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Great Depression in the United Kingdom

The Great Depression in the United Kingdom also known as the Great Slump, was a period of national economic downturn in the 1930s, which had its origins in the global Great Depression. It was Britain's largest and most profound economic depression of the 20th century. The Great Depression originated in the United States in late 1929 and quickly spread to the world. Britain did not experience the boom that had characterized the U.S., Germany, Canada and Australia in the 1920s, so its effect appeared less severe. Britain's world trade fell by half (1929–33), the output of heavy industry fell by a third, employment profits plunged in nearly all sectors. At the depth in summer 1932, registered unemployed numbered 3.5 million, and many more had only part-time employment. However at the same time, from 1929 to 1933 employment dipped only to 94.9% relative to 1929 employment metrics and recovery was seen as early at 1933 (numbers are across the entire country, and unemployment did double over this period relative to 1929 metrics). The positive trend continued across real national income and wages. New houses built increased by 33% from 1929 to 1933, while profits, prices, export volume and value, and imports volume and value dropped. Overall, while all these metrics were concerning to parliament and businessmen along with devastating industrial regions, the common person especially in areas around London did not experience major hardship and even prospered.

Particularly hardest hit by economic problems were the industrial and mining areas in the north of England, Scotland, Northern Ireland and Wales. Unemployment reached 70% in some areas at the start of the 1930s (with more than 3 million out of work nationally) and many families depended entirely on payments from local government known as the dole.

Background
The Great Depression of 1929–32 broke out at a time when the United Kingdom was still far from having recovered from the effects of the First World War. Economist Lee Ohanian showed that economic output fell by 25% between 1918 and 1921 and did not recover until the end of the Great Depression, arguing that the United Kingdom suffered a twenty-year great depression beginning in 1918. Relative to the rest of the world, economic output declined mildly in the UK between 1929 and 1934.

Heavy industries which formed the bedrock of Britain's export trade (such as coal mining, shipbuilding and steel) were heavily concentrated in certain areas of Britain, such as northern England, South Wales, Northern Ireland and central Scotland, while the newer industries were heavily concentrated in southern and central England. British industrial output during the 1920s ran at about 80–100%, and exports at about 80% of their pre-war levels.

Gold standard
From 1921 Britain began a slow economic recovery from the war and the subsequent slump. But in April 1925, the Conservative Chancellor of the Exchequer, Winston Churchill, on advice from the Bank of England, restored the Pound Sterling to the gold standard at its prewar exchange rate of $4.86 US dollars to one pound. This made the pound convertible to its value in gold, but at a level that made British exports more expensive on world markets. The price of gold was over-estimated by 10–14% leading to coal and steel as an export becoming less competitive. The economic recovery immediately slowed. To offset the effects of the high exchange rate, the export industries tried to cut costs by lowering workers' wages.

The industrial areas were in recession during the rest of the 1920s. These industries received little investment or modernization. Throughout the 1920s, unemployment stayed at a steady one million.

Economic crisis and the Labour minority government

In May 1929, a minority Labour government headed by Ramsay MacDonald came to office with Liberal support. This was only the second time a Labour government had been in office (they had briefly been in office in 1924). Few of the government's members had any deep knowledge of economics or experience of running the economy. MacDonald's Labour Party was not radical in economic thinking, and was wedded to the orthodoxy of classical economics with its emphasis on maintaining a balanced budget at any cost.

In October 1929, the Stock Market Crash in New York heralded the worldwide Great Depression. John Maynard Keynes, who had not predicted the slump, said, "'There will be no serious direct consequences in London. We find the look ahead decidedly encouraging."

Doomsayers on the left such as Sidney and Beatrice Webb, J.A. Hobson, and G.D.H. Cole repeated the dire warnings they had been making for years about the imminent death of capitalism, only now far more people paid attention. Starting in 1935 the Left Book Club provided a new warning every month, and built up the credibility of Soviet-style socialism as an alternative.

The ensuing American economic collapse shook the world: World trade contracted, prices fell and governments faced financial crisis as the supply of American credit dried up. Many countries adopted an emergency response to the crisis by erecting trade barriers and tariffs, which worsened the crisis by further hindering global trade. The British Empire tried to hang together by lower tariffs among the members while raising them against the U.S. and others.

The effects on the industrial areas of Britain were immediate and devastating, as demand for British products collapsed. By the end of 1930, unemployment had more than doubled from 1 million to 2.5 million (from 12% to 20% of the insured workforce), and exports had fallen in value by 50%. During this time there were little to no unemployment benefits, so this mass unemployment led to many of Britain's population becoming impoverished. Government revenues contracted as national income fell, while the cost of assisting the jobless rose. The industrial areas were hardest hit, along with the coal mining districts. London and the south-east of England were hurt less. In 1933, 30% of Glaswegians were unemployed due to the severe decline in heavy industry.

Under pressure from its Liberal allies as well as the Conservative opposition, the Labour government appointed a committee to review the state of public finances. The May Report of July 1931 urged public sector wage cuts and large cuts in public spending (notably in benefit payments ("dole") to the unemployed) to avoid incurring a budget deficit. The sense was that the deficit was dangerous and had to be reduced; the proposal was to meet £24 million by increased taxes on the rich, and £96 million by economies, of which £64 million would come from unemployment relief. This proposal proved deeply unpopular within the Labour Party and among its main supporters, the trade unions, which along with several government ministers refused to support any such measures. The Chancellor of the Exchequer, Philip Snowden, insisted that the Report's recommendations be adopted to avoid incurring a budget deficit.

In a memorandum in January 1930, one junior government minister, Oswald Mosley, proposed that the government take control of banking and exports, as well as increase pensions to boost purchasing power. When his ideas were turned down, he left Labour to form the New Party, and later the British Union of Fascists.

National Government
The dispute over spending and wage cuts split the Labour government: as it turned out, beyond recovery. The political deadlock that resulted caused investors to take fright, and a flight of capital and gold further de-stabilised the economy. In response, MacDonald, on the urging of King George V, decided to form a "National Government" with the Conservatives and the Liberals.

On 24 August, MacDonald submitted the resignation of his ministers and led his senior colleagues in forming the new National Government. MacDonald and his supporters were expelled from the Labour Party and adopted the label "National Labour". The Labour Party and some Liberals, led by David Lloyd George, went into opposition. The Labour Party denounced MacDonald as a "traitor" and a "rat" for what they saw as his betrayal.

Soon after this, a general election was called. The 1931 general election resulted in a Conservative landslide victory, with the now leaderless Labour Party winning only 46 seats in Parliament. After the 1931 election the national government was Conservative-dominated, although MacDonald continued as prime minister until 1935.

Emergency measures
In an effort to balance the budget and restore confidence in the pound, on 10 September 1931 with Philip Snowden still as Chancellor, the new national government issued an emergency budget, which immediately instituted a round of cuts in public spending and wages. Public sector wages and unemployment pay were cut by 10%, and income tax was raised from 4s 6d to 5s on the pound (from 22.5% to 25%). The pay cuts did not go down well, however, and resulted in a non-violent "mutiny" in the Royal Navy protesting the pay cut.

These measures were deflationary and merely reduced purchasing power in the economy, worsening the situation, and by the end of 1931 unemployment had reached nearly 3 million. The measures were also unsuccessful at defending the gold standard, which the National Government had ostensibly been created to defend.

The flight of gold continued, however, and the Treasury finally was forced to abandon the gold standard in September 1931. Until now the government had religiously followed orthodox policies which demanded balanced budgets and the gold standard. Instead of the predicted disaster, cutting loose from gold proved a major advantage. Immediately the exchange rate of the pound fell by 25%, from $4.86 for one pound to $3.40. British exports were now much more competitive, which laid the ground for a gradual economic recovery. The worst was over.

Also, in 1932 following the Ottawa Agreement, Neville Chamberlain, who had become Chancellor after the 1931 election, introduced tariffs on industrial and agricultural imports at a rate of 10% on all imports except those from the countries of the British Empire. The introduction of tariffs caused a split in the Liberal Party, some of whom, along with Phillip Snowden, withdrew support for the National Government.

During the recession
Although the overall picture for the British economy in the 1930s was bleak, the effects of the depression were uneven. Some parts of the country, and some industries, fared better than others. Some parts of the country such as the South Wales Valleys experienced mass unemployment and poverty, while some areas in the Home Counties did not.

The brightest spot was in home building. From 1926 through 1939 over 200,000 new houses were built every year, with the peak reaching 365,000 in 1936. Many suburban districts in London and other cities were built at this time, and Brighton shows many signs of more "high deco" home architecture.

The South and the Midlands
In London and the south east of England unemployment was initially as high as 13.5%, the later 1930s were a prosperous time in these areas, as a suburban house-building boom was fuelled by the low interest rates which followed the abolition of the gold standard, and as London's growing population buoyed the economy of the Home Counties.

The south was also the home of new developing industries such as the electrical industry, which prospered from the large-scale electrification of housing and industry. Mass production methods brought new products such as electrical cookers and radios into the reach of the middle classes, and the industries which produced these prospered. Nearly half of all new factories that opened in Britain between 1932 and 1937 were in the Greater London area.

Another industry that prospered during the 1930s was the British motor industry. For cities that had a developed motor industry such as Birmingham, Coventry and Oxford, the 1930s were also a boom time. Manufacturers such as Austin, Morris and Ford dominated the motor industry during the 1930s, and the number of cars on British roads doubled within the decade. British Agriculture also flourished in the 1930s.

In the North and industrial heartlands
Northern England, however, was a quite different matter. The north was the home to most of Britain's traditional heavy industries, such as coal mining in Yorkshire and Nottinghamshire, shipbuilding on Tyneside and Wearside, steel in Sheffield and textiles in Lancashire which were heavily export orientated. The north bore the brunt of the depression, and the '30s were the most difficult time in living memory for people in these areas. The north was hit so hard in the Great Depression because of the structural decline in British industry. Staple industries such as coal, steel and shipbuilding were smaller, less modern and efficient and over-staffed compared to continental rivals.

In the north east (including Sunderland, Middlesbrough and Newcastle-upon-Tyne) this was especially so. The north east was a major centre of the shipbuilding industry. The Depression caused a collapse in demand for ships. Between 1929 and 1932 ship production declined by 90%, and this in turn affected all the supply industries such as steel and coal. In some towns and cities in the north east, unemployment reached as high as 70%. Among the worst affected towns was Jarrow, where unemployment led to the famous Jarrow March, in which unemployed workers marched 300 mi to London to protest against unemployment.

The north west, a centre of the textile industries, was also hard hit, with places such as Manchester and Lancashire suffering a slump. The South Wales Valleys, a centre of the coal mining and steel industries, was also devastated by the depression where towns such as Merthyr Tydfil and Swansea had unemployment rates reaching above 25% at certain times. The industrial belt of central Scotland, also a major shipbuilding centre in Glasgow, was also hard hit by the slump.

In these areas, millions of unemployed and their families were left destitute, and queueing at soup kitchens became a way of life. A government report in the mid-1930s estimated that around 25% of the UK's population existed on a subsistence diet, often with signs of child malnutrition such as scurvy, rickets and tuberculosis. In his book The Road to Wigan Pier, George Orwell described life for the unemployed in northern England during the depression: "Several hundred men risk their lives and several hundred women scrabble in the mud for hours... searching eagerly for tiny chips of coal in slagheaps so they could heat their own homes. For them, this arduously-gained 'free' coal was more important almost than food."

Welfare state during the 1930s
In the 1920s and 1930s, Britain had a relatively advanced welfare system compared to many of the industrialised countries. In 1911 a compulsory national unemployment and health insurance scheme had been put in place by the Liberal government of H. H. Asquith (see Liberal reforms). This scheme had been funded through contributions from the government, the employers and the workers. At first the scheme only applied to certain trades but, in 1920, it was expanded to include most manual workers.

However, the scheme only paid out according to the level of contributions made rather than according to need, and was only payable for 15 weeks. Anyone unemployed for longer than that had to rely on poor law relief paid by their local authority. In effect, millions of workers who had been too poorly paid to make contributions, or who had been unemployed long term, were left destitute by the scheme. With the mass unemployment of the 1930s, contributions to the insurance scheme dried up, resulting in a funding crisis.

In August 1931, the 1911 scheme was replaced by a fully government-funded unemployment benefit system. This system, for the first time, paid out according to need rather than the level of contributions. This unemployment benefit was subject to a strict means test, and anyone applying for unemployment pay had to have an inspection by a government official to make sure that they had no hidden earnings or savings, undisclosed source(s) of income or other means of support. For many poor people, this was a humiliating experience and was much resented.

Slow recovery
Following Britain's withdrawal from the gold standard and the devaluation of the pound, interest rates were reduced from 6% to 2%. As a result, British exports became more competitive on world markets than those of countries that remained on the gold standard. This led to a modest economic recovery, and a fall in unemployment from 1933 onwards. Although exports were still a fraction of their pre-depression levels, they recovered slightly.

Unemployment began a modest fall in 1934 and fell further in 1935 and 1936, but the rise in employment levels occurred mostly in the south, where lower interest rates had spurred the house building boom, which in turn spurred a recovery in domestic industry. The North and Wales remained severely depressed for most of the decade. In severely depressed parts of the country, the government enacted a number of policies to stimulate growth and reduce unemployment, including road building, loans to shipyards, and tariffs on steel imports. These policies helped but were not, however, on a sufficiently large scale to make a huge impact on the unemployment levels.

Rearmament and recovery
Since Britain's debt was 180% of the national GDP economic recovery was difficult. The United Kingdom was able to recover more quickly than other countries that were equally as developed, because their economic growth had been stagnant for some time. This meant that they did not have exponential growth, as the United States did, leaving them with less room to fall. Due to the abandonment of the gold standard in 1931 Britain was able to cut interest rates which led to a drop in real interest rates. This drop in interests rates subsequently led to a boom in construction in the south of Britain; stimulating some renewed economic growth. Also, the government began spending money on goods and services within Britain which aided in the foundation of financial recovery. From 1936 onwards, the National Government followed a policy of mass rearmament in the face of the rise of Nazi Germany. By 1937 unemployment had fallen to 1.5 million, but rose again to 1,810,000 by January 1938 suggesting that the recovery was to be short lived.

Consequences of the Great Depression
By the end of the Second World War in 1945, the majority of the British people, and particularly the working class and returning servicemen and women, were keenly dissatisfied. They rejected a return to pre-war Conservative economic policies, which they blamed for the hardship of the 1930s. They demanded widespread social change. At the 1945 general election, to the surprise of most observers, Conservatives led by Winston Churchill were defeated by the Labour Party headed by Clement Attlee.

The Labour government built up from pre-war foundations what was to become a comprehensive 'cradle-to-grave' welfare state, and established a tax funded National Health Service, which gave treatment according to need rather than ability to pay as the previous tax funded system had been. The Labour government also enacted Keynesian economic policies, to create artificial economic demand leading to full employment. These policies became known as the "post-war consensus", and were accepted by all major political parties at different times.

There were noted disagreements about the involvement of the state with the steel industry. With one government, it was state-owned, to then be sold off with the following Conservative ministry only to be then re-nationalised by the following Labour government. For the most part, the post-war consensus lasted until the late-1970s. Throughout the 1970s, it was becoming clear from all sides that radical change was needed as a result of such economic crises as the 1973 oil shock, high inflation, industrial unrest and sterling devaluation.

Historic evaluation
The events of the 1930s, and the response of the Labour and National governments to the depression, have generated much historical controversy.

In the decades immediately following the Second World War, most historical opinion was critical of the governments of the period. Certain historians, such as Robert Skidelsky in his Politicians and the Slump, compared the orthodox policies of the Labour and National governments unfavourably with the more radical proto-Keynesian measures advocated by David Lloyd George and Oswald Mosley, and the more interventionist and Keynesian responses in other economies: Franklin Roosevelt's New Deal in the United States, the Labour government in New Zealand, and the Social Democratic government in Sweden. Since the 1970s opinion has become less uniformly hostile. In the preface to the 1994 edition, Skidelsky argues that recent experience of currency crises and capital flight make it hard to be so critical of the politicians who wanted to achieve stability by cutting labour costs and defending the value of the currency.

title: Great Depression in the United Kingdom


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Robert Hyde Greg

Robert Hyde Greg (24 September 1795 – 21 February 1875), was an English industrialist, economist, antiquary, and - briefly - a Member of Parliament.

Born in Manchester, he was the son of Samuel Greg and Hannah Lightbody, the creators of Quarry Bank Mill, a pioneering factory of the early Industrial Revolution. His family were Unitarians, part of the prosperous dissenting community that characterised the entrepreneurial class of factory owners. He was brother to William Rathbone Greg and the junior Samuel Greg. He attended the University of Edinburgh and, after the obligatory Grand Tour of the antiquities of Continental Europe, joined his father's textile manufacturing enterprise.

He was active in the city's intellectual life as a member of the Manchester Literary and Philosophical Society and was a founder of its Mechanics' Institute. He was an active member of the Liberal Party and the Anti-Corn Law League. Though he was elected to Parliament for Manchester in 1839, it was without his consent and he resigned in the following year. He was an opponent of factory reform, trades unions and worker health and safety legislation.

He died at Norcliffe Hall, Styal, Cheshire and is buried at the Dean Row Unitarian Chapel, Wilmslow.

Greg was also a slaveholder; tenant-in-common of Cane Garden, St Vincent Island, with 82 enslaved people.

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/

title: Robert Hyde Greg


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Percy Greg

Percy Greg used the pseudonym 'Lionel H. Holdreth' when writing for George Jacob Holyoake's freethinking periodical, The Reasoner, in the 1850s, and he edited the paper for a while in 1859 when Holyoake was ill. Obituary in Manchester Guardian, 30 December 1889; see also more generally, Edward Royle, Victorian Infidels (Manchester UP 1974), p. 311 and passim.

Percy Greg (7 January 1836 Bury – 24 December 1889, Chelsea), son of William Rathbone Greg, was an English writer.

Percy Greg, like his father, wrote about politics, but his views were violently reactionary: his History of the United States to the Reconstruction of the Union (1887) can be said to be more of a polemic, rather than a history.

His Across the Zodiac (1880) is an early science fiction novel, said to be the progenitor of the sword-and-planet genre. For that novel, Greg created what may have been the first artistic language that was described with linguistic and grammatical terminology. It also contained what is possibly the first instance in the English language of the word "astronaut".

In 2010 a crater on Mars was named Greg in recognition of his contribution to the lore of Mars.

title: Percy Greg


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Sarcoidosis

Sarcoidosis (also known as Besnier–Boeck–Schaumann disease) is a disease involving abnormal collections of inflammatory cells that form lumps known as granulomata. The disease usually begins in the lungs, skin, or lymph nodes. Less commonly affected are the eyes, liver, heart, and brain, though any organ can be affected. The signs and symptoms depend on the organ involved. Often, no, or only mild, symptoms are seen. When it affects the lungs, wheezing, coughing, shortness of breath, or chest pain may occur. Some may have Löfgren syndrome with fever, large lymph nodes, arthritis, and a rash known as erythema nodosum.

The cause of sarcoidosis is unknown. Some believe it may be due to an immune reaction to a trigger such as an infection or chemicals in those who are genetically predisposed. Those with affected family members are at greater risk. Diagnosis is partly based on signs and symptoms, which may be supported by biopsy. Findings that make it likely include large lymph nodes at the root of the lung on both sides, high blood calcium with a normal parathyroid hormone level, or elevated levels of angiotensin-converting enzyme in the blood. The diagnosis should be made only after excluding other possible causes of similar symptoms such as tuberculosis.

Sarcoidosis may resolve without any treatment within a few years. However, some people may have long-term or severe disease. Some symptoms may be improved with the use of anti-inflammatory drugs such as ibuprofen. In cases where the condition causes significant health problems, steroids such as prednisone are indicated. Medications such as methotrexate, chloroquine, or azathioprine may occasionally be used in an effort to decrease the side effects of steroids. The risk of death is 1–7%. The chance of the disease returning in someone who has had it previously is less than 5%.

In 2015, pulmonary sarcoidosis and interstitial lung disease affected 1.9 million people globally and they resulted in 122,000 deaths. It is most common in Scandinavians, but occurs in all parts of the world. In the United States, risk is greater among black people as opposed to white people. It usually begins between the ages of 20 and 50. It occurs more often in women than men. Sarcoidosis was first described in 1877 by the English doctor Jonathan Hutchinson as a non-painful skin disease.

Signs and symptoms
Sarcoidosis is a systemic inflammatory disease that can affect any organ, although it can be asymptomatic and is discovered by accident in about 5% of cases. Common symptoms, which tend to be vague, include fatigue (unrelieved by sleep; occurs in up to 85% of cases ), lack of energy, weight loss, joint aches and pains (which occur in about 70% of cases), arthritis (14–38% of cases), dry eyes, swelling of the knees, blurry vision, shortness of breath, a dry, hacking cough, or skin lesions. Less commonly, people may cough up blood. Sarcoidosis is also accompanied by psychological distress and symptoms of anxiety and depression, which are also associated with fatigue. The cutaneous symptoms vary, and range from rashes and noduli (small bumps) to erythema nodosum, granuloma annulare, or lupus pernio. Sarcoidosis and cancer may mimic one another, making the distinction difficult.

The combination of erythema nodosum, bilateral hilar lymphadenopathy, and joint pain is called Löfgren syndrome, which has a relatively good prognosis. This form of the disease occurs significantly more often in Scandinavian patients than in those of non-Scandinavian origin.

Respiratory tract
Localization to the lungs is by far the most common manifestation of sarcoidosis. At least 90% of those affected experience lung involvement. Overall, about 50% develop permanent pulmonary abnormalities, and 5 to 15% have progressive fibrosis of the lung parenchyma. Sarcoidosis of the lung is primarily an interstitial lung disease in which the inflammatory process involves the alveoli, small bronchi, and small blood vessels. In acute and subacute cases, physical examination usually reveals dry crackles. At least 5% of cases include pulmonary arterial hypertension. The upper respiratory tract (including the larynx, pharynx, and sinuses) may be affected, which occurs in between 5 and 10% of cases.

The four stages of pulmonary involvement are based on radiological stage of the disease, which is helpful in prognosis:
 * Stage I: bilateral hilar lymphadenopathy (BHL) alone
 * Stage II: BHL with pulmonary infiltrates
 * Stage III: pulmonary infiltrates without BHL
 * Stage IV: fibrosis

Use of the Scadding scale only provides general information regarding the prognosis of the pulmonary disease over time. Caution is recommended, as it only shows a general relation with physiological markers of the disease and the variation is such that it has limited applicability in individual assessments, including treatment decisions.

Skin
Sarcoidosis involves the skin in between 9 and 37% of cases and is more common in African Americans than in European Americans. The skin is the second-most commonly affected organ after the lungs. The most common lesions are erythema nodosum, plaques, maculopapular eruptions, subcutaneous nodules, and lupus pernio. Treatment is not required, since the lesions usually resolve spontaneously in 2–4 weeks. Although it may be disfiguring, cutaneous sarcoidosis rarely causes major problems. Sarcoidosis of the scalp presents with diffuse or patchy hair loss.

Heart
Histologically, sarcoidosis of the heart is an active granulomatous inflammation surrounded by reactive oedema. The distribution of affected areas is patchy with localised enlargement of heart muscles. This causes scarring and remodelling of the heart, which leads to dilatation of heart cavities and thinning of heart muscles. As the situation progresses, it leads to aneurysm of heart chambers. When the distribution is diffuse, there would be dilatation of both ventricles of the heart, causing heart failure and arrhythmia. When the conduction system in the intraventricular septum is affected, it would lead to heart block, ventricular tachycardia and ventricular arrhythmia, causing sudden death. Nevertheless, the involvement of pericardium and heart valves are uncommon.

The frequency of cardiac involvement varies and is significantly influenced by race; in Japan, more than 25% of those with sarcoidosis have symptomatic cardiac involvement, whereas in the US and Europe, only about 5% of cases present with cardiac involvement. Autopsy studies in the US have revealed a frequency of cardiac involvement of about 20–30%, whereas autopsy studies in Japan have shown a frequency of 60%. The presentation of cardiac sarcoidosis can range from asymptomatic conduction abnormalities to fatal ventricular arrhythmia.

Conduction abnormalities are the most common cardiac manifestations of sarcoidosis in humans and can include complete heart block. Second to conduction abnormalities, in frequency, are ventricular arrhythmias, which occurs in about 23% of cases with cardiac involvement. Sudden cardiac death, either due to ventricular arrhythmias or complete heart block is a rare complication of cardiac sarcoidosis. Cardiac sarcoidosis can cause fibrosis, granuloma formation, or the accumulation of fluid in the interstitium of the heart, or a combination of the former two. Cardiac sarcoidosis may also cause congestive heart failure when granulomas cause myocardial fibrosis and scarring. Congestive heart failure affects 25-75% of those with cardiac sarcoidosis. Diabetes mellitus and sarcoidosis-related arrhythmias are believed to be strong risk factors of heart failure in sarcoidosis. A small (20-40%) increased risk of acute myocardial infarction has also been described. Pulmonary arterial hypertension occurs by two mechanisms in cardiac sarcoidosis: reduced left heart function due to granulomas weakening the heart muscle or from impaired blood flow.

Eye
Eye involvement occurs in about 10–90% of cases. Manifestations in the eye include uveitis, uveoparotitis, and retinal inflammation, which may result in loss of visual acuity or blindness. The most common ophthalmologic manifestation of sarcoidosis is uveitis. The combination of anterior uveitis, parotitis, VII cranial nerve paralysis and fever is called uveoparotid fever or Heerfordt syndrome. Development of scleral nodule associated with sarcoidosis has been observed.

Nervous system
Any of the components of the nervous system can be involved. Sarcoidosis affecting the nervous system is known as neurosarcoidosis. Cranial nerves are most commonly affected, accounting for about 5–30% of neurosarcoidosis cases, and peripheral facial nerve palsy, often bilateral, is the most common neurological manifestation of sarcoidosis. It occurs suddenly and is usually transient. The central nervous system involvement is present in 10–25% of sarcoidosis cases. Other common manifestations of neurosarcoidosis include optic nerve dysfunction, papilledema, palate dysfunction, neuroendocrine changes, hearing abnormalities, hypothalamic and pituitary abnormalities, chronic meningitis, and peripheral neuropathy. Myelopathy, that is spinal cord involvement, occurs in about 16–43% of neurosarcoidosis cases and is often associated with the poorest prognosis of the neurosarcoidosis subtypes. Whereas facial nerve palsies and acute meningitis due to sarcoidosis tend to have the most favourable prognosis, another common finding in sarcoidosis with neurological involvement is autonomic or sensory small-fiber neuropathy. Neuroendocrine sarcoidosis accounts for about 5–10% of neurosarcoidosis cases and can lead to diabetes insipidus, changes in menstrual cycle and hypothalamic dysfunction. The latter can lead to changes in body temperature, mood, and prolactin (see the endocrine and exocrine section for details).

Endocrine and exocrine
Prolactin is frequently increased in sarcoidosis, between 3 and 32% of cases have hyperprolactinemia this frequently leads to amenorrhea, galactorrhea, or nonpuerperal mastitis in women. It also frequently causes an increase in 1,25-dihydroxy vitamin D, the active metabolite of vitamin D, which is usually hydroxylated within the kidney, but in sarcoidosis patients, hydroxylation of vitamin D can occur outside the kidneys, namely inside the immune cells found in the granulomas the condition produces. 1,25-dihydroxy vitamin D is the main cause for hypercalcemia in sarcoidosis and is overproduced by sarcoid granulomata. Gamma-interferon produced by activated lymphocytes and macrophages plays a major role in the synthesis of 1 alpha, 25(OH)2D3. Hypercalciuria (excessive secretion of calcium in one's urine) and hypercalcemia (an excessively high amount of calcium in the blood) are seen in <10% of individuals and likely results from the increased 1,25-dihydroxy vitamin D production.

Thyroid dysfunction is seen in 4.2–4.6% of cases.

Parotid enlargement occurs in about 5–10% of cases. Bilateral involvement is the rule. The gland is usually not tender, but firm and smooth. Dry mouth can occur; other exocrine glands are affected only rarely. The eyes, their glands, or the parotid glands are affected in 20–50% of cases.

Gastrointestinal and genitourinary
Symptomatic gastrointestinal (GI) involvement occurs in less than 1% of cases (if one excludes the liver), and most commonly the stomach is affected, although the small or large intestine may also be affected in a small portion of cases. Studies at autopsy have revealed GI involvement in less than 10% of people. These cases would likely mimic Crohn's disease, which is a more commonly intestine-affecting granulomatous disease. About 1–3% of people have evidence of pancreatic involvement at autopsy. Symptomatic kidney involvement occurs in just 0.7% of cases, although evidence of kidney involvement at autopsy has been reported in up to 22% of people and occurs exclusively in cases of chronic disease. Symptomatic kidney involvement is usually nephrocalcinosis, although granulomatous interstitial nephritis that presents with reduced creatinine clearance and little proteinuria is a close second. Less commonly, the epididymis, testicles, prostate, ovaries, fallopian tubes, uterus, or the vulva may be affected, the latter may cause vulva itchiness. Testicular involvement has been reported in about 5% of people at autopsy. In males, sarcoidosis may lead to infertility.

Around 70% of people have granulomas in their livers, although only in about 20–30% of cases, liver function test anomalies reflecting this fact are seen. About 5–15% of patients exhibit hepatomegaly. Only 5–30% of cases of liver involvement are symptomatic. Usually, these changes reflect a cholestatic pattern and include raised levels of alkaline phosphatase (which is the most common liver function test anomaly seen in those with sarcoidosis), while bilirubin and aminotransferases are only mildly elevated. Jaundice is rare.

Blood
Abnormal blood tests are frequent, accounting for over 50% of cases, but are not diagnostic. Lymphopenia is the most common blood anomaly in sarcoidosis. Anemia occurs in about 20% of people with sarcoidosis. Leukopenia is less common and occurs in even fewer cases but is rarely severe. Thrombocytopenia and hemolytic anemia are fairly rare. In the absence of splenomegaly, leukopenia may reflect bone marrow involvement, but the most common mechanism is a redistribution of blood T cells to sites of disease. Other nonspecific findings include monocytosis, occurring in the majority of sarcoidosis cases, increased hepatic enzymes or alkaline phosphatase. People with sarcoidosis often have immunologic anomalies like allergies to test antigens such as Candida or purified protein derivative. Polyclonal hypergammaglobulinemia is also a fairly common immunologic anomaly seen in sarcoidosis.

Lymphadenopathy (swollen glands) is common in sarcoidosis and occurs in 15% of cases. Intrathoracic nodes are enlarged in 75 to 90% of all people; usually this involves the hilar nodes, but the paratracheal nodes are commonly involved. Peripheral lymphadenopathy is very common, particularly involving the cervical (the most common head and neck manifestation of the disease), axillary, epitrochlear, and inguinal nodes. Approximately 75% of cases show microscopic involvement of the spleen, although only in about 5–10% of cases does splenomegaly appear.

Bone, joints, and muscles
Sarcoidosis can be involved with the joints, bones, and muscles. This causes a wide variety of musculoskeletal complaints that act through different mechanisms. About 5–15% of cases affect the bones, joints, or muscles.

Arthritic syndromes can be categorized as acute or chronic. Sarcoidosis patients with acute arthritis often also have bilateral hilar lymphadenopathy and erythema nodosum. These three associated syndromes often occur together in Löfgren syndrome. The arthritis symptoms of Löfgren syndrome occur most frequently in the ankles, followed by the knees, wrists, elbows, and metacarpophalangeal joints. Usually, true arthritis is not present, but instead, periarthritis appears as a swelling in the soft tissue around the joints that can be seen by ultrasonographic methods. These joint symptoms tend to precede or occur at the same time as erythema nodosum develops. Even when erythema nodosum is absent, it is believed that the combination of hilar lymphadenopathy and ankle periarthritis can be considered as a variant of Löfgren syndrome. Enthesitis also occurs in about one-third of patients with acute sarcoid arthritis, mainly affecting the Achilles tendon and heels. Soft-tissue swelling of the ankles can be prominent, and biopsy of this soft tissue reveals no granulomas, but does show panniculitis similar to erythema nodosum.

Chronic sarcoid arthritis usually occurs in the setting of more diffuse organ involvement. The ankles, knees, wrists, elbows, and hands may all be affected in the chronic form and often this presents itself in a polyarticular pattern. Dactylitis similar to that seen in psoriatic arthritis, that is associated with pain, swelling, overlying skin erythema, and underlying bony changes may also occur. Development of Jaccoud arthropathy (a nonerosive deformity) is very rarely seen.

Bone involvement in sarcoidosis has been reported in 1–13% of cases. The most frequent sites of involvement are the hands and feet, whereas the spine is less commonly affected. Half of the patients with bony lesions experience pain and stiffness, whereas the other half remain asymptomatic. Periostitis is rarely seen in sarcoidosis and has been found to present itself at the femoral bone.

Cause
The exact cause of sarcoidosis is not known. The current working hypothesis is, in genetically susceptible individuals, sarcoidosis is caused through alteration to the immune response after exposure to an environmental, occupational, or infectious agent. Some cases may be caused by treatment with tumor necrosis factor (TNF) inhibitors like etanercept.

Genetics
The heritability of sarcoidosis varies according to ethnicity. About 20% of African Americans with sarcoidosis have a family member with the condition, whereas the same figure for European Americans is about 5%. Additionally, in African Americans, who seem to experience more severe and chronic disease, siblings and parents of sarcoidosis cases have about a 2.5-fold increased risk for developing the disease. In Swedish individuals heritability was found to be 39%. In this group, if a first-degree family member was affected, a person has a four-fold greater risk of being affected.

Investigations of genetic susceptibility yielded many candidate genes, but only few were confirmed by further investigations and no reliable genetic markers are known. Currently, the most interesting candidate gene is BTNL2; several HLA-DR risk alleles are also being investigated. In persistent sarcoidosis, the HLA haplotype HLA-B7-DR15 is either cooperating in disease or another gene between these two loci is associated. In nonpersistent disease, a strong genetic association exists with HLA DR3-DQ2. Cardiac sarcoid has been connected to tumor necrosis factor alpha (TNFA) variants.

Infectious agents
Several infectious agents appear to be significantly associated with sarcoidosis, but none of the known associations is specific enough to suggest a direct causative role. The major implicated infectious agents include: mycobacteria, fungi, borrelia, and rickettsia. A meta-analysis investigating the role of mycobacteria in sarcoidosis found it was present in 26.4% of cases, but they also detected a possible publication bias, so the results need further confirmation. Mycobacterium tuberculosis catalase-peroxidase has been identified as a possible antigen catalyst of sarcoidosis. The disease has also been reported by transmission via organ transplants. A large epidemiological study found little evidence that infectious diseases spanning years before sarcoidosis diagnosis could confer measurable risks for sarcoidosis diagnosis in the future.

Autoimmune
Association of autoimmune disorders has been frequently observed. The exact mechanism of this relation is not known, but some evidence supports the hypothesis that this is a consequence of Th1 lymphokine prevalence. Tests of delayed cutaneous hypersensitivity have been used to measure progression.

Pathophysiology
Granulomatous inflammation is characterized primarily by the accumulation of macrophages and activated T-lymphocytes, with increased production of key inflammatory mediators, tumor necrosis factor alpha (TNF), interferon gamma, interleukin 2 (IL-2), IL-8, IL-10, IL-12, IL-18, IL-23 and transforming growth factor beta (TGF-β), indicative of a T helper cell-mediated immune response. Sarcoidosis has paradoxical effects on inflammatory processes; it is characterized by increased macrophage and CD4 helper T-cell activation, resulting in accelerated inflammation, but immune response to antigen challenges such as tuberculin is suppressed. This paradoxic state of simultaneous hyper- and hypoactivity is suggestive of a state of anergy. The anergy may also be responsible for the increased risk of infections and cancer. The regulatory T-lymphocytes in the periphery of sarcoid granulomas appear to suppress IL-2 secretion, which is hypothesized to cause the state of anergy by preventing antigen-specific memory responses.

While TNF is widely believed to play an important role in the formation of granulomas (this is further supported by the finding that in animal models of mycobacterial granuloma formation inhibition of either TNF or IFN-γ production inhibits granuloma formation), sarcoidosis can and does still develop in those being treated with TNF antagonists like etanercept. B cells also likely play a role in the pathophysiology of sarcoidosis. Serum levels of soluble human leukocyte antigen (HLA) class I antigens and angiotensin converting enzyme (ACE) are higher in people with sarcoidosis. Likewise the ratio of CD4/CD8 T cells in bronchoalveolar lavage is usually higher in people with pulmonary sarcoidosis (usually >3.5), although it can be normal or even abnormally low in some cases. Serum ACE levels have been found to usually correlate with total granuloma load.

Cases of sarcoidosis have also been reported as part of the immune reconstitution syndrome of HIV, that is, when people receive treatment for HIV, their immune system rebounds and the result is that it starts to attack the antigens of opportunistic infections caught prior to said rebound and the resulting immune response starts to damage healthy tissue.

Histopathology
Sarcoidosis is characterized by the formation of non-necrotizing ("non-caseating") granulomas in various organs and tissues. Giant cells, specifically Langhans giant cells, are often seen in sarcoidosis. Schaumann bodies seen in sarcoidosis are calcium and protein inclusions inside of giant cells as part of a granuloma. Asteroid bodies can be seen in sarcoidosis. Hamazaki–Wesenberg bodies can be seen in lymph nodes and more rarely in lung biopsies with sarcoidosis and are inclusion bodies of lysosomes with protein, glycoprotein and iron.

Diagnosis
Diagnosis of sarcoidosis is a matter of exclusion, as there is no specific test for the condition other than the Kveim-Siltzbach test. To exclude sarcoidosis in a case presenting with pulmonary symptoms might involve a chest radiograph, CT scan of chest, PET scan, CT-guided biopsy, mediastinoscopy, open lung biopsy, bronchoscopy with biopsy, endobronchial ultrasound, and endoscopic ultrasound with fine-needle aspiration of mediastinal lymph nodes (EBUS FNA). Tissue from biopsy of lymph nodes is subjected to both flow cytometry to rule out cancer and special stains (acid fast bacilli stain and Gömöri methenamine silver stain) to rule out microorganisms and fungi.

Serum markers of sarcoidosis, include: serum amyloid A, soluble interleukin-2 receptor, lysozyme, angiotensin converting enzyme, and the glycoprotein KL-6. Angiotensin-converting enzyme blood levels are used in the monitoring of sarcoidosis. A bronchoalveolar lavage can show an elevated (of at least 3.5) CD4/CD8 T cell ratio, which is indicative (but not proof) of pulmonary sarcoidosis. In at least one study the induced sputum ratio of CD4/CD8 and level of TNF was correlated to those in the lavage fluid. A sarcoidosis-like lung disease called granulomatous–lymphocytic interstitial lung disease can be seen in patients with common variable immunodeficiency (CVID) and therefore serum antibody levels should be measured to exclude CVID.

Differential diagnosis includes metastatic disease, lymphoma, septic emboli, rheumatoid nodules, granulomatosis with polyangiitis, varicella infection, tuberculosis, and atypical infections, such as Mycobacterium avium complex, cytomegalovirus, and cryptococcus. Sarcoidosis is confused most commonly with neoplastic diseases, such as lymphoma, or with disorders characterized also by a mononuclear cell granulomatous inflammatory process, such as the mycobacterial and fungal disorders.

Chest radiograph changes are divided into four stages: Although people with stage 1 radiographs tend to have the acute or subacute, reversible form of the disease, those with stages 2 and 3 often have the chronic, progressive disease; these patterns do not represent consecutive "stages" of sarcoidosis. Thus, except for epidemiologic purposes, this categorization is mostly of historic interest.
 * 1) bihilar lymphadenopathy
 * 2) bihilar lymphadenopathy and reticulonodular infiltrates
 * 3) bilateral pulmonary infiltrates
 * 4) fibrocystic sarcoidosis typically with upward hilar retraction, cystic and bullous changes

In sarcoidosis presenting in the Caucasian population, hilar adenopathy and erythema nodosum are the most common initial symptoms. In this population, a biopsy of the gastrocnemius muscle is a useful tool in correctly diagnosing the person. The presence of a noncaseating epithelioid granuloma in a gastrocnemius specimen is definitive evidence of sarcoidosis, as other tuberculoid and fungal diseases extremely rarely present histologically in this muscle.

Cardiac magnetic resonance imaging (CMR) is one modality for diagnosing cardiac sarcoidosis. It has 78% specificity in diagnosing cardiac sarcoidosis. Its T2-weighted imaging can detect acute inflammation. Meanwhile, late gadolinium contrast (LGE) can detect fibrosis or scar. Lesions at the subpericardium and midwall enhancement of basal septum or inferolateral wall is strongly suggestive of sarcoidosis. MRI can also follow up on the treatment efficacy of corticosteroids and prognosis of cardiac sarcoidosis.

PET scan is able to quantify disease activity which cannot be performed by CMR.

Classification
Sarcoidosis may be divided into the following types:

 * Annular sarcoidosis
 * Erythrodermic sarcoidosis
 * Ichthyosiform sarcoidosis
 * Hypopigmented sarcoidosis
 * Löfgren syndrome
 * Lupus pernio
 * Morpheaform sarcoidosis
 * Mucosal sarcoidosis
 * Neurosarcoidosis
 * Papular sarcoid
 * Scar sarcoid
 * Subcutaneous sarcoidosis
 * Systemic sarcoidosis
 * Ulcerative sarcoidosis

Treatment
Treatments for sarcoidosis vary greatly depending on the patient. At least half of patients require no systemic therapy. Most people (>75%) only require symptomatic treatment with nonsteroidal anti-inflammatory drugs (NSAIDs) like ibuprofen or aspirin. For those presenting with lung symptoms, unless the respiratory impairment is devastating, active pulmonary sarcoidosis is observed usually without therapy for two to three months; if the inflammation does not subside spontaneously, therapy is instituted.

Major categories of drug interventions include glucocorticoids, antimetabolites, biologic agents especially monoclonal anti-tumor necrosis factor antibodies. Investigational treatments include specific antibiotic combinations and mesenchymal stem cells. If drug intervention is indicated, a step-wise approach is often used to explore alternatives in order of increasing side effects and to monitor potentially toxic effects.

Corticosteroids, most commonly prednisone or prednisolone, have been the standard treatment for many years. In some people, this treatment can slow or reverse the course of the disease, but other people do not respond to steroid therapy. The use of corticosteroids in mild disease is controversial because in many cases the disease remits spontaneously.

Antimetabolites
Antimetabolites, also categorized as steroid-sparing agents, such as azathioprine, methotrexate, mycophenolic acid, and leflunomide are often used as alternatives to corticosteroids. Of these, methotrexate is most widely used and studied. Methotrexate is considered a first-line treatment in neurosarcoidosis, often in conjunction with corticosteroids. Long-term treatment with methotrexate is associated with liver damage in about 10% of people and hence may be a significant concern in people with liver involvement and requires regular liver function test monitoring. Methotrexate can also lead to pulmonary toxicity (lung damage), although this is fairly uncommon and more commonly it can confound the leukopenia caused by sarcoidosis. Due to these safety concerns it is often recommended that methotrexate is combined with folic acid in order to prevent toxicity. Azathioprine treatment can also lead to liver damage. However, the risk of infection appears to be about 40% lower in those treated with methotrexate instead of azathioprine. Leflunomide is being used as a replacement for methotrexate, possibly due to its purportedly lower rate of pulmonary toxicity. Mycophenolic acid has been used successfully in uveal sarcoidosis, neurosarcoidosis (especially CNS sarcoidosis; minimally effective in sarcoidosis myopathy), and pulmonary sarcoidosis.

Immunosuppressants
As the granulomas are caused by collections of immune system cells, particularly T cells, there has been some success using immunosuppressants (like cyclophosphamide, cladribine, chlorambucil, and cyclosporine), immunomodulatory (pentoxifylline and thalidomide), and anti-tumor necrosis factor treatment (such as infliximab, etanercept, golimumab, and adalimumab).

In a clinical trial cyclosporine added to prednisone treatment failed to demonstrate any significant benefit over prednisone alone in people with pulmonary sarcoidosis, although there was evidence of increased toxicity from the addition of cyclosporine to the steroid treatment including infections, malignancies (cancers), hypertension, and kidney dysfunction. Likewise chlorambucil and cyclophosphamide are seldom used in the treatment of sarcoidosis due to their high degree of toxicity, especially their potential for causing malignancies. Infliximab has been used successfully to treat pulmonary sarcoidosis in clinical trials in a number of cases. Etanercept, on the other hand, has failed to demonstrate any significant efficacy in people with uveal sarcoidosis in a couple of clinical trials. Likewise golimumab has failed to show any benefit in those with pulmonary sarcoidosis. One clinical trial of adalimumab found treatment response in about half of subjects, which is similar to that seen with infliximab, but as adalimumab has better tolerability profile it may be preferred over infliximab.

Specific organ treatments
Ursodeoxycholic acid has been used successfully as a treatment for cases with liver involvement. Thalidomide has also been tried successfully as a treatment for treatment-resistant lupus pernio in a clinical trial, which may stem from its anti-TNF activity, although it failed to exhibit any efficacy in a pulmonary sarcoidosis clinical trial. Cutaneous disease may be successfully managed with antimalarials (such as chloroquine and hydroxychloroquine) and the tetracycline antibiotic, minocycline. Antimalarials have also demonstrated efficacy in treating sarcoidosis-induced hypercalcemia and neurosarcoidosis. Long-term use of antimalarials is limited, however, by their potential to cause irreversible blindness and hence the need for regular ophthalmologic screening. This toxicity is usually less of a problem with hydroxychloroquine than with chloroquine, although hydroxychloroquine can disturb the glucose homeostasis.

Recently selective phosphodiesterase 4 (PDE4) inhibitors like apremilast (a thalidomide derivative), roflumilast, and the less subtype-selective PDE4 inhibitor, pentoxifylline, have been tried as a treatment for sarcoidosis, with successful results being obtained with apremilast in cutaneous sarcoidosis in a small open-label study. Pentoxifylline has been used successfully to treat acute disease although its use is greatly limited by its gastrointestinal toxicity (mostly nausea, vomiting, and diarrhea). Case reports have supported the efficacy of rituximab, an anti-CD20 monoclonal antibody and a clinical trial investigating atorvastatin as a treatment for sarcoidosis is under-way. ACE inhibitors have been reported to cause remission in cutaneous sarcoidosis and improvement in pulmonary sarcoidosis, including improvement in pulmonary function, remodeling of lung parenchyma and prevention of pulmonary fibrosis in separate case series'. Nicotine patches have been found to possess anti-inflammatory effects in sarcoidosis patients, although whether they had disease-modifying effects requires further investigation. Antimycobacterial treatment (drugs that kill off mycobacteria, the causative agents behind tuberculosis and leprosy) has also proven itself effective in treating chronic cutaneous (that is, it affects the skin) sarcoidosis in one clinical trial. Quercetin has also been tried as a treatment for pulmonary sarcoidosis with some early success in one small trial.

Because of its uncommon nature, the treatment of male reproductive tract sarcoidosis is controversial. Since the differential diagnosis includes testicular cancer, some recommend orchiectomy, even if evidence of sarcoidosis in other organs is present. In the newer approach, testicular, epididymal biopsy and resection of the largest lesion has been proposed.

Symptoms
People with sarcoidosis may have a range of symptoms that do not correspond with objective physical evidence of disease but that still decrease quality of life.

Physical therapy, rehabilitation, and counseling can help avoid deconditioning, and improve social participation, psychological well-being, and activity levels. Key aspects are avoiding exercise intolerance and muscle weakness.

Low or moderate-intensity physical training has been shown to improve fatigue, psychological health, and physical functioning in people sarcoidosis without adverse effects. Inspiratory muscle training has also decreased severe fatigue perception in subjects with early stages of sarcoidosis, as well as improving functional and maximal exercise capacity and respiratory muscle strength. The duration, frequency, and physical intensity of exercise needs to accommodate impairments such as joint pain, muscle pain, and fatigue.

Neurostimulants such as methylphenidate and modafinil have shown some effectiveness as an adjunct for treatment of sarcoidosis fatigue.

Treatments for symptomatic neuropathic pain in sarcoidosis patients is similar to that for other causes, and include antidepressants, anticonvulsants and prolonged-release opioids, however, only 30 to 60% of patients experience limited pain relief.

Prognosis
The disease can remit spontaneously or become chronic, with exacerbations and remissions. In some cases, it can progress to pulmonary fibrosis and death. In benign cases, remission can occur in 24 to 36 months without treatment but regular follow ups are required. Some cases, however, may persist several decades. Two-thirds of people with the condition achieve a remission within 10 years of the diagnosis. When the heart is involved, the prognosis is generally less favourable, though corticosteroids appear effective in improving AV conduction. The prognosis tends to be less favourable in African Americans than in white Americans. In a Swedish population-based analysis, the majority of cases who did not have severe disease at diagnosis had comparable mortality to the general population. The risk for premature death was markedly (2.3-fold) increased compared to the general population for a smaller group of cases with severe disease at diagnosis. Serious infections, sometimes multiple during the course of disease, and heart failure might contribute to the higher risk of early death in some patients with sarcoidosis.

Some 1990s studies indicated that people with sarcoidosis appear to be at significantly increased risk for cancer, in particular lung cancer, lymphomas, and cancer in other organs known to be affected in sarcoidosis. In sarcoidosis-lymphoma syndrome, sarcoidosis is followed by the development of a lymphoproliferative disorder such as non-Hodgkin lymphoma. This may be attributed to the underlying immunological abnormalities that occur during the sarcoidosis disease process. Sarcoidosis can also follow cancer or occur concurrently with cancer. There have been reports of hairy cell leukemia, acute myeloid leukemia, and acute myeloblastic leukemia associated with sarcoidosis. Sometimes, sarcoidosis, even untreated, can be complicated by opportunistic infections although these are rare.

Epidemiology
Sarcoidosis most commonly affects young adults of both sexes, although studies have reported more cases in females. Incidence is highest for individuals younger than 40 and peaks in the age-group from 20 to 29 years; a second peak is observed for women over 50.

Sarcoidosis occurs throughout the world in all races with an average incidence of 16.5 per 100,000 in men and 19 per 100,000 in women. The disease is most common in Northern European countries and the highest annual incidence of 60 per 100,000 is found in Sweden and Iceland. In the United Kingdom the prevalence is 16 in 100,000. In the United States, sarcoidosis is more common in people of African descent than Caucasians, with annual incidence reported as 35.5 and 10.9 per 100,000, respectively. Sarcoidosis is less commonly reported in South America, Spain, India, Canada, and the Philippines. There may be a higher susceptibility to sarcoidosis in those with celiac disease. An association between the two disorders has been suggested.

There also has been a seasonal clustering observed in sarcoidosis-affected individuals. In Greece about 70% of diagnoses occur between March and May every year, in Spain about 50% of diagnoses occur between April and June, and in Japan it is mostly diagnosed during June and July.

The differing incidence across the world may be at least partially attributable to the lack of screening programs in certain regions of the world, and the overshadowing presence of other granulomatous diseases, such as tuberculosis, that may interfere with the diagnosis of sarcoidosis where they are prevalent. There may also be differences in the severity of the disease between people of different ethnicities. Several studies suggest the presentation in people of African origin may be more severe and disseminated than for Caucasians, who are more likely to have asymptomatic disease. Manifestation appears to be slightly different according to race and sex. Erythema nodosum is far more common in men than in women and in Caucasians than in other races. In Japanese people, ophthalmologic and cardiac involvement are more common than in other races.

It is more common in certain occupations, namely firefighters, educators, military personnel, those who work in industries where pesticides are used, law enforcement, and healthcare personnel. In the year after the September 11 attacks, the rate of sarcoidosis incidence went up four-fold (to 86 cases per 100,000).

History
It was first described in 1877 by Dr. Jonathan Hutchinson, a dermatologist as a condition causing red, raised rashes on the face, arms, and hands. In 1889 the term lupus pernio was coined by Dr. Ernest Besnier, another dermatologist. Later in 1892 lupus pernio's histology was defined. In 1902 bone involvement was first described by a group of three doctors. Between 1909 and 1910 uveitis in sarcoidosis was first described, and later in 1915 it was emphasised, by Dr. Jörgen Nielsen Schaumann, that it was a systemic condition. This same year lung involvement was also described. In 1937 uveoparotid fever was first described and likewise in 1941 Löfgren syndrome was first described. In 1958 the first international conference on sarcoidosis was called in London, likewise the first USA sarcoidosis conference occurred in Washington, D.C., in the year 1961. It has also been called Besnier–Boeck disease or Besnier–Boeck–Schaumann disease.

Etymology
The word "sarcoidosis" comes from Greek [σάρκο-] sarco- meaning "flesh", the suffix -(e)ido (from the Greek εἶδος -eidos [usually omitting the initial e in English as the diphthong epsilon-iota in Classic Greek stands for a long "i" = English ee]) meaning "type", " resembles" or "like", and -sis, a common suffix in Greek meaning "condition". Thus the whole word means "a condition that resembles crude flesh". The first cases of sarcoïdosis, which were recognised as a new pathological entity, in Scandinavia, at the end of the 19th century exhibited skin nodules resembling cutaneous sarcomas, hence the name initially given.

Society and culture
The World Association of Sarcoidosis and Other Granulomatous Disorders (WASOG) is an organisation of physicians involved in the diagnosis and treatment of sarcoidosis and related conditions. WASOG publishes the journal Sarcoidosis, Vasculitis and Diffuse Lung Diseases. Additionally, the Foundation for Sarcoidosis Research (FSR) is devoted to supporting research into sarcoidosis and its possible treatments.

There have been concerns that World Trade Center rescue workers are at a heightened risk for sarcoidosis.

Comedian and actor Bernie Mac had sarcoidosis. In 2005, he mentioned that the disease was in remission. His death on August 9, 2008, was caused by complications from pneumonia, though Mac's agent states the sarcoidosis was not related to his fatal pneumonia.

Karen "Duff" Duffy, MTV personality and actress, was diagnosed with neurosarcoidosis in 1995.

American football player Reggie White died in 2004, with pulmonary and cardiac sarcoidosis being contributing factors to his fatal heart arrhythmia.

Singer Sean Levert died in 2008 of sarcoidosis complications.

Manning Marable, a professor of public policy at Columbia University, died of pneumonia in 2011, less than a year after undergoing a double lung transplant following a diagnosis of sarcoidosis. In 2012, he was posthumously awarded a Pulitzer Prize in history for his biography "Malcolm X: A Life of Reinvention."

Joseph Rago, Pulitzer Prize-winning writer known for his work at The Wall Street Journal, died of sarcoidosis complications in 2017.

Several historical figures are suspected of having sarcoidosis. In a 2014 letter to the British medical journal The Lancet, it was suggested that the French Revolution leader Maximilien Robespierre may have had sarcoidosis, causing him impairment during his time as head of the Reign of Terror. The symptoms associated with Ludwig van Beethoven's 1827 death have been described as possibly consistent with sarcoidosis. Author Robert Louis Stevenson (1850–1894) had a history of chronic coughs and chest complaints, and sarcoidosis has been suggested as a diagnosis.

Pregnancy
Sarcoidosis generally does not prevent successful pregnancy and delivery; the increase in estrogen levels during pregnancy may even have a slightly beneficial immunomodulatory effect. In most cases, the course of the disease is unaffected by pregnancy, with improvement in a few cases and worsening of symptoms in very few cases, although it is worth noting that a number of the immunosuppressants (such as methotrexate, cyclophosphamide) used in corticosteroid-refractory sarcoidosis are known teratogens. Increased risks associated with sarcoidosis ranging from 30 to 70% have been reported for preeclampsia/eclampsia, cesarian or preterm delivery as well as (non-cardiac) birth defects in first singleton pregnancies. In absolute numbers, birth defects and other complications such as maternal death, cardiac arrest, placental abruption or venous thromboembolism are extremely rare in sarcoidosis pregnancies.

title: Sarcoidosis


text:
Allen Newell

Allen Newell (March 19, 1927 – July 19, 1992) was an American researcher in computer science and cognitive psychology at the RAND Corporation and at Carnegie Mellon University's School of Computer Science, Tepper School of Business, and Department of Psychology. He contributed to the Information Processing Language (1956) and two of the earliest AI programs, the Logic Theorist (1956) and the General Problem Solver (1957) (with Herbert A. Simon). He was awarded the ACM's A.M. Turing Award along with Herbert A. Simon in 1975 for their contributions to artificial intelligence and the psychology of human cognition.

Early studies
Newell completed his bachelor's degree in physics from Stanford in 1949. He was a graduate student at Princeton University from 1949 to 1950, where he studied mathematics. Due to his early exposure to an unknown field known as game theory and the experiences from the study of mathematics, he was convinced that he would prefer a combination of experimental and theoretical research to pure mathematics.

In 1950, he left Princeton and joined the RAND Corporation in Santa Monica where he worked for "a group that was studying logistics problems of the Air Force" (Simon). His work with Joseph Kruskal led to the creation of two theories: A Model for Organization Theory and Formulating Precise Concepts in Organization Theory. Newell eventually earned his PhD from the now Tepper School of Business at Carnegie Mellon with Herbert Simon serving as his advisor.

Afterwards, Newell "turned to the design and conduct of laboratory experiments on decision making in small groups" (Simon). He was dissatisfied, however, with the accuracy and validity of their findings produced from small-scale laboratory experiments. He joined with fellow RAND teammates John Kennedy, Bob Chapman, and Bill Biel at an Air Force Early Warning Station to study organizational processes in flight crews. They received funding from the Air Force in 1952 to build a simulator that would enable them to examine and analyze the interactions in the cockpit related to decision-making and information-handling. From these studies, Newell came to believe that information processing is the central activity in organizations.

Artificial intelligence
In September 1954, Newell enrolled in a seminar where Oliver Selfridge "described a running computer program that learned to recognize letters and other patterns" (Simon). This was when Allen came to believe that systems may be created and contain intelligence and have the ability to adapt. With this in mind, Allen, after a couple of months, wrote in 1955 The Chess Machine: An Example of Dealing with a Complex Task by Adaptation, which "outlined an imaginative design for a computer program to play chess in humanoid fashion" (Simon).

His work came to the attention of economist (and future nobel laureate) Herbert A. Simon, and, together with programmer J. C. Shaw, they developed the first true artificial intelligence program (see notes), the Logic Theorist. Newell's work on the program laid the foundations of the field. His inventions included: list processing, the most important programming paradigm used by AI ever since; the application of means-ends analysis to general reasoning (or "reasoning as search"); and the use of heuristics to limit the search space.

They presented the program at the Dartmouth conference of 1956, an informal gathering of researchers who were interested in simulating intelligence with machines. The conference, now widely considered the "birth of artificial intelligence", was enormously influential and those who attended became the leaders of AI research for the next two decades, Newell included.

Later achievements
Newell and Simon formed a lasting partnership. They founded an artificial intelligence laboratory at Carnegie Mellon University and produced a series of important programs and theoretical insights throughout the late fifties and sixties. This work included the General Problem Solver, a highly influential implementation of means–ends analysis, and the physical symbol systems hypothesis, the controversial philosophical assertion that all intelligent behavior could be reduced to the kind of symbol manipulation that Newell's programs demonstrated.

Newell's work culminated in the development of a cognitive architecture known as Soar and his unified theory of cognition, published in 1990, but their improvement was the objective of his efforts up to his death (one of the last Newell's letters ). The field of cognitive architectures, that he initiated, is still active in both the artificial intelligence and computational cognitive science communities.

Awards and honors

 * 1971 — John Danz Lecturer, University of Washington
 * 1971 — Harry Goode Memorial Award, American Federation of Information Processing Societies
 * 1972 — Elected to member of the United States National Academy of Sciences
 * 1972 — Elected to Fellow of the American Academy of Arts and Sciences
 * 1975 — A. M. Turing Award (with Herbert A. Simon), Association for Computing Machinery
 * 1976–77 — Guggenheim Fellowship, John Simon Guggenheim Memorial Foundation
 * 1979 — Alexander C. Williams Jr. Award (with William C. Biel, Robert Chapman and John L. Kennedy), Human Factors Society
 * 1980 — Elected to member of the United States National Academy of Engineering
 * 1980 — First President, American Association for Artificial Intelligence
 * 1981 — Charter recipient of the Computer Pioneer Award from the IEEE Computer Society
 * 1985 — Distinguished Scientific Contribution Award, American Psychological Association
 * 1986 — Doctor of Science (Honorary), University of Pennsylvania
 * 1987 — William James Lectures, Harvard University
 * 1989 — Award for Research Excellence, International Joint Conference on Artificial Intelligence
 * 1989 — Doctor in the Behavioral and Social Sciences (Honorary), University of Groningen, The Netherlands
 * 1989 — William James Fellow Award (charter recipient), American Psychological Society
 * 1990 — IEEE Emanuel R. Piore Award
 * 1990 — IEEE W.R.G. Baker Prize Paper Award
 * 1990 — Fellow of the Association for the Advancement of Artificial Intelligence
 * 1992 — U.S. National Medal of Science
 * 1992 — The Franklin Institute's Louis E. Levy Medal

The ACM - AAAI Allen Newell Award was named in his honor. The Award for Research Excellence of the Carnegie Mellon School of Computer Science was also named in his honor.

title: Allen Newell


text:
Photoflash capacitor

A photoflash capacitor is a high-voltage electrolytic capacitor used in camera flashes and in solid-state laser power supplies. Their usual purpose is to briefly power a flash lamp, used to illuminate a photographic subject or optically pump a laser rod. As flash tubes require very high current for a very short time to operate, photoflash capacitors are designed to supply high discharge current pulses without excessive internal heating.

Fundamentals
The principal properties of a capacitor are capacitance, working voltage, equivalent series resistance (ESR), equivalent series inductance (ESL), and working temperature

Compared with electrolytic capacitors usually used for power supply filtering at power frequency, a photoflash capacitor is designed to have lower ESR, ESL, and capacitance manufacturing tolerance, but does not need as high a working temperature.

Design
The light energy emitted by a flash is supplied by the capacitor, and is proportional to the product of the capacitance and the voltage squared; photoflash capacitors may have capacitance in the range 80-240 microfarads (μF) and voltages from 180 to 330 volts for flash units built into small disposable and compact cameras, increasing for units delivering higher light energy. A typical manufacturer's range includes capacitors operating at 330–380V, with capacitance from 80 to 1,500 μF While normal electrolytic capacitors are often operated at not more than half their nominal voltage due to their high derating, photoflash capacitors are typically operated at their nominal working voltage (labelled as "WV" or "W.V." rather than just "V").

Photoflash capacitors are not subject to the high temperatures of cased electronic equipment in continuous operation, with nearby components and sometimes the capacitors themselves dissipating heat; they are often rated at a maximum operating temperature rate of typically 55 °C, compared to 85 °C–105 °C or more for capacitors for continuous use in electronic equipment. In most electronic applications an electrolytic capacitor can have a capacitance much larger than its nominal value without detracting from circuit performance; general-purpose electrolytics are often specified to have capacitance between 20% below and 80% above rated value, although tighter tolerances are available. The light energy of a flash is proportional to the capacitance and large variations are not acceptable, typical tolerance is -10+20%.

Photoflash capacitors are designed to deliver a brief pulse of very high current, and are consequently sometimes used in railgun and coilgun designs.

title: Photoflash capacitor


text:
Alan Newell

Alan Newell may refer to:

 * Alan C. Newell (born 1941), Irish/American mathematician
 * Alan Newell (English computer scientist), professor emeritus of computer science and human-computer interaction at the University of Dundee

title: Alan Newell


text:
Jack Jones

Jack Jones may refer to:

Music

 * Jack Jones (American singer) (born 1938), American jazz and pop singer
 * Jack Jones, stage name of Australian singer Irwin Thomas (born 1971)
 * Jack Jones (Welsh musician) (born 1992), Welsh musician, songwriter and poet

Other media

 * Jack Jones (novelist) (1884–1970), Welsh novelist and playwright
 * Jack Jones (journalist) (1924–2011), American journalist
 * Jack Jones (TV journalist) (1949–1991), American television journalist

Fictional characters

 * Lance-Corporal Jack Jones, a character in the sitcom Dad's Army
 * Jack Jones, a banker in the Oliver Stone film Nixon

Politics

 * Jack Jones (Silvertown MP) (John Joseph Jones, 1873–1941), British Labour MP for Silvertown
 * Jack Jones (Rotherham MP) (John Henry Jones, 1894–1962), British Labour MP for Bolton, later MP for Rotherham
 * Jack Jones (Australian politician) (John Joseph Jones, 1907–1997), member of the Victorian Legislative Council for Ballarat
 * Jack Jones (trade unionist) (1913–2009), British trade union leader

Association football (soccer)

 * Jack Jones (footballer, born 1869) (1866–1931), Wales international footballer who played for Grimsby Town, Sheffield United and Tottenham
 * Jack Jones (footballer, born 1874) (1874–1904), English football forward for Small Heath, Bristol Rovers and Tottenham
 * Jack Jones (footballer, born 1891) (1891–1948), English football defender for Birmingham, Nelson and Crewe
 * Jack Jones (1920s Welsh footballer), footballer for Wrexham and Crewe Alexandra
 * Jack Jones (footballer, born 1907), Irish football defender for Linfield, Hibernian, Glenavon, Bath City and Ireland (IFA)
 * Jack Jones (footballer, born 1913) (1913–1995), English football player for Everton and Sunderland
 * Jack Jones (footballer, born 1916) (1916–1999), Scottish footballer
 * Jack Jones (footballer, born 1921) (1921–2001), Welsh footballer for Wrexham, Doncaster Rovers and New Brighton
 * Jack Jones (soccer, born 1987) (born 1987), American soccer player

Australian rules football

 * Jack Jones (footballer, born 1887) (1887–1964), Australian rules footballer for South Melbourne
 * Jack Jones (footballer, born 1888) (1888–1960), Australian rules footballer for University
 * Jack Jones (footballer, born 1924) (1924–2020), Australian rules footballer for Essendon

Rugby

 * Jack Jones (rugby union, born 1886) (1886–1951), Welsh international rugby union player
 * Jack Jones (rugby, born 1890) (1890–?), rugby union and league footballer for Wales (RU), Abertillery, and Oldham (RL)
 * Jack Jones (Australian rugby league) (fl. 1925–1933), Australian rugby league player

Other sports

 * Jumping Jack Jones (1860–1936), American baseball pitcher
 * Jack Jones (cricketer) (1899–1991), cricketer for Western Australia and Australian rules football player and coach
 * Jack Jones (water polo) (1925–2016), English Olympic water polo player
 * Jack Jones (American football) (born 1997), American football player

Other

 * Jack Harold Jones (1964–2017), American serial killer

title: Jack Jones


text:
All Hail, Liberia, Hail!

"All Hail, Liberia, Hail!" is the national anthem of Liberia. The lyrics were written by Daniel Bashiel Warner (1815–1880), who later became the third president of Liberia, and the music was composed by Olmstead Luca (1826–1869). It became the official national anthem upon Liberia's independence in 1847.

1974 proposed change to lyrics
On 22 July 1974, the Legislature of Liberia passed an act giving authorization to the president to establish a commission to give consideration to possible changes to a number of national symbols, including "All Hail, Liberia, Hail!" and the flag. President William Tolbert appointed 51 members to the Commission on National Unity. The commission was headed by McKinley Alfred Deshield Sr., and was also called the Deshield Commission. The commission sought to reexamine the symbols and remove divisive aspects of them. The commission submitted their report on 24 January 1978. The report recommended changing the word "benighted" in the anthem to the word "undaunted". The proposed change to the anthem was never made.

title: All Hail, Liberia, Hail!