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Francis Ysidro Edgeworth

Francis Ysidro Edgeworth (8 February 1845 – 13 February 1926) was an Anglo-Irish philosopher and political economist who made significant contributions to the methods of statistics during the 1880s. From 1891 onward, he was appointed the founding editor of The Economic Journal.

Life
Ysidro Francis Edgeworth – the order of his forenames later reversed – was born in Edgeworthstown, County Longford, Ireland, the son of Francis Beaufort Edgeworth and his wife, Rosa Florentina, daughter of exiled Catalan general Antonio Eroles. Francis Beaufort Edgeworth, when "a restless philosophy student at Cambridge on his way to Germany", had met Rosa, a teenage Spanish refugee, on the steps of the British Museum, and they subsequently eloped. Francis Beaufort Edgeworth was the son of politician, writer, and inventor Richard Lovell Edgeworth (father also of the writer Maria Edgeworth), by his fourth wife, the botanical artist and memoirist Frances Anne, daughter of the Anglican clergyman and geographer Daniel Augustus Beaufort, of French Huguenot origin. The Edgeworth family, which settled in Ireland in the 1580s, was distinguished, descending from Francis Edgeworth, joint Clerk of the Crown and Hanaper in 1606, who inherited a fortune from his brother Edward Edgeworth, Bishop of Down and Connor. Richard Lovell Edgeworth was a descendant, through his mother, of the English judge Sir Salathiel Lovell.

The youngest of seven children, Edgeworth did not attend school, but was educated by private tutors at the Edgeworthstown estate until he reached the age to enter university.

As a student at Trinity College Dublin he studied classics getting a scholarship in 1863 and graduating in 1865. In 1867, he went to Oxford and was admitted to Balliol College, Oxford in 1868. At Oxford, Edgeworth studied ancient and modern languages. During his studies, he was influenced by Jeremy Bentham's writings.

A voracious autodidact, he studied mathematics and economics only after he had completed university. He qualified as a barrister in London in 1877 but did not practise.

On the basis of his publications in economics and mathematical statistics in the 1880s, Edgeworth was appointed to a chair in economics at King's College London in 1888, and in 1891, he was appointed Drummond Professor of Political Economy at Oxford University. In 1891, he was also appointed the founding editor of The Economic Journal. He continued as editor or joint-editor until his death 35 years later.

The Royal Statistical Society awarded him the Guy Medal in Gold in 1907. Edgeworth served as the president of the Royal Statistical Society, 1912–14. In 1928, Arthur Lyon Bowley published a book entitled and devoted to F. Y. Edgeworth's Contributions to Mathematical Statistics.

Contributions to economics
Edgeworth was a highly influential figure in the development of neo-classical economics. He was the first to apply certain formal mathematical techniques to individual decision making in economics. He developed utility theory, introducing the indifference curve and the famous Edgeworth box, which is now familiar to undergraduate students of microeconomics. He is also known for the Edgeworth conjecture, which states that the core of an economy shrinks to the set of competitive equilibria as the number of agents in the economy gets larger. In statistics, Edgeworth is most prominently remembered by having his name on the Edgeworth series.

Though Edgeworth's economic ideas were original and in depth, his contemporaries frequently complained of his manner of expression for lack of clarity. He was prone to verbosity and coining obscure words without providing definition for the reader.

Mathematical Psychics (1881)
His most original and creative book on economics was Mathematical Psychics: An Essay on the Application of Mathematics to the Moral Sciences, published in 1881 at the beginning of his long career in the subject.

In the book, he criticised Jevons's theory of barter exchange, showing that under a system of "recontracting" there will be, in fact, many solutions, an "indeterminacy of contract". Edgeworth's "range of final settlements" was later resurrected by Martin Shubik (1959) to be the game-theoretic concept of "the core". The book contained the first instance of the indifference curve, as level sets of the generalised utility function, U(x, y, z, ...).

The book was notoriously difficult to read. He frequently referenced literary sources and interspersed the writing with passages in a number of languages, including Latin, French and Ancient Greek. The mathematics was similarly difficult, and a number of his creative applications of mathematics to economic or moral issues were judged as incomprehensible. However, one of the most influential economists of the time, Alfred Marshall, commented in his review of Mathematical Psychics:
 * This book shows clear signs of genius, and is a promise of great things to come... His readers may sometimes wish that he had kept his work by him a little longer till he had worked it out a little more fully, and obtained that simplicity which comes only through long labour. But taking it as what it claims to be, 'a tentative study', we can only admire its brilliancy, force, and originality.

Edgeworth's close friend, William Stanley Jevons, said of Mathematical Psychics:

 * Whatever else readers of this book may think about it, they would probably all agree that it is a very remarkable one.... There can be no doubt that in the style of his composition Mr. Edgeworth does not do justice to his matter. His style, if not obscure, is implicit, so that the reader is left to puzzle out every important sentence like an enigma.

Edgeworth's limit theorem
When the number of agents in an economy increases, the degree of indeterminacy is reduced. In the limit case of an infinite number of agents (perfect competition), the set of possible contract becomes fully determinate and identical to the 'equilibrium' of economists. The only way of resolving this indeterminacy of contract would be to appeal to the utilitarian principle of maximising the sum of the utilities of traders over the range of final settlements.

International trade
He was the first one to use offer curves and community indifference curves to illustrate its main propositions, including the "optimal tariff".

Taxation paradox
Taxation of a good may actually result in a decrease in price.

He set the utilitarian foundations for highly progressive taxation, arguing that the optimal distribution of taxes should be such that 'the marginal disutility incurred by each taxpayer should be the same' (Edgeworth, 1897).

Monopoly pricing
In 1897, in an article on monopoly pricing, Edgeworth criticised Cournot's exact solution to the duopoly problem with quantity adjustments as well as Bertrand's "instantly competitive" result in a duopoly model with price adjustment. At the same time, Edgeworth showed how price competition between two firms with capacity constraints and/or rising marginal cost curves resulted in indeterminacy. This gave rise to the Bertrand–Edgeworth model of oligopoly.

Marginal productivity theory
Edgeworth criticised the marginal productivity theory in several articles (1904, 1911), and tried to refine the neo-classical theory of distribution on a more solid basis. Although his work in questions of war finance during World War I was original, they were a bit too theoretical and did not achieve the practical influence he had hoped.

Collections/selections

 * F. Y. Edgeworth (1925) Papers relating to political economy 3 vols. Available online at Gallica
 * Charles R. McCann Jr. (ed.) (1966) F.Y. Edgeworth: Writings in Probability, Statistics and Economics, 3 vols. Cheltenham, Glos.: Elgar.
 * Charles R. McCann Jr. (ed.) (1966) F.Y. Edgeworth: Writings in Probability, Statistics and Economics, 3 vols. Cheltenham, Glos.: Elgar.

Individual works

 * "Mr. Matthew Arnold on Bishop Butler's Doctrine of Self-Love", 1876, Mind
 * New and Old Methods of Ethics, 1877.
 * "The Hedonical Calculus", 1879, Mind, pp. 394–408
 * "Mr. Leslie Stephen on Utilitarianism", 1882, Mind
 * "The Law of Error", 1883, Phil Mag, pp. 300–309
 * "The Method of Least Squares", 1883, Phil Mag
 * "The Physical Basis of Probability", 1883, Phil Mag
 * "On the Method of Ascertaining a Change in the Value of Gold", 1883, JRSS
 * "Review of Jevons's Investigations", 1884, Academy
 * "The Rationale of Exchange", 1884, JRSS
 * "The Philosophy of Chance", 1884, Mind
 * "On the Reduction of Observations", 1884, Phil Mag, pp. 135–141
 * "A Priori Probabilities", 1884, Phil Mag
 * "Chance and Law", 1884, Hermathena, pp. 154–163
 * "Methods of Statistics", 1885, Jubilee Volume of RSS.
 * "The Calculus of Probabilities Applied to Psychic Research, I & II", 1885, 1886, Proceedings of Society for Psychic Research
 * "On Methods of Ascertaining Variations in the Rate of Births, Deaths and Marriages", 1885, JRSS
 * "Progressive Means", 1886, JRSS
 * "The Law of Error and the Elimination of Chance", 1886 Phil Mag
 * "On the Determination of the Modulus of Errors", 1886, Phil Mag
 * "Problems in Probabilities", 1886, Phil Mag
 * "Review of Sidgwick's Scope and Method", 1886, Academy
 * "Review of Jevons's Journals", 1886, Academy
 * "Four Reports by the committee investigating best method of ascertaining and measuring variations in the monetary standard", 1887, Reports of the BAAS (Parts I & 3; Part 2)
 * "Observations and Statistics: An essay on the theory of errors of observation and the first principles of statistics", 1887, Transactions of Cambridge Society.
 * Metretike, or the method of measuring probability and utility, 1887.
 * "On Observations Relating to Several Quantities", 1887, Hermathena
 * "The Law of Error", 1887, Nature
 * "The Choice of Means", 1887, Phil Mag
 * "On Discordant Observations", 1887, Phil Mag
 * "The Empirical Proof of the Law of Error", 1887, Phil Mag
 * "On a New Method of Reducing Observations Relating to Several Quantities", 1888, Phil Mag
 * "New Methods of Measuring Variation in General Prices, 1888, JRSS
 * "The Statistics of Examinations", 1888, JRSS
 * "The Value of Authority Tested by Experiment", 1888, Mind
 * "Mathematical Theory of Banking", 1888, JRSS
 * "On the Application of Mathematics to Political Economy: Address of the President of Section F of the British Association for the Advancement of Science", 1889, JRSS
 * "The Mathematical Theory of Political Economy: Review of Walras's Elements", 1889, Nature
 * "Review of Wicksteed's Alphabet", 1889, Academy
 * "Review of Bohm-Bawerk's Kapital und Kapitalismus", 1889, Academy
 * "Review of Bertrand's Calcul des Probabilites", 1889, J of Education
 * "Points at which Mathematical Reasoning is Applicable to Political Economy", 1889, Nature
 * "Appreciation of Gold", 1889, QJE
 * "The Element of Chance in Competitive Examinations", 1890, JRSS
 * "Economic Science and Statistics", 1889, Nature
 * "Review of Marshall's Principles", 1890, Nature
 * "Review of Jevons's Pure Logic", 1890, Academy
 * "Review of Walras's Elements", 1890, Academy
 * "Review of Bohm-Bawerk's Capital and Interest", 1890, Academy
 * "La Théorie mathématique de l'offre et de la demande et le côut de production", 1891, Revue d'Economie Politique
 * "Osservazioni sulla teoria matematica dell' economica politica", 1891, GdE (trans. "On the Determinateness of Economic Equilibrium")
 * "Ancora a proposito della teoria del baratto", 1891, GdE
 * "Review of Ricardo's Principles", 1891, J of Education
 * "The British Economic Association", 1891, In: The Economic Journal (EJ), Vol. 1, pp. 1–14 (in [[Image:wikisource-logo.svg|16x16px]] Wikisource)
 * "Review of Keynes's Scope and Method", 1891, EJ
 * "An Introductory Lecture on Political Economy", 1891, EJ
 * "Review of Sidgwick's Elements of Politics", 1891, EJ
 * "Review of Second Edition of Marshall's Principles", 1891, EJ
 * "Mathematical Investigations in the Theory of Value and Prices," Connecticut Academy, 1892.
 * "Correlated Averages", 1892, Phil Mag
 * "The Law of Error and Correlated Averages", 1892, Phil Mag.
 * "Recent Attempts to Evaluate the Amount of Coin Circulating in a Country", 1892, EJ
 * "Review of Marshall's Economics of Industry", 1892, Nature
 * "Review of Cantillon's Essai", 1892, EJ
 * "Review of Palgrave's Dictionary", 1892, EJ
 * "Review of Bohm-Bawerk's Positive Theory of Capital", 1892, EJ
 * "Review of Smart's Introduction to the Theory of Value", 1892, EJ
 * "Review of Dusing's Das Geschlechtverhaltniss", 1892, EJ
 * "Review of Benson's Capital, Labor and Trade", 1892, EJ
 * "Review of Smart's Women's Wages", 1893
 * "Review of Bonar's Philosophy", 1893, Mind
 * "Review of Walsh's Bimetallism", 1893, EJ
 * "Review of Fisher's Mathematical Investigations", 1893, EJ
 * "Professor Böhm-Bawerk on the Ultimate Standard of Value", 1894, EJ
 * "One More Word on the Ultimate Standard of Value", 1894, EJ
 * "Review of Wiser's Natural Value", 1894, EJ
 * "Theory of International Values: Parts I, II and III", 1894, EJ
 * "Recent Writings on Index Numbers", 1894, EJ
 * "The Measurement of Utility by Money", 1894, EJ
 * "Asymmetric Correlation between Social Phenomenon", 1894, JRSS
 * Entries: "Average", "Census", "Cournot", "Curves", "Demand Curves", Difficulty of Attainment", "Distance in Time", "Error", 1894, in Palgrave, editor, Dictionary of Political Economy, Vol. 1.
 * "Review of the Webbs' History of Trade Unionism", 1894, EJ
 * "Review of Third Edition of Marshall's Principles", 1895, EJ
 * "Mr. Pierson on the Scarcity of Gold", 1895, EJ
 * "Thoughts on Monetary Reform", 1895, EJ
 * "The Stationary State in Japan", 1895, EJ
 * "A Defense of Index-Numbers", 1896, EJ
 * "Statistics on Unprogressive Communities", 1896, JRSS
 * "The Asymmetrical Probability Curve (Abstract)", 1894, Proceedings of the Royal Society
 * "The Asymmetrical Probability Curve", 1896, Phil Mag
 * "The Compound law of Error", 1896, Phil Mag
 * Entries: "Gossen", "Index Numbers", "Intrinsic Value", "Jenkin", "Jennings", "Least Squares" and "Mathematical Method", 1896, in Palgrave, editor, Dictionary of Political Economy, Vol. 2.
 * "Review of Price's Money", 1896, EJ
 * "Review of Nicholson's Strikes and Social Problems", 1896, EJ
 * "Review of Pierson's Leerboek, Vol. 1", 1896, EJ
 * "Review of Pierson's Leerkook, Vol. 2", 1897, EJ
 * "Review of Bastable, Theory of International Trade", 1897, EJ
 * "Review of Grazani's Istituzioni", 1897, EJ
 * "La teoria pura del monopolio", 1897, GdE, (trans."The Pure Theory of Monopoly")
 * "The Pure Theory of Taxation: Parts I, II and III", 1897, EJ
 * "Miscellaneous Applications of the Calculus of Probabilities", Parts 1, 2, 3, 1897, 1898, JRSS
 * "Review of Cournot's Recherches", 1898, EJ
 * "Professor Graziani on the Mathematical Theory of Monopoly", 1898, EJ
 * "Review of Darwin's Bimetallism", 1898, EJ
 * "On the Representation of Statistics by Mathematical Formulae", Part 1 (1898), Parts 2, 3, 4 (1899)
 * "On a Point in the Theory of International Trade", 1899, EJ
 * "Review of Davidson, Bargain Theory of Wages", 1899, EJ
 * "Professor Seligman on the Mathematical Method in Political Economy", 1899, EJ
 * Entries: "Pareto", "Pareto's Law", "Probability", Supply Curve" and "Utility", 1899, in Palgrave, editor, Dictionary of Political Economy, Vol. 3
 * "Answers to Questions by Local Taxation Commission", 1899, Reprint of Royal Commission for Local Taxation
 * "The Incidence of Urban Rates, Parts I, II and III" 1900, EJ
 * "Defence of Mr. Harrison's Calculation of the Rupee Circulation", 1900, EJ
 * "Review of J.B. Clark's Theory of Distribution", 1900, EJ
 * "Review of Smart's Taxation of Land-Values", 1900, EJ
 * "Review of Bastable, Theory of International Trade (3rd edition)", 1897, EJ
 * "Review of Bonar and Hollander, Letters of Ricardo", 1900, EJ
 * "Mr. Walsh on the Measurement of General Exchange Value", 1901, EJ
 * "Disputed Points in the Theory of International Trade", 1901, EJ
 * "Review of Gide's Cooperation", 1902, EJ
 * "Review of Wells's Anticipations", 1902, EJ
 * "Methods of Representing Statistics of Wages and Other Groups Not *"Fulfilling the Normal Law of Error", with A.L. Bowley, 1902, JRSS
 * "The Law of Error", 1902, Encycl Britannica
 * "Review of Cannan's History of Theories of Production", 1903, EJ
 * "Review of Bortkiewicz's Anwendungen and Pareto's Anwendungen", 1903, EJ
 * "Review of Bastable's Public Finance", 1903, EJ
 * "Review of Bastable's Cartels et Trusts", 1903, EJ
 * "Review of Pigou's Riddle of the Tariff", 1904, EJ
 * "Review of Nicholson's Elements", 1904, EJ
 * "Review of Bowley's National Progress", 1904, EJ
 * "Review of Plunkett's Ireland", 1904, EJ
 * "Review of Northon's Loan Credit", 1904, EJ
 * "Review of Graziani's Istituzione", 1904, EJ
 * "Review of Dietzel's Vergeltungzolle", 1904, EJ
 * "Preface", 1904, in J.R. MacDonald, editor, Women in the Printing Trades.
 * "The Theory of Distribution", 1904, QJE
 * "The Law of Error", 1905, Transactions of Cambridge Society
 * "Review of Nicholson's History of English Corn Laws", 1905, EJ
 * "Review of Cunynghame's Geometrical Political Economy", 1905, EJ
 * "Review of Carver's Theory of Distribution", 1905, EJ
 * "Review of Taussig's Present Position", 1905, EJ
 * "Review of Henry Sidgwick: A memoir", 1906, EJ
 * "The Generalised Law of Error, or Law of Great Numbers", 1906, JRSS
 * "Recent Schemes for Rating Urban Land Values", 1906, EJ
 * "On the Representation of Statistical Frequency by a Series", 1907, JRSS
 * "Statistical Observations on Wasps and Bees", 1907, Biometrika
 * "Review of de Foville's Monnaie and Guyot's Science economique", 1907, EJ
 * "Appreciations of Mathematical Theories", Parts I & II (1907), Parts III & IV (1908), EJ
 * "On the Probable Errors of Frequency Constants", I, II & III (1908), Add. (1909), JRSS
 * "Review of Andreades's Lecture on the Census", 1908, EJ
 * "Review of Rea's Free Trade", 1908, EJ
 * "Review of Withers's Meaning of Money", 1909, EJ
 * "Review of Mitchell's Gold Prices", 1909, EJ
 * "Review of Jevons's Investigations", 1909, EJ
 * "Application du calcul des probabilités à la Statistique", 1909, Bulletin de l'Institut international de statistique
 * "On the Use of the Differential Calculus in Economics to Determine Conditions of Maximum Advantage", 1909, Scientia
 * "Applications of Probabilities to Economics, Parts I & II", 1910, EJ.
 * "The Subjective Element in the First Principles of Taxation", 1910, QJE
 * "Review of John Stuart Mill's Principles", 1910, EJ
 * "Review of Colson's Cours", 1910, EJ
 * "Review of J. Maurice Clark's Local Freight Discriminations", 1910, EJ
 * "Review of Hammond's Railway Rate Theories", 1911, EJ
 * "Probability and Expectation", 1911, Encycl Britannica
 * "Monopoly and Differential Prices", 1911, EJ
 * "Contributions to the Theory of Railway Rates", Part I & II (1911), Part III (1912), Part IV (1913), EJ
 * "Review of Moore's Laws of Wages", 1912, EJ
 * "Review of Pigou's Wealth and Welfare", 1913, EJ
 * "On the Use of the Theory of Probabilities in Statistics Relating to Society", 1913, J of RSS
 * "A Variant Proof of the Distribution of Velocities in a Molecular Chaos", 1913, PhilMag
 * "On the Use of Analytical Geometry to Represent Certain Kinds of Statistics", Parts I–V, 1914, J of RSS
 * "Recent Contributions to Mathematical Economics, I & II", 1915, EJ
 * On the Relations of Political Economy to War, 1915.
 * The Cost of War and ways of reducing it suggested by economic theory, 1915.
 * "Economists on War: Review of Sombart, etc.", 1915, EJ
 * "Review of Pigou's Economy and Finance of War", 1916, EJ
 * "Review of Preziosi's La Germania alla Conquista dell' Italia", 1916, EJ
 * "British Incomes and Property", 1916, EJ
 * "On the Mathematical Representation of Statistical Data", Part I (1916), Parts II–IV (1917), J of RSS
 * "Review of Gill's National Power and Prosperity", 1917, EJ
 * "Review of Lehfeldt's Economics in Light of War", 1917, EJ
 * "Some German Economic Writings about the War", 1917, EJ
 * "After-War Problems: Review of Dawson at al.", 1917, EJ
 * "Review of Westergaard's Scope and Methods of Statistics", 1917, JRSS
 * "Review of Anderson's Value of Money", 1918, EJ
 * "Review of Moulton and Phillips on Money and Banking", 1918, EJ
 * "Review of Loria's Economic Causes of War", 1918, EJ
 * "Review of Arias's Principii", 1918, EJ
 * "Review of Smith-Gordon, Rural Reconstruction of Ireland and Russell's National Being", 1918, EJ
 * "On the Value of a Mean as Calculated from a Sample", 1918, EJ
 * "An Astronomer on the Law of Error", 1918, PhilMag
 * Currency and Finance in Time of War, 1918.
 * "The Doctrine of Index-Numbers According to Prof. Wesley Mitchell", 1918, EJ
 * "Psychical Research and Statistical Method", 1919, JRSS
 * "Methods of Graduating Taxes on Income and Capital", 1919, EJ
 * "Review of Cannan's Money", 1919, EJ
 * "Review of Andreades's Historia", 1919, EJ
 * "Review of Lehfeldt's Gold Prices", 1919, EJ
 * A Levy on Capital for the Discharge of the Debt, 1919.
 * "Mathematical Formulae and the National Commission on Income Tax", 1920, EJ
 * "On the Application of Probabilities to the Movement of Gas Molecules", Part I (1920), Part II (1922), Phil Mag
 * "Entomological Statistics", 1920, Metron, pp. 75–80
 * "Review of Gustav Cassel's Theory of Social Economy", 1920, EJ
 * "Review of Bowley's Change in Distribution of National Income", 1920, JRSS
 * "Review of the Webbs' History of Trade Unionism", 1920, EJ
 * "Molecular Statistics", Part I (1921), Part II (1922), JRSS
 * "On the Genesis of the Law of Eror", 1921, PhilMag
 * "The Philosophy of Chance", 1922, Mind
 * "The Mathematical Economics of Professor Amoroso", 1922, EJ
 * "Equal Pay to Men and Women for Equal Work", 1922, EJ
 * "Review of Keynes's Treatise on Probability", 1922, JRSS
 * "Review of Pigou's Political Economy of War", 1922, EJ
 * "Statistics of Examinations", 1923, JRSS
 * "On the Use of Medians for Reducing Observations Relating to Several Quantities", 1923, Phil Mag
 * "Mr. Correa Walsh on the Calculation of Index Numbers", 1923, JRSS
 * "Index Numbers According to Mr. Walsh", 1923, EJ
 * "Women's Wages in Relation to Economic Welfare", 1923, EJ
 * Also available as:
 * Also available as:

 * "Review of Marshall's Money, Credit and Commerce", 1923, EJ
 * "Review of The Labour Party's Aim", 1923, EJ
 * "Review of Bowley's Mathematical Groundwork", 1924, EJ
 * "Review of Fisher's Economic Position of the Married Woman", 1924, EJ
 * "Untried Methods of Representing Frequency", 1924, JRSS
 * Papers Relating to Political Economy, 3 volumes, 1925.
 * "The Plurality of Index-Numbers", 1925, EJ
 * "The Element of Probability in Index-Numbers", 1925, JRSS
 * "The Revised Doctrine of Marginal Social Product", 1925, EJ
 * "Review of J.M. Clark's Overhead Costs", 1925, EJ.
 * "mathematical method in political economy," 1926, Palgrave's Dictionary of Political Economy, reprinted in 1987, The New Palgrave: A Dictionary of Economics, v. 3.
 * "Mr Rhode's Curve and the Method of Adjustment", 1926, JRSS

title: Francis Ysidro Edgeworth


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Viscount Brackley

The title Viscount Brackley has been created twice for members of the Egerton family; once in the Peerage of England and once in the Peerage of the United Kingdom.

The first creation in the Peerage of England was in 1616 for Thomas Egerton, 1st Baron Ellesmere (1540–1617), who had been created 1st Baron Ellesmere in 1603. He died a year later and his barony and viscountcy merged with the earldom of Bridgewater, which was created for his son, John Egerton. The earldom had been meant for Thomas Egerton, but he died before he could receive it.

The second creation in the Peerage of the United Kingdom was in 1846 for Francis Egerton (1800–1857) as a subsidiary title of the earldom of Ellesmere. In 1963, the 5th Earl of Ellesmere (1915–2000) succeeded as Duke of Sutherland and the title of Viscount Brackley merged with the dukedom.

Viscounts Brackley, first Creation (1616)
For further succession, see Earl of Bridgewater, second creation
 * Thomas Egerton, 1st Baron Ellesmere (1540–1617) (created Viscount Brackley)
 * John Egerton, 2nd Viscount Brackley (1579–1649) (created Earl of Bridgewater in 1617)

Viscounts Brackley, second Creation (1846)

 * see Earl of Ellesmere

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

title: Viscount Brackley


text:
Earl of Ellesmere

Earl of Ellesmere, of Ellesmere in the County of Shropshire, is a title in the Peerage of the United Kingdom. It was created in 1846 for the Conservative politician Lord Francis Egerton. He was granted the subsidiary title of Viscount Brackley, of Brackley in the County of Northampton, at the same time, also in the Peerage of the United Kingdom. Born Lord Francis Leveson-Gower, he was the third son of George Leveson-Gower, 1st Duke of Sutherland and Elizabeth Gordon, 19th Countess of Sutherland. In 1803 his father had inherited the substantial estates of his maternal uncle Francis Egerton, 3rd Duke of Bridgewater. On his father's death in 1833, Lord Francis succeeded to the Egerton estates according to the will of the late Duke of Bridgewater, and assumed by Royal licence the surname of Egerton in lieu of Leveson-Gower. The Brackley and Ellesmere titles created for him in 1846 were revivals of titles held by the Dukes of Bridgewater. In 1963 his great-great-grandson, the fifth Earl, succeeded his kinsman as 6th Duke of Sutherland. The earldom of Ellesmere and viscountcy of Brackley are now subsidiary titles of the dukedom.

The Hon. Alfred Egerton, younger son of the second Earl, represented Eccles in Parliament.

The family seat was Worsley New Hall.

Earls of Ellesmere (1846)
For further Earls of Ellesmere, see the Duke of Sutherland
 * Francis Egerton, 1st Earl of Ellesmere (1800–1857)
 * George Granville Francis Egerton, 2nd Earl of Ellesmere (1823–1862)
 * Francis Charles Granville Egerton, 3rd Earl of Ellesmere (1847–1914)
 * John Francis Granville Scrope Egerton, 4th Earl of Ellesmere (1872–1944)
 * John Sutherland Egerton, 5th Earl of Ellesmere (1915–2000) (succeeded as Duke of Sutherland in 1963)

title: Earl of Ellesmere


text:
Talk:Conservative bias

Not created because it was important, just because it was referenced but empty. I carefully avoided mentioning my own belief that the entire liberal/conservative dichotomy is severely outdated and that I find discussion of liberal or conservative bias to be more quaint than relivent. Also becuase I thought the topic was mildly funny. --soto 01:43, 8 May 2004 (UTC)

This really needs to be expanded with specific examples of this claim being made. I don't think that should be hard to do, but I'm up to my neck in other projects. -- Jmabel 05:17, 8 May 2004 (UTC)

Under NPOV tutorial/guidelines. I am creating a outline in favor of conservative bias. Please do not delete anything. Simply add or arrange. Thank you.--dis- 14:13, 9 Feb 2005 (UTC)

This article seems to be mainly about denial of claims of liberal bias, rather than claims of conservative bias itself. Ironically, liberal bias has more on the latter than this article. This also seems to imply that denial of claims of liberal bias originated in the blogosphere, which is ridiculous. There isn't even a link to Manufacturing Consent here. — Gwalla | Talk 00:17, 16 Mar 2005 (UTC)

I reworked the article for -- clarity, sources, NPOV and factual basis of demonstrated conservative bias in media. It's not a question of claims, that's a weasele's word. The questions of conservative bias center on that which has been substantiated and is based on fact-checking, content analysis, accurate references to quotes and source documentation and empolyment of the standards of ethical journalism. Calicocat 17:23, 10 July 2005 (UTC)

title: Talk:Conservative bias


text:
Generalized anxiety disorder

Generalized anxiety disorder (GAD) is a mental and behavioral disorder, specifically an anxiety disorder characterized by excessive, uncontrollable and often irrational worry about events or activities. Worry often interferes with daily functioning, and individuals with GAD are often overly concerned about everyday matters such as health, finances, death, family, relationship concerns, or work difficulties. Symptoms may include excessive worry, restlessness, trouble sleeping, exhaustion, irritability, sweating, and trembling.

Symptoms must be consistent and ongoing, persisting at least six months, for a formal diagnosis of GAD. Individuals with GAD often have other disorders including other psychiatric disorders (e.g., major depressive disorder), substance use disorder, obesity, and may have a history of trauma or family with GAD. Clinicians use screening tools such as the GAD-7 and GAD-2 questionnaires to determine if individuals may have GAD and warrant formal evaluation for the disorder. Additionally, sometimes screening tools may enable clinicians to evaluate the severity of GAD symptoms.

GAD is believed to have a hereditary or genetic basis (e.g., first-degree relatives of an individual who has GAD are themselves more likely to have GAD), but the exact nature of this relationship is not fully appreciated. Genetic studies of individuals who have anxiety disorders (including GAD) suggest that the hereditary contribution to developing anxiety disorders is only approximately 30–40%, which suggests that environmental factors may be more important to determining whether an individual develops GAD. There is a strong overlapping relationship between GAD and major depressive disorder (MDD), with 72% of those with a lifelong diagnosis of GAD also being diagnosed with MDD at some point in their lives.

The pathophysiology of GAD implicates several regions of the brain that mediate the processing of stimuli associated with fear, anxiety, memory, and emotion (i.e., the amygdala, insula and the frontal cortex). The amygdala is part of the brain that is associated with experiencing emotions. In the amygdala, the basolateral amygdala complex recognizes sensory information and activates GABAergic neurons which can cause somatic symptoms of anxiety. GABAergic neurons control the nervous system by reducing feelings of stress, anxiety, and fear. When there is an inadequate number of GABAergic neurons, those negative feelings become apparent and can release somatic responses of stress. It has been suggested that individuals with GAD have greater amygdala and medial prefrontal cortex (mPFC) activity in response to stimuli than individuals who do not have GAD. However, the relationship between GAD and activity levels in other parts of the frontal cortex is the subject of ongoing research with some literature suggesting greater activation in specific regions for individuals who have GAD but where other research suggests decreased activation levels in individuals who have GAD as compared to individuals who do not have GAD.

Treatment includes psychotherapy (e.g., cognitive behavioral therapy [CBT] or metacognitive therapy) and pharmacological intervention (e.g., cannabis, citalopram, escitalopram, sertraline, duloxetine, and venlafaxine). CBT and selective serotonin reuptake inhibitors (SSRIs) are first-line psychological and pharmacological treatments; other options include selective norepinephrine reuptake inhibitors (SNRIs). In Europe, pregabalin is also used. The positive effects (if any) of complementary and alternative medications (CAMs), exercise, therapeutic massage and other interventions have been studied.

Estimates regarding prevalence of GAD or lifetime risk (i.e., lifetime morbid risk [LMR]) for GAD vary depending upon which criteria are used for diagnosing GAD (e.g., DSM-5 versus ICD-10) although estimates do not vary widely between diagnostic criteria. In general, ICD-10 is more inclusive than DSM-5, so estimates regarding prevalence and lifetime risk tend to be greater using ICD-10. In regard to prevalence, in a given year, about two (2%) percent of adults in the United States and Europe have been suggested to have GAD. However, the risk of developing GAD at any point in life has been estimated at 9.0%. Although it is possible to experience a single episode of GAD during one's life, most people who experience GAD experience it repeatedly over the course of their lives as a chronic or ongoing condition. GAD is diagnosed twice as frequently in women as in men.

DSM-5 criteria
The diagnostic criteria for GAD as defined by the Diagnostic and Statistical Manual of Mental Disorders DSM-5 (2013), published by the American Psychiatric Association, are paraphrased as follows: 1. "Excessive anxiety or worry" experienced most days over at least six months and which involve a plurality of concerns.

2. Inability to manage worry.

3. At least three of the following occur:

Note that in children, only one of the above items is required.

4. One experiences significant distress in functioning (e.g., work, school, social life).

5. Symptoms are not due to a substance use disorder, prescription medication, or other medical condition(s).

6. Symptoms do not fit better with another psychiatric condition such as panic disorder.No major changes to GAD have occurred since publication of the Diagnostic and Statistical Manual of Mental Disorders (2004); minor changes include wording of diagnostic criteria.

ICD-10 criteria
The 10th revision of the International Statistical Classification of Disease (ICD-10) provides a different set of diagnostic criteria for GAD than the DSM-5 criteria described above. In particular, ICD-10 allows diagnosis of GAD as follows:

See ICD-10 F41.1 Note: For children different ICD-10 criteria may be applied for diagnosing GAD (see F93.80).

History of diagnostic criteria
The American Psychiatric Association introduced GAD as a diagnosis in the DSM-III in 1980, when anxiety neurosis was split into GAD and panic disorder. The definition in the DSM-III required uncontrollable and diffuse anxiety or worry that is excessive and unrealistic and persists for 1 month or longer. High rates in comorbidity of GAD and major depression led many commentators to suggest that GAD would be better conceptualized as an aspect of major depression instead of an independent disorder. Many critics stated that the diagnostic features of this disorder were not well established until the DSM-III-R. Since comorbidity of GAD and other disorders decreased with time, the DSM-III-R changed the time requirement for a GAD diagnosis to 6 months or longer. The DSM-IV changed the definition of excessive worry and the number of associated psychophysiological symptoms required for a diagnosis. Another aspect of the diagnosis the DSM-IV clarified was what constitutes a symptom as occurring "often". The DSM-IV also required difficulty controlling the worry to be diagnosed with GAD. The DSM-5 emphasized that excessive worrying had to occur more days than not and on a number of different topics. It has been stated that the constant changes in the diagnostic features of the disorder have made assessing epidemiological statistics such as prevalence and incidence difficult, as well as increasing the difficulty for researchers in identifying the biological and psychological underpinnings of the disorder. Consequently, making specialized medications for the disorder is more difficult as well. This has led to the continuation of GAD being medicated heavily with SSRIs.

Genetics, family and environment
The relationship between genetics and anxiety disorders is an ongoing area of research. It is broadly understood that there exists a hereditary basis for GAD, but the exact nature of this hereditary basis is not fully understood. While investigators have identified several genetic loci that are regions of interest for further study, there is no singular gene or set of genes that have been identified as causing GAD. Nevertheless, genetic factors may play a role in determining whether an individual is at greater risk for developing GAD, structural changes in the brain related to GAD, or whether an individual is more or less likely to respond to a particular treatment modality. Genetic factors that may play a role in development of GAD are usually discussed in view of environmental factors (e.g., life experience or ongoing stress) that might also play a role in development of GAD. The traditional methods of investigating the possible hereditary basis of GAD include using family studies and twin studies (there are no known adoption studies of individuals who have anxiety disorders, including GAD). Meta-analysis of family and twin studies suggests that there is strong evidence of a hereditary basis for GAD in that GAD is more likely to occur in first-degree relatives of individuals who have GAD than in non-related individuals in the same population. Twin studies also suggest that there may be a genetic linkage between GAD and major depressive disorder (MDD), which may explain the common occurrence of MDD in individuals who have GAD (e.g., comorbidity of MDD in individuals with GAD has been estimated at 60% ). When GAD is considered among all anxiety disorders (e.g., panic disorder, social anxiety disorder), genetic studies suggest that hereditary contribution to the development of anxiety disorders amounts to only approximately 30–40%, which suggests that environmental factors are likely more important to determining whether an individual may develop GAD. In regard to environmental influences in the development of GAD, it has been suggested that parenting behaviour may be an important influence since parents potentially model anxiety-related behaviours. It has also been suggested that individuals with GAD have experienced a greater number of minor stress-related events in life and that the number of stress-related events may be important in development of GAD (irrespective of other individual characteristics).

Studies of possible genetic contributions to the development of GAD have examined relationships between genes implicated in brain structures involved in identifying potential threats (e.g., in the amygdala) and also implicated in neurotransmitters and neurotransmitter receptors known to be involved in anxiety disorders. More specifically, genes studied for their relationship to development of GAD or demonstrated to have had a relationship to treatment response include:

 * PACAP (A54G polymorphism): remission after 6-month treatment with Venlafaxine suggested to have a significant relationship with the A54G polymorphism (Cooper et al. (2013))
 * HTR2A gene (rs7997012 SNP G allele): HTR2A allele suggested to be implicated in a significant decrease in anxiety symptoms associated with response to 6 months of Venlafaxine treatment (Lohoff et al. (2013))
 * SLC6A4 promoter region (5-HTTLPR): Serotonin transporter gene suggested to be implicated in significant reduction in anxiety symptoms in response to 6 months of Venlafaxine treatment (Lohoff et al. (2013))

Pathophysiology
The pathophysiology of GAD is an active and ongoing area of research often involving the intersection of genetics and neurological structures. Generalized anxiety disorder has been linked to changes in functional connectivity of the amygdala and its processing of fear and anxiety. Sensory information enters the amygdala through the nuclei of the basolateral complex (consisting of lateral, basal and accessory basal nuclei). The basolateral complex processes the sensory-related fear memories and communicates information regarding threat importance to memory and sensory processing elsewhere in the brain, such as the medial prefrontal cortex and sensory cortices. Neurological structures traditionally appreciated for their roles in anxiety include the amygdala, insula and orbitofrontal cortex (OFC). It is broadly postulated that changes in one or more of these neurological structures are believed to allow greater amygdala response to emotional stimuli in individuals who have GAD as compared to individuals who do not have GAD.

Individuals with GAD have been suggested to have greater amygdala and medial prefrontal cortex (mPFC) activation in response to stimuli than individuals who do not have GAD. However, the exact relationship between the amygdala and the frontal cortex (e.g., prefrontal cortex or the orbitofrontal cortex [OFC]) is not fully understood because there are studies that suggest increased or decreased activity in the frontal cortex in individuals who have GAD. Consequently, because of the tenuous understanding of the frontal cortex as it relates to the amygdala in individuals who have GAD, it's an open question as to whether individuals who have GAD bear an amygdala that is more sensitive than an amygdala in an individual without GAD or whether frontal cortex hyperactivity is responsible for changes in amygdala responsiveness to various stimuli. Recent studies have attempted to identify specific regions of the frontal cortex (e.g., dorsomedial prefrontal cortex [dmPFC]) that may be more or less reactive in individuals who have GAD or specific networks that may be differentially implicated in individuals who have GAD. Other lines of study investigate whether activation patterns vary in individuals who have GAD at different ages with respect to individuals who do not have GAD at the same age (e.g., amygdala activation in adolescents with GAD).

Treatment
Traditional treatment modalities broadly fall into two categories, i.e., psychotherapeutic and pharmacological intervention. In addition to these two conventional therapeutic approaches, areas of active investigation include complementary and alternative medications (CAMs), brain stimulation, exercise, therapeutic massage and other interventions that have been proposed for further study. Treatment modalities can, and often are, utilized concurrently so that an individual may pursue psychological therapy (i.e., psychotherapy) and pharmacological therapy. Both cognitive behavioral therapy (CBT) and medications (such as SSRIs) have been shown to be effective in reducing anxiety. A combination of both CBT and medication is generally seen as the most desirable approach to treatment. Use of medication to lower extreme anxiety levels can be important in enabling patients to engage effectively in CBT.

Psychotherapy
Psychotherapeutic interventions include a plurality of therapy types that vary based upon their specific methodologies for enabling individuals to gain insight into the working of the conscious and subconscious mind and which sometimes focus on the relationship between cognition and behavior. Cognitive behavioral therapy (CBT) is widely regarded as the first-line psychological therapy for treating GAD. Additionally, many of these psychological interventions may be delivered in an individual or group therapy setting. While individual and group settings are broadly both considered effective for treating GAD, individual therapy tends to promote longer-lasting engagement in therapy (i.e., lower attrition over time).

Psychodynamic therapy
Psychodynamic therapy is a type of therapy premised upon Freudian psychology in which a psychologist enables an individual explore various elements in their subconscious mind to resolve conflicts that may exist between the conscious and subconscious elements of the mind. In the context of GAD, the psychodynamic theory of anxiety suggests that the unconscious mind engages in worry as a defense mechanism to avoid feelings of anger or hostility because such feelings might cause social isolation or other negative attribution toward oneself. Accordingly, the various psychodynamic therapies attempt to explore the nature of worry as it functions in GAD in order to enable individuals to alter the subconscious practice of using worry as a defense mechanism and to thereby diminish GAD symptoms. Variations of psychotherapy include a near-term version of therapy, "short-term anxiety-provoking psychotherapy (STAPP).

Behavioral therapy
Behavioral therapy is therapeutic intervention premised upon the concept that anxiety is learned through classical conditioning (e.g., in view of one or more negative experiences) and maintained through operant conditioning (e.g., one finds that by avoiding a feared experience that one avoids anxiety). Thus, behavioral therapy enables an individual to re-learn conditioned responses (behaviors) and to thereby challenge behaviors that have become conditioned responses to fear and anxiety, and which have previously given rise to further maladaptive behaviors.

Cognitive therapy
Cognitive therapy (CT) is premised upon the idea that anxiety is the result of maladaptive beliefs and methods of thinking. Thus, CT involves assisting individuals to identify more rational ways of thinking and to replace maladaptive thinking patterns (i.e., cognitive distortions) with healthier thinking patterns (e.g., replacing the cognitive distortion of catastrophizing with a more productive pattern of thinking). Individuals in CT learn how to identify objective evidence, test hypotheses, and ultimately identify maladaptive thinking patterns so that these patterns can be challenged and replaced.

Acceptance and commitment therapy
Acceptance and commitment therapy (ACT) is a behavioral treatment based on acceptance-based models. ACT is designed with the purpose to target three therapeutic goals: (1) reduce the use of avoiding strategies intended to avoid feelings, thoughts, memories, and sensations; (2) decreasing a person's literal response to their thoughts (e.g., understanding that thinking "I'm hopeless" does not mean that the person's life is truly hopeless), and (3) increasing the person's ability to keep commitments to changing their behaviors. These goals are attained by switching the person's attempt to control events to working towards changing their behavior and focusing on valued directions and goals in their lives as well as committing to behaviors that help the individual accomplish those personal goals. This psychological therapy teaches mindfulness (paying attention on purpose, in the present, and in a nonjudgmental manner) and acceptance (openness and willingness to sustain contact) skills for responding to uncontrollable events and therefore manifesting behaviors that enact personal values.

Intolerance of uncertainty therapy
Intolerance of uncertainty (IU) refers to a consistent negative reaction to uncertain and ambiguous events regardless of their likelihood of occurrence. Intolerance of uncertainty therapy (IUT) is used as a stand-alone treatment for GAD patients. Thus, IUT focuses on helping patients in developing the ability to tolerate, cope with and accept uncertainty in their life in order to reduce anxiety. IUT is based on the psychological components of psychoeducation, awareness of worry, problem-solving training, re-evaluation of the usefulness of worry, imagining virtual exposure, recognition of uncertainty, and behavioral exposure. Studies have shown support for the efficacy of this therapy with GAD patients with continued improvements in follow-up periods.

Motivational interviewing
A promising innovative approach to improving recovery rates for the treatment of GAD is to combine CBT with motivational interviewing (MI). Motivational interviewing is a strategy centered on the patient that aims to increase intrinsic motivation and decrease ambivalence about change due to the treatment. MI contains four key elements: (1) express empathy, (2) heighten dissonance between behaviors that are not desired and values that are not consistent with those behaviors, (3) move with resistance rather than direct confrontation, and (4) encourage self-efficacy. It is based on asking open-ended questions and listening carefully and reflectively to patients' answers, eliciting "change talk", and talking with patients about the pros and cons of change. Some studies have shown the combination of CBT with MI to be more effective than CBT alone.

Cognitive behavioral therapy
Cognitive behavioral therapy (CBT) is an evidence-based type of psychotherapy that demonstrates efficacy in treating GAD and which integrates the cognitive and behavioral therapeutic approaches. The objective of CBT is to enable individuals to identify irrational thoughts that cause anxiety and to challenge dysfunctional thinking patterns by engaging in awareness techniques such as hypothesis testing and journaling. Because CBT involves the practice of worry and anxiety management, CBT includes a plurality of intervention techniques that enable individuals to explore worry, anxiety and automatic negative thinking patterns. These interventions include anxiety management training, cognitive restructuring, progressive relaxation, situational exposure and self-controlled desensitization. Several modes of delivery are effective in treating GAD, including internet-delivered CBT, or iCBT.

Emotion-focused therapy
Emotion-focused therapy (EFT) is a short-term psychotherapy that is focused on humanistic needs of emotions when treating individuals with GAD. EFT can incorporate numerous practices such as experimental therapy, systemic therapy, and elements of CBT to allow individuals to work through difficult emotional states. The primary goal of EFT is assisting individuals in living with their vulnerable emotions and overcoming avoidance so that adaptive experiences such as compassion and protective anger can be generated in response to the emotional needs that are embedded in core emotional vulnerability.

Sandplay therapy
Sandplay therapy (SPT) is an intervention based on nonverbal therapeutic practices. The main objective of SPT is to allow the individual the ability to work through their emotional problems from childhood traumas (CT) through play using sand and toy figures. Although the therapy is mainly focused on nonverbal cues, verbal cues are also observed and documented during the rehabilitation process of the individual. SPT allows a multisensory experience through a safe and protected space allowing the individual the opportunity to regulate their mind and emotions. This therapeutic practice is offered in both adults and children.

Exposure therapy
There is empirical evidence that exposure therapy can be an effective treatment for people with GAD, citing specifically in vivo exposure therapy (exposure through a real-life situation), which has greater effectiveness than imaginal exposure in regards to generalized anxiety disorder. The aim of in vivo exposure treatment is to promote emotional regulation using systematic and controlled therapeutic exposure to traumatic stimuli. Exposure is used to promote fear tolerance.

Exposure therapy is also a preferred method for children who struggle with anxiety.

Other forms of psychological therapy

 * Relaxation techniques (e.g., relaxing imagery, meditational relaxation)
 * Metacognitive therapy (MCT) : The objective of MCT is to alter thinking patterns regarding worry so that worry is no longer used as a coping strategy. It has promising results in treatment of GAD as well as other mental issues.
 * Mindfulness based stress reduction (MBSR)
 * Mindfulness based cognitive therapy (MBCT): The goal of MBCT is to be used as an alternative or adjunctive to Cognitive Behavior Therapy (CBT).
 * Supportive therapy : This is a Rogerian method of therapy in which subjects experience empathy and acceptance from their therapist to facilitate increasing awareness. Variations of active supportive therapy include Gestalt therapy, Transactional analysis and Counseling.
 * Internet-delivered interpretation training: The focus of this training is to reduce worry and anxiety while promoting positive outcomes and positive interpretations.

Pharmacotherapy
Medications that have been studied were reviewed in a recent network meta-analysis that compared all studied medications with placebo and also with each other and another compared the rates of remission between different medications. Benzodiazepines (BZs) have been used to treat anxiety starting in the 1960s. There is a risk of dependence and tolerance to benzodiazepines. BZs have a number of effects that make them a good option for treating anxiety including anxiolytic, hypnotic (induce sleep), myorelaxant (relax muscles), anticonvulsant, and amnestic (impair short-term memory) properties. While BZs work well to alleviate anxiety shortly after administration, they are also known for their ability to promote dependence and are frequently used recreationally or non-medically. Antidepressants (e.g., SSRIs / SNRIs) have become a mainstay in treating GAD in adults. First-line medications from any drug category often include those that have been approved by the Food and Drug Administration (FDA) or other similar regulatory body such as the EMA or TGA for treating GAD because these drugs have been shown to be safe and effective.

FDA-approved medications for treating GAD
FDA-approved medications for treating GAD include:    1. SSRIs

2. SNRIs

3. Benzodiazepines

4. Azapirones

5.

6.

Non-FDA approved medications
While certain medications are not specifically FDA approved for treatment of GAD, there are a number of medications that historically have been used or studied for treating GAD. Other medications that have been used or evaluated for treating GAD include:

 * SSRIs (antidepressants)
 * Citalopram
 * Fluoxetine
 * Sertraline
 * Fluvoxamine
 * Benzodiazepines
 * Clonazepam
 * Lorazepam
 * Diazepam
 * GABA analogs
 * Pregabalin
 * Tiagabine
 * Second-generation antipsychotics (SGAs)
 * Olanzapine (evidence of effectiveness is merely a trend)
 * Ziprasidone
 * Risperidone
 * Aripiprazole (studied as an adjunctive measure in concert with other treatment)
 * Quetiapine (atypical antipsychotic studied as an adjunctive measure in adults and geriatric patients)
 * Antihistamines
 * Hydroxyzine (H1 receptor antagonist)
 * Vilazodone (atypical antidepressant)
 * Agomelatine (antidepressant, MT1/2 receptor agonist, 5-HT2C antagonist)
 * Clonidine (noted to cause decreased blood pressure and other AEs)
 * Guanfacine (α2A receptor agonist, studied in pediatric patients with GAD)
 * Mirtazapine (atypical antidepressant having 5-HT2A and 5-HT2C receptor affinity)
 * Vortioxetine (multimodal antidepressant)
 * Eszopiclone (non-benzodiazepine hypnotic)
 * Tricyclic antidepressants
 * Amitriptyline
 * Clomipramine
 * Doxepin
 * Imipramine
 * Trimipramine
 * Desipramine
 * Nortriptyline
 * Protriptyline
 * Opipramol (atypical TCA)
 * Trazodone
 * Monamine oxidase inhibitors (MAOIs)
 * Tranylcypromine
 * Phenelzine
 * Homeopathic preparations (discussed below, see complementary and alternative medications [CAMs])

Selective serotonin reuptake inhibitors
Pharmaceutical treatments for GAD include selective serotonin reuptake inhibitors (SSRIs). SSRIs increase serotonin levels through inhibition of serotonin reuptake receptors.

FDA approved SSRIs used for this purpose include escitalopram and paroxetine. However, guidelines suggest using sertraline first due to its cost-effectiveness compared to other SSRIs used for generalized anxiety disorder and a lower risk of withdrawal compared to SNRIs. If sertraline is found to be ineffective, then it is recommended to try another SSRI or SNRI.

Common side effects include nausea, sexual dysfunction, headache, diarrhea, constipation, restlessness, increased risk of suicide in young adults and adolescents, among others. Sexual side effects, weight gain, and higher risk of withdrawal are more common in paroxetine than escitalopram and sertraline. In older populations or those taking concomitant medications that increase risk of bleeding, SSRIs may further increase the risk of bleeding. Overdose of an SSRI or concomitant use with another agent that causes increased levels of serotonin can result in serotonin syndrome, which can be life-threatening.

Serotonin norepinephrine reuptake inhibitors
First line pharmaceutical treatments for GAD also include serotonin-norepinephrine reuptake inhibitors (SNRIs). These inhibit the reuptake of serotonin and noradrenaline to increase their levels in the CNS.

FDA approved SNRIs used for this purpose include duloxetine (Cymbalta) and venlafaxine (Effexor). While SNRIs have similar efficacy as SSRIs, many psychiatrists prefer to use SSRIs first in the treatment of Generalized Anxiety Disorder. The slightly higher preference for SSRIs over SNRIs as a first choice for treatment of anxiety disorders may have been influenced by the observation of poorer tolerability of the SNRIs in comparison to SSRIs in systematic reviews of studies of depressed patients.

Side effects common to both SNRIs include anxiety, restlessness, nausea, weight loss, insomnia, dizziness, drowsiness, sweating, dry mouth, sexual dysfunction and weakness. In comparison to SSRIs, the SNRIs have a higher prevalence of the side effects of insomnia, dry mouth, nausea and high blood pressure. Both SNRIs have the potential for discontinuation syndrome after abrupt cessation, which can precipitate symptoms including motor disturbances and anxiety and may require tapering. Like other serotonergic agents, SNRIs have the potential to cause serotonin syndrome, a potentially fatal systemic response to serotonergic excess that causes symptoms including agitation, restlessness, confusion, tachycardia, hypertension, mydriasis, ataxia, myoclonus, muscle rigidity, diaphoresis, diarrhea, headache, shivering, goose bumps, high fever, seizures, arrhythmia and unconsciousness. SNRIs like SSRIs carry a black box warning for suicidal ideation, but it is generally considered that the risk of suicide in untreated depression is far higher than the risk of suicide when depression is properly treated.

Pregabalin and gabapentin
Pregabalin (Lyrica) is effective for treating GAD. It acts on the voltage-dependent calcium channel to decrease the release of neurotransmitters such as glutamate, norepinephrine and substance P. Its therapeutic effect appears after 1 week of use and is similar in effectiveness to lorazepam, alprazolam and venlafaxine but pregabalin has demonstrated superiority by producing more consistent therapeutic effects for psychic and somatic anxiety symptoms. Long-term trials have shown continued effectiveness without the development of tolerance and additionally, unlike benzodiazepines, it does not disrupt sleep architecture and produces less severe cognitive and psychomotor impairment. It also has a low potential for misuse and dependency and may be preferred over the benzodiazepines for these reasons. The anxiolytic effects of pregabalin appear to persist for at least six months continuous use, suggesting tolerance is less of a concern; this gives pregabalin an advantage over certain anxiolytic medications such as benzodiazepines.

Gabapentin (Neurontin), a closely related medication to pregabalin with the same mechanism of action, has also demonstrated effectiveness in the treatment of GAD, though unlike pregabalin, it has not been approved specifically for this indication. Nonetheless, it is likely to be of similar usefulness in the management of this condition, and by virtue of being off-patent, it has the advantage of being significantly less expensive in comparison. In accordance, gabapentin is frequently prescribed off-label to treat GAD.

Complementary and alternative medicines studied for potential in treating GAD
Complementary and alternative medicines (CAMs) are widely used by individuals with GAD despite having no evidence or varied evidence regarding efficacy. Efficacy trials for CAM medications often have various types of bias and low quality reporting in regard to safety. In regard to efficacy, critics point out that CAM trials sometimes predicate claims of efficacy based on a comparison of a CAM against a known drug after which no difference in subjects is found by investigators and which is used to suggest an equivalence between a CAM and a drug. Because this equates a lack of evidence with the positive assertion of efficacy, a "lack of difference" assertion is not a proper claim for efficacy. Moreover, an absence of strict definitions and standards for CAM compounds further burdens the literature regarding CAM efficacy in treating GAD. CAMs academically studied for their potential in treating GAD or GAD symptoms along with a summary of academic findings are given below. What follows is a summary of academic findings. Accordingly, none of the following should be taken as offering medical guidance or an opinion as to the safety or efficacy of any of the following CAMs.

 * 1) Kava Kava (Piper methysticum) extracts: Meta analysis does not suggest efficacy of Kava extracts due to few data available yielding inconclusive results or non-statistically significant results. Nearly a quarter (25.8%) of subjects experienced adverse effects (AEs) from Kava Kava extracts during six trials. Kava Kava may cause liver toxicity.
 * 2) Lavender (Lavandula angustifolia) extracts: Small and varied studies may suggest some level of efficacy as compared to placebo or other medication; claims of efficacy are regarded as needing further evaluation.  Silexan is an oil derivative of Lavender studied in pediatric patients with GAD. Concern exists regarding the question as to whether Silexan may cause unopposed estrogen exposure in boys due to disruption of steroid signaling.
 * 3) Galphimia glauca extracts: While Galphima glauca extracts have been the subject of two randomised controlled trials (RCTs) comparing Galphima glauca extracts to lorazepam, efficacy claims are regarded as "highly uncertain."
 * 4) Chamomile (Matricaria chamomilla) extracts: Poor quality trials have trends that may suggest efficacy but further study is needed to establish any claim of efficacy.
 * 5) Crataegus oxycantha and Eschscholtzia californica extracts combined with magnesium: A single 12-week trial of Crataegus oxycantha and Eschscholtzia californica compared to placebo has been used to suggest efficacy. However, efficacy claims require confirmation studies. For the minority of subjects who experienced AEs from extracts, most AEs implicated gastrointestinal tract (GIT) intolerance.
 * 6) Echium amoneum extract: A single, small trial used this extract as a supplement to fluoxetine (vs using a placebo to supplement fluoxetine); larger studies are needed to substantiate efficacy claims.
 * 7) Gamisoyo-San: Small trials of this herbal mixture compared to placebo have suggested no efficacy of the herbal mixture over placebo but further study is necessary to allow definitive conclusion of a lack of efficacy.
 * 8) Passiflora incarnata extract: Claims of efficacy or benzodiazepam equivalence are regarded as "highly uncertain."
 * 9) Valeriana extract: A single 4-week trial suggests no effect of Valeriana extract on GAD but is regarded as "uninformative" on the topic of efficacy in view of its finding that the benzodiazepine diazepam also had no effect. Further study may be warranted.

Other possible modalities discussed in literature for potential in treating GAD
Other modalities that have been academically studied for their potential in treating GAD or symptoms of GAD are summarised below. What follows is a summary of academic findings. Accordingly, none of the following should be taken as offering medical guidance or an opinion as to the safety or efficacy of any of the following modalities.

 * 1) Acupuncture : A single, very small trial revealed a trend toward efficacy but flaws in the trial design suggest uncertainty regarding efficacy.
 * 2) Balneotherapy : Data from a single non-blinded study suggested possible efficacy of balneotherapy as compared to paroxetine. However, efficacy claims need confirmation.
 * 3) Therapeutic massage : A single, small, possibly biased study revealed inconclusive results.
 * 4) Resistance and aerobic exercise : When compared to no treatment, a single, small, potentially unrepresentative trial suggested a trend toward GAD remission and reduction of worry.
 * 5) Chinese bloodletting : When added to paroxetine, a single, small, imprecise trial that lacked a sham procedure for comparison suggested efficacy at 4-weeks. However, larger trials are needed to evaluate this technique as compared to a sham procedure.
 * 6) Floating in water : When compared to no treatment, a single, imprecise, non-blinded trial suggested a trend toward efficacy (findings were statistically insignificant).
 * 7) Swedish massage : When compared to a sham procedure, a single trial showed a trend toward efficacy (i.e., findings were statistically insignificant).
 * 8) Ayurvedic medications : a single non-blinded trial was inconclusive as to whether Ayurvedic medications were effective in treating GAD.
 * 9) Multifaith spiritually-based intervention : a single, small, non-blinded study was inconclusive regarding efficacy.

Lifestyle
Lifestyle factors including: stress management, stress reduction, relaxation, sleep hygiene, and caffeine and alcohol reduction can influence anxiety levels. Physical activity has shown to have a positive impact whereas low physical activity may be a risk factor for anxiety disorders.

There has also been increasing evidence behind exercise substantially alleviating anxiety. Early primates, such as the Homo Erectus, developed Achilles tendons and foot arches from its earlier ancestor, the tree-swinging Austrlopithecus. These features allowed the Homo Erectus to run and compete against other carnivores also scavenging for meat. Additionally, in a study examining humans and primates, scientists found how evolution has favored low levels of the alpha-2C adrenergic receptor. This protein coding gene helps inhibit the sympathetic nervous system, simultaneously suppressing anxiety. However, humans and their living ancestors, chimpanzees, lacked this gene. This led to a more active nervous system needed for fight-or-flight behavior in ancestral scavenging techniques and for fleeing predators.

Exercise has ancestral ties to human lifestyle; humans are built for exercise physically and neurologically. More studies are being conducted to investigate this claim and examine exercise's benefit on GAD.

Substances and anxiety in GAD
While there are no substances that are known to cause generalized anxiety disorder (GAD), certain substances or the withdrawal from certain substances have been implicated in promoting the experience of anxiety. For example, even while benzodiazepines may afford individuals with GAD relief from anxiety, withdrawal from benzodiazepines is associated with the experience of anxiety among other adverse events like sweating and tremor.

Tobacco withdrawal symptoms may provoke anxiety in smokers and excessive caffeine use has been linked to aggravating and maintaining anxiety.

Depression
A longitudinal cohort study found 12% of 972 participants had GAD comorbid with major depressive disorder. Accumulating evidence indicates that patients with comorbid depression and anxiety tend to have greater illness severity and a lower treatment response than those with either disorder alone. In addition, social function and quality of life are more greatly impaired.

For many, the symptoms of both depression and anxiety are not severe enough (i.e., are subsyndromal) to justify a primary diagnosis of either major depressive disorder (MDD) or an anxiety disorder. However, dysthymia is the most prevalent comorbid diagnosis of GAD clients. Patients can also be categorized as having mixed anxiety-depressive disorder, though this is an unstable diagnosis that typically either goes away or shifts to a different diagnosis later on.

Various explanations for the high comorbidity between GAD and depressive disorders have been suggested, ranging from genetic pleiotropy (i.e., GAD and nonbipolar depression might represent different phenotypic expressions of a common etiology ) to impaired executive control or sleep problems and fatigue as potential bridging mechanisms between the two disorders.

Comorbidity and treatment
Therapy has been shown to have equal efficacy in patients with GAD and patients with GAD and comorbid disorders. Patients with comorbid disorders have more severe symptoms when starting therapy but demonstrated a greater improvement than patients with simple GAD.

Pharmacological approaches, i.e., the use of antidepressants, must be adapted for different comorbidities. For example, serotonin reuptake inhibitors and short-acting benzodiazepines (BZDs) are used for depression and anxiety. However, for patients with anxiety and a substance use disorder, BZDs should be avoided due to their addictive properties. CBT has been found an effective treatment since it improves symptoms of GAD and substance use.

Compared to the general population, patients with internalizing disorders such as depression, generalized anxiety disorder (GAD) and post-traumatic stress disorder (PTSD) have higher mortality rates, but die of the same age-related diseases as the population, such as heart disease, cerebrovascular disease and cancer.

GAD often coexists with conditions associated with stress, such as muscle tension and irritable bowel syndrome.

Patients with GAD can sometimes present with symptoms such as insomnia or headaches as well as pain and interpersonal problems.

There is also observed comorbidity between GAD and attention deficit hyperactivity disorder. Anxiety disorders and major depressive disorder occur in a minority of individuals with ADHD, but more often than in the general population. Further research suggests that about 20 to 40 percent of individuals with attention deficit hyperactivity disorder have comorbid anxiety disorders, with GAD being the most prevalent.

Those with GAD have a lifetime comorbidity prevalence of 30% to 35% with alcohol use disorder and 25% to 30% for another substance use disorder. People with both GAD and a substance use disorder also have a higher lifetime prevalence for other comorbidities. A study found that GAD was the primary disorder in slightly more than half of the 18 participants that were comorbid with alcohol use disorder.

Epidemiology
GAD is often estimated to affect approximately 3–6% of adults and 5% of children and adolescents. Although estimates have varied to suggest a GAD prevalence of 3% in children and 10.8% in adolescents. When GAD manifests in children and adolescents, it typically begins around 8 to 9 years of age.

Estimates regarding prevalence of GAD or lifetime risk (i.e., lifetime morbid risk [LMR]) for GAD vary depending upon which criteria are used for diagnosing GAD (e.g., DSM-5 vs ICD-10) although estimates do not vary widely between diagnostic criteria. In general, ICD-10 is more inclusive than DSM-5, so estimates regarding prevalence and lifetime risk tend to be greater using ICD-10. In regard to prevalence, in a given year, about two (2%) percent of adults in the United States and Europe have been suggested to have GAD. However, the risk of developing GAD at any point in life has been estimated at 9.0%. Although it is possible to experience a single episode of GAD during one's life, most people who experience GAD experience it repeatedly over the course of their lives as a chronic or ongoing condition. GAD is diagnosed twice as frequently in women as in men and is more often diagnosed in those who are separated, divorced, unemployed, widowed or have low levels of education, and among those with low socioeconomic status. African Americans have higher odds of having GAD and the disorder often manifests itself in different patterns. It has been suggested that greater prevalence of GAD in women may be because women are more likely than men to live in poverty, are more frequently the subject of discrimination, and be sexually and physically abused more often than men. In regard to the first incidence of GAD in an individual's life course, a first manifestation of GAD usually occurs between the late teenage years and the early twenties with the median age of onset being approximately 31 and mean age of onset being 32.7. However, GAD can begin or reoccur at any point in life. Indeed, GAD is common in the elderly population.

United States
United States: Approximately 3.1 percent of people age 18 and over in a given year (9.5 million).

UK
5.9 percent of adults were affected by GAD in 2019.

Other

 * Australia: 3 percent of adults
 * Canada: 2.5 percent
 * Italy: 2.9 percent
 * Taiwan: 0.4 percent

title: Generalized anxiety disorder


text:
Earl of Bridgewater

Earl of Bridgewater was a title that has been created twice in the Peerage of England, once for the Daubeny family (1538) and once for the Egerton family (1617). From 1720 to 1803, the Earls of Bridgewater also held the title of Duke of Bridgewater. The 3rd Duke of Bridgewater is famously known as the "Canal Duke", for his creation of a series of canals in North West England.

Creation for the Daubeny family (1538)
The title Earl of Bridgewater was first created in 1538 for Henry Daubeny, 9th Baron Daubeny. The Daubeney (or Dabney ) family descended from Elias Daubeny, who in 1295 was summoned by writ to the Model Parliament as Lord Daubeny. The eighth Baron was created Baron Daubeny by letters patent in the Peerage of England in 1486 and was also made a Knight of the Garter the following year. All three titles became extinct on the first Earl of Bridgewater's death in 1548.

Creation for the Egerton family (1617)
The title Earl of Bridgewater was created secondly in 1617 for John Egerton, Baron Ellesmere and Viscount Brackley, after the town of Bridgwater in Somerset, where he owned estates. The Egerton family descended from Sir Richard Egerton of Ridley, Cheshire, whose illegitimate son Sir Thomas Egerton was a prominent lawyer who served as Master of the Rolls from 1594 to 1603, as Lord Keeper of the Great Seal from 1593 to 1603 and as Lord High Chancellor of England from 1603 to 1617. Thomas Egerton was knighted in 1594, admitted to the Privy Council in 1596 and in 1603 he was raised to the Peerage of England as Baron Ellesmere, in the County of Shropshire, and in 1616 to Viscount Brackley. In 1598 he had inherited the Tatton estate in Cheshire from his brother-in-law Richard Brereton. He was succeeded by his son, John who represented Callington and Shropshire in the House of Commons and served as Lord-Lieutenant of several counties in Wales and western England and who in 1617 was made Earl of Bridgewater in the Peerage of England.

He was succeeded by his eldest surviving son, the second Earl. He was Lord-Lieutenant of Buckinghamshire, Lancashire, Cheshire and Herefordshire. On his death the titles passed to his eldest son, the third Earl. He was a Whig politician and served as First Lord of Trade and as First Lord of the Admiralty. His eldest son from his first marriage, John Egerton, died as an infant, while his two elder sons from his second marriage, Charles Egerton, Viscount Brackley, and the Hon. Thomas Egerton, both died in the fire which destroyed Bridgwater House in London. Lord Bridgewater was succeeded by his eldest surviving son from his second marriage, the fourth Earl. He served as Lord-Lieutenant of Buckinghamshire and also held several positions at court. In 1720 he was created Marquess of Brackley, in the County of Northampton, and Duke of Bridgewater, in the County of Somerset. Both titles were in the Peerage of Great Britain.

The first Duke outlived his two elder sons and was succeeded by his second but eldest surviving son from his second marriage, the second Duke. He died from fever at an early age. On his death the titles passed to his younger brother, the third Duke. He is remembered as the father of British inland navigation and commissioned the Bridgewater Canal, said to be the first true canal in Britain and the modern world. Bridgewater never married and on his death in 1803 the marquessate and dukedom became extinct.

The last Duke was succeeded in the other titles by his first cousin once removed, the seventh Earl. He was the son of the Right Reverend the Hon. John Egerton, Bishop of Durham, son of the Right Reverend the Hon. Henry Egerton, Bishop of Hereford, youngest son of the third Earl. Lord Bridgewater was a General in the Army and also sat as Tory Member of Parliament for Morpeth and for Brackley. He was childless and on his death in 1823 the titles passed to his younger brother, the eighth Earl. He was known as a patron of science as well as a great eccentric. Lord Bridgewater never married and on his death in 1829 his titles became extinct.

In the early 17th century, Thomas Egerton, 1st Viscount Brackley, had purchased Ashridge House in Hertfordshire, one of the largest country houses in England, from Queen Elizabeth I, who had inherited it from her father who had appropriated it after the dissolution of the monasteries in 1539. Ashridge House served the Egerton family as a residence until the 19th century. The Egertons later had a family chapel (the Bridgewater Chapel) with burial vault in Little Gaddesden Church, where many monuments commemorate the Dukes and Earls of Bridgewater and their families. Among those buried here is the 3rd Duke of Bridgewater.

Lady Amelia Egerton, sister of the seventh and eighth Earls, married Sir Abraham Hume, 2nd Baronet. Their daughter Sophia Hume married John Cust, 1st Earl Brownlow. Their grandson John William Spencer Brownlow Egerton-Cust, 2nd Earl Brownlow (1842–1867), assumed the additional surname of Egerton and inherited the Bridgewater estates after a lengthy lawsuit (see the Baron Brownlow for additional information on the Cust family). Also, Lady Louisa Egerton, daughter of the first Duke of Bridgewater, married Granville Leveson-Gower, 1st Marquess of Stafford. Their son George Leveson-Gower, 2nd Marquess of Stafford, was created Duke of Sutherland in 1833. His second son Lord Francis Leveson-Gower assumed by Royal licence the surname of Egerton in lieu of Leveson-Gower according to the will of the third Duke of Bridgewater. In 1846 the Brackley and Ellesmere titles were revived when he was made Viscount Brackley and Earl of Ellesmere. The Hon. Thomas Egerton, of Tatton Park, Cheshire, youngest son of the second Earl of Bridgewater, was the grandfather of Hester Egerton (d. 1780). She married William Tatton. In 1780 they assumed by Royal licence the surname of Egerton in lieu of Tatton. Their great-grandson William Tatton Egerton was created Baron Egerton in 1859.

A scoundrel claiming to be the long-lost but rightful Duke of Bridgewater appears in the 1885 novel Adventures of Huckleberry Finn by Mark Twain, which is set before the American Civil War.

The original spelling is likely to have been Bridgwater, meaning the burg of Water, and the same as Bridgwater in Somerset (see archive reference 2/79).

Holders of the title
Arms of Daubeney.svg and Abney-Hastings family. Coat of arms: Gules, 4 fusils conjoined in fess argent.

The arms are derived from their ancestral home of Saint-Aubin-d'Aubigné. ]]

Barons Daubeney (1486)

 * Giles Daubeney, 1st Baron Daubeney (d. 1508)
 * Henry Daubeney, 2nd Baron Daubeney (1494–1548) (created Earl of Bridgewater in 1538)

Earls of Bridgewater, First Creation (1538)

 * Henry Daubeney, 1st Earl of Bridgewater (1493–1548)

Egerton family

Earls of Bridgewater, Second Creation (1617)

 * Other titles: Baron Ellesmere (1603) and Viscount Brackley (1616)

 * John Egerton, 1st Earl of Bridgewater, 2nd Viscount Brackley (1579–1649), second son of Thomas Egerton, 1st Viscount Brackley and 1st Baron Ellesmere
 * James Egerton, Viscount Brackley (1616–1620), his eldest son, who died in childhood
 * Charles Egerton, Viscount Brackley (c. 1617–1623), his next brother, who also died in childhood
 * John Egerton, 2nd Earl of Bridgewater (1623–1686), his only adult brother
 * John Egerton, 3rd Earl of Bridgewater (1646–1701), his eldest son
 * Hon. John Egerton (1669–1670), his eldest son, who died in infancy
 * Charles Egerton, Viscount Brackley (1675–1687), his younger half-brother, who died in childhood
 * Scroop Egerton, 4th Earl of Bridgewater (1681–1745), his younger brother, who was created Duke of Bridgewater and Marquess of Brackley in 1720
 * John Egerton, Viscount Brackley (1704–1719), his eldest son, who died before adulthood

Dukes of Bridgewater (1720)

 * Other titles: Baron Ellesmere (1603), Viscount Brackley (1616), Earl of Bridgewater (1617) and Marquess of Brackley (1720)

 * Scroop Egerton, 1st Duke of Bridgewater, 4th Earl of Bridgewater (1681–1745)
 * John Egerton, 2nd Duke of Bridgewater, 5th Earl of Bridgewater (1727–1748), his son, who died young and unmarried
 * Francis Egerton, 3rd Duke of Bridgewater, 6th Earl of Bridgewater (1736–1803), his younger brother, who also died unmarried

Earls of Bridgewater, Second creation (1617; Reverted)

 * Other titles: Baron Ellesmere (1603) and Viscount Brackley (1616)

 * John William Egerton, 7th Earl of Bridgewater (1753–1823), great-grandson of the 3rd Earl (via John Egerton, Bishop of Durham, and Henry Egerton, Bishop of Hereford)
 * Francis Henry Egerton, 8th Earl of Bridgewater (1756–1829), his younger brother, who died without heirs

title: Earl of Bridgewater


text:
Talk:John Digweed

Untitled
I added a snippet about Bedrock as a production alias. I'll try and remember to expand on that later. --Starx 01:57, 8 May 2004 (UTC)

Suggestion
Hi I don't know if this is the place to suggest this, but it would be nice for DJs like Digweed to go a bit into just what they do, like do they actually create music, add sounds to music, just adjust tempos and mix, or what? This would be interesting on a DJ by DJ basis, which is why my comment is here in the Talk:John Digweed page. Daniel Rosenstark 04:39, 19 October 2007 (UTC)
 * Aye, when I get around to putting some work in on this article there will almost certainly be a "Techniques" section or something like that. I did a similar section in the Sasha article.  Wickethewok 13:17, 19 October 2007 (UTC)

Which birth decade?
Intro says "born ... on 1 January 1977" while the fact box says "Born 	1 January 1967 (1967-01-01) (age 44)". Which is it? -- 25 March 2011 —Preceding unsigned comment added by 94.140.49.163 (talk) 18:16, 25 March 2011 (UTC)

Image
I saw this page listed on WikiProject_Electronic_music. I have a great image that I took of John at his show in Honolulu. I will upload it to wikimedia commons asap and put it up there.- Check out my user page for the rest of my photos. Photocyclone (talk) 21:22, 7 November 2014 (UTC)

External links modified
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title: Talk:John Digweed


text:
Limaçon

In geometry, a limaçon or limacon, also known as a limaçon of Pascal or Pascal's Snail, is defined as a roulette curve formed by the path of a point fixed to a circle when that circle rolls around the outside of a circle of equal radius. It can also be defined as the roulette formed when a circle rolls around a circle with half its radius so that the smaller circle is inside the larger circle. Thus, they belong to the family of curves called centered trochoids; more specifically, they are epitrochoids. The cardioid is the special case in which the point generating the roulette lies on the rolling circle; the resulting curve has a cusp.

Depending on the position of the point generating the curve, it may have inner and outer loops (giving the family its name), it may be heart-shaped, or it may be oval.

A limaçon is a bicircular rational plane algebraic curve of degree 4.

History
The earliest formal research on limaçons is generally attributed to Étienne Pascal, father of Blaise Pascal. However, some insightful investigations regarding them had been undertaken earlier by the German Renaissance artist Albrecht Dürer. Dürer's Underweysung der Messung (Instruction in Measurement) contains specific geometric methods for producing limaçons. The curve was named by Gilles de Roberval when he used it as an example for finding tangent lines.

Equations
The equation (up to translation and rotation) of a limaçon in polar coordinates has the form

 * $$r = b + a \cos \theta.$$

This can be converted to Cartesian coordinates by multiplying by r (thus introducing a point at the origin which in some cases is spurious), and substituting $$r^2 = x^2+y^2$$ and $$r \cos \theta = x$$ to obtain

 * $$\left(x^2 + y^2 - ax\right)^2 = b^2\left(x^2 + y^2\right).$$

Applying the parametric form of the polar to Cartesian conversion, we also have

 * $$x = (b + a\cos \theta)\cos \theta = {a\over 2} + b \cos \theta + {a\over 2} \cos 2 \theta,$$
 * $$y = (b + a\cos \theta)\sin \theta = b \sin \theta + {a\over 2} \sin 2 \theta;$$

while setting

 * $$z = x + i y = ( b + a \cos \theta )( \cos \theta + i \sin \theta )$$

yields this parameterization as a curve in the complex plane:

 * $$z = {a \over 2} + b e^{i\theta} + {a\over 2} e^{2i\theta}.$$

If we were to shift horizontally by $-\frac{1}{2}a$, i.e.,

 * $$z = b e^{it} + {a \over 2} e^{2it}$$,

we would, by changing the location of the origin, convert to the usual form of the equation of a centered trochoid. Note the change of independent variable at this point to make it clear that we are no longer using the default polar coordinate parameterization $$\theta = \arg z$$.

Special cases
In the special case $$a = b$$, the polar equation is

 * $$r = b(1 + \cos \theta) = 2b\cos^2 \frac{\theta}{2}$$

or

 * $$r^{1 \over 2} = (2b)^{1 \over 2} \cos \frac{\theta}{2},$$

making it a member of the sinusoidal spiral family of curves. This curve is the cardioid.

In the special case $$a = 2b$$, the centered trochoid form of the equation becomes

 * $$z = b \left(e^{it} + e^{2it}\right) = b e^{3it\over 2} \left(e^{it\over 2} + e^{-it\over 2}\right) = 2b e^{3it\over 2} \cos{t \over 2},$$

or, in polar coordinates,

 * $$r = 2b\cos{\theta \over 3}$$

making it a member of the rose family of curves. This curve is a trisectrix, and is sometimes called the limaçon trisectrix.

Form
When $$b > a$$, the limaçon is a simple closed curve. However, the origin satisfies the Cartesian equation given above, so the graph of this equation has an acnode or isolated point.

When $$b > 2a$$, the area bounded by the curve is convex, and when $$a < b < 2a$$, the curve has an indentation bounded by two inflection points. At $$b = 2a$$, the point $$(-a, 0)$$ is a point of 0 curvature.

As $$b$$ is decreased relative to $$a$$, the indentation becomes more pronounced until, at $$b = a$$, the curve becomes a cardioid, and the indentation becomes a cusp. For $$0 < b < a$$, the cusp expands to an inner loop, and the curve crosses itself at the origin. As $$b$$ approaches 0, the loop fills up the outer curve and, in the limit, the limaçon becomes a circle traversed twice.

Measurement
The area enclosed by the limaçon $$r = b + a \cos \theta$$ is $\left(b^2 + {{a^2} \over 2}\right)\pi$. When $$b < a$$ this counts the area enclosed by the inner loop twice. In this case the curve crosses the origin at angles $\pi \pm \arccos {b \over a}$, the area enclosed by the inner loop is

 * $$ \left (b^2 + {{a^2}\over 2} \right )\arccos {b \over a} - {3\over 2} b \sqrt{a^2 - b^2},$$

the area enclosed by the outer loop is

 * $$ \left(b^2 + {{a^2}\over 2} \right ) \left (\pi - \arccos {b \over a} \right ) + {3\over 2} b \sqrt{a^2 -b^2},$$

and the area between the loops is

 * $$ \left (b^2 + {{a^2}\over 2} \right ) \left (\pi - 2\arccos {b \over a} \right ) + 3b \sqrt{a^2 -b^2}.$$

The circumference of the limaçon is given by a complete elliptic integral of the second kind:

 * $$ 4(a + b)E\left({{2\sqrt{ab}} \over a + b}\right).$$

Relation to other curves

 * Let $$P$$ be a point and $$C$$ be a circle whose center is not $$P$$. Then the envelope of those circles whose center lies on $$C$$ and that pass through $$P$$ is a limaçon.

 * A pedal of a circle is a limaçon. In fact, the pedal with respect to the origin of the circle with radius $$b$$ and center $$(a, 0)$$ has polar equation $$r = b + a \cos \theta$$.

 * The inverse with respect to the unit circle of $$r = b + a \cos \theta$$ is

 * $$r = {1 \over {b + a \cos \theta}}$$

 * which is the equation of a conic section with eccentricity $$\tfrac{a}{b}$$ and focus at the origin. Thus a limaçon can be defined as the inverse of a conic where the center of inversion is one of the foci. If the conic is a parabola then the inverse will be a cardioid, if the conic is a hyperbola then the corresponding limaçon will have an inner loop, and if the conic is an ellipse then the corresponding limaçon will have no loop.

 * The conchoid of a circle with respect to a point on the circle is a limaçon.

 * A particular special case of a Cartesian oval is a limaçon.

title: Limaçon


text:
Ill (France)

The Ill is a river in Alsace, in north-eastern France, and a left-bank, or western, tributary of the Rhine. It is 217 km long.

It starts down from its source near the village of Winkel, in the Jura mountains, with a resurgence near Ligsdorf, turns around Ferrette on its east side, and then runs northward through Alsace, flowing parallel to the Rhine. Taking apart the Largue, also coming from the Jura mountains near Illfurth, it receives several tributaries from the west bank Vosges mountains after passing through Altkirch: the Doller in Mulhouse, the Thur near Ensisheim, the Lauch in Colmar, the Fecht in Illhaeusern, the Giessen in Sélestat, the Andlau near Fegersheim, the Ehn near Geispolsheim, the Bruche next to Strasbourg and the Souffel upstream from La Wantzenau before meeting with the Rhine downstream from Gambsheim's lock.

As the Ill nears the city of Mulhouse, most of its flow is diverted into a discharge channel leading to the Doller, protecting the historical center of the town from floods.

Flowing through the city of Strasbourg, the river forms part of the 17th-century fortifications and passes through a series of locks and channels in the picturesque old town, including the Petite France quarter, where its waters were once used to power mills and tanneries. One of these channels is the Canal du Faux-Rempart that, together with the main channel of the Ill, surrounds the Grande Île or historic centre of Strasbourg.

Navigation
The Ill is currently navigable from a junction with the Canal de la Marne au Rhin for a distance of just under 10 km upstream to a head of navigation at Nachtweid. This stretch of river passes through the centre of Strasbourg, and makes connection with the Canal du Faux-Rempart, the Canal du Rhone au Rhine and the, no longer navigable, Canal de la Bruche. There is a single lock, in the Petite France quarter of central Strasbourg.

Navigation through the section of the central part of this section, through Petite France, is restricted to small pleasure craft in the downstream direction only; upstream traffic and commercial traffic must use an indirect route from the Canal de la Marne au Rhin to the Canal du Rhone au Rhine via the Port of Strasbourg. Passenger trip boats use this section in the opposite direction, completing their loop via the Canal du Faux-Rempart that is closed to all other traffic.

Other stretches of the Ill, downstream of the Canal de la Marne au Rhin to the confluence with the Rhine, and upstream of Nachtweid, are not navigable by powered craft, although they may be used by canoes and similar craft.

title: Ill (France)


text: Talk:Kirpal Singh

title: Talk:Kirpal Singh


text:
Robert T. Bakker

Robert Thomas Bakker (born March 24, 1945) is an American paleontologist who helped reshape modern theories about dinosaurs, particularly by adding support to the theory that some dinosaurs were endothermic (warm-blooded). Along with his mentor John Ostrom, Bakker was responsible for initiating the ongoing "dinosaur renaissance" in paleontological studies, beginning with Bakker's article "Dinosaur Renaissance" in the April 1975 issue of Scientific American. His specialty is the ecological context and behavior of dinosaurs.

Bakker has been a major proponent of the theory that dinosaurs were warm-blooded, smart, fast, and adaptable. He published his first paper on dinosaur endothermy in 1968. His seminal work, The Dinosaur Heresies, was published in 1986. He revealed the first evidence of parental care at nesting sites for Allosaurus. He also observed evidence in support of Eldredge and Gould's theory of punctuated equilibrium in dinosaur populations. Bakker currently serves as the Curator of Paleontology for the Houston Museum of Natural Science.

Biography
Bakker was born in Bergen County, New Jersey. He attributes his interest in dinosaurs to his reading an article in the September 7, 1953, issue of Life magazine. He graduated from Ridgewood High School in 1963.

At Yale University Bakker studied under John Ostrom, an early proponent of the new view of dinosaurs, and later earned his PhD at Harvard. He began by teaching anatomy at Johns Hopkins University in Baltimore, Maryland and Earth and Space Sciences, where future artist Gregory S. Paul worked and collaborated informally under his guidance. Most of Bakker's fieldwork has been done in Wyoming, especially at Como Bluff. Still, he has traveled as far as Mongolia and South Africa in search of dinosaur habitats. He also worked as an assistant at the University of Colorado.

Theories
In his 1986 work The Dinosaur Heresies, Bakker puts forth the theory that dinosaurs were warm-blooded. His evidence for this includes:
 * Almost all modern animals that walk upright are warm-blooded, and dinosaurs walked upright.
 * The hearts of warm-blooded animals can pump much more effectively than the hearts of cold-blooded animals. Therefore, the giant Brachiosaurus must have had the type of heart associated with warm-blooded animals in order to pump blood up to its head.
 * Dinosaurs such as Deinonychus led a very active life, behavior which is much more compatible with a warm-blooded animal.
 * Some dinosaurs lived in northern latitudes where it would have been impossible for cold-blooded dinosaurs to maintain their body temperature.
 * The rapid rate of speciation and evolution found in dinosaurs is typical of warm-blooded animals and atypical of cold-blooded animals.
 * The hypothesized population ratios of predatory dinosaurs to their prey is a signature trait of warm-blooded predators rather than cold-blooded ones.
 * Birds are warm-blooded and evolved from dinosaurs; therefore, a change to a warm-blooded metabolism must have taken place at some point. There is far more change between dinosaurs and their ancestors (basal archosaurs) than between non-avian dinosaurs and birds.
 * A warm-blooded metabolism is an evolutionary advantage for top predators and large herbivores; if dinosaurs had not been warm-blooded there should be fossil evidence of warm-blooded animals evolving to fill these ecological niches. No such evidence exists; in fact, by the end of the Cretaceous, mammals had become much smaller than their stem-mammal ancestors.
 * Dinosaurs grew rapidly, evidence for which can be found by observing cross-sections of their bones. Warm-blooded animals grow at a similar rate.

Bakker is also a proponent of the idea that flowering plants evolved because of their interactions with dinosaurs. He also believes the principal cause of extinction for all non-avian dinosaurs was in fact a plague caused by invasive species crossing land bridges, retorting that, had the comet been large enough to kill off every non-avian dinosaur, it would have also wiped out the various taxa known to have survived the K-T extinction event.

Writing
Bakker's fictional novel Raptor Red tells of a year in the life of a female Utahraptor during the lower Cretaceous. In the story, Bakker elaborates on his knowledge of the behavior of dromaeosaurids ("raptor" dinosaurs) and life at the time of their existence.

Religious beliefs
As a Pentecostal, Ecumenical Christian minister, Bakker has said there is no real conflict between religion and science, and that evolution of species and geologic history is compatible with religious belief. Bakker views the Bible as an ethical and moral guide, rather than a literal timetable of events in the history of life. He has advised non-believers and creationists to read the views put forward by Saint Augustine, who argued against a literal understanding of the Book of Genesis.

Influence on popular media
Bakker's earliest known appearance was in the 1976 BBC Nova episode The Hot-Blooded Dinosaurs aired on WGBH Boston.

Bakker appears in the 1989 BBC series Lost Worlds, Vanished Lives presented by David Attenborough, in the third episode Dinosaur discussing his theory regarding Tyrannosaurus rex and other theropods being warm-blooded animals. Bakker later renamed Attenborosaurus, a species of plesiosaur after Sir David.

Bakker was an advisor for the 1992 PBS series, The Dinosaurs!. He had many appearances in the TLC television series Paleoworld, and was also among the advisors for the film Jurassic Park, with some of the early concept art being informed by Bakker's works. Bakker also appeared in the Sega CD version of Jurassic Park.

Dr. Bakker was a guest in episode 27 ("Surprise") of the Williams Street original Space Ghost Coast to Coast.

Bakker appeared in the 1992 VHS Whatever Happened to the Dinosaurs?

He was profiled on location at his Wyoming dinosaur excavation site in an episode of the Discover Magazine (TV series) on The Disney Channel in 1992.

Bakker and his 1986 book are mentioned in the original Jurassic Park. The bearded paleontologist Dr. Robert Burke, who is eaten by a Tyrannosaurus rex in Steven Spielberg's film The Lost World: Jurassic Park, is an affectionate caricature of Bakker. In real life, Bakker has argued for a predatory T. rex, while Bakker's rival paleontologist Jack Horner views it as primarily a scavenger. According to Horner, Spielberg wrote the character of Burke and had him killed by the T. rex as a favor for Horner. After the film came out, Bakker recognized himself in Burke, loved the caricature, and actually sent Horner a message saying, "See, I told you T. rex was a hunter!"

title: Robert T. Bakker