edit]

text: Limited notes in an ancient Egyptian document known as the Ebers papyrus appear to describe the affected states of concentration, attention, and emotional distress in the heart or mind.[7] Some of these were interpreted later, and renamed as hysteria and melancholy. Somatic treatments included applying bodily fluids while reciting magical spells. Hallucinogens may have been used as a part of the healing rituals. Religious temples may have been used as therapeutic retreats, possibly for the induction of receptive states to facilitate sleep and the interpretation of dreams.[8]

text: India[edit]

text: This section relies largely or entirely on a single source. Relevant discussion may be found on the talk page. Please help improve this article by introducing citations to additional sources. (December 2016)

text: Ancient Hindu scriptures-Ramayana and Mahabharata-contain fictional descriptions of depression and anxiety.[9] Mental disorders were generally thought to reflect abstract metaphysical entities, supernatural agents, sorcery and witchcraft. The Charaka Samhita from circa 600 BC, which is a part of the Hindu Ayurveda ("knowledge of life"), saw ill health as resulting from an imbalance among the three body fluids or forces called Tri-Dosha. These also affected the personality types among people. Suggested causes included inappropriate diet, disrespect towards the gods, teachers or others, mental shock due to excessive fear or joy, and faulty bodily activity. Treatments included the use of herbs and ointments, charms and prayers, and moral or emotional persuasion.[10]

text: China[edit]

text: The earliest known record of mental illness in ancient China dates back to 1100 B.C.[11] Mental disorders were treated mainly under Traditional Chinese Medicine using herbs, acupuncture or "emotional therapy". The Inner Canon of the Yellow Emperor described symptoms, mechanisms and therapies for mental illness, emphasizing connections between bodily organs and emotions. The ancient Chinese believed that demonic possession played a role in mental illness during this time period. They felt that areas of emotional outbursts such as funeral homes could open up the Wei Chi and allow entities to possess an individual. Trauma was also considered to be something that caused high levels of emotion. Thus, trauma is a possible catalyst for mental illness, due to its ability to allow the Wei Chi open to possession. This explains why the ancient Chinese believed that a mental illness was in reality a demonic possession.[12] According to Chinese thought, five stages or elements comprised the conditions of imbalance between Yin and yang. Mental illness, according to the Chinese perspective is thus considered as an imbalance of the yin and yang because optimum health arises from balance with nature.[13]

text: China was one of the earliest developed civilizations in which medicine and attention to mental disorders were introduced (Soong, 2006)As in the West, Chinese views of mental disorders regressed to a belief in supernatural forces as causal agents. From the later part of the second century through the early part of the ninth century, ghosts and devils were implicated in “ghostevil” insanity, which presumably resulted from possession by evil spirits. The “Dark Ages” in China, however, were neither so severe (in terms of the treatment of mental patients) nor as long-lasting as in the West. A return to biological, somatic (bodily) views and an emphasis on psychosocial factors occurred in the centuries that followed. Over the past 50 years, China has been experiencing a broadening of ideas in mental health services and has been incorporating many ideas from Western psychiatry (Zhang & Lu, 2006) [14]

text: Greece and Rome[edit]

text: In ancient Greece and Rome, madness was associated stereotypically with aimless wandering and violence. However, Socrates considered positive aspects including prophesying (a 'manic art'); mystical initiations and rituals; poetic inspiration; and the madness of lovers. Now often seen as the very epitome of rational thought and as the founder of philosophy, Socrates freely admitted to experiencing what are now called "command hallucinations" (then called his 'daemon'). Pythagoras also heard voices.[15] Hippocrates (470–ca. 360 BC) classified mental disorders, including paranoia, epilepsy, mania and melancholia.[16]

text: Through long contact with Greek culture, and their eventual conquest of Greece, the Romans absorbed many Greek (and other) ideas on medicine.[17] The humoral theory fell out of favor in some quarters. The Greek physician Asclepiades (ca. 124–40 BC), who practiced in Rome, discarded it and advocated humane treatments, and had insane persons freed from confinement and treated them with natural therapy, such as diet and massages. Arateus (ca. AD 30–90) argued that it is hard to pinpoint from where a mental illness comes. However, Galen (AD 129–ca. 200), practicing in Greece and Rome, revived humoral theory.[18] Galen, however, adopted a single symptom approach rather than broad diagnostic categories, for example studying separate states of sadness, excitement, confusion and memory loss.[15]

text: Playwrights such as Homer, Sophocles and Euripides described madmen driven insane by the gods, imbalanced humors or circumstances. As well as the triad (of which mania was often used as an overarching term for insanity) there were a variable and overlapping range of terms for such things as delusion, eccentricity, frenzy, and lunacy. Physician Celsus argued that insanity is really present when a continuous dementia begins due to the mind being at the mercy of imaginings. He suggested that people must heal their own souls through philosophy and personal strength. He described common practices of dietetics, bloodletting, drugs, talking therapy, incubation in temples, exorcism, incantations and amulets, as well as restraints and "tortures" to restore rationality, including starvation, being terrified suddenly, agitation of the spirit, and stoning and beating. Most, however, did not receive medical treatment but stayed with family or wandered the streets, vulnerable to assault and derision. Accounts of delusions from the time included people who thought themselves to be famous actors or speakers, animals, inanimate objects, or one of the gods. Some were arrested for political reasons, such as Jesus ben Ananias who was eventually released as a madman after showing no concern for his own fate during torture.

text: Israel and the Hebrew diaspora[edit]

text: Passages of the Hebrew Bible/Old Testament have been interpreted as describing mood disorders in figures such as Job, King Saul and in the Psalms of David.[18] In the Book of Daniel, King Nebuchadnezzar is described as temporarily losing his sanity.[19] Mental disorder was not a problem like any other, caused by one of the gods, but rather caused by problems in the relationship between the individual and God.[citation needed] They believed that abnormal behavior was the result of possessions that represented the wrath and punishment from God. This punishment was seen as a withdrawal of God's protection and the abandonment of the individual to evil forces.[20]

text: Middle ages[edit]

text: Persia, Arabia and the Muslim empire[edit]

text: Persian and Arabic scholars were heavily involved in translating, analyzing and synthesizing Greek texts and concepts. As the Muslim world expanded, Greek concepts were integrated with religious thought and over time, new ideas and concepts were developed. Arab texts from this period contain discussions of melancholia, mania, hallucinations, delusions, and other mental disorders. Mental disorder was generally connected to loss of reason, and writings covered links between the brain and disorders, and spiritual/mystical meaning of disorders.[21] wrote about fear and anxiety, anger and aggression, sadness and depression, and obsessions.

text: Authors who wrote on mental disorders and/or proposed treatments during this period include Al-Balkhi, Al-Razi, Al-Farabi, Ibn-Sina, Al-Majusi[22] Abu al-Qasim al-Zahrawi, Averroes,[23] and Unhammad.[24]

text: Some thought mental disorder could be caused by possession by a djinn (genie), which could be either good or demon-like. There were sometimes beatings to exorcise the djin, or alternatively over-zealous attempts at cures.[25] Islamic views often merged with local traditions. In Morocco the traditional Berber people were animists and the concept of sorcery was integral to the understanding of mental disorder; it was mixed with the Islamic concepts of djin and often treated by religious scholars combining the roles of holy man, sage, seer and sorcerer.[26]

text: The first psychiatric hospital ward was founded in Baghdad in 705, and insane asylums were built in Fes in the early 8th century, Cairo in 800 and in Damascus and Aleppo in 1270. Insane patients were treated using baths, drugs, music and activities.[citation needed] In the centuries to come, The Muslim world would eventually serve as a critical way station of knowledge for Renaissance Europe, through the Latin translations of many scientific Islamic texts. Ibn-Sina's (Avicenna's) Canon of Medicine became the standard of medical science in Europe for centuries, together with works of Hippocrates and Galen.[27]

text: Christian Europe[edit]

text: Conceptions of madness in the Middle Ages in Europe were a mixture of the divine, diabolical, magical and transcendental. Theories of the four humors (black bile, yellow bile, phlegm, and blood) were applied, sometimes separately (a matter of "physic") and sometimes combined with theories of evil spirits (a matter of "faith"). Arnaldus de Villanova (1235–1313) combined "evil spirit" and Galen-oriented "four humours" theories and promoted trephining as a cure to let demons and excess humours escape. Other bodily remedies in general use included purges, bloodletting and whipping. Madness was often seen as a moral issue, either a punishment for sin or a test of faith and character. Christian theology endorsed various therapies, including fasting and prayer for those estranged from God and exorcism of those possessed by the devil.[28] Thus, although mental disorder was often thought to be due to sin, other more mundane causes were also explored, including intemperate diet and alcohol, overwork, and grief.[29] The Franciscan monk Bartholomeus Anglicus (ca. 1203 – 1272) described a condition which resembles depression in his encyclopedia, De Proprietatibis Rerum, and he suggested that music would help. A semi-official tract called the Praerogativa regis distinguished between the "natural born idiot" and the "lunatic". The latter term was applied to those with periods of mental disorder; deriving from either Roman mythology describing people "moonstruck" by the goddess Luna[30] or theories of an influence of the moon.[31][32]

text: Episodes of mass dancing mania are reported from the Middle Ages, "which gave to the individuals affected all the appearance of insanity".[33] This was one kind of mass delusion or mass hysteria/panic that has occurred around the world through the millennia.[34]

text: The care of lunatics was primarily the responsibility of the family. In England, if the family were unable or unwilling, an assessment was made by crown representatives in consultation with a local jury and all interested parties, including the subject himself or herself. The process was confined to those with real estate or personal estate, but it encompassed poor as well as rich and took into account psychological and social issues. Most of those considered lunatics at the time probably had more support and involvement from the community than people diagnosed with mental disorders today.[35] As in other eras, visions were generally interpreted as meaningful spiritual and visionary insights; some may have been causally related to mental disorders, but since hallucinations were culturally supported they may not have had the same connections as today.[36]

text: Modern period[edit]

text: The examples and perspective in this section deal primarily with Western culture and do not represent a worldwide view of the subject. You may improve this article, discuss the issue on the talk page. (December 2016) (Learn how and when to remove this template message)

text: 16th to 18th centuries[edit]

text: Some mentally disturbed people may have been victims of the witch-hunts that spread in waves in early modern Europe.[37] However, those judged insane were increasingly admitted to local workhouses, poorhouses and jails (particularly the "pauper insane") or sometimes to the new private madhouses.[38] Restraints and forcible confinement were used for those thought dangerously disturbed or potentially violent to themselves, others or property.[28] The latter likely grew out of lodging arrangements for single individuals (who, in workhouses, were considered disruptive or ungovernable) then there were a few catering each for only a handful of people, then they gradually expanded (e.g. 16 in London in 1774, and 40 by 1819). By the mid-19th century there would be 100 to 500 inmates in each. The development of this network of madhouses has been linked to new capitalist social relations and a service economy, that meant families were no longer able or willing to look after disturbed relatives.[39]

text: Madness was commonly depicted in literary works, such as the plays of Shakespeare.[40][41]

text: By the end of the 17th century and into the Enlightenment, madness was increasingly seen as an organic physical phenomenon, no longer involving the soul or moral responsibility. The mentally ill were typically viewed as insensitive wild animals. Harsh treatment and restraint in chains was seen as therapeutic, helping suppress the animal passions. There was sometimes a focus on the management of the environment of madhouses, from diet to exercise regimes to number of visitors. Severe somatic treatments were used, similar to those in medieval times.[28] Madhouse owners sometimes boasted of their ability with the whip. Treatment in the few public asylums was also barbaric, often secondary to prisons. The most notorious was Bedlam where at one time spectators could pay a penny to watch the inmates as a form of entertainment.[42][43]

text: Concepts based in humoral theory gradually gave way to metaphors and terminology from mechanics and other developing physical sciences. Complex new schemes were developed for the classification of mental disorders, influenced by emerging systems for the biological classification of organisms and medical classification of diseases.

text: The term "crazy" (from Middle English meaning cracked) and insane (from Latin insanus meaning unhealthy) came to mean mental disorder in this period. The term "lunacy", long used to refer to periodic disturbance or epilepsy, came to be synonymous with insanity. "Madness", long in use in root form since at least the early centuries AD, and originally meaning crippled, hurt or foolish, came to mean loss of reason or self-restraint. "Psychosis", from Greek "principle of life/animation", had varied usage referring to a condition of the mind/soul. "Nervous", from an Indo-European root meaning to wind or twist, meant muscle or vigor, was adopted by physiologists to refer to the body's electrochemical signalling process (thus called the nervous system), and was then used to refer to nervous disorders and neurosis. "Obsession", from a Latin root meaning to sit on or sit against, originally meant to besiege or be possessed by an evil spirit, came to mean a fixed idea that could decompose the mind.[44]

text: With the rise of madhouses and the professionalization and specialization of medicine, there was considerable incentive for medical doctors to become involved. In the 18th century, they began to stake a claim to a monopoly over madhouses and treatments. Madhouses could be a lucrative business, and many made a fortune from them. There were some bourgeois ex-patient reformers who opposed the often brutual regimes, blaming both the madhouse owners and the medics, who in turn resisted the reforms.[39]

text: Towards the end of the 18th century, a moral treatment movement developed, that implemented more humane, psychosocial and personalized approaches. Notable figures included the medic Vincenzo Chiarugi in Italy under Enlightenment leadership; the ex-patient superintendent Pussin and the psychologically inclined medic Philippe Pinel in revolutionary France; the Quakers in England, led by businessman William Tuke; and later, in the United States, campaigner Dorothea Dix.

text: 19th century[edit]

text: The 19th century, in the context of industrialization and population growth, saw a massive expansion of the number and size of insane asylums in every Western country, a process called "the great confinement" or the "asylum era". Laws were introduced to compel authorities to deal with those judged insane by family members and hospital superintendents. Although originally based on the concepts and structures of moral treatment, they became large impersonal institutions overburdened with large numbers of people with a complex mix of mental and social-economic problems.[38] The success of moral treatment had cast doubt on the approach of medics, and many had opposed it, but by the mid-19th century many became advocates of it but argued that the mad also often had physical/organic problems, so that both approaches were necessary. This argument has been described as an important step in the profession's eventual success in securing a monopoly on the treatment of lunacy. However, it is well documented that very little therapeutic activity occurred in the new asylum system, that medics were little more than administrators who seldom attended to patients, and then mainly for other physical problems.[39]

text: Clear descriptions of some syndromes, such as the condition that would later be termed schizophrenia, have been identified as relatively rare prior to the 19th century,[45] although interpretations of the evidence and its implications are inconsistent.[46]

text: Numerous different classification schemes and diagnostic terms were developed by different authorities, taking an increasingly anatomical-clinical descriptive approach. The term "psychiatry" was coined as the medical specialty became more academically established. Asylum superintendents, later to be psychiatrists, were generally called "alienists" because they were thought to deal with people alienated from society; they adopted largely isolated and managerial roles in the asylums while milder "neurotic" conditions were dealt with by neurologists and general physicians, although there was overlap for conditions such as neurasthenia.[47]

text: In the United States it was proposed that black slaves who tried to escape were suffering from a mental disorder termed drapetomania. It was then argued in scientific journals that mental disorders were rare under conditions of slavery but became more common following emancipation, and later that mental illness in African Americans was due to evolutionary factors or various negative characteristics, and that they were not suitable for therapeutic intervention.[48]

text: By the 1870s in North America, officials who ran Lunatic Asylums renamed them Insane Asylums. By the late century, the term "asylum" had lost its original meaning as a place of refuge, retreat or safety, and was associated with abuses that had been widely publicized in the media, including by ex-patient organization the Alleged Lunatics' Friend Society and ex-patients like Elizabeth Packard.[30]

text: The relative proportion of the public officially diagnosed with mental disorders was increasing, however. This has been linked to various factors, including possibly humanitarian concern; incentives for professional status/money; a lowered tolerance of communities for unusual behavior due to the existence of asylums to place them in (this affected the poor the most); and the strain placed on families by industrialization.[39]

text: 20th century[edit]

text: The turn of the 20th century saw the development of psychoanalysis, which came to the fore later. Kraepelin's classification gained popularity, including the separation of mood disorders from what would later be termed schizophrenia.[49][page needed]

text: Asylum superintendents sought to improve the image and medical status of their profession. Asylum "inmates" were increasingly referred to as "patients" and asylums renamed as hospitals. Referring to people as having a "mental illness" dates from this period in the early 20th century.[30]

text: In the United States, a "mental hygiene" movement, originally defined in the 19th century, gained momentum and aimed to "prevent the disease of insanity" through public health methods and clinics.[50] The term mental health became more popular, however. Clinical psychology and social work developed as professions alongside psychiatry. Theories of eugenics led to compulsory sterilization movements in many countries around the world for several decades, often encompassing patients in public mental institutions.[51] World War I saw a massive increase of conditions that came to be termed "shell shock".

text: In Nazi Germany, the institutionalized mentally ill were among the earliest targets of sterilization campaigns and covert "euthanasia" programs.[52] It has been estimated that over 200,000 individuals with mental disorders of all kinds were put to death, although their mass murder has received relatively little historical attention. Despite not being formally ordered to take part, psychiatrists and psychiatric institutions were at the center of justifying, planning and carrying out the atrocities at every stage, and "constituted the connection" to the later annihilation of Jews and other "undesirables" such as homosexuals in the Holocaust.[53]

text: In other areas of the world, funding was often cut for asylums, especially during periods of economic decline, and during wartime in particular many patients starved to death.[54] Soldiers received increased psychiatric attention, and World War II saw the development in the US of a new psychiatric manual for categorizing mental disorders, which along with existing systems for collecting census and hospital statistics led to the first Diagnostic and Statistical Manual of Mental Disorders (DSM). The International Classification of Diseases (ICD) followed suit with a section on mental disorders.

text: Previously restricted to the treatment of severely disturbed people in asylums, psychiatrists cultivated clients with a broader range of problems, and between 1917 and 1970 the number practicing outside institutions swelled from 8 percent to 66 percent.[55] The term stress, having emerged from endocrinology work in the 1930s, was popularized with an increasingly broad biopsychosocial meaning, and was increasingly linked to mental disorders.[56] "Outpatient commitment" laws were gradually expanded or introduced in some countries.

text: Lobotomies, Insulin shock therapy, Electro convulsive therapy, and the "neuroleptic" chlorpromazine came into use mid-century.

text: An antipsychiatry movement came to the fore in the 1960s. Deinstitutionalization gradually occurred in the West, with isolated psychiatric hospitals being closed down in favor of community mental health services. However, inadequate services and continued social exclusion often led to many being homeless or in prison.[57] A consumer/survivor movement gained momentum.

text: Other kinds of psychiatric medication gradually came into use, such as "psychic energizers" and lithium. Benzodiazepines gained widespread use in the 1970s for anxiety and depression, until dependency problems curtailed their popularity. Advances in neuroscience and genetics led to new research agendas. Cognitive behavioral therapy was developed. Through the 1990s, new SSRI antidepressants became some of the most widely prescribed drugs in the world.

text: The DSM and then ICD adopted new criteria-based classification, representing a return to a Kraepelin-like descriptive system. The number of "official" diagnoses saw a large expansion, although homosexuality was gradually downgraded and dropped in the face of human rights protests. Different regions sometimes developed alternatives such as the Chinese Classification of Mental Disorders or Latin American Guide for Psychiatric Diagnosis.

text: 21st century[edit]

text: This section needs to be updated. Please update this article to reflect recent events or newly available information. (December 2016)

text: Starting from 2002 DSM-5 Research Agenda researchers were invited to contribute with their publication to the literature basis for the DSM-5, whose draft criteria are now[when?] available to the scientific community.[58] In the meanwhile, serious limits of the current version of the DSM extremely high comorbidity, diagnostic heterogeneity of the categories, unclear boundaries have been interpreted as intrinsic anomalies of the criterial, neopositivistic approach leading the system to a state of scientific crisis.[59] Accordingly, a radical rethinking of the concept of mental disorder and the need of a radical scientific revolution in psychiatric taxonomy was proposed.[60]

text: History of mental health treatment[edit]

text: Trephination[edit]

text: This procedure included removing a part of the skull using an auger, bore or so. It was used 7000 years ago to remove headaches, mental illness and even perceived demonic possession.

text: Bloodletting and purging[edit]

text: This procedures saw its inception in the 1600s. Bleeding, purging and vomiting were thought to keep the balance of humors in the body. According to the Greek philosophy, the imbalance of these humors were considered to cause mental disorders. These techniques were used to treat more than just mental disorders.

text: Isolation and asylums[edit]

text: The confinement of the mentally ill became prevalent in the 17th century. The idea behind these asylums was to isolate the abnormal and keep them separate from the normal. The poor sanitation conditions, and overcrowding along with violent treatment of the mentally ill were serious problems faced in these asylums.

text: Insulin coma therapy[edit]

text: This treatment was introduced in 1927 and was used till 1960. Physicians deliberately put the patient into a low blood sugar coma because they thought that large fluctuations in insulin levels could alter the function of the brain. Risks included prolong coma. Electro Convulsive Therapy (ECT) was later adopted as a substitution to this.

text: Lobotomy[edit]

text: Prefrontal Lobotomies, required the surgical removal of the connections in between the prefrontal cortex and frontal lobes of the brain. The procedure took not more than five minutes to be performed. Though useful for some, it often created further impairments for others. It was discontinued in the mid-1950s.


document_title: Season of Migration to the North

question_text: where does season of migration to the north take place

root

text: Season of Migration to the North

text: Historical context[edit]

text: In January 1899, a condominium, or joint-authority, was established to rule over Sudan by Britain and Egypt.[5] Sudan gained independence in 1956, but was then engulfed in two prolonged civil wars for much of the remainder of the 20th century.[6] This novel is set in the 1960s, a significant and tumultuous time in Sudan's history.

tag: p

text: Summary[edit]

text: The unnamed narrator has returned to his native village in the Sudan after seven years in England furthering his education. It is the 1960s, and he is eager to make a contribution to the new postcolonial life of his country.[4]

text: On his arrival home, the Narrator encounters a new villager named Mustafa Sa'eed who exhibits none of the adulation for his achievements that most others do, and he displays an antagonistically aloof nature. Mustafa betrays his past one drunken evening by wistfully reciting poetry in fluent English, leaving the narrator resolute to discover the stranger's identity. The Narrator later asks Mustafa about his past, and Mustafa tells the Narrator much of his story, often saying "I am no Othello, Othello was a lie," as well as "I am a lie."

text: The Narrator becomes fascinated by Mustafa, and learns that Mustafa was also a precocious student educated in the West but that he held a violent, hateful and complex relationship with his western identity and acquaintances. The story of Mustafa's troubled past in Europe, and in particular his love affairs with British women, form the center of the novel. Mustafa attracts the women by appealing to their Orientalist fantasies. All of the relationships end in tragedy. Three of the women commit suicide and the fourth, Mustafa's wife, is murdered by him. He stands trial for the murder and serves time in an English jail.

text: In the dramatic present, Mustafa drowns in the Nile, and his widow, Hosna, is pressured to remarry. She refuses, because she does not want to marry after her husband. She tries to appeal to the Narrator, who was appointed the guardian of her sons in Mustafa's will. The Narrator does try to foil the marriage before it can take place, but he spends most of his time in Khartoum and therefore cannot exert much influence on the village. Hosna is married to Wad Rayyes against her will, and when he attempts to forcefully consummate the marriage, she kills him first and then proceeds to kill herself. Both are then buried without a funeral.

text: The stories of Mustafa's past life in England, and the repercussions on the village around him, take their toll on the narrator, who is driven to the very edge of sanity. In the final chapter, the Narrator is floating in the Nile, precariously between life and death, and resolves to rid himself of Mustafa's lingering presence, and to stand as an influential individual in his own right. In the middle of the Nile, he yells, "Help! Help!" The novel ends upon that cry and it is unclear whether his decision is too late, whether it is the right one, and whether he, others, and the country itself will receive the help needed.[7]

text: Relation to other texts[edit]

text: The novel can be related in many ways to the seminal works of Frantz Fanon, specifically Black Skin, White Masks. Fanon discusses the politics of desire between black men and white women, as Salih also explores extensively in the relationships of Mustafa Sa'eed.

text: The novel has also been compared in many ways to Joseph Conrad's Heart of Darkness.[8] Both novels explore cultural hybridity, cross-colonial experiences, and Orientalism.

text: The novel is also set in the same village, Wad Hamid, as many of Salih's other works, including The Wedding of Zein, Bandarshah, and others. Many of the novel's character, such as Mahjoub and the Narrator, recur in these other works as well. Ami Elad-Boulaski writes that Salih's depiction of Wad Hamid is more fully realized because a reader can track the development of characters throughout multiple novels and short stories.[9]

text: Characters[edit]

text:
Mustafa Sa'eed
The Narrator*
Jean Morris
Sheila Greenwood
Ann Hammond
Mahjoub
Bint Mahmoud (Hosna)
Bint Majzoub
The Narrator's Wife
The Narrator's Father
Hajj Ahmed (The Narrator's Grandfather)
The Narrator's Mother
Wad Rayyes
Isabella Seymour
Mrs. Robinson
Mr. Robinson

tag: ul

text: *The Narrator is once mistakenly referred to as "Effendi"; however, the word Effendi merely denotes respect for another. The narrator's actual name is never given in the novel. However, in another of Salih's Wad Hamid stories, the Narrator's name is revealed to be Meheimid, a diminutive version of Muhammad.

text: Controversy[edit]

text: The novel was banned in the author's native Sudan for a period of time starting in 1989 because its graphic sexual imagery offended the Islamic government. Today the novel is readily available in Sudan.[2]

text: Theater[edit]

text: Season of Migration to the North, adapted and directed by Ouriel Zohar, starring Mohammed Bakri. Bakri won the award for best actor in the 1993 Acco Festival of Alternative Israeli Theatre.

text: Editions in print[edit]

text:
ISBN 0-435-90630-5 Season of Migration to the North, 1969 Heinemann
ISBN 0-935576-29-0 Season of Migration to the North (hardcover), 1989 M. Kesend Pub. Ltd.
ISBN 0-435-90066-8 Season of Migration to the North (paperback), 1970 Heinemann
ISBN 0-89410-199-4 Season of Migration to the North: A novel (paperback reprint), 1980 Lynne Rienner Publishers
ISBN 0-14-118720-4 Season of Migration to the North, 2003 Penguin Classics Series

text: Notes[edit]

text:
Jump up ^ Johnson-Davies, Memories In Translation: A Life Between The Lines Of Arabic Literature, p 85
^ Jump up to: a b GradeSaver. "Season of Migration to the North Study Guide". www.gradesaver.com. Retrieved 2016-04-08.
Jump up ^ Mahjoub, Jamal (2009-02-19). "Tayeb Salih". The Guardian. ISSN 0261-3077. Retrieved 2016-11-30.
^ Jump up to: a b "Season of Migration to the North (New York Review Books Classics)". Rifflebooks.com. Retrieved 2016-04-08.
Jump up ^ "Sudan – THE ANGLO-EGYPTIAN CONDOMINIUM, 1899–1955". countrystudies.us. Retrieved 2016-04-08.
Jump up ^ "The World Factbook". www.cia.gov. Retrieved 2016-04-08.
Jump up ^ Harss, Marina. "Season of Migration to the North – Words Without Borders". Words Without Borders. Retrieved 2016-04-08.
Jump up ^ Shaheen, Mohammad. "Tayeb Salih and Conrad", Comparative Literature Studies 22.1 (1985): 156–71. Jstor. Web. 1 December 2010.
Jump up ^ Elad-Bouskila, Ami (1998). "Shaping the Cast of Characters: The Case of Al-Tayyib Salih". Journal of Arabic Literature. 29.2: 59–84.

tag: ol


document_title: Son of perdition

question_text: who is the son of destruction in john 17

text: Son of perdition

text: New Testament[edit]

text: The two occurrences of the Greek phrase have traditionally been translated consistently in English Bibles from the Wycliffe Bible, following the Latin Vulgate which has "filius perditionis" (son of perdition) in both instances. However this is not the case in all languages; for example the Luther Bible renders the use in John as "das verlorene Kind" (the lost child), but the use in 2 Thessalonians as "das Kind des Verderbens" (the child of corruption).

text: John 17:12[edit]

text: In John:17:12 KJV Jesus, in reference to Judas Iscariot, says that of all his disciples, none has been lost except the "son of perdition".

text: While I was with them in the world, I kept them in thy name: those that thou gavest me I have kept, and none of them is lost, but the son of perdition; that the scripture might be fulfilled.

text: The New International Version translates the phrase as "the one doomed to destruction." D. A. Carson suggests that this verse refers both to Judas' character and to his destiny.[1]

text: Various Old Testament origins have been suggested for "that the scripture might be fulfilled." These traditionally include Psalm 41:9 "Yea, mine own familiar friend, in whom I trusted, which did eat of my bread, hath lifted up his heel against me."[2] Also Psalm 109:8 "Let his days be few; and let another take his office." which is interpreted by Peter in Acts 1:16-20 as having been prophetic of Judas.

text: 2 Thessalonians 2:3[edit]

text: In 2 Thessalonians 2:3, Paul referred to "the son of perdition".

text: 2 Thessalonians 2:3 "Let no man deceive you by any means: for that day shall not come, except there come a falling away first, and that man of sin be revealed, the son of perdition;" King James Version, 1611

text: He appears to equate this image with the Man of Sin.

text: Some scholars[3] and theologians[4] down through history, including Hippolytus,[5] Luther,[6] Wesley,[7] Manton,[8] Schaff,[9] et al, say that first "Son of Perdition" reference is to Antiochus IV Epiphanes, the man who attacked the Second Temple in Jerusalem and defiled it by sacrificing a pig on the altar, erecting a statue of Zeus as himself in the temple, raiding the Temple treasury and minting coins saying "Theos Epiphanes" (God manifest), etc. Even those theologians who advocate an interpretation of Daniel that includes the Roman Empire in their analysis recognize Antiochus as a prototype.[10]

text: Revelation[edit]

text: Some theologians and scholars also consider "the beast that goes into perdition" mentioned in Revelation 17:8 and 17:11 to be references to the son of perdition."[11][12]

text: Derivation[edit]

text: Similar uses of "son" occur in Hebrew, such as "sons of corruption" (Isaiah 1:4 בָּנִים מַשְׁחִיתִים benim mishchatim), however the exact Hebrew or Greek term "son of perdition" does not occur in Jewish writings prior to the New Testament.

text: According to some modern biblical criticism New Testament writers derived the "son of perdition" (and "man of sin") concepts from Daniel and 1 Maccabees 2:48 "And they did not surrender the horn to the sinner." et al.[13] John related the "Son of Perdition" concepts by language, referring to "the star that fell from heaven" Revelation 9:1 by two names, one Greek, and the other Hebrew. (Revelation 9:11) The Greek name is "Apollyon" (Greek: Aπολλυων), from the Greek root word "apollumi" (Greek:απολλυμι).[14] It refers to utter loss, eternal destruction, and disassociation." [Strong's 622] The Hebrew name is "Abaddon" (Greek: Aβαδδων), from the Aramaic root word "'abad", which means the same thing as the Greek root word. Strong's 07 Daniel 7:11 says that the eventual destiny of the "great beast" is to be slain, and his body "destroyed" ('abad), and given to the eternal flames (generally accepted by religious scholars to be a reference to hell).

text: Matthew Henry wrote:

text: Of the kings that came after Antiochus nothing is here prophesied, for that was the most malicious mischievous enemy to the church, that was a type of the son of perdition, whom the Lord shall consume with the breath of his mouth and destroy with the brightness of his coming, and none shall help him.[15]


document_title: Muscle contraction

question_text: when was the link between muscular contraction and electricity discovered

text: Muscle contraction

text: Types[edit]

text: Muscle contractions can be described based on two variables: force and length. Force itself can be differentiated as either tension or load. Muscle tension is the force exerted by the muscle on an object whereas a load is the force exerted by an object on the muscle.[1] When muscle tension changes without any corresponding changes in muscle length, the muscle contraction is described as isometric.[1][3][4][5] If the muscle length changes while muscle tension remains the same, then the muscle contraction is isotonic.[1][3][4][5] In an isotonic contraction, the muscle length can either shorten to produce a concentric contraction or lengthen to produce an eccentric contraction.[1][6] Furthermore, if the muscle length shortens, the contraction is concentric.[1][6] But if the muscle length lengthens, then the contraction is eccentric. In natural movements that underlie locomotor activity, muscle contractions are multifaceted as they are able to produce changes in length and tension in a time-varying manner.[7] Therefore, neither length nor tension is likely to remain constant when the muscle is active during locomotor activity.

text: Isometric contraction[edit]

text: An isometric contraction of a muscle generates tension without changing length.[1][3][4][5] An example can be found when the muscles of the hand and forearm grip an object; the joints of the hand do not move, but muscles generate sufficient force to prevent the object from being dropped.

text: Isotonic contraction[edit]

text: In isotonic contraction, the tension in the muscle remains constant despite a change in muscle length.[1][3][4][5] This occurs when a muscle's force of contraction matches the total load on the muscle.

text: Concentric contraction[edit]

text: In concentric contraction, muscle tension is sufficient to overcome the load, and the muscle shortens as it contracts.[8] This occurs when the force generated by the muscle exceeds the load opposing its contraction.

text: During a concentric contraction, a muscle is stimulated to contract according to the sliding filament theory. This occurs throughout the length of the muscle, generating a force at the origin and insertion, causing the muscle to shorten and changing the angle of the joint. In relation to the elbow, a concentric contraction of the biceps would cause the arm to bend at the elbow as the hand moved from the leg to the shoulder (a biceps curl). A concentric contraction of the triceps would change the angle of the joint in the opposite direction, straightening the arm and moving the hand towards the leg.

text: Eccentric contraction[edit]

text: In eccentric contraction, the tension generated is insufficient to overcome the external load on the muscle and the muscle fibers lengthen as they contract.[9] Rather than working to pull a joint in the direction of the muscle contraction, the muscle acts to decelerate the joint at the end of a movement or otherwise control the repositioning of a load. This can occur involuntarily (e.g., when attempting to move a weight too heavy for the muscle to lift) or voluntarily (e.g., when the muscle is 'smoothing out' a movement). Over the short-term, strength training involving both eccentric and concentric contractions appear to increase muscular strength more than training with concentric contractions alone.[10] However, exercise-induced muscle damage is also greater during lengthening contractions.[11]

text: During an eccentric contraction of the biceps muscle, the elbow starts the movement while bent and then straightens as the hand moves away from the shoulder. During an eccentric contraction of the triceps muscle, the elbow starts the movement straight and then bends as the hand moves towards the shoulder. Desmin, titin, and other z-line proteins are involved in eccentric contractions, but their mechanism is poorly understood in comparison to crossbridge cycling in concentric contractions.[9]

text: Though the muscle is doing a negative amount of mechanical work, (work is being done on the muscle), chemical energy (in fat, glucose or ATP) is nevertheless consumed, although less than would be consumed during a concentric contraction of the same force. For example, one expends more energy going up a flight of stairs than going down the same flight.

text: Muscles undergoing heavy eccentric loading suffer greater damage when overloaded (such as during muscle building or strength training exercise) as compared to concentric loading. When eccentric contractions are used in weight training, they are normally called negatives. During a concentric contraction, muscle fibers slide across each other, pulling the Z-lines together. During an eccentric contraction, the filaments slide past each other the opposite way, though the actual movement of the myosin heads during an eccentric contraction is not known. Exercise featuring a heavy eccentric load can actually support a greater weight (muscles are approximately 40% stronger during eccentric contractions than during concentric contractions) and also results in greater muscular damage and delayed onset muscle soreness one to two days after training. Exercise that incorporates both eccentric and concentric muscular contractions (i.e., involving a strong contraction and a controlled lowering of the weight) can produce greater gains in strength than concentric contractions alone.[10][12] While unaccustomed heavy eccentric contractions can easily lead to overtraining, moderate training may confer protection against injury.[10]

text: Eccentric contractions in movement[edit]

text: Eccentric contractions normally occur as a braking force in opposition to a concentric contraction to protect joints from damage. During virtually any routine movement, eccentric contractions assist in keeping motions smooth, but can also slow rapid movements such as a punch or throw. Part of training for rapid movements such as pitching during baseball involves reducing eccentric braking allowing a greater power to be developed throughout the movement.

text: Eccentric contractions are being researched for their ability to speed rehabilitation of weak or injured tendons. Achilles tendinitis [13][14] and patellar tendonitis [15] (also known as jumper's knee or patellar tendonosis) have been shown to benefit from high-load eccentric contractions.

text: Vertebrate animals[edit]

text: In vertebrate animals, there are three types of muscle tissues: skeletal, smooth, and cardiac. Skeletal muscle constitutes the majority of muscle mass in the body and is responsible for locomotor activity. Smooth muscle forms blood vessels, gastrointestinal tract, and other areas in the body that produce sustained contractions. Cardiac muscle make up the heart, which pumps blood. Skeletal and cardiac muscles are called striated muscle because of their striped appearance under a microscope, which is due to the highly organized alternating pattern of A bands and I bands.

text: Skeletal muscle[edit]

text: Excluding reflexes, all skeletal muscles contractions occur as a result of conscious effort originating in the brain. The brain sends electrochemical signals through the nervous system to the motor neuron that innervates several muscle fibers.[16] In the case of some reflexes, the signal to contract can originate in the spinal cord through a feedback loop with the grey matter. Other actions such as locomotion, breathing, and chewing have a reflex aspect to them: the contractions can be initiated both consciously or unconsciously.

text: Neuromuscular junction[edit]

text: A neuromuscular junction is a chemical synapse formed by the contact between a motor neuron and a muscle fiber.[17] It is the site in which a motor neuron transmits a signal to a muscle fiber to initiate muscle contraction. The sequence of events that results in the depolarization of the muscle fiber at the neuromuscular junction begins when an action potential is initiated in the cell body of a motor neuron, which is then propagated by saltatory conduction along its axon toward the neuromuscular junction. Once it reaches the terminal bouton, the action potential causes a Ca2+ ion influx into the terminal by way of the voltage-gated calcium channels. The Ca2+ influx causes synaptic vesicles containing the neurotransmitter acetylcholine to fuse with the plasma membrane, releasing acetylcholine into the synaptic cleft between the motor neuron terminal and the neuromuscular junction of the skeletal muscle fiber. Acetylcholine diffuses across the synapse and binds to and activates nicotinic acetylcholine receptors on the neuromuscular junction. Activation of the nicotinic receptor opens its intrinsic sodium/potassium channel, causing sodium to rush in and potassium to trickle out. As a result, the sarcolemma reverses polarity and its voltage quickly jumps from the resting membrane potential of -90mV to as high as +75mV as sodium enters. The membrane potential then becomes hyperpolarized when potassium exits and is then adjusted back to the resting membrane potential. This rapid fluctuation is called the end-plate potential [18] The voltage-gated ion channels of the sarcolemma next to the end plate open in response to the end plate potential. These voltage-gated channels are sodium and potassium specific and only allow one through. This wave of ion movements creates the action potential that spreads from the motor end plate in all directions.[18] If action potentials stop arriving, then acetylcholine ceases to be released from the terminal bouton. The remaining acetylcholine in the synaptic cleft is either degraded by active acetylcholine esterase or reabsorbed by the synaptic knob and none is left to replace the degraded acetylcholine.

text: Excitation-contraction coupling[edit]

text: Excitation–contraction coupling is the process by which a muscular action potential in the muscle fiber causes the myofibrils to contract.[19] In skeletal muscle, excitation–contraction coupling relies on a direct coupling between key proteins, the sarcoplasmic reticulum (SR) calcium release channel (identified as the ryanodine receptor, RyR) and voltage-gated L-type calcium channels (identified as dihydropyridine receptors, DHPRs). DHPRs are located on the sarcolemma (which includes the surface sarcolemma and the transverse tubules), while the RyRs reside across the SR membrane. The close apposition of a transverse tubule and two SR regions containing RyRs is described as a triad and is predominantly where excitation–contraction coupling takes place. Excitation–contraction coupling occurs when depolarization of skeletal muscle cell results in a muscle action potential, which spreads across the cell surface and into the muscle fiber's network of T-tubules, thereby depolarizing the inner portion of the muscle fiber. Depolarization of the inner portions activates dihydropyridine receptors in the terminal cisternae, which are in close proximity to ryanodine receptors in the adjacent sarcoplasmic reticulum. The activated dihydropyridine receptors physically interact with ryanodine receptors to activate them via foot processes (involving conformational changes that allosterically activates the ryanodine receptors). As the ryanodine receptors open, Ca2+ is released from the sarcoplasmic reticulum into the local junctional space, which then diffuses into the bulk cytoplasm to cause a calcium spark. Note that the sarcoplasmic reticulum has a large calcium buffering capacity partially due to a calcium-binding protein called calsequestrin. The near synchronous activation of thousands of calcium sparks by the action potential causes a cell-wide increase in calcium giving rise to the upstroke of the calcium transient. The Ca2+ released into the cytosol binds to Troponin C by the actin filaments, to allow crossbridge cycling, producing force and, in some situations, motion. The sarco/endoplasmic reticulum calcium-ATPase (SERCA) actively pumps Ca2+ back into the sarcoplasmic reticulum. As Ca2+ declines back to resting levels, the force declines and relaxation occurs.

text: Sliding filament theory[edit]

text: The sliding filament theory describes a process used by muscles to contract. It is a cycle of repetitive events that cause a thin filament to slide over a thick filament and generate tension in the muscle.[20] It was independently developed by Andrew Huxley and Rolf Niedergerke and by Hugh Huxley and Jean Hanson in 1954.[21][22] Physiologically, this contraction is not uniform across the sarcomere; the central position of the thick filaments becomes unstable and can shift during contraction. However the actions of elastic proteins such as titin are hypothesised to maintain uniform tension across the sarcomere and pull the thick filament into a central position.[23]

text: Crossbridge cycling[edit]

text: Crossbridge cycling is a sequence of molecular events that underlies the sliding filament theory. A crossbridge is a myosin projection, consisting of two myosin heads, that extends from the thick filaments.[1] Each myosin head has two binding sites: one for ATP and another for actin. The binding of ATP to a myosin head detaches myosin from actin, thereby allowing myosin to bind to another actin molecule. Once attached, the ATP is hydrolyzed by myosin, which uses the released energy to move into the "cocked position" whereby it binds weakly to a part of the actin binding site. The remainder of the actin binding site is blocked by tropomyosin.[24] With the ATP hydrolyzed, the cocked myosin head now contains ADP + Pi. Two Ca2+ ions bind to troponin C on the actin filaments. The troponin-Ca2+ complex causes tropomyosin to slide over and unblock the remainder of the actin binding site. Unblocking the rest of the actin binding sites allows the two myosin heads to close and myosin to bind strongly to actin.[24] The myosin head then releases the inorganic phosphate and initiates a power stroke, which generates a force of 2 pN. The power stroke moves the actin filament inwards, thereby shortening the sarcomere. Myosin then releases ADP but still remains tightly bound to actin. At the end of the power stroke, ADP is released from the myosin head, leaving myosin attached to actin in a rigor state until another ATP binds to myosin. A lack of ATP would result in the rigor state characteristic of rigor mortis. Once another ATP binds to myosin, the myosin head will again detach from actin and another crossbridges cycle occurs.

text: Crossbridge cycling is able to continue as long as there are sufficient amounts of ATP and Ca2+ in the cytoplasm.[24] Termination of crossbridge cycling can occur when Ca2+ is actively pumped back into the sarcoplasmic reticulum. When Ca2+ is no longer present on the thin filament, the tropomyosin changes conformation back to its previous state so as to block the binding sites again. The myosin ceases binding to the thin filament, and the muscle relaxes. The Ca2+ ions leave the troponin molecule in order to maintain the Ca2+ ion concentration in the sarcoplasm. The active pumping of Ca2+ ions into the sarcoplasmic reticulum creates a deficiency in the fluid around the myofibrils. This causes the removal of Ca2+ ions from the troponin. Thus, the tropomyosin-troponin complex again covers the binding sites on the actin filaments and contraction ceases.

text: Gradation of skeletal muscle contractions[edit]

text: The strength of skeletal muscle contractions can be broadly separated into twitch, summation, and tetanus. A twitch is a single contraction and relaxation cycle produced by an action potential within the muscle fiber itself.[25] The time between a stimulus to the motor nerve and the subsequent contraction of the innervated muscle is called the latent period, which usually takes about 10 ms and is caused by the time taken for nerve action potential to propagate, the time for chemical transmission at the neuromuscular junction, then the subsequent steps in excitation-contraction coupling.[26]

text: If another muscle action potential were to be produced before the complete relaxation of a muscle twitch, then the next twitch will simply sum onto the previous twitch, thereby producing a summation. Summation can be achieved in two ways:[27] frequency summation and multiple fiber summation. In frequency summation, the force exerted by the skeletal muscle is controlled by varying the frequency at which action potentials are sent to muscle fibers. Action potentials do not arrive at muscles synchronously, and, during a contraction, some fraction of the fibers in the muscle will be firing at any given time. In a typical circumstance, when a human is exerting a muscle as hard as he/she is consciously able, roughly one-third of the fibers in that muscle will be firing at once, though this ratio can be affected by various physiological and psychological factors (including Golgi tendon organs and Renshaw cells). This 'low' level of contraction is a protective mechanism to prevent avulsion of the tendon—the force generated by a 95% contraction of all fibers is sufficient to damage the body. In multiple fiber summation, if the central nervous system sends a weak signal to contract a muscle, the smaller motor units, being more excitable than the larger ones, are stimulated first. As the strength of the signal increases, more motor units are excited in addition to larger ones, with the largest motor units having as much as 50 times the contractile strength as the smaller ones. As more and larger motor units are activated, the force of muscle contraction becomes progressively stronger. A concept known as the size principle, allows for a gradation of muscle force during weak contraction to occur in small steps, which then become progressively larger when greater amounts of force are required.

text: Finally, if the frequency of muscle action potentials increases such that the muscle contraction reaches its peak force and plateaus at this level, then the contraction is a tetanus.

text: Length-tension relationship[edit]

text: Length-tension relationship relates the strength of an isometric contraction to the length of the muscle at which the contraction occurs. Muscles operate with greatest active tension when close to an ideal length (often their resting length). When stretched or shortened beyond this (whether due to the action of the muscle itself or by an outside force), the maximum active tension generated decreases.[28] This decrease is minimal for small deviations, but the tension drops off rapidly as the length deviates further from the ideal. Due to the presence of elastic proteins within a muscle cell (such as titin) and extracellular matrix, as the muscle is stretched beyond a given length, there is an entirely passive tension, which opposes lengthening. Combined together, there is a strong resistance to lengthening an active muscle far beyond the peak of active tension.

text: Force-velocity relationships[edit]

text: Force–velocity relationship relates the speed at which a muscle changes its length (usually regulated by external forces, such as load or other muscles) to the amount of force that it generates. Force declines in a hyperbolic fashion relative to the isometric force as the shortening velocity increases, eventually reaching zero at some maximum velocity. The reverse holds true for when the muscle is stretched – force increases above isometric maximum, until finally reaching an absolute maximum. This has strong implications for the rate at which muscles can perform mechanical work (power). Since power is equal to force times velocity, the muscle generates no power at either isometric force (due to zero velocity) or maximal velocity (due to zero force). Instead, the optimal shortening velocity for power generation is approximately one-third of maximum shortening velocity.

text: These two fundamental properties of muscle have numerous biomechanical consequences, including limiting running speed, strength, and jumping distance and height.

text: Smooth muscle[edit]

text: Smooth muscles can be divided into two subgroups: single-unit (unitary) and multi-unit. Single-unit smooth muscle cells can be found in the gut and blood vessels. Because these cells are linked together by gap junctions, they are able to contract as a syncytium. Single-unit smooth muscle cells contract myogenically, which can be modulated by the autonomic nervous system.

text: Unlike single-unit smooth muscle cells, multi-unit smooth muscle cells are found in the muscle of the eye and in the base of hair follicles. Multi-unit smooth muscle cells contract by being separately stimulated by nerves of the autonomic nervous system. As such, they allow for fine control and gradual responses, much like motor unit recruitment in skeletal muscle.

text: Mechanisms of smooth muscle contraction[edit]

text: The contractile activity of smooth muscle cells is influenced by multiple inputs such as spontaneous electrical activity, neural and hormonal inputs, local changes in chemical composition, and stretch.[1] This is in contrast to the contractile activity of skeletal muscle cells, which relies on a single neural input. Some types of smooth muscle cells are able to generate their own action potentials spontaneously, which usually occur following a pacemaker potential or a slow wave potential. These action potentials are generated by the influx of extracellular Ca2+, and not Na+. Like skeletal muscles, cytosolic Ca2+ ions are also required for crossbridge cycling in smooth muscle cells.

text: The two sources for cytosolic Ca2+ in smooth muscle cells are the extracellular Ca2+ entering through calcium channels and the Ca2+ ions that are released from the sarcoplasmic reticulum. The elevation of cytosolic Ca2+ results in more Ca2+ binding to calmodulin, which then binds and activates myosin light-chain kinase. The calcium-calmodulin-myosin light-chain kinase complex phosphorylates myosin on the 20 kilodalton (kDa) myosin light chains on amino acid residue-serine 19, initiating contraction and activating the myosin ATPase. Unlike skeletal muscle cells, smooth muscle cells lack troponin, even though they contain the thin filament protein tropomyosin and other notable proteins – caldesmon and calponin. Thus, smooth muscle contractions are initiated by the Ca2+-activated phosphorylation of myosin rather than Ca2+ binding to the troponin complex that regulates myosin binding sites on actin like in skeletal and cardiac muscles.

text: Termination of crossbridge cycling (and leaving the muscle in latch-state) occurs when myosin light chain phosphatase removes the phosphate groups from the myosin heads. Phosphorylation of the 20 kDa myosin light chains correlates well with the shortening velocity of smooth muscle. During this period, there is a rapid burst of energy utilization as measured by oxygen consumption. Within a few minutes of initiation, the calcium level markedly decreases, the 20 kDa myosin light chains' phosphorylation decreases, and energy utilization decreases; however, force in tonic smooth muscle is maintained. During contraction of muscle, rapidly cycling crossbridges form between activated actin and phosphorylated myosin, generating force. It is hypothesized that the maintenance of force results from dephosphorylated "latch-bridges" that slowly cycle and maintain force. A number of kinases such as rho kinase, ZIP kinase, and protein kinase C are believed to participate in the sustained phase of contraction, and Ca2+ flux may be significant.

text: Neuromodulation[edit]

text: Although smooth muscle contractions are myogenic, the rate and strength of their contractions can be modulated by the autonomic nervous system. Postganglionic nerve fibers of parasympathetic nervous system release the neurotransmitter acetylcholine, which binds to muscarinic acetylcholine receptors (mAChRs) on smooth muscle cells. These receptors are metabotropic, or G-protein coupled receptors that initiate a second messenger cascade. Conversely, postganglionic nerve fibers of the sympathetic nervous system release the neurotransmitters epinephrine and norepinephrine, which bind to adrenergic receptors that are also metabotropic. The exact effects on the smooth muscle depend on the specific characteristics of the receptor activated—both parasympathetic input and sympathetic input can be either excitatory (contractile) or inhibitory (relaxing).

text: Cardiac muscle[edit]

text: There are two types of cardiac muscle cells: autorhythmic and contractile. Autorhythmic cells do not contract, but instead set the pace of contraction for other cardiac muscle cells, which can be modulated by the autonomic nervous system. In contrast, contractile muscle cells (cardiomyocytes) constitute the majority of the heart muscle and are able to contract.

text: Excitation-contraction coupling[edit]

text: Unlike skeletal muscle, excitation–contraction coupling in cardiac muscle is thought to depend primarily on a mechanism called calcium-induced calcium release.[29] Though the proteins involved are similar, the L-type calcium channels and ryanodine receptors (RyRs) are not physically coupled. Instead, RyRs are activated by a calcium trigger, which is brought about by the flow of Ca2+through the L-type calcium channels. Furthermore, cardiac muscle tend to exhibit diad (or dyad) structures, rather than triads.

text: Excitation-contraction coupling in cardiac muscle cells occurs when an action potential is initiated by pacemaker cells in the sinoatrial node or Atioventricular node and conducted to all cells in the heart via gap junctions. The action potential travels along the surface membrane into T-tubules (the latter are not seen in all cardiac cell types) and the depolarisation causes extracellular Ca2+ to enter the cell via L-type calcium channels and possibly sodium-calcium exchanger (NCX) during the early part of the plateau phase. This Ca2+ influx causes a small local increase in intracellular Ca2+. The increase in Ca2+ is detected by ryanodine receptors in the membrane of the sarcoplasmic reticulum which releaes Ca2+ in a positive feedback physiological response. This positive feedback is known as calcium-induced calcium release [29] and gives rise to calcium sparks (Ca2+ sparks[30]). The spatial and temporal summation of ~30,000 Ca2+ sparks gives a cell-wide increase in cytoplasmic calcium concentration.[31] The increase in cytosolic calcium following the flow of calcium through the cell membrane and sarcoplasmic reticulum is moderated by calcium buffers which bind a large proportion of intracellular calcium. As a result, a large increase in total calcium leads to a relatively small rise in free Ca2+.[32]

text: The cytoplasmic calcium binds to Troponin C, moving the tropomyosin complex off the actin binding site allowing the myosin head to bind to the actin filament. From this point on, the contractile mechanism is essentially the same as for skeletal muscle (above). Briefly, using ATP hydrolysis, the myosin head pulls the actin filament toward the centre of the sarcomere.

text: Following systole, intracellular calcium is taken up by the sarco/endoplasmic reticulum ATPase (SERCA) pump back into the sarcoplasmic reticulum ready for the next cycle to begin. Calcium is also ejected from the cell mainly by the sodium-calcium exchanger (NCX) and, to a lesser extent, a plasma membrane calcium ATPase. Some calcium is also taken up by the mitochondria.[33] An enzyme, phospholamban, serves as a brake for SERCA. At low heart rates, phospholamban is active and slows down the activity of the ATPase so that Ca2+ does not have to leave the cell entirely. At high heart rates, phospholamban is phosphorylated and deactivated thus taking most Ca2+ from the cytoplasm back into the sarcoplasmic reticulum. Once again, calcium buffers moderate this fall in Ca2+concentration, permitting a relatively small decrease in free Ca2+concentration in response to a large change in total calcium. The falling Ca2+concentration allows the troponin complex to dissociate from the actin filament thereby ending contraction. The heart relaxes, allowing the ventricles to fill with blood and begin the cardiac cycle again.

text: Invertebrate animals[edit]

text: Circular and longitudinal muscles[edit]

text: In annelids such as earthworms and leeches, circular and longitudinal muscles cells form the body wall of these animals and are responsible for their movement.[34] In an earthworm that is moving through a soil, for example, contractions of circular and longitudinal muscles occur reciprocally while the coelomic fluid serves as a hydroskeleton by maintaining turgidity of the earthworm.[35] When the circular muscles in the anterior segments contract, the anterior portion of animal's body begins to constrict radially, which pushes the incompressible coelomic fluid forward and increasing the length of the animal. As a result, the front end of the animal moves forward. As the front end of the earthworm becomes anchored and the circular muscles in the anterior segments become relaxed, a wave of longitudinal muscle contractions passes backwards, which pulls the rest of animal's trailing body forward.[34][35] These alternating waves of circular and longitudinal contractions is called peristalsis, which underlies the creeping movement of earthworms.

text: Obliquely striated muscles[edit]

text: Invertebrates such as annelids, mollusks, and nematodes, possess obliquely striated muscles, which contain bands of thick and thin filaments that are arranged helically rather than transversely, like in vertebrate skeletal or cardiac muscles.[36] In bivalves, the obliquely striated muscles can maintain tension over long periods without using too much energy. Bivalves use these muscles to keep their shells closed.

text: Asynchronous muscles[edit]

text: Advanced insects such as wasps, flies, bees, and beetles possess asynchronous muscles that constitute the flight muscles in these animals.[36] These flight muscles are often called fibrillar muscles because they contain myofibrils that are thick and conspicuous.[37] A remarkable feature of these muscles is that they do not require stimulation for each muscle contraction. Hence, they are called asynchronous muscles because the number of contractions in these muscles do not correspond (or synchronize) with the number of action potentials. For example, a wing muscle of a tethered fly may receive action potentials at a frequency of 3 Hz but it is able to beat at a frequency of 120 Hz.[36] The high frequency beating is made possible because the muscles are connected to a resonant system, which is driven to a natural frequency of vibration.

text: History[edit]

text: In 1780, Luigi Galvani discovered that the muscles of dead frogs' legs twitched when struck by an electrical spark.[39] This was one of the first forays into the study of bioelectricity, a field that still studies the electrical patterns and signals in tissues such as nerves and muscles.

text: In 1952, the term excitation–contraction coupling was coined to describe the physiological process of converting an electrical stimulus to a mechanical response.[19] This process is fundamental to muscle physiology, whereby the electrical stimulus is usually an action potential and the mechanical response is contraction. Excitation–contraction coupling can be dysregulated in many diseases.Though excitation–contraction coupling has been known for over half a century, it is still an active area of biomedical research. The general scheme is that an action potential arrives to depolarize the cell membrane. By mechanisms specific to the muscle type, this depolarization results in an increase in cytosolic calcium that is called a calcium transient. This increase in calcium activates calcium-sensitive contractile proteins that then use ATP to cause cell shortening.

text: The mechanism for muscle contraction evaded scientists for years and requires continued research and updating.[40] The sliding filament theory was independently developed by Andrew F. Huxley and Rolf Niedergerke and by Hugh Huxley and Jean Hanson. Their findings were published as two consecutive papers published in the 22 May 1954 issue of Nature under the common theme "Structural Changes in Muscle During Contraction".[21][22]