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Acantharia	Table of Content	Short description, Morphology, Taxonomy, Symbiosis, Life cycle, References
African National Congress	Short description	The African National Congress (ANC) is a political party in South Africa. It originated as a liberation movement known for its opposition to apartheid and has governed the country since 1994, when the first post-apartheid election resulted in Nelson Mandela being elected as President of South Africa. Cyril Ramaphosa, the incumbent national president, has served as president of the ANC since 18 December 2017. Founded on 8 January 1912 in Bloemfontein as the South African Native National Congress, the organisation was formed to advocate for the rights of black South Africans. When the National Party government came to power in 1948, the ANC's central purpose became to oppose the new government's policy of institutionalised apartheid. To this end, its methods and means of organisation shifted; its adoption of the techniques of mass politics, and the swelling of its membership, culminated in the Defiance Campaign of civil disobedience in 1952–53. The ANC was banned by the South African government between April 1960 – shortly after the Sharpeville massacre – and February 1990. During this period, despite periodic attempts to revive its domestic political underground, the ANC was forced into exile by increasing state repression, which saw many of its leaders imprisoned on Robben Island. Headquartered in Lusaka, Zambia, the exiled ANC dedicated much of its attention to a campaign of sabotage and guerrilla warfare against the apartheid state, carried out under its military wing, uMkhonto we Sizwe, which was founded in 1961 in partnership with the South African Communist Party (SACP). The ANC was condemned as a terrorist organisation by the governments of South Africa, the United States, and the United Kingdom. However, it positioned itself as a key player in the negotiations to end apartheid, which began in earnest after the ban was repealed in 1990. For much of that time, the ANC leadership, along with many of its most active members, operated from abroad. After the Soweto Uprising of 1976, the ANC remained committed to achieving its objectives through armed struggle, led by its military wing, Umkhonto we Sizwe. These circumstances significantly shaped the ANC during its years in exile. In the post-apartheid era, the ANC continues to identify itself foremost as a liberation movement, although it is also a registered political party. Partly due to its Tripartite Alliance with the South African Communist Party (SACP) and the Congress of South African Trade Unions, it had retained a comfortable electoral majority at the national level and in most provinces, and has provided each of South Africa's five presidents since 1994. South Africa is considered a dominant-party state. However, the ANC's electoral majority has declined consistently since 2004, and in the 2021 local elections, its share of the national vote dropped below 50% for the first time ever. Over the last decade, the party has been embroiled in a number of controversies, particularly relating to widespread allegations of political corruption among its members. Following the 2024 general election, the ANC lost its majority in parliament for the first time in South Africa's democratic history. However, it still remained the largest party, with just over 40% of the vote. The party also lost its majority in Kwa-Zulu Natal, Gauteng and Northern Cape. Despite these setbacks, the ANC retained power at the national level through a grand coalition referred to as the Government of National Unity, including parties which together have 72% of the seats in Parliament.
African National Congress	History	History
African National Congress	Origins	Origins thumb\|A South African Native National Congress delegation to England, June 1914. L–R: Thomas Mtobi Mapikela, Walter Rubusana, John Dube, Saul Msane, and Sol Plaatje.\|left A successor of the Cape Colony's Imbumba Yamanyama organisation, the ANC was founded as the South African Native National Congress in Bloemfontein on 8 January 1912, and was renamed the African National Congress in 1923. Pixley ka Isaka Seme, Sol Plaatje, John Dube, and Walter Rubusana founded the organisation, who, like much of the ANC's early membership, were from the conservative, educated, and religious professional classes of black South African society. Although they would not take part, Xhosa chiefs would show huge support for the organisation; as a result, King Jongilizwe donated 50 cows to it during its founding. Around 1920, in a partial shift away from its early focus on the "politics of petitioning", the ANC developed a programme of passive resistance directed primarily at the expansion and entrenchment of pass laws. When Josiah Gumede took over as ANC president in 1927, he advocated for a strategy of mass mobilisation and cooperation with the Communist Party, but was voted out of office in 1930 and replaced with the traditionalist Seme, whose leadership saw the ANC's influence wane. In the 1940s, Alfred Bitini Xuma revived some of Gumede's programmes, assisted by a surge in trade union activity and by the formation in 1944 of the left-wing ANC Youth League under a new generation of activists, among them Walter Sisulu, Nelson Mandela, and Oliver Tambo. After the National Party was elected into government in 1948 on a platform of apartheid, entailing the further institutionalisation of racial segregation, this new generation pushed for a Programme of Action which explicitly advocated African nationalism and led the ANC, for the first time, to the sustained use of mass mobilisation techniques like strikes, stay-aways, and boycotts. This culminated in the 1952–53 Defiance Campaign, a campaign of mass civil disobedience organised by the ANC, the Indian Congress, and the coloured Franchise Action Council in protest of six apartheid laws. The ANC's membership swelled. In June 1955, it was one of the groups represented at the multi-racial Congress of the People in Kliptown, Soweto, which ratified the Freedom Charter, from then onwards a fundamental document in the anti-apartheid struggle. The Charter was the basis of the enduring Congress Alliance, but was also used as a pretext to prosecute hundreds of activists, among them most of the ANC's leadership, in the Treason Trial. Before the trial was concluded, the Sharpeville massacre occurred on 21 March 1960. In the aftermath, the ANC was banned by the South African government. It was not unbanned until February 1990, almost three decades later.
African National Congress	Exile in Lusaka	Exile in Lusaka After its banning in April 1960, the ANC was driven underground, a process hastened by a barrage of government banning orders, by an escalation of state repression, and by the imprisonment of senior ANC leaders pursuant to the Rivonia trial and Little Rivonia trial. From around 1963, the ANC effectively abandoned much of even its underground presence inside South Africa and operated almost entirely from its external mission, with headquarters first in Morogoro, Tanzania, and later in Lusaka, Zambia. For the entirety of its time in exile, the ANC was led by Tambo – first de facto, with president Albert Luthuli under house arrest in Zululand; then in an acting capacity, after Luthuli's death in 1967; and, finally, officially, after a leadership vote in 1985. Also notable about this period was the extremely close relationship between the ANC and the reconstituted South African Communist Party (SACP), which was also in exile.
African National Congress	uMkhonto we Sizwe	uMkhonto we Sizwe In 1961, partly in response to the Sharpeville massacre, leaders of the SACP and the ANC formed a military body, Umkhonto we Sizwe (MK, Spear of the Nation), as a vehicle for armed struggle against the apartheid state. Initially, MK was not an official ANC body, nor had it been directly established by the ANC National Executive: it was considered an autonomous organisation, until such time as the ANC formally recognised it as its armed wing in October 1962. In the first half of the 1960s, MK was preoccupied with a campaign of sabotage attacks, especially bombings of unoccupied government installations. As the ANC reduced its presence inside South Africa, however, MK cadres were increasingly confined to training camps in Tanzania and neighbouring countries – with such exceptions as the Wankie Campaign, a momentous military failure. In 1969, Tambo was compelled to call the landmark Morogoro Conference to address the grievances of the rank-and-file, articulated by Chris Hani in a memorandum which depicted MK's leadership as corrupt and complacent. Although MK's malaise persisted into the 1970s, conditions for armed struggle soon improved considerably, especially after the Soweto uprising of 1976 in South Africa saw thousands of students – inspired by Black Consciousness ideas – cross the borders to seek military training. MK guerrilla activity inside South Africa increased steadily over this period, with one estimate recording an increase from 23 incidents in 1977 to 136 incidents in 1985. In the latter half of the 1980s, a number of South African civilians were killed in these attacks, a reversal of the ANC's earlier reluctance to incur civilian casualties. Fatal attacks included the 1983 Church Street bombing, the 1985 Amanzimtoti bombing, the 1986 Magoo's Bar bombing, and the 1987 Johannesburg Magistrate's Court bombing. Partly in retaliation, the South African Defence Force increasingly crossed the border to target ANC members and ANC bases, as in the 1981 raid on Maputo, 1983 raid on Maputo, and 1985 raid on Gaborone.thumb\|Oliver Tambo, ANC president in exile from 1967 to 1991. During this period, MK activities led the governments of Margaret Thatcher and Ronald Reagan to condemn the ANC as a terrorist organisation. In fact, neither the ANC nor Mandela were removed from the U.S. terror watch list until 2008. The animosity of Western regimes was partly explained by the Cold War context, and by the considerable amount of support – both financial and technical – that the ANC received from the Soviet Union.
African National Congress	Negotiations to end apartheid	Negotiations to end apartheid From the mid-1980s, as international and internal opposition to apartheid mounted, elements of the ANC began to test the prospects for a negotiated settlement with the South African government, although the prudence of abandoning armed struggle was an extremely controversial topic within the organisation. Following preliminary contact between the ANC and representatives of the state, business, and civil society, President F. W. de Klerk announced in February 1990 that the government would unban the ANC and other banned political organisations, and that Mandela would be released from prison. Some ANC leaders returned to South Africa from exile for so-called "talks about talks", which led in 1990 and 1991 to a series of bilateral accords with the government establishing a mutual commitment to negotiations. Importantly, the Pretoria Minute of August 1990 included a commitment by the ANC to unilaterally suspend its armed struggle. This made possible the multi-party Convention for a Democratic South Africa and later the Multi-Party Negotiating Forum, in which the ANC was regarded as the main representative of the interests of the anti-apartheid movement. However, ongoing political violence, which the ANC attributed to a state-sponsored third force, led to recurrent tensions. Most dramatically, after the Boipatong massacre of June 1992, the ANC announced that it was withdrawing from negotiations indefinitely. It faced further casualties in the Bisho massacre, the Shell House massacre, and in other clashes with state forces and supporters of the Inkatha Freedom Party (IFP). However, once negotiations resumed, they resulted in November 1993 in an interim Constitution, which governed South Africa's first democratic elections on 27 April 1994. In the elections, the ANC won an overwhelming 62.65% majority of the vote. Mandela was elected president and formed a coalition Government of National Unity, which, under the provisions of the interim Constitution, also included the National Party and IFP. The ANC has controlled the national government since then.
African National Congress	Breakaways	Breakaways In the post-apartheid era, several significant breakaway groups have been formed by former ANC members. The first is the Congress of the People, founded by Mosiuoa Lekota in 2008 in the aftermath of the Polokwane elective conference, when the ANC declined to re-elect Thabo Mbeki as its president and instead compelled his resignation from the national presidency. The second breakaway is the Economic Freedom Fighters, founded in 2013 after youth leader Julius Malema was expelled from the ANC. Before these, the most important split in the ANC's history occurred in 1959, when Robert Sobukwe led a splinter faction of African nationalists to the new Pan Africanist Congress. uMkhonto weSizwe rose to prominence in December 2023, when former president Jacob Zuma announced that, while planning to remain a lifelong member of the ANC, he would not be campaigning for the ANC in the 2024 South African general election, and would instead be voting for MK. In July 2024, Jacob Zuma was expelled from the ANC, because of campaigning for a rival party (MK party) in the 29 May general election.
African National Congress	Current structure and composition	Current structure and composition thumb\|205x205px\|Cyril Ramaphosa was elected ANC president at the 2017 conference.
African National Congress	Leadership	Leadership Under the ANC constitution, every member of the ANC belongs to a local branch, and branch members select the organisation's policies and leaders. They do so primarily by electing delegates to the National Conference, which is currently convened every five years. Between conferences, the organisation is led by its 86-member National Executive Committee, which is elected at each conference. The most senior members of the National Executive Committee are the so-called Top Six officials, the ANC president primary among them. A symmetrical process occurs at the subnational levels: each of the nine provincial executive committees and regional executive committees are elected at provincial and regional elective conferences respectively, also attended by branch delegates; and branch officials are elected at branch general meetings.
African National Congress	Leagues	Leagues The ANC has three leagues: the Women's League, the Youth League and the Veterans' League. Under the ANC constitution, the leagues are autonomous bodies with the scope to devise their own constitutions and policies; for the purpose of national conferences, they are treated somewhat like provinces, with voting delegates and the power to nominate leadership candidates.
African National Congress	Tripartite Alliance	Tripartite Alliance The ANC is recognised as the leader of a three-way alliance, known as the Tripartite Alliance, with the SACP and Congress of South African Trade Unions (COSATU). The alliance was formalised in mid-1990, after the ANC was unbanned, but has deeper historical roots: the SACP had worked closely with the ANC in exile, and COSATU had aligned itself with the Freedom Charter and Congress Alliance in 1987. The membership and leadership of the three organisations has traditionally overlapped significantly. The alliance constitutes a de facto electoral coalition: the SACP and COSATU do not contest in government elections, but field candidates through the ANC, hold senior positions in the ANC, and influence party policy. However, the SACP, in particular, has frequently threatened to field its own candidates, and in 2017 it did so for the first time, running against the ANC in by-elections in the Metsimaholo municipality, Free State.thumb\|203x203px\|The logo of the ANC in 1990, since updated.
African National Congress	Electoral candidates	Electoral candidates Under South Africa's closed-list proportional representation electoral system, parties have immense power in selecting candidates for legislative bodies. The ANC's internal candidate selection process is overseen by so-called "list committees" and tends to involve a degree of broad democratic participation, especially at the local level, where ANC branches vote to nominate candidates for the local government elections. Between 2003 and 2008, the ANC also gained a significant number of members through the controversial floor crossing process, which occurred especially at the local level. The leaders of the executive in each sphere of government – the president, the provincial premiers, and the mayors – are indirectly elected after each election. In practice, the selection of ANC candidates for these positions is highly centralised, with the ANC caucus voting together to elect a pre-decided candidate. Although the ANC does not always announce whom its caucuses intend to elect, the National Assembly has thus far always elected the ANC president as the national president.
African National Congress	Cadre deployment	Cadre deployment The ANC has adhered to a formal policy of cadre deployment since 1985. In the post-apartheid era, the policy includes but is not exhausted by selection of candidates for elections and government positions: it also entails that the central organisation "deploys" ANC members to various other strategic positions in the party, state, and economy.
African National Congress	Ideology and policies	Ideology and policies left\|thumb\|190x190px\|As ANC president (1991–97), Nelson Mandela saw the ANC expand and informally absorb other anti-apartheid groups. The ANC prides itself on being a broad church, and, like many dominant parties, resembles a catch-all party, accommodating a range of ideological tendencies. As Mandela told The Washington Post in 1990: The ANC has never been a political party. It was formed as a parliament of the African people. Right from the start, up to now, the ANC is a coalition, if you want, of people of various political affiliations. Some will support free enterprise, others socialism. Some are conservatives, others are liberals. We are united solely by our determination to oppose racial oppression. That is the only thing that unites us. There is no question of ideology as far as the odyssey of the ANC is concerned, because any question approaching ideology would split the organization from top to bottom. Because we have no connection whatsoever except at this one, of our determination to dismantle apartheid. The post-apartheid ANC continues to identify itself foremost as a liberation movement, pursuing "the complete liberation of the country from all forms of discrimination and national oppression". It also continues to claim the Freedom Charter of 1955 as "the basic policy document of the ANC". However, as NEC member Jeremy Cronin noted in 2007, the various broad principles of the Freedom Charter have been given different interpretations, and emphasised to differing extents, by different groups within the organisation. Nonetheless, some basic commonalities are visible in the policy and ideological preferences of the organisation's mainstream.
African National Congress	Non-racialism	Non-racialism The ANC is committed to the ideal of non-racialism and to opposing "any form of racial, tribalistic or ethnic exclusivism or chauvinism".
African National Congress	National Democratic Revolution	National Democratic Revolution The 1969 Morogoro Conference committed the ANC to a "national democratic revolution [which] – destroying the existing social and economic relationship – will bring with it a correction of the historical injustices perpetrated against the indigenous majority and thus lay the basis for a new – and deeper internationalist – approach". For the movement's intellectuals, the concept of the National Democratic Revolution (NDR) was a means of reconciling the anti-apartheid and anti-colonial project with a second goal, that of establishing domestic and international socialism – the ANC is a member of the Socialist International, and its close partner the SACP traditionally conceives itself as a vanguard party. Specifically, and as implied by the 1969 document, NDR doctrine entails that the transformation of the domestic political system (national struggle, in Joe Slovo's phrase) is a precondition for a socialist revolution (class struggle). The concept remained important to ANC intellectuals and strategists after the end of apartheid. Indeed, the pursuit of the NDR is one of the primary objectives of the ANC as set out in its constitution. As with the Freedom Charter, the ambiguity of the NDR has allowed it to bear varying interpretations. For example, whereas SACP theorists tend to emphasise the anti-capitalist character of the NDR, some ANC policymakers have construed it as implying the empowerment of the black majority even within a market-capitalist scheme.
African National Congress	Economic interventionism	Economic interventionism Since 1994, consecutive ANC governments have held a strong preference for a significant degree of state intervention in the economy. The ANC's first comprehensive articulation of its post-apartheid economic policy framework was set out in the Reconstruction and Development Programme (RDP) document of 1994, which became its electoral manifesto and also, under the same name, the flagship policy of Nelson Mandela's government. The RDP aimed both to redress the socioeconomic inequalities created by colonialism and apartheid, and to promote economic growth and development; state intervention was judged a necessary step towards both goals. Specifically, the state was to intervene in the economy through three primary channels: a land reform programme; a degree of economic planning, through industrial and trade policy; and state investments in infrastructure and the provision of basic services, including health and education. Although the RDP was abandoned in 1996, these three channels of state economic intervention have remained mainstays of subsequent ANC policy frameworks.
African National Congress	Neoliberal turn	Neoliberal turn In 1996, Mandela's government replaced the RDP with the Growth Employment and Redistribution (GEAR) programme, which was maintained under President Thabo Mbeki, Mandela's successor. GEAR has been characterised as a neoliberal policy, and it was disowned by both COSATU and the SACP. While some analysts viewed Mbeki's economic policy as undertaking the uncomfortable macroeconomic adjustments necessary for long-term growth, others – notably Patrick Bond – viewed it as a reflection of the ANC's failure to implement genuinely radical transformation after 1994. Debate about ANC commitment to redistribution on a socialist scale has continued: in 2013, the country's largest trade union, the National Union of Metalworkers of South Africa, withdrew its support for the ANC on the basis that "the working class cannot any longer see the ANC or the SACP as its class allies in any meaningful sense". It is evident, however, that the ANC never embraced free-market capitalism, and continued to favour a mixed economy: even as the debate over GEAR raged, the ANC declared itself (in 2004) a social-democratic party,The Mail & Guardian A-Z of South African Politics by Barbara Ludman, Paul Stober, and Ferial Haffagee and it was at that time presiding over phenomenal expansions of its black economic empowerment programme and the system of social grants..
African National Congress	Developmental state	Developmental state As its name suggests, the RDP emphasised state-led development – that is, a developmental state – which the ANC has typically been cautious, at least in its rhetoric, to distinguish from the neighbouring concept of a welfare state. In the mid-2000s, during Mbeki's second term, the notion of a developmental state was revived in South African political discourse when the national economy worsened; and the 2007 National Conference whole-heartedly endorsed developmentalism in its policy resolutions, calling for a state "at the centre of a mixed economy... which leads and guides that economy and which intervenes in the interest of the people as a whole". The proposed developmental state was also central to the ANC's campaign in the 2009 elections, and it remains a central pillar of the policy of the current government, which seeks to build a "capable and developmental" state. In this regard, ANC politicians often cite China as an aspirational example. A discussion document ahead of the ANC's 2015 National General Council proposed that: China['s] economic development trajectory remains a leading example of the triumph of humanity over adversity. The exemplary role of the collective leadership of the Communist Party of China in this regard should be a guiding lodestar of our own struggle.
African National Congress	Radical economic transformation	Radical economic transformation Towards the end of Jacob Zuma's presidency, an ANC faction aligned to Zuma pioneered a new policy platform referred to as radical economic transformation (RET). Zuma announced the new focus on RET during his February 2017 State of the Nation address, and later that year, explaining that it had been adopted as ANC policy and therefore as government policy, defined it as entailing "fundamental change in the structures, systems, institutions and patterns of ownership and control of the economy, in favour of all South Africans, especially the poor". Arguments for RET were closely associated with the rhetorical concept of white monopoly capital. At the 54th National Conference in 2017, the ANC endorsed a number of policy principles advocated by RET supporters, including their proposal to pursue land expropriation without compensation as a matter of national policy.
African National Congress	Foreign policy and relations	Foreign policy and relations The ANC has long had close ties with China and the Chinese Communist Party (CCP), with the CCP having supported ANC's struggle of apartheid since 1961. In 2008, the two parties signed a memorandum of understanding to train ANC members in China. President Cyril Ramaphosa and the ANC have not condemned the Russian invasion of Ukraine, and have faced criticism from opposition parties, public commentators, academics, civil society organisations, and former ANC members due to this. The ANC youth wing has meanwhile condemned sanctions against Russia and denounced NATO's eastward expansion as "fascistic". Officials representing the ANC Youth League acted as international observers for Russia's staged referendum to annex Ukrainian territory claimed during the war. In February 2024 ANC Secretary-General Fikile Mbalula attend a "forum on combating Western neocolonialism" hosted by Russia, thereby drawing further criticism for the party's perceived support for Russia's invasion. The ANC had received large donations from the Putin linked Russian oligarch Viktor Vekselberg, whilst the party's investment arm, Chancellor House, has a joint investment with Vekselberg in a South African manganese mine.
African National Congress	Symbols and media	Symbols and media thumb\|The tricolour flag of the ANC.
African National Congress	Flag and logo	Flag and logo The logo of the ANC incorporates a spear and shield – symbolising the historical and ongoing struggle, armed and otherwise, against colonialism and racial oppression – and a wheel, which is borrowed from the 1955 Congress of the People campaign and therefore symbolises a united and non-racial movement for freedom and equality. The logo uses the same colours as the ANC flag, which comprises three horizontal stripes of equal width in black, green and gold. The black symbolises the native people of South Africa; the green represents the land of South Africa; and the gold represents the country's mineral and other natural wealth. The black, green and gold tricolour also appeared on the flag of the KwaZulu bantustan and appears on the flag of the ANC's rival, the IFP; and all three colours appear in the post-apartheid South African national flag.
African National Congress	Publications	Publications Since 1996, the ANC Department of Political Education has published the quarterly Umrabulo political discussion journal; and ANC Today, a weekly online newsletter, was launched in 2001 to offset the alleged bias of the press. In addition, since 1972, it has been traditional for the ANC president to publish annually a so-called January 8 Statement: a reflective letter sent to members on 8 January, the anniversary of the organisation's founding. In earlier years, the ANC published a range of periodicals, the most important of which was the monthly journal Sechaba (1967–1990), printed in the German Democratic Republic and banned by the apartheid government. The ANC's Radio Freedom also gained a wide audience during apartheid.
African National Congress	Amandla	Amandla "Amandla ngawethu", or the Sotho variant "Matla ke arona", is a common rallying call at ANC meetings, roughly meaning "power to the people". It is also common for meetings to sing so-called struggle songs, which were sung during anti-apartheid meetings and in MK camps. In the case of at least two of these songs – Dubula ibhunu and Umshini wami – this has caused controversy in recent years.
African National Congress	Criticism and controversy	Criticism and controversy The ANC has received criticism from both internal and external sources. Internally Mandela publicly criticized the party, following the conclusion of his presidency, for ignoring instances of corruption and mismanagement, whilst allowing for the growth of a culture of racial and ideological intolerance.
African National Congress	Corruption controversies	Corruption controversies The most prominent corruption case involving the ANC relates to a series of bribes paid to companies involved in the ongoing R55 billion Arms Deal saga, which resulted in a long term jail sentence to then Deputy President Jacob Zuma's legal adviser Schabir Shaik. Zuma, the former South African President, was charged with fraud, bribery and corruption in the Arms Deal, but the charges were subsequently withdrawn by the National Prosecuting Authority of South Africa due to their delay in prosecution. The ANC has also been criticised for its subsequent abolition of the Scorpions, the multidisciplinary agency that investigated and prosecuted organised crime and corruption, and was heavily involved in the investigation into Zuma and Shaik. Tony Yengeni, in his position as chief whip of the ANC and head of the Parliaments defence committee has recently been named as being involved in bribing the German company ThyssenKrupp over the purchase of four corvettes for the SANDF. Other corruption issues in the 2000s included the sexual misconduct and criminal charges of Beaufort West municipal manager Truman Prince, and the Oilgate scandal, in which millions of Rand in funds from a state-owned company were funnelled into ANC coffers. The ANC has also been accused of using government and civil society to fight its political battles against opposition parties such as the Democratic Alliance. The result has been a number of complaints and allegations that none of the political parties truly represent the interests of the poor. This has resulted in the "No Land! No House! No Vote!" Campaign which became very prominent during elections. In 2018, The New York Times reported on the killings of ANC corruption whistleblowers. During an address on 28 October 2021, former president Thabo Mbeki commented on the history of corruption within the ANC. He reflected that Mandela had already warned in 1997 that the ANC was attracting individuals who viewed the party as "a route to power and self-enrichment." He added that the ANC leadership "did not know how to deal with this problem." During a lecture on 10 December, Mbeki reiterated concerns about "careerists" within the party, and stressed the need to "purge itself of such members". In May 2024, the International Consortium of Investigative Journalists in association with amaBhungane showed in documents that R200 million in the ANC's election fund was siphoned off to the church of controversial archbishop Bheki Lukhele in Eswatini; the Chief Financial Officer of the ANC, Bongani Mahlalela along with the Ambassador of Eswatini to Belgium, Sibusisiwe Mngomezulu, were implicated in the scheme.
African National Congress	Condemnation over Secrecy Bill	Condemnation over Secrecy Bill In late 2011, the ANC was heavily criticised over the passage of the Protection of State Information Bill, which opponents claimed would improperly restrict the freedom of the press. Opposition to the bill included otherwise ANC-aligned groups such as COSATU. Notably, Nelson Mandela and other Nobel laureates Nadine Gordimer, Archbishop Desmond Tutu, and F. W. de Klerk have expressed disappointment with the bill for not meeting standards of constitutionality and aspirations for freedom of information and expression.
African National Congress	Role in the Marikana killings	Role in the Marikana killings The ANC have been criticised for its role in failing to prevent 16 August 2012 massacre of Lonmin miners at Marikana in the Northwest. Some allege that Police Commissioner Riah Phiyega and Police Minister Nathi Mthethwa gave the go ahead for the police action against the miners on that day. Commissioner Phiyega of the ANC came under further criticism as being insensitive and uncaring when she was caught smiling and laughing during the Farlam Commission's video playback of the massacre. In 2014, Archbishop Desmond Tutu announced that he could no longer bring himself to vote for the ANC, as it was no longer the party that he and Nelson Mandela fought for. He stated that the party had lost its way, and was in danger of becoming a corrupt entity in power.
African National Congress	Financial mismanagement	Financial mismanagement Since at least 2017, the ANC has encountered significant problems related to financial mismanagement. According to a report filed by the former treasurer-general Zweli Mkhize in December 2017, the ANC was technically insolvent as its liabilities exceeded its assets. These problems continued into the second half of 2021. By September 2021, the ANC had reportedly amassed a debt exceeding R200-million, including over R100-million owed to the South African Revenue Service. Beginning in May 2021, the ANC failed to pay monthly staff salaries on time. Having gone without pay for three consecutive months, workers planned a strike in late August 2021. In response, the ANC initiated a crowdfunding campaign to raise money for staff salaries. By November 2021, its Cape Town staff was approaching their fourth month without salaries, while medical aid and provident fund contributions had been suspended in various provinces. The party has countered that the Political Party Funding Act, which prohibits anonymous contributions, has dissuaded some donors who previously injected money for salaries.
African National Congress	State capture	State capture In January 2018, then-President Jacob Zuma established the Zondo Commission to investigate allegations of state capture, corruption, and fraud in the public sector. Over the following four years, the Commission heard testimony from over 250 witnesses and collected more than 150,000 pages of evidence. After several extensions, the first part of the final three-part report was published on 4 January 2022. The report found that the ANC, including Zuma and his political allies, had benefited from the extensive corruption of state enterprises, including the South African Revenue Service. It also found that the ANC "simply did not care that state entities were in decline during state capture or they slept on the job – or they simply didn't know what to do."
African National Congress	Electoral history	Electoral history thumb\|Proportion of votes cast for the ANC in the 2014 election, by ward. thumb\|250px\|The ANC's performance by region in the 2024 South African general election.
African National Congress	National Assembly elections	National Assembly elections ElectionParty leaderVotes%Seats+/–PositionResult1994Nelson Mandela12,237,65562.65% 252 1st1999Thabo Mbeki10,601,33066.35% 14 1st200410,880,91569.69% 13 1st2009Jacob Zuma11,650,74865.90% 15 1st201411,436,92162.15% 15 1st2019Cyril Ramaphosa10,026,47557.50% 19 1st20246,459,68340.18% 71 1st
African National Congress	National Council of Provinces elections	National Council of Provinces elections ElectionParty leaderSeats+/–PositionResult1994Nelson Mandela 60 1st1999Thabo Mbeki 3 1st2004 2 1st2009Jacob Zuma 3 1st2014 2 1st2019Cyril Ramaphosa 6 1st2024 11 1st
African National Congress	Provincial legislatures	Provincial legislatures ElectionEastern CapeFree StateGautengKwaZulu-NatalLimpopoMpumalangaNorth-WestNorthern CapeWestern Cape%Seats%Seats%Seats%Seats%Seats%Seats%Seats%Seats%Seats199484.3548/5676.6524/3057.6050/8632.2326/8191.6338/4080.6925/3083.3326/3049.7415/3033.0114/42199973.8047/6380.7925/3067.8750/7339.3832/8088.2944/4984.8326/3078.9727/3364.3220/3042.0718/42200479.2751/6381.7825/3068.4051/7346.9838/8089.1845/4986.3027/3080.7127/3368.8321/3045.2519/42200968.8244/6371.1022/3064.0447/7362.9551/8084.8843/4985.5527/3072.8925/3360.7519/3031.5514/42201470.0945/6369.8522/3053.5940/7364.5252/8078.6039/4978.2324/3067.3923/3364.4020/3032.8914/42201968.7444/6361.1419/3050.1937/7354.2244/8075.4938/4970.5822/3061.8721/3357.5418/3028.6312/422024 62.16 45/73 51.87 16/30 34.76 28/80 16.99 14/80 73.30 48/64 51.31 27/51 57.73 21/38 49.34 15/30 19.55 8/42
African National Congress	Municipal elections	Municipal elections ElectionVotes%Change1995–965,033,85558%2000None released59.4% 1.4%200617,466,94866.3% 6.9%201116,548,82661.9% 4.4%201621,450,33255.7% 6.2%202114,531,90847.5% 8.2%
African National Congress	See also	See also :Category:Members of the African National Congress Democratic Alliance Solomon Mahlangu Freedom College Step-aside rule State v. Ebrahim United Democratic Front
African National Congress	References	References
African National Congress	External links	External links Sechaba archive at JSTOR Mayibuye archive at JSTOR Attacks attributed to the ANC on the START terrorism database List of articles & videos about the ANC Response by the ANC General Secretary to COSATU's assessment, 2004 Category:Anti-apartheid organisations Category:Anti-Zionism in Africa Category:Corruption in South Africa Category:Full member parties of the Socialist International Category:National liberation movements Category:Organisations associated with apartheid Category:Organizations formerly designated as terrorist by the United States Category:Political parties based in Johannesburg Category:Political parties established in 1912 Category:Social democratic parties in South Africa
African National Congress	Table of Content	Short description, History, Origins, Exile in Lusaka, uMkhonto we Sizwe, Negotiations to end apartheid, Breakaways, Current structure and composition, Leadership, Leagues, Tripartite Alliance, Electoral candidates, Cadre deployment, Ideology and policies, Non-racialism, National Democratic Revolution, Economic interventionism, Neoliberal turn, Developmental state, Radical economic transformation, Foreign policy and relations, Symbols and media, Flag and logo, Publications, Amandla, Criticism and controversy, Corruption controversies, Condemnation over Secrecy Bill, Role in the Marikana killings, Financial mismanagement, State capture, Electoral history, National Assembly elections, National Council of Provinces elections, Provincial legislatures, Municipal elections, See also, References, External links
Amphetamine	Short description	Amphetamine (contracted from alpha-methylphenethylamine) is a central nervous system (CNS) stimulant that is used in the treatment of attention deficit hyperactivity disorder (ADHD), narcolepsy, and obesity; it is also used to treat binge eating disorder in the form of its inactive prodrug lisdexamfetamine. Amphetamine was discovered as a chemical in 1887 by Lazăr Edeleanu, and then as a drug in the late 1920s. It exists as two enantiomers: levoamphetamine and dextroamphetamine. Amphetamine properly refers to a specific chemical, the racemic free base, which is equal parts of the two enantiomers in their pure amine forms. The term is frequently used informally to refer to any combination of the enantiomers, or to either of them alone. Historically, it has been used to treat nasal congestion and depression. Amphetamine is also used as an athletic performance enhancer and cognitive enhancer, and recreationally as an aphrodisiac and euphoriant. It is a prescription drug in many countries, and unauthorized possession and distribution of amphetamine are often tightly controlled due to the significant health risks associated with recreational use. The first amphetamine pharmaceutical was Benzedrine, a brand which was used to treat a variety of conditions. Pharmaceutical amphetamine is prescribed as racemic amphetamine, Adderall, dextroamphetamine, or the inactive prodrug lisdexamfetamine. Amphetamine increases monoamine and excitatory neurotransmission in the brain, with its most pronounced effects targeting the norepinephrine and dopamine neurotransmitter systems. At therapeutic doses, amphetamine causes emotional and cognitive effects such as euphoria, change in desire for sex, increased wakefulness, and improved cognitive control. It induces physical effects such as improved reaction time, fatigue resistance, decreased appetite, elevated heart rate, and increased muscle strength. Larger doses of amphetamine may impair cognitive function and induce rapid muscle breakdown. Addiction is a serious risk with heavy recreational amphetamine use, but is unlikely to occur from long-term medical use at therapeutic doses. Very high doses can result in psychosis (e.g., hallucinations, delusions and paranoia) which rarely occurs at therapeutic doses even during long-term use. Recreational doses are generally much larger than prescribed therapeutic doses and carry a far greater risk of serious side effects. Amphetamine belongs to the phenethylamine class. It is also the parent compound of its own structural class, the substituted amphetamines, which includes prominent substances such as bupropion, cathinone, MDMA, and methamphetamine. As a member of the phenethylamine class, amphetamine is also chemically related to the naturally occurring trace amine neuromodulators, specifically phenethylamine and , both of which are produced within the human body. Phenethylamine is the parent compound of amphetamine, while is a positional isomer of amphetamine that differs only in the placement of the methyl group.
Amphetamine	Uses	Uses
Amphetamine	Medical	Medical Amphetamine is used to treat attention deficit hyperactivity disorder (ADHD), narcolepsy, obesity, and, in the form of lisdexamfetamine, binge eating disorder. It is sometimes prescribed for its past medical indications, particularly for depression and chronic pain.
Amphetamine	Pharmaceutical products	Pharmaceutical products Several currently marketed amphetamine formulations contain both enantiomers, including those marketed under the brand names Adderall, Adderall XR, Mydayis, Adzenys ER, , Dyanavel XR, Evekeo, and Evekeo ODT. Of those, Evekeo (including Evekeo ODT) is the only product containing only racemic amphetamine (as amphetamine sulfate), and is therefore the only one whose active moiety can be accurately referred to simply as "amphetamine". Dextroamphetamine, marketed under the brand names Dexedrine and Zenzedi, is the only enantiopure amphetamine product currently available. A prodrug form of dextroamphetamine, lisdexamfetamine, is also available and is marketed under the brand name Vyvanse. As it is a prodrug, lisdexamfetamine is structurally different from dextroamphetamine, and is inactive until it metabolizes into dextroamphetamine. The free base of racemic amphetamine was previously available as Benzedrine, Psychedrine, and Sympatedrine. Levoamphetamine was previously available as Cydril. Many current amphetamine pharmaceuticals are salts due to the comparatively high volatility of the free base. However, oral suspension and orally disintegrating tablet (ODT) dosage forms composed of the free base were introduced in 2015 and 2016, respectively. Some of the current brands and their generic equivalents are listed below. + Amphetamine pharmaceuticals Brandname United StatesAdopted Name (D:L) ratio Dosageform Marketingstart date Sources Adderall – 3:1 (salts) tablet 1996 Adderall XR – 3:1 (salts) capsule 2001 Mydayis – 3:1 (salts) capsule 2017 Adzenys ER amphetamine 3:1 (base) suspension 2017 amphetamine 3:1 (base) ODT 2016 Dyanavel XR amphetamine 3.2:1 (base) suspension 2015 Evekeo amphetamine sulfate 1:1 (salts) tablet 2012 Evekeo ODT amphetamine sulfate 1:1 (salts) ODT 2019 Dexedrine dextroamphetamine sulfate 1:0 (salts) capsule 1976 Zenzedi dextroamphetamine sulfate 1:0 (salts) tablet 2013 Vyvanse lisdexamfetamine dimesylate 1:0 (prodrug) capsule 2007 tablet Xelstrym dextroamphetamine 1:0 (base) patch 2022
Amphetamine	Indications	Indications
Amphetamine	ADHD	ADHD Long-term amphetamine exposure at sufficiently high doses in some animal species is known to produce abnormal dopamine system development or nerve damage, but, in humans with ADHD, long-term use of pharmaceutical amphetamines at therapeutic doses appears to improve brain development and nerve growth. Reviews of magnetic resonance imaging (MRI) studies suggest that long-term treatment with amphetamine decreases abnormalities in brain structure and function found in subjects with ADHD, and improves function in several parts of the brain, such as the right caudate nucleus of the basal ganglia. Reviews of clinical stimulant research have established the safety and effectiveness of long-term continuous amphetamine use for the treatment of ADHD.Figure 3: Treatment benefit by treatment type and outcome group Randomized controlled trials of continuous stimulant therapy for the treatment of ADHD spanning 2 years have demonstrated treatment effectiveness and safety. Two reviews have indicated that long-term continuous stimulant therapy for ADHD is effective for reducing the core symptoms of ADHD (i.e., hyperactivity, inattention, and impulsivity), enhancing quality of life and academic achievement, and producing improvements in a large number of functional outcomes across 9 categories of outcomes related to academics, antisocial behavior, driving, non-medicinal drug use, obesity, occupation, self-esteem, service use (i.e., academic, occupational, health, financial, and legal services), and social function. Additionally, a 2024 meta-analytic systematic review reported moderate improvements in quality of life when amphetamine treatment is used for ADHD. One review highlighted a nine-month randomized controlled trial of amphetamine treatment for ADHD in children that found an average increase of 4.5 IQ points, continued increases in attention, and continued decreases in disruptive behaviors and hyperactivity. Another review indicated that, based upon the longest follow-up studies conducted to date, lifetime stimulant therapy that begins during childhood is continuously effective for controlling ADHD symptoms and reduces the risk of developing a substance use disorder as an adult. Models of ADHD suggest that it is associated with functional impairments in some of the brain's neurotransmitter systems; these functional impairments involve impaired dopamine neurotransmission in the mesocorticolimbic projection and norepinephrine neurotransmission in the noradrenergic projections from the locus coeruleus to the prefrontal cortex. Stimulants like methylphenidate and amphetamine are effective in treating ADHD because they increase neurotransmitter activity in these systems. Approximately 80% of those who use these stimulants see improvements in ADHD symptoms. Children with ADHD who use stimulant medications generally have better relationships with peers and family members, perform better in school, are less distractible and impulsive, and have longer attention spans. The Cochrane reviews on the treatment of ADHD in children, adolescents, and adults with pharmaceutical amphetamines stated that short-term studies have demonstrated that these drugs decrease the severity of symptoms, but they have higher discontinuation rates than non-stimulant medications due to their adverse side effects. However, a 2025 meta-analytic systematic review of 113 randomized controlled trials found that stimulant medications were the only intervention with robust short-term efficacy, and were associated with lower all-cause treatment discontinuation rates than non-stimulant medications (e.g., atomoxetine). A Cochrane review on the treatment of ADHD in children with tic disorders such as Tourette syndrome indicated that stimulants in general do not make tics worse, but high doses of dextroamphetamine could exacerbate tics in some individuals.
Amphetamine	Binge eating disorder	Binge eating disorder Binge eating disorder (BED) is characterized by recurrent and persistent episodes of compulsive binge eating. These episodes are often accompanied by marked distress and a feeling of loss of control over eating. The pathophysiology of BED is not fully understood, but it is believed to involve dysfunctional dopaminergic reward circuitry along the cortico-striatal-thalamic-cortical loop. As of July 2024, lisdexamfetamine is the only USFDA- and TGA-approved pharmacotherapy for BED. Evidence suggests that lisdexamfetamine's treatment efficacy in BED is underpinned at least in part by a psychopathological overlap between BED and ADHD, with the latter conceptualized as a cognitive control disorder that also benefits from treatment with lisdexamfetamine. class=skin-invert-image\|thumb\|right\|370px\|alt=Diagram of TAAR1 organ-specific expression and function\|This diagram illustrates how TAAR1 activation induces incretin-like effects through the release of gastrointestinal hormones and influences food intake, blood glucose levels, and insulin release. TAAR1 expression in the periphery is indicated with "x". Lisdexamfetamine's therapeutic effects for BED primarily involve direct action in the central nervous system after conversion to its pharmacologically active metabolite, dextroamphetamine. Centrally, dextroamphetamine increases neurotransmitter activity of dopamine and norepinephrine in prefrontal cortical regions that regulate cognitive control of behavior. Similar to its therapeutic effect in ADHD, dextroamphetamine enhances cognitive control and may reduce impulsivity in patients with BED by enhancing the cognitive processes responsible for overriding prepotent feeding responses that precede binge eating episodes. In addition, dextroamphetamine's actions outside of the central nervous system may also contribute to its treatment effects in BED. Peripherally, dextroamphetamine triggers lipolysis through noradrenergic signaling in adipose fat cells, leading to the release of triglycerides into blood plasma to be utilized as a fuel substrate. Dextroamphetamine also activates TAAR1 in peripheral organs along the gastrointestinal tract that are involved in the regulation of food intake and body weight. Together, these actions confer an anorexigenic effect that promotes satiety in response to feeding and may decrease binge eating as a secondary effect. While lisdexamfetamine's anorexigenic effects contribute to its efficacy in BED, evidence indicates that the enhancement of cognitive control is necessary and sufficient for addressing the disorder's underlying psychopathology. This view is supported by the failure of anti-obesity medications and other appetite suppressants to significantly reduce BED symptom severity, despite their capacity to induce weight loss. Medical reviews of randomized controlled trials have demonstrated that lisdexamfetamine, at doses between 50–70 mg, is safe and effective for the treatment of moderate-to-severe BED in adults. These reviews suggest that lisdexamfetamine is persistently effective at treating BED and is associated with significant reductions in the number of binge eating days and binge eating episodes per week. Furthermore, a meta-analytic systematic review highlighted an open-label, 12-month extension safety and tolerability study that reported lisdexamfetamine remained effective at reducing the number of binge eating days for the duration of the study. In addition, both a review and a meta-analytic systematic review found lisdexamfetamine to be superior to placebo in several secondary outcome measures, including persistent binge eating cessation, reduction of obsessive-compulsive related binge eating symptoms, reduction of body-weight, and reduction of triglycerides. Lisdexamfetamine, like all pharmaceutical amphetamines, has direct appetite suppressant effects that may be therapeutically useful in both BED and its comorbidities. Based on reviews of neuroimaging studies involving BED-diagnosed participants, therapeautic neuroplasticity in dopaminergic and noradrenergic pathways from long-term use of lisdexamfetamine may be implicated in lasting improvements in the regulation of eating behaviors that are observed.
Amphetamine	Narcolepsy	Narcolepsy Narcolepsy is a chronic sleep-wake disorder that is associated with excessive daytime sleepiness, cataplexy, and sleep paralysis. Patients with narcolepsy are diagnosed as either type 1 or type 2, with only the former presenting cataplexy symptoms. Type 1 narcolepsy results from the loss of approximately 70,000 orexin-releasing neurons in the lateral hypothalamus, leading to significantly reduced cerebrospinal orexin levels; this reduction is a diagnostic biomarker for type 1 narcolepsy. Lateral hypothalamic orexin neurons innervate every component of the ascending reticular activating system (ARAS), which includes noradrenergic, dopaminergic, histaminergic, and serotonergic nuclei that promote wakefulness. Amphetamine’s therapeutic mode of action in narcolepsy primarily involves increasing monoamine neurotransmitter activity in the ARAS. This includes noradrenergic neurons in the locus coeruleus, dopaminergic neurons in the ventral tegmental area, histaminergic neurons in the tuberomammillary nucleus, and serotonergic neurons in the dorsal raphe nucleus. Dextroamphetamine, the more dopaminergic enantiomer of amphetamine, is particularly effective at promoting wakefulness because dopamine release has the greatest influence on cortical activation and cognitive arousal, relative to other monoamines. In contrast, levoamphetamine may have a greater effect on cataplexy, a symptom more sensitive to the effects of norepinephrine and serotonin. Noradrenergic and serotonergic nuclei in the ARAS are involved in the regulation of the REM sleep cycle and function as "REM-off" cells, with amphetamine's effect on norepinephrine and serotonin contributing to the suppression of REM sleep and a possible reduction of cataplexy at high doses. The American Academy of Sleep Medicine (AASM) 2021 clinical practice guideline conditionally recommends dextroamphetamine for the treatment of both type 1 and type 2 narcolepsy. Treatment with pharmaceutical amphetamines is generally less preferred relative to other stimulants (e.g., modafinil) and is considered a third-line treatment option. Medical reviews indicate that amphetamine is safe and effective for the treatment of narcolepsy. Amphetamine appears to be most effective at improving symptoms associated with hypersomnolence, with three reviews finding clinically significant reductions in daytime sleepiness in patients with narcolepsy. Additionally, these reviews suggest that amphetamine may dose-dependently improve cataplexy symptoms. However, the quality of evidence for these findings is low and is consequently reflected in the AASM's conditional recommendation for dextroamphetamine as a treatment option for narcolepsy.
Amphetamine	Enhancing performance	Enhancing performance
Amphetamine	Cognitive performance	Cognitive performance In 2015, a systematic review and a meta-analysis of high quality clinical trials found that, when used at low (therapeutic) doses, amphetamine produces modest yet unambiguous improvements in cognition, including working memory, long-term episodic memory, inhibitory control, and some aspects of attention, in normal healthy adults; these cognition-enhancing effects of amphetamine are known to be partially mediated through the indirect activation of both dopamine D1 receptor and α2-adrenergic receptor in the prefrontal cortex. A systematic review from 2014 found that low doses of amphetamine also improve memory consolidation, in turn leading to improved recall of information. Therapeutic doses of amphetamine also enhance cortical network efficiency, an effect which mediates improvements in working memory in all individuals. Amphetamine and other ADHD stimulants also improve task saliency (motivation to perform a task) and increase arousal (wakefulness), in turn promoting goal-directed behavior. Stimulants such as amphetamine can improve performance on difficult and boring tasks and are used by some students as a study and test-taking aid. Based upon studies of self-reported illicit stimulant use, of college students use diverted ADHD stimulants, which are primarily used for enhancement of academic performance rather than as recreational drugs. However, high amphetamine doses that are above the therapeutic range can interfere with working memory and other aspects of cognitive control.
Amphetamine	Physical performance	Physical performance Amphetamine is used by some athletes for its psychological and athletic performance-enhancing effects, such as increased endurance and alertness; however, non-medical amphetamine use is prohibited at sporting events that are regulated by collegiate, national, and international anti-doping agencies. In healthy people at oral therapeutic doses, amphetamine has been shown to increase muscle strength, acceleration, athletic performance in anaerobic conditions, and endurance (i.e., it delays the onset of fatigue), while improving reaction time. Amphetamine improves endurance and reaction time primarily through reuptake inhibition and release of dopamine in the central nervous system. Amphetamine and other dopaminergic drugs also increase power output at fixed levels of perceived exertion by overriding a "safety switch", allowing the core temperature limit to increase in order to access a reserve capacity that is normally off-limits. At therapeutic doses, the adverse effects of amphetamine do not impede athletic performance; however, at much higher doses, amphetamine can induce effects that severely impair performance, such as rapid muscle breakdown and elevated body temperature.
Amphetamine	Recreational	Recreational class=skin-invert-image\|thumb\|upright=1.35\|Table from the 2010 ISCD study ranking various drugs (legal and illegal) based on statements by drug-harm experts. Amphetamine was found to be the 7th overall most dangerous drug. thumb\|Illicitly produced amphetamine thumb\|lined-up amphetamine Amphetamine, specifically the more dopaminergic dextrorotatory enantiomer (dextroamphetamine), is also used recreationally as a euphoriant and aphrodisiac, and like other amphetamines; is used as a club drug for its energetic and euphoric high. Dextroamphetamine (d-amphetamine) is considered to have a high potential for misuse in a recreational manner since individuals typically report feeling euphoric, more alert, and more energetic after taking the drug. A notable part of the 1960s mod subculture in the UK was recreational amphetamine use, which was used to fuel all-night dances at clubs like Manchester's Twisted Wheel. Newspaper reports described dancers emerging from clubs at 5 a.m. with dilated pupils. Mods used the drug for stimulation and alertness, which they viewed as different from the intoxication caused by alcohol and other drugs. Dr. Andrew Wilson argues that for a significant minority, "amphetamines symbolised the smart, on-the-ball, cool image" and that they sought "stimulation not intoxication [...] greater awareness, not escape" and "confidence and articulacy" rather than the "drunken rowdiness of previous generations." Dextroamphetamine's dopaminergic (rewarding) properties affect the mesocorticolimbic circuit; a group of neural structures responsible for incentive salience (i.e., "wanting"; desire or craving for a reward and motivation), positive reinforcement and positively-valenced emotions, particularly ones involving pleasure. Large recreational doses of dextroamphetamine may produce symptoms of dextroamphetamine overdose. Recreational users sometimes open dexedrine capsules and crush the contents in order to insufflate (snort) it or subsequently dissolve it in water and inject it. Immediate-release formulations have higher potential for abuse via insufflation (snorting) or intravenous injection due to a more favorable pharmacokinetic profile and easy crushability (especially tablets). Injection into the bloodstream can be dangerous because insoluble fillers within the tablets can block small blood vessels. Chronic overuse of dextroamphetamine can lead to severe drug dependence, resulting in withdrawal symptoms when drug use stops.
Amphetamine	Contraindications	Contraindications According to the International Programme on Chemical Safety (IPCS) and the U.S. Food and Drug Administration (FDA), amphetamine is contraindicated in people with a history of drug abuse, cardiovascular disease, severe agitation, or severe anxiety. It is also contraindicated in individuals with advanced arteriosclerosis (hardening of the arteries), glaucoma (increased eye pressure), hyperthyroidism (excessive production of thyroid hormone), or moderate to severe hypertension. These agencies indicate that people who have experienced allergic reactions to other stimulants or who are taking monoamine oxidase inhibitors (MAOIs) should not take amphetamine, although safe concurrent use of amphetamine and monoamine oxidase inhibitors has been documented. These agencies also state that anyone with anorexia nervosa, bipolar disorder, depression, hypertension, liver or kidney problems, mania, psychosis, Raynaud's phenomenon, seizures, thyroid problems, tics, or Tourette syndrome should monitor their symptoms while taking amphetamine. Evidence from human studies indicates that therapeutic amphetamine use does not cause developmental abnormalities in the fetus or newborns (i.e., it is not a human teratogen), but amphetamine abuse does pose risks to the fetus. Amphetamine has also been shown to pass into breast milk, so the IPCS and the FDA advise mothers to avoid breastfeeding when using it. Due to the potential for reversible growth impairments, the FDA advises monitoring the height and weight of children and adolescents prescribed an amphetamine pharmaceutical.
Amphetamine	Adverse effects	Adverse effects The adverse side effects of amphetamine are many and varied, and the amount of amphetamine used is the primary factor in determining the likelihood and severity of adverse effects. Amphetamine products such as Adderall, Dexedrine, and their generic equivalents are currently approved by the U.S. FDA for long-term therapeutic use. Recreational use of amphetamine generally involves much larger doses, which have a greater risk of serious adverse drug effects than dosages used for therapeutic purposes.
Amphetamine	Physical	Physical Cardiovascular side effects can include hypertension or hypotension from a vasovagal response, Raynaud's phenomenon (reduced blood flow to the hands and feet), and tachycardia (increased heart rate). Sexual side effects in males may include erectile dysfunction, frequent erections, or prolonged erections. Gastrointestinal side effects may include abdominal pain, constipation, diarrhea, and nausea. Other potential physical side effects include appetite loss, blurred vision, dry mouth, excessive grinding of the teeth, nosebleed, profuse sweating, rhinitis medicamentosa (drug-induced nasal congestion), reduced seizure threshold, tics (a type of movement disorder), and weight loss. Dangerous physical side effects are rare at typical pharmaceutical doses. Amphetamine stimulates the medullary respiratory centers, producing faster and deeper breaths. In a normal person at therapeutic doses, this effect is usually not noticeable, but when respiration is already compromised, it may be evident. Amphetamine also induces contraction in the urinary bladder sphincter, the muscle which controls urination, which can result in difficulty urinating. This effect can be useful in treating bed wetting and loss of bladder control. The effects of amphetamine on the gastrointestinal tract are unpredictable. If intestinal activity is high, amphetamine may reduce gastrointestinal motility (the rate at which content moves through the digestive system); however, amphetamine may increase motility when the smooth muscle of the tract is relaxed. Amphetamine also has a slight analgesic effect and can enhance the pain relieving effects of opioids. FDA-commissioned studies from 2011 indicate that in children, young adults, and adults there is no association between serious adverse cardiovascular events (sudden death, heart attack, and stroke) and the medical use of amphetamine or other ADHD stimulants. However, amphetamine pharmaceuticals are contraindicated in individuals with cardiovascular disease.
Amphetamine	Psychological	Psychological At normal therapeutic doses, the most common psychological side effects of amphetamine include increased alertness, apprehension, concentration, initiative, self-confidence and sociability, mood swings (elated mood followed by mildly depressed mood), insomnia or wakefulness, and decreased sense of fatigue. Less common side effects include anxiety, change in libido, grandiosity, irritability, repetitive or obsessive behaviors, and restlessness; these effects depend on the user's personality and current mental state. Amphetamine psychosis (e.g., delusions and paranoia) can occur in heavy users. Although very rare, this psychosis can also occur at therapeutic doses during long-term therapy. According to the FDA, "there is no systematic evidence" that stimulants produce aggressive behavior or hostility. Amphetamine has also been shown to produce a conditioned place preference in humans taking therapeutic doses, meaning that individuals acquire a preference for spending time in places where they have previously used amphetamine.
Amphetamine	Reinforcement disorders	Reinforcement disorders
Amphetamine	Addiction	Addiction Addiction is a serious risk with heavy recreational amphetamine use, but is unlikely to occur from long-term medical use at therapeutic doses; in fact, lifetime stimulant therapy for ADHD that begins during childhood reduces the risk of developing substance use disorders as an adult. Pathological overactivation of the mesolimbic pathway, a dopamine pathway that connects the ventral tegmental area to the nucleus accumbens, plays a central role in amphetamine addiction. Individuals who frequently self-administer high doses of amphetamine have a high risk of developing an amphetamine addiction, since chronic use at high doses gradually increases the level of accumbal ΔFosB, a "molecular switch" and "master control protein" for addiction. Once nucleus accumbens ΔFosB is sufficiently overexpressed, it begins to increase the severity of addictive behavior (i.e., compulsive drug-seeking) with further increases in its expression. While there are currently no effective drugs for treating amphetamine addiction, regularly engaging in sustained aerobic exercise appears to reduce the risk of developing such an addiction. Exercise therapy improves clinical treatment outcomes and may be used as an adjunct therapy with behavioral therapies for addiction.
Amphetamine	Biomolecular mechanisms	Biomolecular mechanisms Chronic use of amphetamine at excessive doses causes alterations in gene expression in the mesocorticolimbic projection, which arise through transcriptional and epigenetic mechanisms. The most important transcription factors that produce these alterations are Delta FBJ murine osteosarcoma viral oncogene homolog B (ΔFosB), cAMP response element binding protein (CREB), and nuclear factor-kappa B (NF-κB). ΔFosB is the most significant biomolecular mechanism in addiction because ΔFosB overexpression (i.e., an abnormally high level of gene expression which produces a pronounced gene-related phenotype) in the D1-type medium spiny neurons in the nucleus accumbens is necessary and sufficient for many of the neural adaptations and regulates multiple behavioral effects (e.g., reward sensitization and escalating drug self-administration) involved in addiction. Once ΔFosB is sufficiently overexpressed, it induces an addictive state that becomes increasingly more severe with further increases in ΔFosB expression. It has been implicated in addictions to alcohol, cannabinoids, cocaine, methylphenidate, nicotine, opioids, phencyclidine, propofol, and substituted amphetamines, among others. ΔJunD, a transcription factor, and G9a, a histone methyltransferase enzyme, both oppose the function of ΔFosB and inhibit increases in its expression. Sufficiently overexpressing ΔJunD in the nucleus accumbens with viral vectors can completely block many of the neural and behavioral alterations seen in chronic drug abuse (i.e., the alterations mediated by ΔFosB). Similarly, accumbal G9a hyperexpression results in markedly increased histone 3 lysine residue 9 dimethylation (H3K9me2) and blocks the induction of ΔFosB-mediated neural and behavioral plasticity by chronic drug use, which occurs via H3K9me2-mediated repression of transcription factors for ΔFosB and H3K9me2-mediated repression of various ΔFosB transcriptional targets (e.g., CDK5). ΔFosB also plays an important role in regulating behavioral responses to natural rewards, such as palatable food, sex, and exercise. Since both natural rewards and addictive drugs induce the expression of ΔFosB (i.e., they cause the brain to produce more of it), chronic acquisition of these rewards can result in a similar pathological state of addiction. Consequently, ΔFosB is the most significant factor involved in both amphetamine addiction and amphetamine-induced sexual addictions, which are compulsive sexual behaviors that result from excessive sexual activity and amphetamine use. These sexual addictions are associated with a dopamine dysregulation syndrome which occurs in some patients taking dopaminergic drugs. The effects of amphetamine on gene regulation are both dose- and route-dependent. Most of the research on gene regulation and addiction is based upon animal studies with intravenous amphetamine administration at very high doses. The few studies that have used equivalent (weight-adjusted) human therapeutic doses and oral administration show that these changes, if they occur, are relatively minor. This suggests that medical use of amphetamine does not significantly affect gene regulation.
Amphetamine	Pharmacological treatments	Pharmacological treatments there is no effective pharmacotherapy for amphetamine addiction. Reviews from 2015 and 2016 indicated that TAAR1-selective agonists have significant therapeutic potential as a treatment for psychostimulant addictions; however, the only compounds which are known to function as TAAR1-selective agonists are experimental drugs. Amphetamine addiction is largely mediated through increased activation of dopamine receptors and NMDA receptors in the nucleus accumbens; magnesium ions inhibit NMDA receptors by blocking the receptor calcium channel. One review suggested that, based upon animal testing, pathological (addiction-inducing) psychostimulant use significantly reduces the level of intracellular magnesium throughout the brain. Supplemental magnesium treatment has been shown to reduce amphetamine self-administration (i.e., doses given to oneself) in humans, but it is not an effective monotherapy for amphetamine addiction. A systematic review and meta-analysis from 2019 assessed the efficacy of 17 different pharmacotherapies used in randomized controlled trials (RCTs) for amphetamine and methamphetamine addiction; it found only low-strength evidence that methylphenidate might reduce amphetamine or methamphetamine self-administration. There was low- to moderate-strength evidence of no benefit for most of the other medications used in RCTs, which included antidepressants (bupropion, mirtazapine, sertraline), antipsychotics (aripiprazole), anticonvulsants (topiramate, baclofen, gabapentin), naltrexone, varenicline, citicoline, ondansetron, prometa, riluzole, atomoxetine, dextroamphetamine, and modafinil.
Amphetamine	Behavioral treatments	Behavioral treatments A 2018 systematic review and network meta-analysis of 50 trials involving 12 different psychosocial interventions for amphetamine, methamphetamine, or cocaine addiction found that combination therapy with both contingency management and community reinforcement approach had the highest efficacy (i.e., abstinence rate) and acceptability (i.e., lowest dropout rate). Other treatment modalities examined in the analysis included monotherapy with contingency management or community reinforcement approach, cognitive behavioral therapy, 12-step programs, non-contingent reward-based therapies, psychodynamic therapy, and other combination therapies involving these. Additionally, research on the neurobiological effects of physical exercise suggests that daily aerobic exercise, especially endurance exercise (e.g., marathon running), prevents the development of drug addiction and is an effective adjunct therapy (i.e., a supplemental treatment) for amphetamine addiction. Exercise leads to better treatment outcomes when used as an adjunct treatment, particularly for psychostimulant addictions. In particular, aerobic exercise decreases psychostimulant self-administration, reduces the reinstatement (i.e., relapse) of drug-seeking, and induces increased dopamine receptor D2 (DRD2) density in the striatum. This is the opposite of pathological stimulant use, which induces decreased striatal DRD2 density. One review noted that exercise may also prevent the development of a drug addiction by altering ΔFosB or immunoreactivity in the striatum or other parts of the reward system.
Amphetamine	Dependence and withdrawal	Dependence and withdrawal Drug tolerance develops rapidly in amphetamine abuse (i.e., recreational amphetamine use), so periods of extended abuse require increasingly larger doses of the drug in order to achieve the same effect. According to a Cochrane review on withdrawal in individuals who compulsively use amphetamine and methamphetamine, "when chronic heavy users abruptly discontinue amphetamine use, many report a time-limited withdrawal syndrome that occurs within 24 hours of their last dose." This review noted that withdrawal symptoms in chronic, high-dose users are frequent, occurring in roughly 88% of cases, and persist for weeks with a marked "crash" phase occurring during the first week. Amphetamine withdrawal symptoms can include anxiety, drug craving, depressed mood, fatigue, increased appetite, increased movement or decreased movement, lack of motivation, sleeplessness or sleepiness, and lucid dreams. The review indicated that the severity of withdrawal symptoms is positively correlated with the age of the individual and the extent of their dependence. Mild withdrawal symptoms from the discontinuation of amphetamine treatment at therapeutic doses can be avoided by tapering the dose.
Amphetamine	Overdose	Overdose An amphetamine overdose can lead to many different symptoms, but is rarely fatal with appropriate care. The severity of overdose symptoms increases with dosage and decreases with drug tolerance to amphetamine. Tolerant individuals have been known to take as much as 5 grams of amphetamine in a day, which is roughly 100 times the maximum daily therapeutic dose. Symptoms of a moderate and extremely large overdose are listed below; fatal amphetamine poisoning usually also involves convulsions and coma. In 2013, overdose on amphetamine, methamphetamine, and other compounds implicated in an "amphetamine use disorder" resulted in an estimated 3,788 deaths worldwide ( deaths, 95% confidence). + Overdose symptoms by system System Minor or moderate overdose Severe overdose Cardiovascular Abnormal heartbeat High or low blood pressure Cardiogenic shock (heart not pumping enough blood) Cerebral hemorrhage (bleeding in the brain) Circulatory collapse (partial or complete failure of the circulatory system) Central nervoussystem Confusion Abnormally fast reflexes Severe agitation Tremor (involuntary muscle twitching) Acute amphetamine psychosis (e.g., delusions and paranoia) Compulsive and repetitive movement Serotonin syndrome (excessive serotonergic nerve activity) Sympathomimetic toxidrome (excessive adrenergic nerve activity) Musculoskeletal Muscle pain Rhabdomyolysis (rapid muscle breakdown) Respiratory Rapid breathing Pulmonary edema (fluid accumulation in the lungs) Pulmonary hypertension (high blood pressure in the arteries of the lung) Respiratory alkalosis (reduced blood CO2) Urinary Painful urination Urinary retention (inability to urinate) No urine production Kidney failure Other Elevated body temperature Mydriasis (dilated pupils) Elevated or low blood potassium Hyperpyrexia (extremely elevated core body temperature) Metabolic acidosis (excessively acidic bodily fluids)
Amphetamine	Toxicity	Toxicity In rodents and primates, sufficiently high doses of amphetamine cause dopaminergic neurotoxicity, or damage to dopamine neurons, which is characterized by dopamine terminal degeneration and reduced transporter and receptor function. There is no evidence that amphetamine is directly neurotoxic in humans. However, large doses of amphetamine may indirectly cause dopaminergic neurotoxicity as a result of hyperpyrexia, the excessive formation of reactive oxygen species, and increased autoxidation of dopamine. Animal models of neurotoxicity from high-dose amphetamine exposure indicate that the occurrence of hyperpyrexia (i.e., core body temperature ≥ 40 °C) is necessary for the development of amphetamine-induced neurotoxicity. Prolonged elevations of brain temperature above 40 °C likely promote the development of amphetamine-induced neurotoxicity in laboratory animals by facilitating the production of reactive oxygen species, disrupting cellular protein function, and transiently increasing blood–brain barrier permeability.
Amphetamine	Psychosis	Psychosis An amphetamine overdose can result in a stimulant psychosis that may involve a variety of symptoms, such as delusions and paranoia. A Cochrane review on treatment for amphetamine, dextroamphetamine, and methamphetamine psychosis states that about of users fail to recover completely. According to the same review, there is at least one trial that shows antipsychotic medications effectively resolve the symptoms of acute amphetamine psychosis. Psychosis rarely arises from therapeutic use.
Amphetamine	Drug interactions{{anchor	Drug interactions Many types of substances are known to interact with amphetamine, resulting in altered drug action or metabolism of amphetamine, the interacting substance, or both. Inhibitors of enzymes that metabolize amphetamine (e.g., CYP2D6 and FMO3) will prolong its elimination half-life, meaning that its effects will last longer. Amphetamine also interacts with , particularly monoamine oxidase A inhibitors, since both MAOIs and amphetamine increase plasma catecholamines (i.e., norepinephrine and dopamine); therefore, concurrent use of both is dangerous. Amphetamine modulates the activity of most psychoactive drugs. In particular, amphetamine may decrease the effects of sedatives and depressants and increase the effects of stimulants and antidepressants. Amphetamine may also decrease the effects of antihypertensives and antipsychotics due to its effects on blood pressure and dopamine respectively. Zinc supplementation may reduce the minimum effective dose of amphetamine when it is used for the treatment of ADHD. Norepinephrine reuptake inhibitors (NRIs) like atomoxetine prevent norepinephrine release induced by amphetamines and have been found to reduce the stimulant, euphoriant, and sympathomimetic effects of dextroamphetamine in humans. In general, there is no significant interaction when consuming amphetamine with food, but the pH of gastrointestinal content and urine affects the absorption and excretion of amphetamine, respectively. Acidic substances reduce the absorption of amphetamine and increase urinary excretion, and alkaline substances do the opposite. Due to the effect pH has on absorption, amphetamine also interacts with gastric acid reducers such as proton pump inhibitors and H2 antihistamines, which increase gastrointestinal pH (i.e., make it less acidic).
Amphetamine	Pharmacology	Pharmacology
Amphetamine	Pharmacodynamics	Pharmacodynamics Amphetamine exerts its behavioral effects by altering the use of monoamines as neuronal signals in the brain, primarily in catecholamine neurons in the reward and executive function pathways of the brain. The concentrations of the main neurotransmitters involved in reward circuitry and executive functioning, dopamine and norepinephrine, increase dramatically in a dose-dependent manner by amphetamine because of its effects on monoamine transporters. The reinforcing and motivational salience-promoting effects of amphetamine are due mostly to enhanced dopaminergic activity in the mesolimbic pathway. The euphoric and locomotor-stimulating effects of amphetamine are dependent upon the magnitude and speed by which it increases synaptic dopamine and norepinephrine concentrations in the striatum. Amphetamine potentiates monoaminergic neurotransmission by entering the presynaptic neuron both as a substrate for monoamine transporters (DAT, NET, and, SERT) and by passive diffusion across the neuronal membrane. Transporter-mediated uptake competes with reabsorption of endogenous neurotransmitters from the synaptic cleft and produces competitive reuptake inhibition as a consequence. Once inside the neuronal cytosol, amphetamine initiates intracellular signaling cascades that activate protein kinase C (PKC), leading to phosphorylation of DAT, NET, and SERT. PKC-dependent phosphorylation of monoamine transporters can either reverse their direction to induce efflux of cytosolic neurotransmitters into the synaptic cleft, or trigger the withdrawal of transporters into the presynaptic neuron (internalization), thereby ceasing their reuptake function in a non-competitive manner. Amphetamine also causes a rise in intracellular calcium, an effect associated with transporter phosphorylation through a Ca²⁺/calmodulin-dependent protein kinase II alpha (CaMKIIα) signaling cascade. Unlike PKC, CaMKIIα-mediated transporter phosphorylation appears to reverse the direction of DAT and NET without triggering internalization. Amphetamine has been identified as a full agonist of trace amine-associated receptor 1 (TAAR1), a and G protein-coupled receptor (GPCR) discovered in 2001, which is important for regulation of brain monoamines. Several reviews have linked amphetamine’s agonism at TAAR1 to modulation of monoamine transporter function and subsequent neurotransmitter efflux and reuptake inhibition at monoaminergic synapses. Activation of increases production via adenylyl cyclase activation, which triggers protein kinase A (PKA)- and PKC-mediated transporter phosphorylation. Monoamine autoreceptors (e.g., D2 short, presynaptic α2, and presynaptic 5-HT1A) have the opposite effect of TAAR1, and together these receptors provide a regulatory system for monoamines. Notably, amphetamine and trace amines possess high binding affinities for TAAR1, but not for monoamine autoreceptors. Although TAAR1 is implicated in amphetamine-induced transporter phosphorylation, the magnitude of TAAR1-mediated monoamine release in humans remains unclear. Findings from studies using TAAR1 gene knockout models suggest that, despite facilitating monoamine release through reverse transport, TAAR1 activation may paradoxically attenuate amphetamine’s psychostimulant effects in part by opening G protein-coupled inwardly rectifying potassium channels, an action that reduces neuronal firing. Amphetamine is also a substrate for the vesicular monoamine transporters VMAT1 and VMAT2. Under normal conditions, VMAT2 transports cytosolic monoamines into synaptic vesicles for storage and later exocytotic release. When amphetamine accumulates in the presynaptic terminal, it collapses the vesicular pH gradient and releases vesicular monoamines into the neuronal cytosol. These displaced monoamines expand the cytosolic pool available for reverse transport, thereby increasing the capacity for monoamine efflux beyond that achieved by amphetamine-mediated transporter phosphorylation alone. Although VMAT2 is recognized as a major target in amphetamine-induced monoamine release at higher doses, some reviews have challenged its relevance at therapeutic doses. In addition to membrane and vesicular monoamine transporters, amphetamine also inhibits SLC1A1, SLC22A3, and SLC22A5. SLC1A1 is excitatory amino acid transporter 3 (EAAT3), a glutamate transporter located in neurons, SLC22A3 is an extraneuronal monoamine transporter that is present in astrocytes, and SLC22A5 is a high-affinity carnitine transporter. Amphetamine is known to strongly induce cocaine- and amphetamine-regulated transcript (CART) gene expression, a neuropeptide involved in feeding behavior, stress, and reward, which induces observable increases in neuronal development and survival in vitro. The CART receptor has yet to be identified, but there is significant evidence that CART binds to a unique . Amphetamine also inhibits monoamine oxidases at very high doses, resulting in less monoamine and trace amine metabolism and consequently higher concentrations of synaptic monoamines. In humans, the only post-synaptic receptor at which amphetamine is known to bind is the receptor, where it acts as an agonist with low micromolar affinity. The full profile of amphetamine's short-term drug effects in humans is mostly derived through increased cellular communication or neurotransmission of dopamine, serotonin, norepinephrine, epinephrine, histamine, CART peptides, endogenous opioids, adrenocorticotropic hormone, corticosteroids, and glutamate, which it affects through interactions with , , , , , , and possibly other biological targets. Amphetamine also activates seven human carbonic anhydrase enzymes, several of which are expressed in the human brain. Dextroamphetamine displays higher binding affinity for DAT than levoamphetamine, whereas both enantiomers share comparable affinity at NET; Consequently, dextroamphetamine produces greater stimulation than levoamphetamine, roughly three to four times more, but levoamphetamine has slightly stronger cardiovascular and peripheral effects. Dextroamphetamine is also a more potent agonist of than levoamphetamine.
Amphetamine	Dopamine	Dopamine In certain brain regions, amphetamine increases the concentration of dopamine in the synaptic cleft by modulating through several overlapping processes. Amphetamine can enter the presynaptic neuron either through or by diffusing across the neuronal membrane directly. As a consequence of DAT uptake, amphetamine produces competitive reuptake inhibition at the transporter. Upon entering the presynaptic neuron, amphetamine provokes the release of Ca²⁺ from endoplasmic reticulum stores, an effect that raises intracellular calcium to levels sufficient for downstream kinase-dependent signalling. Subsequently, amphetamine initiates kinase-dependent signaling cascades that activate both protein kinase A (PKA) and protein kinase C (PKC). Phosphorylation of DAT by either kinase induces transporter internalization ( reuptake inhibition), but phosphorylation alone induces the reversal of dopamine transport through DAT (i.e., dopamine efflux). is a biomolecular target of amphetamine that can trigger the activation of PKA- and PKC-dependent pathways. TAAR1 agonism also activates Ras homolog A (RhoA) and its downstream effector, Rho-associated coiled-coil kinase (ROCK), which results in transient internalization of DAT and EAAT3; as intracellular accumulates, PKA is activated and inhibits RhoA activity, thereby terminating ROCK-mediated transporter internalization. Importantly, TAAR1 has been demonstrated to also produce inhibitory effects on dopamine release that may attenuate amphetamine's psychostimulant effects. Through direct activation of G protein-coupled inwardly-rectifying potassium channels, reduces the firing rate of dopamine neurons, preventing a hyper-dopaminergic state. Amphetamine's effect on intracellular calcium is associated with DAT phosphorylation through Ca²⁺/calmodulin-dependent protein kinase II alpha (CAMKIIα), in turn producing dopamine efflux. Notably, because conventional PKC isoforms can be activated by calcium ions, the rise in intracellular calcium can also promote PKC activation and subsequent DAT phosphorylation independent of TAAR1. + Effects of amphetamine on membrane transport proteins in dopamine neurons Trigger mechanism Secondary effectorprotein kinase Phosphorylatedtransporter Effect on transporter function Effect on neurotransmission Sources Ca²⁺ release† Reverse transport of dopamine Dopamine efflux into synaptic cleft activation ROCK‡ DAT Transporter internalization Dopamine reuptake inhibition TAAR1 activation ROCK‡ Transporter internalization Glutamate reuptake inhibition TAAR1 activation DAT Transporter internalization Dopamine reuptake inhibition TAAR1 activation DAT Reverse transport of dopamineTransporter internalization Dopamine efflux into synaptic cleftDopamine reuptake inhibition Ca²⁺ release†DATReverse transport of dopamineTransporter internalizationDopamine efflux into synaptic cleftDopamine reuptake inhibition † Amphetamine interacts with an unidentified intracellular target to trigger release of endoplasmic reticulum Ca²⁺ stores, thereby supplying the cytosolic Ca²⁺ required for protein kinase activation. ‡ ROCK-mediated transporter internalization is transient due to the inactivation of RhoA (which activates ROCK) by PKA. Amphetamine is also a substrate for the presynaptic vesicular monoamine transporter, . Following amphetamine uptake at VMAT2, amphetamine induces the collapse of the vesicular pH gradient, which results in a dose-dependent release of dopamine molecules from synaptic vesicles into the cytosol via dopamine efflux through VMAT2. Subsequently, the cytosolic dopamine molecules are released from the presynaptic neuron into the synaptic cleft via reverse transport at .
Amphetamine	Norepinephrine	Norepinephrine Similar to dopamine, amphetamine dose-dependently increases the level of synaptic norepinephrine, the direct precursor of epinephrine. Amphetamine is believed to affect norepinephrine analogously to dopamine. In other words, amphetamine induces competitive reuptake inhibition, non-competitive reuptake inhibition and efflux at phosphorylated NET via PKC activation, CAMKIIα-mediated NET efflux without internalization, and norepinephrine release from .
Amphetamine	Serotonin	Serotonin Amphetamine exerts analogous, yet less pronounced, effects on serotonin as on dopamine and norepinephrine. Amphetamine affects serotonin via and is thought to phosphorylate via a PKC-dependent signaling cascade. Like dopamine, amphetamine has low, micromolar affinity at the human 5-HT1A receptor.
Amphetamine	Other neurotransmitters, peptides, hormones, and enzymes	Other neurotransmitters, peptides, hormones, and enzymes + Human carbonic anhydraseactivation potency Enzyme KA () Sources hCA4 94 hCA5A 810 hCA5B 2560 hCA7 910 hCA12 640 hCA13 24100 hCA14 9150 Acute amphetamine administration in humans increases endogenous opioid release in several brain structures in the reward system. Extracellular levels of glutamate, the primary excitatory neurotransmitter in the brain, have been shown to increase in the striatum following exposure to amphetamine. This increase in extracellular glutamate presumably occurs via the amphetamine-induced internalization of EAAT3, a glutamate reuptake transporter, in dopamine neurons. This internalization is mediated by RhoA activation and its downstream effector ROCK. Amphetamine also induces the selective release of histamine from mast cells and efflux from histaminergic neurons through . Acute amphetamine administration can also increase adrenocorticotropic hormone and corticosteroid levels in blood plasma by stimulating the hypothalamic–pituitary–adrenal axis. In December 2017, the first study assessing the interaction between amphetamine and human carbonic anhydrase enzymes was published; of the eleven carbonic anhydrase enzymes it examined, it found that amphetamine potently activates seven, four of which are highly expressed in the human brain, with low nanomolar through low micromolar activating effects. Based upon preclinical research, cerebral carbonic anhydrase activation has cognition-enhancing effects; but, based upon the clinical use of carbonic anhydrase inhibitors, carbonic anhydrase activation in other tissues may be associated with adverse effects, such as ocular activation exacerbating glaucoma.
Amphetamine	Pharmacokinetics	Pharmacokinetics The oral bioavailability of amphetamine varies with gastrointestinal pH; it is well absorbed from the gut, and bioavailability is typically 90%. Amphetamine is a weak base with a pKa of 9.9; consequently, when the pH is basic, more of the drug is in its lipid soluble free base form, and more is absorbed through the lipid-rich cell membranes of the gut epithelium. Conversely, an acidic pH means the drug is predominantly in a water-soluble cationic (salt) form, and less is absorbed. Approximately of amphetamine circulating in the bloodstream is bound to plasma proteins. Following absorption, amphetamine readily distributes into most tissues in the body, with high concentrations occurring in cerebrospinal fluid and brain tissue. The half-lives of amphetamine enantiomers differ and vary with urine pH. At normal urine pH, the half-lives of dextroamphetamine and levoamphetamine are hours and hours, respectively. Highly acidic urine will reduce the enantiomer half-lives to 7 hours; highly alkaline urine will increase the half-lives up to 34 hours. The immediate-release and extended release variants of salts of both isomers reach peak plasma concentrations at 3 hours and 7 hours post-dose respectively. Amphetamine is eliminated via the kidneys, with of the drug being excreted unchanged at normal urinary pH. When the urinary pH is basic, amphetamine is in its free base form, so less is excreted. When urine pH is abnormal, the urinary recovery of amphetamine may range from a low of 1% to a high of 75%, depending mostly upon whether urine is too basic or acidic, respectively. Following oral administration, amphetamine appears in urine within 3 hours. Roughly 90% of ingested amphetamine is eliminated 3 days after the last oral dose. CYP2D6, dopamine β-hydroxylase (DBH), flavin-containing monooxygenase 3 (FMO3), butyrate-CoA ligase (XM-ligase), and glycine N-acyltransferase (GLYAT) are the enzymes known to metabolize amphetamine or its metabolites in humans. Amphetamine has a variety of excreted metabolic products, including , , , benzoic acid, hippuric acid, norephedrine, and phenylacetone. Among these metabolites, the active sympathomimetics are , , and norephedrine. The main metabolic pathways involve aromatic para-hydroxylation, aliphatic alpha- and beta-hydroxylation, N-oxidation, N-dealkylation, and deamination. The known metabolic pathways, detectable metabolites, and metabolizing enzymes in humans include the following:
Amphetamine	Pharmacomicrobiomics	Pharmacomicrobiomics The human metagenome (i.e., the genetic composition of an individual and all microorganisms that reside on or within the individual's body) varies considerably between individuals. Since the total number of microbial and viral cells in the human body (over 100 trillion) greatly outnumbers human cells (tens of trillions), there is considerable potential for interactions between drugs and an individual's microbiome, including: drugs altering the composition of the human microbiome, drug metabolism by microbial enzymes modifying the drug's pharmacokinetic profile, and microbial drug metabolism affecting a drug's clinical efficacy and toxicity profile. The field that studies these interactions is known as pharmacomicrobiomics. Similar to most biomolecules and other orally administered xenobiotics (i.e., drugs), amphetamine is predicted to undergo promiscuous metabolism by human gastrointestinal microbiota (primarily bacteria) prior to absorption into the blood stream. The first amphetamine-metabolizing microbial enzyme, tyramine oxidase from a strain of E. coli commonly found in the human gut, was identified in 2019. This enzyme was found to metabolize amphetamine, tyramine, and phenethylamine with roughly the same binding affinity for all three compounds.
Amphetamine	Related endogenous compounds	Related endogenous compounds Amphetamine has a very similar structure and function to the endogenous trace amines, which are naturally occurring neuromodulator molecules produced in the human body and brain. Among this group, the most closely related compounds are phenethylamine, the parent compound of amphetamine, and , a structural isomer of amphetamine (i.e., it has an identical molecular formula). In humans, phenethylamine is produced directly from by the aromatic amino acid decarboxylase (AADC) enzyme, which converts into dopamine as well. In turn, is metabolized from phenethylamine by phenylethanolamine N-methyltransferase, the same enzyme that metabolizes norepinephrine into epinephrine. Like amphetamine, both phenethylamine and regulate monoamine neurotransmission via ; unlike amphetamine, both of these substances are broken down by monoamine oxidase B, and therefore have a shorter half-life than amphetamine.
Amphetamine	Chemistry	Chemistry Amphetamine is a methyl homolog of the mammalian neurotransmitter phenethylamine with the chemical formula . The carbon atom adjacent to the primary amine is a stereogenic center, and amphetamine is composed of a racemic 1:1 mixture of two enantiomers. This racemic mixture can be separated into its optical isomers: levoamphetamine and dextroamphetamine. At room temperature, the pure free base of amphetamine is a mobile, colorless, and volatile liquid with a characteristically strong amine odor, and acrid, burning taste. Frequently prepared solid salts of amphetamine include amphetamine adipate, aspartate, hydrochloride, phosphate, saccharate, sulfate, and tannate. Dextroamphetamine sulfate is the most common enantiopure salt. Amphetamine is also the parent compound of its own structural class, which includes a number of psychoactive derivatives. In organic chemistry, amphetamine is an excellent chiral ligand for the stereoselective synthesis of .
Amphetamine	Substituted derivatives	Substituted derivatives The substituted derivatives of amphetamine, or "substituted amphetamines", are a broad range of chemicals that contain amphetamine as a "backbone"; specifically, this chemical class includes derivative compounds that are formed by replacing one or more hydrogen atoms in the amphetamine core structure with substituents. The class includes amphetamine itself, stimulants like methamphetamine, serotonergic empathogens like MDMA, and decongestants like ephedrine, among other subgroups.
Amphetamine	Synthesis	Synthesis Since the first preparation was reported in 1887, numerous synthetic routes to amphetamine have been developed. The most common route of both legal and illicit amphetamine synthesis employs a non-metal reduction known as the Leuckart reaction (method 1). In the first step, a reaction between phenylacetone and formamide, either using additional formic acid or formamide itself as a reducing agent, yields . This intermediate is then hydrolyzed using hydrochloric acid, and subsequently basified, extracted with organic solvent, concentrated, and distilled to yield the free base. The free base is then dissolved in an organic solvent, sulfuric acid added, and amphetamine precipitates out as the sulfate salt. A number of chiral resolutions have been developed to separate the two enantiomers of amphetamine. For example, racemic amphetamine can be treated with to form a diastereoisomeric salt which is fractionally crystallized to yield dextroamphetamine. Chiral resolution remains the most economical method for obtaining optically pure amphetamine on a large scale. In addition, several enantioselective syntheses of amphetamine have been developed. In one example, optically pure is condensed with phenylacetone to yield a chiral Schiff base. In the key step, this intermediate is reduced by catalytic hydrogenation with a transfer of chirality to the carbon atom alpha to the amino group. Cleavage of the benzylic amine bond by hydrogenation yields optically pure dextroamphetamine. A large number of alternative synthetic routes to amphetamine have been developed based on classic organic reactions. One example is the Friedel–Crafts alkylation of benzene by allyl chloride to yield beta chloropropylbenzene which is then reacted with ammonia to produce racemic amphetamine (method 2). Another example employs the Ritter reaction (method 3). In this route, allylbenzene is reacted acetonitrile in sulfuric acid to yield an organosulfate which in turn is treated with sodium hydroxide to give amphetamine via an acetamide intermediate. A third route starts with which through a double alkylation with methyl iodide followed by benzyl chloride can be converted into acid. This synthetic intermediate can be transformed into amphetamine using either a Hofmann or Curtius rearrangement (method 4). A significant number of amphetamine syntheses feature a reduction of a nitro, imine, oxime, or other nitrogen-containing functional groups. In one such example, a Knoevenagel condensation of benzaldehyde with nitroethane yields . The double bond and nitro group of this intermediate is reduced using either catalytic hydrogenation or by treatment with lithium aluminium hydride (method 5). Another method is the reaction of phenylacetone with ammonia, producing an imine intermediate that is reduced to the primary amine using hydrogen over a palladium catalyst or lithium aluminum hydride (method 6). +Amphetamine synthetic routes
Amphetamine	Detection in body fluids	Detection in body fluids Amphetamine is frequently measured in urine or blood as part of a drug test for sports, employment, poisoning diagnostics, and forensics. Techniques such as immunoassay, which is the most common form of amphetamine test, may cross-react with a number of sympathomimetic drugs. Chromatographic methods specific for amphetamine are employed to prevent false positive results. Chiral separation techniques may be employed to help distinguish the source of the drug, whether prescription amphetamine, prescription amphetamine prodrugs, (e.g., selegiline), over-the-counter drug products that contain levomethamphetamine, or illicitly obtained substituted amphetamines. Several prescription drugs produce amphetamine as a metabolite, including benzphetamine, clobenzorex, famprofazone, fenproporex, lisdexamfetamine, mesocarb, methamphetamine, prenylamine, and selegiline, among others. These compounds may produce positive results for amphetamine on drug tests. Amphetamine is generally only detectable by a standard drug test for approximately 24 hours, although a high dose may be detectable for days. For the assays, a study noted that an enzyme multiplied immunoassay technique (EMIT) assay for amphetamine and methamphetamine may produce more false positives than liquid chromatography–tandem mass spectrometry. Gas chromatography–mass spectrometry (GC–MS) of amphetamine and methamphetamine with the derivatizing agent chloride allows for the detection of methamphetamine in urine. GC–MS of amphetamine and methamphetamine with the chiral derivatizing agent Mosher's acid chloride allows for the detection of both dextroamphetamine and dextromethamphetamine in urine. Hence, the latter method may be used on samples that test positive using other methods to help distinguish between the various sources of the drug.
Amphetamine	History, society, and culture	History, society, and culture thumb\|Tickets and benzedrine tubes linked to Jack Kerouac's life Amphetamine was first synthesized in 1887 in Germany by Romanian chemist Lazăr Edeleanu who named it phenylisopropylamine; its stimulant effects remained unknown until 1927, when it was independently resynthesized by Gordon Alles and reported to have sympathomimetic properties. Amphetamine had no medical use until late 1933, when Smith, Kline and French began selling it as an inhaler under the brand name Benzedrine as a decongestant. Benzedrine sulfate was introduced 3 years later and was used to treat a wide variety of medical conditions, including narcolepsy, obesity, low blood pressure, low libido, and chronic pain, among others. During World War II, amphetamine and methamphetamine were used extensively by both the Allied and Axis forces for their stimulant and performance-enhancing effects. As the addictive properties of the drug became known, governments began to place strict controls on the sale of amphetamine. For example, during the early 1970s in the United States, amphetamine became a schedule II controlled substance under the Controlled Substances Act. In spite of strict government controls, amphetamine has been used legally or illicitly by people from a variety of backgrounds, including authors, musicians, mathematicians, and athletes. Amphetamine is illegally synthesized in clandestine labs and sold on the black market, primarily in European countries. Among European Union (EU) member states 11.9 million adults of ages have used amphetamine or methamphetamine at least once in their lives and 1.7 million have used either in the last year. During 2012, approximately 5.9 metric tons of illicit amphetamine were seized within EU member states; the "street price" of illicit amphetamine within the EU ranged from per gram during the same period. Outside Europe, the illicit market for amphetamine is much smaller than the market for methamphetamine and MDMA.
Amphetamine	Legal status	Legal status As a result of the United Nations 1971 Convention on Psychotropic Substances, amphetamine became a schedule II controlled substance, as defined in the treaty, in all 183 state parties. Consequently, it is heavily regulated in most countries. Some countries, such as South Korea and Japan, have banned substituted amphetamines even for medical use. In other nations, such as Brazil (class A3), Canada (schedule I drug), the Netherlands (List I drug), the United States (schedule II drug), Australia (schedule 8), Thailand (category 1 narcotic), and United Kingdom (class B drug), amphetamine is in a restrictive national drug schedule that allows for its use as a medical treatment.
Amphetamine	Notes	Notes Image legend
Amphetamine	Reference notes	Reference notes
Amphetamine	References	References
Amphetamine	External links	External links – Dextroamphetamine – Levoamphetamine Comparative Toxicogenomics Database entry: Amphetamine Comparative Toxicogenomics Database entry: CARTPT Category:Products introduced in 1887 Category:5-HT1A agonists Category:Anorectics Category:Aphrodisiacs Category:Attention deficit hyperactivity disorder management Category:Carbonic anhydrase activators Category:Drugs acting on the cardiovascular system Category:Drugs acting on the nervous system Category:Drugs in sport Category:Ergogenic aids Category:Euphoriants Category:Excitatory amino acid reuptake inhibitors Category:German inventions Category:Human drug metabolites Category:Monoaminergic activity enhancers Category:Narcolepsy Category:Nootropics Category:Norepinephrine-dopamine releasing agents Category:Stimulants Category:Substituted amphetamines Category:TAAR1 agonists Category:VMAT inhibitors Category:World Anti-Doping Agency prohibited substances
Amphetamine	Table of Content	Short description, Uses, Medical, Pharmaceutical products, Indications, ADHD, Binge eating disorder, Narcolepsy, Enhancing performance, Cognitive performance, Physical performance, Recreational, Contraindications, Adverse effects, Physical, Psychological, Reinforcement disorders, Addiction, Biomolecular mechanisms, Pharmacological treatments, Behavioral treatments, Dependence and withdrawal, Overdose, Toxicity, Psychosis, Drug interactions{{anchor, Pharmacology, Pharmacodynamics, Dopamine, Norepinephrine, Serotonin, Other neurotransmitters, peptides, hormones, and enzymes, Pharmacokinetics, Pharmacomicrobiomics, Related endogenous compounds, Chemistry, Substituted derivatives, Synthesis, Detection in body fluids, History, society, and culture, Legal status, Notes, Reference notes, References, External links
Asynchronous communication	Short description	In telecommunications, asynchronous communication is transmission of data, generally without the use of an external clock signal, where data can be transmitted intermittently rather than in a steady stream. Any timing required to recover data from the communication symbols is encoded within the symbols. The most significant aspect of asynchronous communications is that data is not transmitted at regular intervals, thus making possible variable bit rate, and that the transmitter and receiver clock generators do not have to be exactly synchronized all the time. In asynchronous transmission, data is sent one byte at a time and each byte is preceded by start and stop bits.
Asynchronous communication	Physical layer	Physical layer In asynchronous serial communication in the physical protocol layer, the data blocks are code words of a certain word length, for example octets (bytes) or ASCII characters, delimited by start bits and stop bits. A variable length space can be inserted between the code words. No bit synchronization signal is required. This is sometimes called character oriented communication. Examples include MNP2 and modems older than V.2.
Asynchronous communication	Data link layer and higher	Data link layer and higher Asynchronous communication at the data link layer or higher protocol layers is known as statistical multiplexing, for example Asynchronous Transfer Mode (ATM). In this case, the asynchronously transferred blocks are called data packets, for example ATM cells. The opposite is circuit switched communication, which provides constant bit rate, for example ISDN and SONET/SDH. The packets may be encapsulated in a data frame, with a frame synchronization bit sequence indicating the start of the frame, and sometimes also a bit synchronization bit sequence, typically 01010101, for identification of the bit transition times. Note that at the physical layer, this is considered as synchronous serial communication. Examples of packet mode data link protocols that can be/are transferred using synchronous serial communication are the HDLC, Ethernet, PPP and USB protocols.
Asynchronous communication	Application layer	Application layer An asynchronous communication service or application does not require a constant bit rate. Examples are file transfer, email and the World Wide Web. An example of the opposite, a synchronous communication service, is realtime streaming media, for example IP telephony, IPTV and video conferencing.
Asynchronous communication	Electronically mediated communication	Electronically mediated communication Electronically mediated communication often happens asynchronously in that the participants do not communicate concurrently. Examples include email and bulletin-board systems, where participants send or post messages at different times than they read them. The term "asynchronous communication" acquired currency in the field of online learning, where teachers and students often exchange information asynchronously instead of synchronously (that is, simultaneously), as they would in face-to-face or in telephone conversations.
Asynchronous communication	See also	See also Synchronization in telecommunications Asynchronous serial communication Asynchronous system Asynchronous circuit Anisochronous Baud rate Plesiochronous Plesiochronous Digital Hierarchy (PDH)
Asynchronous communication	References	References Category:Synchronization Category:Telecommunications techniques
Asynchronous communication	Table of Content	Short description, Physical layer, Data link layer and higher, Application layer, Electronically mediated communication, See also, References
Artillery	short description	thumb\|upright=1.35\|US artillerymen test fire an M777 Lightweight 155-millimeter Howitzer at Marine Corps Air Ground Combat Center Twentynine Palms (2005) Artillery consists of ranged weapons that launch munitions far beyond the range and power of infantry firearms. Early artillery development focused on the ability to breach defensive walls and fortifications during sieges, and led to heavy, fairly immobile siege engines. As technology improved, lighter, more mobile field artillery cannons were developed for battlefield use. This development continues today; modern self-propelled artillery vehicles are highly mobile weapons of great versatility generally providing the largest share of an army's total firepower. Originally, the word "artillery" referred to any group of soldiers primarily armed with some form of manufactured weapon or armour. Since the introduction of gunpowder and cannon, "artillery" has largely meant cannon, and in contemporary usage, usually refers to shell-firing guns, howitzers, and mortars (collectively called barrel artillery, cannon artillery or gun artillery) and rocket artillery. In common speech, the word "artillery" is often used to refer to individual devices, along with their accessories and fittings, although these assemblages are more properly called "equipment". However, there is no generally recognized generic term for a gun, howitzer, mortar, and so forth: the United States uses "artillery piece", but most English-speaking armies use "gun" and "mortar". The projectiles fired are typically either "shot" (if solid) or "shell" (if not solid). Historically, variants of solid shot including canister, chain shot and grapeshot were also used. "Shell" is a widely used generic term for a projectile, which is a component of munitions. By association, artillery may also refer to the arm of service that customarily operates such engines. In some armies, the artillery arm has operated field, coastal, anti-aircraft, and anti-tank artillery; in others these have been separate arms, and with some nations coastal has been a naval or marine responsibility. In the 20th century, target acquisition devices (such as radar) and techniques (such as sound ranging and flash spotting) emerged, primarily for artillery. These are usually utilized by one or more of the artillery arms. The widespread adoption of indirect fire in the early 20th century introduced the need for specialist data for field artillery, notably survey and meteorological, and in some armies, provision of these are the responsibility of the artillery arm. The majority of combat deaths in the Napoleonic Wars, World War I, and World War II were caused by artillery. In 1944, Joseph Stalin said in a speech that artillery was "the god of war".
Artillery	Artillery piece	Artillery piece thumb\|right\|French soldiers in the Franco-Prussian War 1870–71 thumb\|British 64 Pounder Rifled Muzzle-Loaded (RML) Gun on a Moncrieff disappearing mount, at Scaur Hill Fort, Bermuda. This is a part of a fixed battery, meant to protect against over-land attack and to serve as coastal artillery. Although not called by that name, siege engines performing the role recognizable as artillery have been employed in warfare since antiquity. The first known catapult was developed in Syracuse in 399 BC. Until the introduction of gunpowder into western warfare, artillery was dependent upon mechanical energy, which not only severely limited the kinetic energy of the projectiles, but also required the construction of very large engines to accumulate sufficient energy. A 1st-century BC Roman catapult launching stones achieved a kinetic energy of 16 kilojoules, compared to a mid-19th-century 12-pounder gun, which fired a round, with a kinetic energy of 240 kilojoules, or a 20th-century US battleship that fired a projectile from its main battery with an energy level surpassing 350 megajoules. From the Middle Ages through most of the modern era, artillery pieces on land were moved by horse-drawn gun carriages. In the contemporary era, artillery pieces and their crew relied on wheeled or tracked vehicles as transportation. These land versions of artillery were dwarfed by railway guns; the largest of these large-calibre guns ever conceived – Project Babylon of the Supergun affair – was theoretically capable of putting a satellite into orbit. Artillery used by naval forces has also changed significantly, with missiles generally replacing guns in surface warfare. Over the course of military history, projectiles were manufactured from a wide variety of materials, into a wide variety of shapes, using many different methods in which to target structural/defensive works and inflict enemy casualties. The engineering applications for ordnance delivery have likewise changed significantly over time, encompassing some of the most complex and advanced technologies in use today. In some armies, the weapon of artillery is the projectile, not the equipment that fires it. The process of delivering fire onto the target is called gunnery. The actions involved in operating an artillery piece are collectively called "serving the gun" by the "detachment" or gun crew, constituting either direct or indirect artillery fire. The manner in which gunnery crews (or formations) are employed is called artillery support. At different periods in history, this may refer to weapons designed to be fired from ground-, sea-, and even air-based weapons platforms.
Artillery	Crew	Crew Some armed forces use the term "gunners" for the soldiers and sailors with the primary function of using artillery. thumb\|7-person gun crew firing a US M777 Light Towed Howitzer, War in Afghanistan, 2009 The gunners and their guns are usually grouped in teams called either "crews" or "detachments". Several such crews and teams with other functions are combined into a unit of artillery, usually called a battery, although sometimes called a company. In gun detachments, each role is numbered, starting with "1" the Detachment Commander, and the highest number being the Coverer, the second-in-command. "Gunner" is also the lowest rank, and junior non-commissioned officers are "Bombardiers" in some artillery arms. Batteries are roughly equivalent to a company in the infantry, and are combined into larger military organizations for administrative and operational purposes, either battalions or regiments, depending on the army. These may be grouped into brigades; the Russian army also groups some brigades into artillery divisions, and the People's Liberation Army has artillery corps. The term "artillery" also designates a combat arm of most military services when used organizationally to describe units and formations of the national armed forces that operate the weapons.
Artillery	Tactics	Tactics thumb\|Artillery illuminating ammunition used in a shooting exercise on Simplon Pass, Switzerland. The illuminated mountain is Mount Fletschhorn, 9 km from the photographer's position. During military operations, field artillery has the role of providing support to other arms in combat or of attacking targets, particularly in-depth. Broadly, these effects fall into two categories, aiming either to suppress or neutralize the enemy, or to cause casualties, damage, and destruction. This is mostly achieved by delivering high-explosive munitions to suppress, or inflict casualties on the enemy from casing fragments and other debris and from blast, or by destroying enemy positions, equipment, and vehicles. Non-lethal munitions, notably smoke, can also suppress or neutralize the enemy by obscuring their view. Fire may be directed by an artillery observer or another observer, including crewed and uncrewed aircraft, or called onto map coordinates. Military doctrine has had a significant influence on the core engineering design considerations of artillery ordnance through its history, in seeking to achieve a balance between the delivered volume of fire with ordnance mobility. However, during the modern period, the consideration of protecting the gunners also arose due to the late-19th-century introduction of the new generation of infantry weapons using conoidal bullet, better known as the Minié ball, with a range almost as long as that of field artillery. The gunners' increasing proximity to and participation in direct combat against other combat arms and attacks by aircraft made the introduction of a gun shield necessary. The problems of how to employ a fixed or horse-towed gun in mobile warfare necessitated the development of new methods of transporting the artillery into combat. Two distinct forms of artillery were developed: the towed gun, used primarily to attack or defend a fixed-line; and the self-propelled gun, intended to accompany a mobile force and to provide continuous fire support and/or suppression. These influences have guided the development of artillery ordnance, systems, organizations, and operations until the present, with artillery systems capable of providing support at ranges from as little as 100 m to the intercontinental ranges of ballistic missiles. The only combat in which artillery is unable to take part is close-quarters combat, with the possible exception of artillery reconnaissance teams.
Artillery	Etymology	Etymology The word as used in the current context originated in the Middle Ages. One suggestion is that it comes from French atelier, meaning the place where manual work is done. Another suggestion is that it originates from the 13th century and the Old French artillier, designating craftsmen and manufacturers of all materials and warfare equipments (spears, swords, armor, war machines); and, for the next 250 years, the sense of the word "artillery" covered all forms of military weapons. Hence, the naming of the Honourable Artillery Company, which was essentially an infantry unit until the 19th century. Another suggestion is that it comes from the Italian arte de tirare (art of shooting), coined by one of the first theorists on the use of artillery, Niccolò Tartaglia. The term was used by Girolamo Ruscelli (died 1566) in his Precepts of Modern Militia published posthumously in 1572.