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Talk:Cushing's syndrome

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Merging is wrong
Cushing's Disease and Cushing's Syndrome are two different entities. So they should be separate. I would suggest to unmerge. Thanks -- Abhijeet Safai (talk) 09:55, 22 February 2013 (UTC)

Imaging in ectopic Cushing's syndrome
10.1210/JC.2015-1589 - various modalities discussed. JFW | T@lk  18:01, 12 July 2015 (UTC)

Endocrine society guideline
10.1210/jc.2015-1818 JFW | T@lk  08:35, 3 August 2015 (UTC)

Lancet seminar
10.1016/S0140-6736(14)61375-1 JFW | T@lk  17:02, 1 September 2015 (UTC)

Diagnosis?
No diagnosis section...Jobonki (talk) 16:39, 4 September 2016 (UTC)
 * Feel free to find some good sources and add that section. Doc James  (talk · contribs · email) 16:42, 4 September 2016 (UTC)

Text
Visibly obvious Cushing’s syndrome is associated with 83% of the patients in older peer reviewed medical literature that have been described as either abusing corticosteroids or having a corticosteroid addiction, which would now be more correctly described as having a corticosteroid use disorder. Newer peer reviewed medical literature uses the term Factitious Cushing’s Syndrome to characterize what used to be termed abuse and by definition the correlation is 100% with a 0.7% incidence having no supporting underlying medical condition, however, the more modern literature fails to address the concept of medically prescribed addiction where the DSM V criteria of a Corticosteroid Use Disorder is met while having an active prescription for an underlying medical condition.

Removed a mass of old primary sources. Editor needs to read WP:MEDRS Doc James  (talk · contribs · email) 08:21, 6 September 2016 (UTC)

Images used might be illegal
The immages used are sourced from a journal article. While the article may be open content, this does not mean that the immages may be copied. This is even more true given that the pictures in the original article were published under strict consent forms that may or, and this far more likely, may not have allowed publication in a third source. The consent forms are not publicized, so the obvious thing to assume is that consent is **not** given! — Preceding unsigned comment added by 62.58.236.32 (talk) 05:25, 12 October 2016 (UTC)

Glucose homeostasis
Reviewed: 10.1210/er.2016-1105 JFW | T@lk  18:53, 12 June 2017 (UTC)

External links modified
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Fluticasone ad at the top of this page
Why is there an ad for Fluticasone at the top of the page with an unverified picture of someone who supposedly took it and had relief of symptoms? Wikipedia is supposed to be ad free. After four attempts to remove this ad unsuccessfully I end up here discussing something that should be obvious to everyone. Advertisements for anything, including drugs,have no place in a wiki page. — Preceding unsigned comment added by 2600:1003:B11D:8018:93A:E38F:D82A:9741 (talk) 23:13, 25 March 2018 (UTC)
 * I don't understand why you think the image is an advertisement. Wikipedia should describe the results of drugs and the image is showing an adverse effect of from the use of a drug. How does showing this adverse effect advertise the drug anyway?  And why do you call it an unverified picture?  It is referenced to a peer-reviewed medical journal.  What greater verification do you expect?  ChemNerd (talk) 17:17, 26 March 2018 (UTC)

Inconsistent first sentence
Hi,

The opening sentence of the article reads "Cushing's syndrome is a collection of signs and symptoms due to prolonged exposure to cortisol." which is consistent with the its inline citations. However, this proposition is clearly contradicted later in the article; Cushing's syndrome can also be caused by glucocorticoid medications that mimic the physiological effects of cortisol while not being, well, cortisol. The sentence is thus inaccurate.

Since inline citations are not required for the lead section, and since the detailed explanation of CS etiology (endogenous vs. medication-induced CS) is clearly delineated in the article body, I propose the first paragraph be rewritten as e.g. "Cushing's syndrome is a collection of signs and symptoms caused by prolonged exposure to cortisol or other glucocorticoids." or "... cortisol or glucocorticoid medications." and the current inline citations be removed.

Kind regards, -J Jay Hodec (talk) 21:48, 16 April 2019 (UTC)

 * Muddle, and potential muddle, between Cushing’s Syndrome and Cushing’s Disease is a bit of a theme - within the article as it stands, and as a thread through the article’s history. Unless I’m misunderstanding something, the point being made here is the same issue turning up again.  The sooner we can deal with it, so the article ceases to prompt controversy or puzzlement about this, the better.

 * But I’m not sure the proposed amendment is the way to do it. The opening sentence as it stands is clear and, for what it’s worth, accurate.  (The Syndrome is a collection of signs and symptoms, and the common feature which those signs and symptoms share is that they arise from prolonged exposure to cortisol.)  The snag, the weakness of the sentence, is tht it’s apt to be misunderstood: as saying tht that’s the *only* thing that causes them, they arise *only* from exposure to cortisol.  It doesn’t say that, but it’s easily misread and gives that impression.

 * The proposed change avoids the misunderstanding - but loses the crispness and clarity of the sentence. It kind-of risks substituting *no* understanding for *mis*understanding!  And that is sooo not what u want at the start of a lede!

 * To me, the better route is to clarify by amplifying, immediately but in a separate following sentence. (Or two, actually.)  And to use the opportunity to tackle the Syndrome / Disease muddle up-front and head-on.

 * How about

Cushing's syndrome is a collection of signs and symptoms which arise from prolonged exposure to cortisol. Cushing’s Disease is a condition which causes a raised level of cortisol in the body, and so causes Cushing’s syndrome. The syndrome itself can also be [? is often? source?] caused instead by medication such as prednisone.

 * - SquisherDa (talk) 13:42, 17 April 2019 (UTC)

 * Cushing's disease is generally defined as a subcategory of CS caused specifically by excess ACTH release. The syndrome encompasses, at least as set forth in the article, CD, ACTH-independent CS, and the medication-induced condition. I'm noticing that sources are a bit divided as to the precise definitions also, however, since the article defines medication-induced CS within the scope of "Cushing's syndrome", the wording of the first sentence should be changed to reflect article content. If we wish to distinguish exogeneous CS from endogeneous CS "proper" (as some sources do), the distinction should likewise be made in the article text.

 * I went ahead and checked how the term is defined in a dozen sources chosen at random (definition excerpts below). You'll notice that there's an interesting pattern; scientific sources tend to point out that CS is caused by *any* glucocorticoid excess (whether endogenous cortisol or exogenous glucocorticoids) while non-scientific sources fail to make the distinction. However, here's the crucial point; glucocorticoids=/=cortisol, and failing to point that out leads to an inaccurate definition. I understand why you would simplify the thing for the general public on a health information website, however, as far as I know, Wikipedia should strive for greater accuracy instead of greater comprehensibility.

*"Cushing’s syndrome is a rare disorder resulting from prolonged exposure to excess glucocorticoids." - S. T. Sharma (2015) *"Cushing syndrome is caused by prolonged exposure to high circulating levels of cortisol. The most common cause of cushingoid features is iatrogenic corticosteroid use [...] There are two main etiologies of Cushing syndrome: endogenous hypercortisolism and exogenous hypercortisolism. Exogenous hypercortisolism, the most common cause of Cushing syndrome, is mostly iatrogenic and results from the prolonged use of glucocorticoids. Endogenous Cushing Syndrome results from excessive production of cortisol by adrenal glands and can be ACTH-dependent and ACTH-independent." - C. S. Hammad, G. Singh (2019) *"Cushing’s Syndrome results from chronic exposure to excessive circulating levels of glucocorticoids." - A. Juszczak, P. Sulentic, A. Grossman (2017) *"Endogenous pathologic hypercortisolism, or Cushing’s syndrome ..." L. K. Nieman (2015) *"Cushing’s syndrome (CS) is the state of hypercortisolism that results from endogenous or exogenous glucocorticoid excess." J. M. Pappachan, et al. (2017) *"Cushing's syndrome, or chronic hypercortisolism, is a severe endocrine disease due to the prolonged exposure to glucocorticoid excess" - A. M. Isidori, et al. (2015)

*"Cushing syndrome occurs when your body is exposed to high levels of the hormone cortisol for a long time. Cushing syndrome, sometimes called hypercortisolism, may be caused by the use of oral corticosteroid medication. The condition can also occur when your body makes too much cortisol on its own. [...] Excess levels of the hormone cortisol are responsible for Cushing syndrome. [...] Cushing syndrome can develop from a cause outside of your body (exogenous Cushing syndrome)." - Mayo Clinic *"Cushing’s syndrome is a disorder that occurs when your body makes too much of the hormone cortisol over a long period of time. [...] Endogenous Cushing’s syndrome is rare. “Endogenous” means something inside your body is causing the disorder rather than something outside your body, such as medicine. [...] People who take medicines called glucocorticoids, which are similar to cortisol, also can develop Cushing’s syndrome." - National Institute of Diabetes and Digestive and Kidney Diseases *"Cushing syndrome occurs due to abnormally high levels of the hormone cortisol. This can happen for a variety of reasons. The most common cause is overuse of corticosteroid medications." - Healthline *"You can get Cushing's syndrome when there’s too much cortisol in your body for too long. Cortisol comes from your adrenal glands, which sit on top of your kidneys. The most common cause is related to medications called glucocorticoids, also commonly known as steroids or prednisone." - WebMD *"Cushing syndrome is a rare endocrine disorder caused by abnormally excessive amounts of the hormone cortisol. Many people develop Cushing syndrome as a result of exogenous, long-term administration of a cortisol-like drug therapy [...] Cushing syndrome can also be due to endogenous causes; approximately 70% of Cushing syndrome is the result of Cushing disease." - National Organization for Rare Disorders *"Cushing's syndrome is a condition caused by having too much of a hormone called cortisol in your body. [...] Cushing's syndrome is uncommon. It mostly affects people who have been taking steroid medicine, especially steroid tablets, for a long time. Steroids contain a man-made version of cortisol. Very rarely, it can be caused by the body producing too much cortisol." - NHS

 * I think the wiki article should use the wider definition which also appears to be the preferred definition in scientific literature.

 * Sincerely, -J Jay Hodec (talk) 10:07, 18 April 2019 (UTC)

 * Mmm - looking at the references U’ve pulled together there, I’m seeing more clearly why U want to get the exogenous syndrome more up-front and into the first sentence.

 * I want to make changes too, of course.

 * And that’s not the only thing we agree on! Ur observation tht Wikipedia should strive for greater accuracy seems to me entirely right, and absolutely central.  In fact I’d suggest this particular article is mainly important for its value to refugees from the non-scientific sources U point to: because yes, that is a really *very* interesting pattern; and u’d really think, for example, tht the Mayo Clinic would do a bit better than that!

 * I also agree with Ur view tht the wider, scientific definition is the more encyclopaedic - so tht where endogenous CS is caused by CD, but exogenous-CS cases are not CD cases.

 * I might attach greater priority than I think U do, though, to greater comprehensibility. I hesitate to settle for “instead”!  I’d try really hard to get *both*.

 * In that connection, Ur plan to drop citations out of the lede is also obviously good.

 * And should we drop the reference to “signs and symptoms”? The distinction doesn’t seem helpful here - signs aren’t much involved where CS is concerned - if I understand the distinction correctly?  (My impression is tht signs are abnormalities tht declare the condition even to people without medical knowledge: make the diagnosis obvious, in the way tht a bent limb can declare a fracture.  In this sense, there aren’t going to be many signs of an endocrine disorder - whether or not iatrogenic!)

 * How about refocusing the opening sentence - on the distinction itself? That way, our reader / refugee gets the distinction clear, as a rather necessary preliminary; and the sentence functions naturally to introduce a pair of following sentences which handle the details:

Cushing's syndrome is a collection of symptoms which can arise from an endocrine disorder, or, more often, as a side-effect of medication. Cushing’s Disease is a rare condition which causes a raised level of cortisol in the body, resulting in endogenous Cushing’s syndrome. The syndrome itself is more often exogenous - caused by prolonged use of glucocorticoid medication such as prednisone.

 * - SquisherDa (talk) 20:52, 19 April 2019 (UTC)

 * Attesting from my own personal experience, I usually use Wikipedia as a semi-scientific framework to get a feel for a subject before building upon that knowledge; individual scientific articles often do not give a good enough overview of a subject to give a reader the basis for initial comprehension. Wikipedia, in contrast, often offers a comprehensive initial aggregate of relevant scholarly information to help you get started on a deeper dive on a subject. That's why "pop-sci" inconsistencies in wiki articles really throw me off and "grind my gears" since you have to go back and compare sources to figure out where the inconsistency lies.

 * Regarding "Signs and symptoms"; I much prefer to use the terms "Presentation" and "Features" since the former are as you have pointed out a bit murky. "Symptoms" generally refers to disease features that are internal/subjective (pain, fatigue, nausea, tingling, numbness, etc.) while "signs" refers to objective/observable features, and particularly those that are observed during medical examination (e.g. abnormal heart/lung sounds, abnormal lab/radiological findings, a palpable lump, abnormal gait, tremor, etc.). The terms are often used interchangeably, however, and the "Signs and symptoms" phrasing is generally preferred on wiki ... In this case, I think there are plenty outwardly/objective signs of disease, even if not immediately suggestive of the cause to casual observers.

 * I generally agree with your formulation, however, there are some inaccuracies in your phrasing, namely that exogenous disorder could still be tentatively defined as an endocrine disorder as it still affects the "endocrine mechanisms" at the target receptor end. Furthermore, CD is a subset of endogenous CS, and not all endogenous CS is CD.

 * I'm gonna go ahead an just rewrite the Causes section and the first sentence so that we can get a feel for the situation as it stands and we can then discuss it further.

 * Kind regards, -J Jay Hodec (talk) 11:53, 20 April 2019 (UTC)

 * This "causes a raised level of cortisol in the body" is not really accurate. It is a result of a high cortisol level.

 * For medical articles we references the lead.

 * How common the condition is is discussed in the 4 paragraph of the lead and in the infobox. We do not need to state how common it is as we give the numbers. Doc James  (talk · contribs · email) 19:45, 20 April 2019 (UTC)

Definition

 * The NIH says "Cushing's syndrome is a hormonal disorder caused by prolonged exposure of the body's tissues to high levels of the hormone cortisol"

 * This can reasonably be summarized as "due to prolonged exposure to glucocorticoids such as cortisol."

 * I agree with the usefulness of mentioning glucocorticoids and have added that to the first sentence.  Doc James  (talk · contribs · email) 19:49, 20 April 2019 (UTC)

Etiology

 * We try to use English not Latin / Greek. The English word is cause. We use easier to understand language per WP:MEDMOS.

 * There is no NEED for 7 references here. Expecially not two reference that are the same. It is not that controversial. Doc James  (talk · contribs · email) 19:31, 20 April 2019 (UTC)

Regarding NIH/NEMDIS's definition see discussion above (I found your version acceptable and did not contest it).

To address the two sections I actually reversed to my version ... Though I generally understand the utility of avoiding jargon, I think @DocJames's drive for plain English goes a bit too far. Just as an off-point, "cause" comes from Latin ("causare"), but is just as much an English word as "etiology". Admittedly, etiology is a more "advanced" word, however, I don't see the point in reducing everything down to a second grade English level, especially when it comes at the cost of accurate language ("cause" and "etiology" are not synonyms, please, see context). I've noticed multiple times that your simplifications made sections less precise and more ambiguous. From a scholarly standpoint this is quite problematic. I've tried to find the guideline that directs medical editors towards the plainest of English but cannot find it, even in the WP:MEDMOS you've referenced (anyway, I thought that's what Simple English wiki is for).

I may have accidentally inserted a source twice (my bad). However, as already mentioned, the handful of references was intended to establish a trend to bolster the "glucocorticoids" definition since no secondary source for a meta-definition of CS can be found.

I've already addressed the reason for re-inserting "... or the dose can be adjusted downward to limit Cushing's symptoms."

Kind regards, -J Jay Hodec (talk) 21:02, 20 April 2019 (UTC)
 * We are not writing for graduate students. We can barely get our content down to a grade 12 reading level at the best of times. MEDMOS says "The lead of an article, if not the entire article, should be written as simply as possible without introducing errors or ambiguity." Doc James  (talk · contribs · email) 04:21, 22 April 2019 (UTC)

 * "If due to medications, these can often be slowly stopped or decreased." → " If due to medications, these can often be slowly stopped, or, if the medication is needed to treat an ongoing chronic condition, the dose can sometimes be reduced to minimize Cushing's symptoms." Emphasis on the fact that it is not always possible to completely avoid CS if no alternative exists and that it may be necessary to balance exogenous CS against underlying disorder. Note that reducing the dose is not mentioned in the originally cited source (I reinserted the needed source). If you leave "stopped or decreased" while removing the source, the "decreased" may be removed as unsourced in the future.

 * "The cause of Cushing's syndrome include all reasons for increased glucocorticoid levels leading to a diseased state." → "Cushing's syndrome may be defined broadly as disease resulting from any cause of increased glucocorticoid levels, whether due to medication or internal processes." Your version makes the sentence nonsensical when contrasted to the following one. (i.e. "Some sources however do not consider the glucocorticoid medication-induced condition as "Cushing's syndrome" proper, instead using the term "Cushingoid" to describe the medication's side effects which mimic the endogenous condition.") I rephrased the sentence to remove "etiology" while preserving the intended meaning. Emphasis on the fact that not all sources define endogenous CS as CS (important in context of definitions that regard cortisol exposure as sole possible cause; future editors may challenge the definition without this clarification/disclaimer). I did not restore the sources since that was a minor point of contention.

 * Kind regards, -J Jay Hodec (talk) 15:50, 21 April 2019 (UTC)

 * Yah the original source sort did not cover it as clearly.
 * "If Cushing’s syndrome is caused by glucocorticoid medicine taken to treat another disorder, your health care provider will slowly and carefully decrease your dose and give you another medication so that your body can go back to making its own cortisol. However, if you need to continue taking the glucocorticoid, your health care provider will closely monitor you and treat symptoms that might develop, such as high blood sugar, high cholesterol levels, bone thinning, or osteoporosis"
 * Have condensed it to "Cushing's syndrome may result from any cause of increased glucocorticoid levels"
 * Doc James (talk · contribs · email) 04:18, 22 April 2019 (UTC)

 * Alright ... Your new condensed version is better than previous one, but still quite a bit off (when read together with following sentence). However, I really don't wanna argue about this anymore, so I leave it up to (potential) other editors to decide.

 * Take care. -J Jay Hodec (talk) 17:32, 22 April 2019 (UTC)

Genetics behind Cushing
Please, can someone add some information about the genetics behind this syndrome? Now is quite known that there are some relevant mutations in PRKACA gene. Reviewed: https://advances.sciencemag.org/content/7/8/eabd4176.full — Preceding unsigned comment added by Aldhairmedico (talk • contribs) 01:39, 9 March 2021 (UTC)

title: Talk:Cushing's syndrome


text:
Canonization of Joan of Arc

Joan of Arc (1412–1431) was formally canonized as a saint of the Roman Catholic Church on 16 May 1920 by Pope Benedict XV in his bull Divina disponente, which concluded the canonization process that the Sacred Congregation of Rites instigated after a petition of 1869 of the French Catholic hierarchy. Although pro-English clergy had Joan burnt at the stake for heresy in 1431, she was rehabilitated in 1456 after a posthumous retrial. Subsequently, she became a folk saint among French Catholics and soldiers inspired by her story of being commanded by God to fight for France against England. Many French regimes encouraged her cult, and the Third Republic was sympathetic to the canonization petition prior to the 1905 separation of church and state.

Death and 15th century
As with other saints who were excommunicated or investigated by ecclesiastic courts, such as Athanasius, Teresa of Ávila, and John of the Cross, Joan was put on trial by an Inquisitorial court. In her case, the court was influenced by the English, which occupied northern France, leading to her execution in the marketplace of Rouen. When the French retook Rouen in 1449, a series of investigations were launched. Her now-widowed mother Isabelle Romée and Joan's brothers Jéan and Pierre, who were with Joan at the Siege of Orléans, petitioned Pope Nicholas V to reopen her case. The formal appeal was conducted in 1455 by Jean Bréhal, Inquisitor-General of France, under the aegis of Pope Callixtus III. Isabelle addressed the opening session of the appellate trial at Notre Dame with an impassioned plea to clear her daughter's name. Joan was exonerated on 7 July 1456, with Bréhal's summary of case evidence describing her as being executed by a court which itself had violated Church law.

The city of Orléans had commemorated her death each year beginning in 1432, and from 1435 onward performed a religious play centered on the lifting of the siege. The play represented her as a divinely-sent savior guided by angels. In 1452, during one of the postwar investigations into her execution, Cardinal d'Estouteville declared that this play would merit qualification as a pilgrimage site by which attendees could gain an indulgence.

Not long after the appeal, Pope Pius II, who died in 1464, wrote an approving piece about her in his memoirs.

16th century
An anonymous author wrote a biography of Joan's life, stating that it was compiled "By order of the King, Louis XII of that name" in circa 1500.

18th and 19th centuries
Joan's cult of personality was opposed by the leaders of the French Revolution as she was a devout Catholic who had served the monarchy. They banned the yearly celebration of the lifting of the Siege of Orléans, and Joan's relics, including her sword and banner, were destroyed. A statue of Joan erected by the people of Orléans in 1571 (to replace one destroyed by Protestants in 1568) was melted down and made into a cannon.

Recognizing he could use Joan for his nationalist purposes, Napoleon allowed Orléans to resume its yearly celebration of the lifting of the siege, commissioned Augustin Dupré to strike a commemorative coin, and had Jean-Antoine Chaptal inform the mayor of Orléans that he approved of a resolution by the municipal council for Edme-François-Étienne Gois to erect his statue of Joan: "'The illustrious career of Joan of Arc proves that there is no miracle French genius cannot perform in the face of a threat against national freedom.'" Gois's work was relocated to Place Dauphiné in 1855, replaced with a statue of Joan by Denis Foyatier.

Although Nicolas Lenglet Du Fresnoy and Clément Charles François de Laverdy are credited with the first full-length biographies of Joan, several English authors ironically sparked a movement which led to her canonization. Harvard University English literature professor Herschel Baker noted in his introduction to Henry VI for The Riverside Shakespeare how appalled William Warburton was by the depiction of Joan in Henry VI, Part 1, and that Edmond Malone sought in "Dissertation on the Three Parts of Henry VI" (1787) to prove Shakespeare had no hand in its authorship (1974; p. 587). Charles Lamb chided Samuel Taylor Coleridge for reducing Joan to "a pot girl" in the first drafts of The Destiny of Nations, initially part of Robert Southey's Joan of Arc. She was the subject of essays by Lord Mahon for The Quarterly Review, and by Thomas De Quincey for Tait's. In 1890, the Joan of Arc Church was dedicated to her.

As Joan found her way further into popular culture, the Government of France commissioned Emmanuel Frémiet to erect a statue of her in the Place des Pyramides—the only public commission of the state from 1870 to 1914. The French Navy dedicated four vessels to her: a 52-gun frigate (1820); a 42-gun frigate (1852); an ironclad corvette warship (1867); and an armored cruiser (1899). Philippe-Alexandre Le Brun de Charmettes's biography (1817), and Jules Quicherat's account of her trial and rehabilitation (1841–1849) seemed to have inspired canonization efforts.

In 1869, to celebrate the 440th anniversary of the lifting of the Siege, Félix Dupanloup, Bishop of Orléans, delivered a second panegyric on Joan, attended by: Jean-François-Anne Landriot; Guillaume-René Meignan; Georges Darboy; Joseph-Alfred Foulon; Henri-Marie-Gaston Boisnormand de Bonnechose; Louis-Édouard-François-Desiré Pie; Joseph-Hippolyte Guibert; Charles Lavigerie; Charles-Amable de La Tour d'Auvergne-Lauraguais, Bishop of Bourges; Félix-Joseph-François-Barthélemy de Las Cases, Bishop of Constantine; Joseph-Armand Gignoux, Bishop of Beauvais; Louis-Marie-Joseph-Eusèbe, Bishop of Saint-Dié; Louis-Théophile Pallu du Parc, Bishop of Blois; Emmanuel-Jules Ravinet, Bishop of Troyes; Augustin Hacquard, Bishop of Verdun; and Pierre-Marie-Gervais Lacarrière, former Bishop of Basse-Terre and Guadeloupe. Supported by Henri-Alexandre Wallon, Dupanloup submitted a petition to Pope Pius IX, signed by the aforementioned bishops, and other dignitaries, for Joan to be canonized, but the Franco-Prussian War postponed further action.

In 1874, depositions began to be collected, received by Cardinal Luigi Bilio in 1876. Dupanloup's successor, Bishop Pierre-Hector Coullié, directed an inquest to authenticate her acts and testimony from her trial and rehabilitation. On 27 January 1894, the Curia (Cardinals Benedetto Aloisi-Masella, Angelo Bianchi, Benoît-Marie Langénieux, Luigi Macchi, Camillo Mazzella, Paul Melchers, Mario Mocenni, Lucido Parocchi, Fulco Luigi Ruffo-Scilla, and Isidoro Verga) voted unanimously that Pope Leo XIII sign the Commissio Introductionis Causæ Servæ Dei Joannæ d'Arc, which he did that afternoon.

20th century to present
However, the path to sainthood did not go smoothly. On 20 August 1902, the papal consistory rejected adding Joan to the Calendar of saints, citing: she launched the assault on Paris on the birthday of Mary, mother of Jesus; her capture ("proof" her claim that she was sent by God was false); her attempts to escape from prison; her abjure after being threatened with death; and doubts of her purity. On 17 November 1903, the Sacred Congregation of Rites met to discuss Joan's cause at the behest of Pope Pius X. A decree proclaiming Joan's heroic virtue was issued on 6 January 1904 by Cardinal Serafino Cretoni, and Pius proclaimed her venerable on 8 January. The Decree of the Three Miracles was issued on 13 December 1908, and The Decree of Beatification was read five days later, which was issued formally by the Congregation of Rites on 24 January 1909.

The beatification ceremony was held on 18 April 1909, presided by Cardinals Sebastiano Martinelli and Mariano Rampolla. Bishop Stanislas Touchet performed the Mass. Cardinals Serafino Vannutelli, Pierre Andrieu, Louis Luçon, Coullié, Girolamo Maria Gotti, José Calassanç Vives y Tuto, then-Monsignor Rafael Merry del Val, Bishop John Patrick Farrelly, Bishop Thomas Kennedy, Monsignor Robert Seton, Count Giulio Porro-Lambertenghi (grandson of Luigi Porro Lambertenghi) with tribunes from The Knights of Malta, The Duke of Alençon and The Duke of Vendôme, then-Archbishop William Henry O'Connell, and The Duke of Norfolk attended. Pius—who was determined that the ceremony would not be used by Legitimists to attack the Third Republic —venerated the relics that afternoon, flanked by 70 French prelates.

Her beatification approximately coincided with the French invention of the Janvier transfer engraving machine (also called a die engraving pantograph), which facilitates the creation of minted coins and commemorative medallions. This invention, together with the already well-established French sculptural tradition, added another element to Joan's beatification: a series of well-made religious art medals featuring scenes from her life.

Edmond Richer's La première histoire en date de Jeanne d'Arc: histoire de la Pucelle d'Orléans, written between 1625 and 1630, was published in two volumes in 1911 by Henri and Jules Desclée.

During World War I, French troops carried her image into battle with them. During one battle, they interpreted a German searchlight image projected onto low-lying clouds as an appearance by Joan, which bolstered their morale greatly. [see: The Maid of Orléans: The Story of Joan of Arc Told to American Soldiers by Charles Saroléa (1918)]

Her canonization was held on 16 May 1920. Over 60,000 people attended the ceremony, including 140 descendants of Joan's family. Dignitaries included: Vendôme, Lambertenghi with The Knights of Malta, now-Bishop O'Connell, Gabriel Hanotaux, Princess Zinaida Yusupova, Princess Irina Alexandrovna, Prince Feodor Alexandrovich, The Duke of Braganza, The Count de Salis-Soglio, Rafael Valentín Errázuriz, Diego von Bergen, Bishop John Patrick Carroll, Archbishop Edward Joseph Hanna, Bishop Daniel Mary Gorman, Bishop Paul Joseph Nussbaum, the student body of The American College of Rome, and now-Cardinal Merry del Val, who greeted Pope Benedict XV as Benedict entered St. Peter's Basilica to preside over the rites. The Latin bull of Pope Benedict XV effecting her canonization was Divina Disponente of the same date. Approximately 100,000 persons celebrated at Westminster Cathedral and French churches throughout London.

In the 18 May 1920 Le Matin, former President of France Raymond Poincaré wrote that Joan's canonization "fulfills the last part of her mission in bringing together forever in the sacredness of her memory" one-time mortal enemies England and France: "In her spirit, let us remain united for the good of Mankind".

Popularity
Joan of Arc's feast day is 30 May. Although reforms in 1968 moved many medieval European saints' days off the general calendar in order to make room for more non-Europeans, her feast day is still celebrated on many local and regional Church calendars, especially in France. Many Catholic churches around the globe have been named after her in the decades since her canonization.

She has become especially popular among Traditional Catholics, particularly in France—both because of her obvious connection to this country as well as the fact that the Traditional Catholic movement is strongest there. This movement within the church, which includes those few orders and societies which refused to accept the changes made by the Second Vatican Council, has compared the 1988 excommunication of Archbishop Marcel Lefebvre (one of the founders of the Society of Saint Pius X) to Joan of Arc's excommunication by a corrupt pro-English bishop in 1431.

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title: Canonization of Joan of Arc


text:
Cardiovascular disease

Cardiovascular disease (CVD) is any disease involving the heart or blood vessels. CVDs constitute a class of diseases that includes: coronary artery diseases (e.g. angina, heart attack), heart failure, hypertensive heart disease, rheumatic heart disease, cardiomyopathy, arrhythmia, congenital heart disease, valvular heart disease, carditis, aortic aneurysms, peripheral artery disease, thromboembolic disease, and venous thrombosis.

The underlying mechanisms vary depending on the disease. It is estimated that dietary risk factors are associated with 53% of CVD deaths. Coronary artery disease, stroke, and peripheral artery disease involve atherosclerosis. This may be caused by high blood pressure, smoking, diabetes mellitus, lack of exercise, obesity, high blood cholesterol, poor diet, excessive alcohol consumption, and poor sleep,  among other things. High blood pressure is estimated to account for approximately 13% of CVD deaths, while tobacco accounts for 9%, diabetes 6%, lack of exercise 6%, and obesity 5%. Rheumatic heart disease may follow untreated strep throat.

It is estimated that up to 90% of CVD may be preventable. Prevention of CVD involves improving risk factors through: healthy eating, exercise, avoidance of tobacco smoke and limiting alcohol intake. Treating risk factors, such as high blood pressure, blood lipids and diabetes is also beneficial. Treating people who have strep throat with antibiotics can decrease the risk of rheumatic heart disease. The use of aspirin in people who are otherwise healthy is of unclear benefit.

Cardiovascular diseases are the leading cause of death worldwide except Africa. Together CVD resulted in 17.9 million deaths (32.1%) in 2015, up from 12.3 million (25.8%) in 1990. Deaths, at a given age, from CVD are more common and have been increasing in much of the developing world, while rates have declined in most of the developed world since the 1970s. Coronary artery disease and stroke account for 80% of CVD deaths in males and 75% of CVD deaths in females. Most cardiovascular disease affects older adults. In the United States 11% of people between 20 and 40 have CVD, while 37% between 40 and 60, 71% of people between 60 and 80, and 85% of people over 80 have CVD. The average age of death from coronary artery disease in the developed world is around 80, while it is around 68 in the developing world. CVD is typically diagnosed seven to ten years earlier in men than in women.

Types
There are many cardiovascular diseases involving the blood vessels. They are known as vascular diseases.
 * Coronary artery disease (coronary heart disease or ischemic heart disease)
 * Peripheral arterial disease – a disease of blood vessels that supply blood to the arms and legs
 * Cerebrovascular disease – a disease of blood vessels that supply blood to the brain (includes stroke)
 * Renal artery stenosis
 * Aortic aneurysm

There are also many cardiovascular diseases that involve the heart.
 * Cardiomyopathy – diseases of cardiac muscle
 * Hypertensive heart disease – diseases of the heart secondary to high blood pressure or hypertension
 * Heart failure – a clinical syndrome caused by the inability of the heart to supply sufficient blood to the tissues to meet their metabolic requirements
 * Pulmonary heart disease – a failure at the right side of the heart with respiratory system involvement
 * Cardiac dysrhythmias – abnormalities of heart rhythm
 * Inflammatory heart diseases
 * Endocarditis – inflammation of the inner layer of the heart, the endocardium. The structures most commonly involved are the heart valves.
 * Inflammatory cardiomegaly
 * Myocarditis – inflammation of the myocardium, the muscular part of the heart, caused most often by viral infection and less often by bacterial infections, certain medications, toxins, and autoimmune disorders. It is characterized in part by infiltration of the heart by lymphocyte and monocyte types of white blood cells.
 * Eosinophilic myocarditis – inflammation of the myocardium caused by pathologically activated eosinophilic white blood cells. This disorder differs from myocarditis in its causes and treatments.
 * Valvular heart disease
 * Congenital heart disease – heart structure malformations existing at birth
 * Rheumatic heart disease – heart muscles and valves damage due to rheumatic fever caused by Streptococcus pyogenes a group A streptococcal infection.

Risk factors
There are many risk factors for heart diseases: age, sex, tobacco use, physical inactivity, non-alcoholic fatty liver disease, excessive alcohol consumption, unhealthy diet, obesity, genetic predisposition and family history of cardiovascular disease, raised blood pressure (hypertension), raised blood sugar (diabetes mellitus), raised blood cholesterol (hyperlipidemia), undiagnosed celiac disease, psychosocial factors, poverty and low educational status, air pollution, and poor sleep. While the individual contribution of each risk factor varies between different communities or ethnic groups the overall contribution of these risk factors is very consistent. Some of these risk factors, such as age, sex or family history/genetic predisposition, are immutable; however, many important cardiovascular risk factors are modifiable by lifestyle change, social change, drug treatment (for example prevention of hypertension, hyperlipidemia, and diabetes). People with obesity are at increased risk of atherosclerosis of the coronary arteries.

Genetics
Cardiovascular disease in a person's parents increases their risk by ~3 fold, and genetics is an important risk factor for cardiovascular diseases. Genetic cardiovascular disease can occur either as a consequence of single variant (Mendelian) or polygenic influences. There are more than 40 inherited cardiovascular disease that can be traced to a single disease-causing DNA variant, although these conditions are rare. Most common cardiovascular diseases are non-Mendelian and are thought to be due to hundreds or thousands of genetic variants (known as single nucleotide polymorphisms), each associated with a small effect.

Age

Age is the most important risk factor in developing cardiovascular or heart diseases, with approximately a tripling of risk with each decade of life. Coronary fatty streaks can begin to form in adolescence. It is estimated that 82 percent of people who die of coronary heart disease are 65 and older. Simultaneously, the risk of stroke doubles every decade after age 55.

Multiple explanations are proposed to explain why age increases the risk of cardiovascular/heart diseases. One of them relates to serum cholesterol level. In most populations, the serum total cholesterol level increases as age increases. In men, this increase levels off around age 45 to 50 years. In women, the increase continues sharply until age 60 to 65 years.

Aging is also associated with changes in the mechanical and structural properties of the vascular wall, which leads to the loss of arterial elasticity and reduced arterial compliance and may subsequently lead to coronary artery disease.

Sex
Men are at greater risk of heart disease than pre-menopausal women. Once past menopause, it has been argued that a woman's risk is similar to a man's although more recent data from the WHO and UN disputes this. If a female has diabetes, she is more likely to develop heart disease than a male with diabetes. Women who have high blood pressure and had complications in their pregnancy have three times the risk of developing cardiovascular disease compared to women with normal blood pressure who had no complications in pregnancy.

Coronary heart diseases are 2 to 5 times more common among middle-aged men than women. In a study done by the World Health Organization, sex contributes to approximately 40% of the variation in sex ratios of coronary heart disease mortality. Another study reports similar results finding that sex differences explains nearly half the risk associated with cardiovascular diseases One of the proposed explanations for sex differences in cardiovascular diseases is hormonal difference. Among women, estrogen is the predominant sex hormone. Estrogen may have protective effects on glucose metabolism and hemostatic system, and may have direct effect in improving endothelial cell function. The production of estrogen decreases after menopause, and this may change the female lipid metabolism toward a more atherogenic form by decreasing the HDL cholesterol level while increasing LDL and total cholesterol levels.

Among men and women, there are differences in body weight, height, body fat distribution, heart rate, stroke volume, and arterial compliance. In the very elderly, age-related large artery pulsatility and stiffness are more pronounced among women than men. This may be caused by the women's smaller body size and arterial dimensions which are independent of menopause.

Tobacco
Cigarettes are the major form of smoked tobacco. Risks to health from tobacco use result not only from direct consumption of tobacco, but also from exposure to second-hand smoke. Approximately 10% of cardiovascular disease is attributed to smoking; however, people who quit smoking by age 30 have almost as low a risk of death as never smokers.

Physical inactivity
Insufficient physical activity (defined as less than 5 x 30 minutes of moderate activity per week, or less than 3 x 20 minutes of vigorous activity per week) is currently the fourth leading risk factor for mortality worldwide. In 2008, 31.3% of adults aged 15 or older (28.2% men and 34.4% women) were insufficiently physically active. The risk of ischemic heart disease and diabetes mellitus is reduced by almost a third in adults who participate in 150 minutes of moderate physical activity each week (or equivalent). In addition, physical activity assists weight loss and improves blood glucose control, blood pressure, lipid profile and insulin sensitivity. These effects may, at least in part, explain its cardiovascular benefits.

Diet
High dietary intakes of saturated fat, trans-fats and salt, and low intake of fruits, vegetables and fish are linked to cardiovascular risk, although whether all these associations indicate causes is disputed. The World Health Organization attributes approximately 1.7 million deaths worldwide to low fruit and vegetable consumption. Frequent consumption of high-energy foods, such as processed foods that are high in fats and sugars, promotes obesity and may increase cardiovascular risk. The amount of dietary salt consumed may also be an important determinant of blood pressure levels and overall cardiovascular risk. There is moderate quality evidence that reducing saturated fat intake for at least two years reduces the risk of cardiovascular disease. High trans-fat intake has adverse effects on blood lipids and circulating inflammatory markers, and elimination of trans-fat from diets has been widely advocated. In 2018 the World Health Organization estimated that trans fats were the cause of more than half a million deaths per year. There is evidence that higher consumption of sugar is associated with higher blood pressure and unfavorable blood lipids, and sugar intake also increases the risk of diabetes mellitus. High consumption of processed meats is associated with an increased risk of cardiovascular disease, possibly in part due to increased dietary salt intake.

Alcohol
The relationship between alcohol consumption and cardiovascular disease is complex, and may depend on the amount of alcohol consumed. There is a direct relationship between high levels of drinking alcohol and cardiovascular disease. Drinking at low levels without episodes of heavy drinking may be associated with a reduced risk of cardiovascular disease, but there is evidence that associations between moderate alcohol consumption and protection from stroke are non-causal. At the population level, the health risks of drinking alcohol exceed any potential benefits.

Celiac disease
Untreated celiac disease can cause the development of many types of cardiovascular diseases, most of which improve or resolve with a gluten-free diet and intestinal healing. However, delays in recognition and diagnosis of celiac disease can cause irreversible heart damage.

Sleep
A lack of good sleep, in amount or quality, is documented as increasing cardiovascular risk in both adults and teens. Recommendations suggest that Infants typically need 12 or more hours of sleep per day, adolescent at least eight or nine hours, and adults seven or eight. About one-third of adult Americans get less than the recommended seven hours of sleep per night, and in a study of teenagers, just 2.2 percent of those studied got enough sleep, many of whom did not get good quality sleep. Studies have shown that short sleepers getting less than seven hours sleep per night have a 10 percent to 30 percent higher risk of cardiovascular disease.

Sleep disorders such as sleep-disordered breathing and insomnia, are also associated with a higher cardiometabolic risk. An estimated 50 to 70 million Americans have insomnia, sleep apnea or other chronic sleep disorders.

In addition, sleep research displays differences in race and class. Short sleep and poor sleep tend to be more frequently reported in ethnic minorities than in whites. African-Americans report experiencing short durations of sleep five times more often than whites, possibly as a result of social and environmental factors. Black children and children living in disadvantaged neighborhoods have much higher rates of sleep apnea.

Socioeconomic disadvantage
Cardiovascular disease has a greater impact on low- and middle-income countries compared to those with higher income. Although data on the social patterns of cardiovascular disease in low- and middle-income countries is limited, reports from high-income countries consistently demonstrate that low educational status or income are associated with a greater risk of cardiovascular disease. Policies that have resulted in increased socio-economic inequalities have been associated with greater subsequent socio-economic differences in cardiovascular disease implying a cause and effect relationship. Psychosocial factors, environmental exposures, health behaviours, and health-care access and quality contribute to socio-economic differentials in cardiovascular disease. The Commission on Social Determinants of Health recommended that more equal distributions of power, wealth, education, housing, environmental factors, nutrition, and health care were needed to address inequalities in cardiovascular disease and non-communicable diseases.

Air pollution
Particulate matter has been studied for its short- and long-term exposure effects on cardiovascular disease. Currently, airborne particles under 2.5 micrometers in diameter (PM2.5) are the major focus, in which gradients are used to determine CVD risk. Overall, long-term PM exposure increased rate of atherosclerosis and inflammation. In regards to short-term exposure (2 hours), every 25 μg/m3 of PM2.5 resulted in a 48% increase of CVD mortality risk. In addition, after only 5 days of exposure, a rise in systolic (2.8 mmHg) and diastolic (2.7 mmHg) blood pressure occurred for every 10.5 μg/m3 of PM2.5. Other research has implicated PM2.5 in irregular heart rhythm, reduced heart rate variability (decreased vagal tone), and most notably heart failure. PM2.5 is also linked to carotid artery thickening and increased risk of acute myocardial infarction.

Cardiovascular risk assessment
Existing cardiovascular disease or a previous cardiovascular event, such as a heart attack or stroke, is the strongest predictor of a future cardiovascular event. Age, sex, smoking, blood pressure, blood lipids and diabetes are important predictors of future cardiovascular disease in people who are not known to have cardiovascular disease. These measures, and sometimes others, may be combined into composite risk scores to estimate an individual's future risk of cardiovascular disease. Numerous risk scores exist although their respective merits are debated. Other diagnostic tests and biomarkers remain under evaluation but currently these lack clear-cut evidence to support their routine use. They include family history, coronary artery calcification score, high sensitivity C-reactive protein (hs-CRP), ankle–brachial pressure index, lipoprotein subclasses and particle concentration, lipoprotein(a), apolipoproteins A-I and B, fibrinogen, white blood cell count, homocysteine, N-terminal pro B-type natriuretic peptide  (NT-proBNP), and markers of kidney function. High blood phosphorus is also linked to an increased risk.

Depression and traumatic stress
There is evidence that mental health problems, in particular depression and traumatic stress, is linked to cardiovascular diseases. Whereas mental health problems are known to be associated with risk factors for cardiovascular diseases such as smoking, poor diet, and a sedentary lifestyle, these factors alone do not explain the increased risk of cardiovascular diseases seen in depression, stress, and anxiety. Moreover, posttraumatic stress disorder is independently associated with increased risk for incident coronary heart disease, even after adjusting for depression and other covariates.

Occupational exposure
Little is known about the relationship between work and cardiovascular disease, but links have been established between certain toxins, extreme heat and cold, exposure to tobacco smoke, and mental health concerns such as stress and depression.

Non-chemical risk factors
A 2015 SBU-report looking at non-chemical factors found an association for those:
 * with mentally stressful work with a lack of control over their working situation — with an effort-reward imbalance
 * who experience low social support at work; who experience injustice or experience insufficient opportunities for personal development; or those who experience job insecurity
 * those who work night schedules; or have long working weeks
 * those who are exposed to noise

Specifically the risk of stroke was also increased by exposure to ionizing radiation. Hypertension develops more often in those who experience job strain and who have shift-work. Differences between women and men in risk are small, however men risk having and dying of heart attacks or stroke twice as often as women during working life.

Chemical risk factors
A 2017 SBU report found evidence that workplace exposure to silica dust, engine exhaust or welding fumes is associated with heart disease. Associations also exist for exposure to arsenic, benzopyrenes, lead, dynamite, carbon disulphide, carbon monoxide, metalworking fluids and occupational exposure to tobacco smoke. Working with  the  electrolytic production of  aluminium  or  the  production  of  paper  when  the  sulphate pulping  process  is  used  is  associated with heart disease. An association was also found between  heart  disease  and  exposure  to  compounds  which  are  no  longer  permitted  in certain  work  environments,  such  as  phenoxy acids containing TCDD(dioxin) or asbestos.

Workplace exposure to silica dust or asbestos is also associated with pulmonary heart disease. There is evidence that workplace exposure to lead, carbon disulphide, phenoxyacids containing  TCDD, as well as working in an environment where aluminum is being electrolytically produced, is associated with stroke.

Somatic mutations
As of 2017, evidence suggests that certain leukemia-associated mutations in blood cells may also lead to increased risk of cardiovascular disease. Several large-scale research projects looking at human genetic data have found a robust link between the presence of these mutations, a condition known as clonal hematopoiesis, and cardiovascular disease-related incidents and mortality.

Radiation therapy
Radiation treatments (RT) for cancer can increase the risk of heart disease and death, as observed in breast cancer therapy. Therapeutic radiation increases the risk of a subsequent heart attack or stroke by 1.5 to 4 times; the increase depends on the dose strength, volume, and location. Use of concomitant chemotherapy, e.g. anthracyclines, is an aggravating risk factor. The occurrence rate of RT induced cardiovascular disease is estimated between 10% and 30%.

Side-effects from radiation therapy for cardiovascular diseases have been termed radiation-induced heart disease or radiation-induced cardiovascular disease. Symptoms are dose-dependent and include cardiomyopathy, myocardial fibrosis, valvular heart disease, coronary artery disease, heart arrhythmia and peripheral artery disease. Radiation-induced fibrosis, vascular cell damage and oxidative stress can lead to these and other late side-effect symptoms.

Pathophysiology
Population-based studies show that atherosclerosis, the major precursor of cardiovascular disease, begins in childhood. The Pathobiological Determinants of Atherosclerosis in Youth (PDAY) study demonstrated that intimal lesions appear in all the aortas and more than half of the right coronary arteries of youths aged 7–9 years.

Obesity and diabetes mellitus are linked to cardiovascular disease, as are a history of chronic kidney disease and hypercholesterolaemia. In fact, cardiovascular disease is the most life-threatening of the diabetic complications and diabetics are two- to four-fold more likely to die of cardiovascular-related causes than nondiabetics.

Screening
Screening ECGs (either at rest or with exercise) are not recommended in those without symptoms who are at low risk. This includes those who are young without risk factors. In those at higher risk the evidence for screening with ECGs is inconclusive. Additionally echocardiography, myocardial perfusion imaging, and cardiac stress testing is not recommended in those at low risk who do not have symptoms. Some biomarkers may add to conventional cardiovascular risk factors in predicting the risk of future cardiovascular disease; however, the value of some biomarkers is questionable. Ankle-brachial index (ABI), high-sensitivity C-reactive protein (hsCRP), and coronary artery calcium, are also of unclear benefit in those without symptoms as of 2018.

The NIH recommends lipid testing in children beginning at the age of 2 if there is a family history of heart disease or lipid problems. It is hoped that early testing will improve lifestyle factors in those at risk such as diet and exercise.

Screening and selection for primary prevention interventions has traditionally been done through absolute risk using a variety of scores (ex. Framingham or Reynolds risk scores). This stratification has separated people who receive the lifestyle interventions (generally lower and intermediate risk) from the medication (higher risk). The number and variety of risk scores available for use has multiplied, but their efficacy according to a 2016 review was unclear due to lack of external validation or impact analysis. Risk stratification models often lack sensitivity for population groups and do not account for the large number of negative events among the intermediate and low risk groups. As a result, future preventative screening appears to shift toward applying prevention according to randomized trial results of each intervention rather than large-scale risk assessment.

Prevention
Up to 90% of cardiovascular disease may be preventable if established risk factors are avoided. Currently practised measures to prevent cardiovascular disease include:
 * Maintaining a healthy diet, such as the Mediterranean diet, a vegetarian, vegan or another plant-based diet.
 * Replacing saturated fat with healthier choices: Clinical trials show that replacing saturated fat with polyunsaturated vegetable oil reduced CVD by 30%. Prospective observational studies show that in many populations lower intake of saturated fat coupled with higher intake of polyunsaturated and monounsaturated fat is associated with lower rates of CVD.
 * Decrease body fat if overweight or obese. The effect of weight loss is often difficult to distinguish from dietary change, and evidence on weight reducing diets is limited. In observational studies of people with severe obesity, weight loss following bariatric surgery is associated with a 46% reduction in cardiovascular risk.
 * Limit alcohol consumption to the recommended daily limits. People who moderately consume alcoholic drinks have a 25–30% lower risk of cardiovascular disease. However, people who are genetically predisposed to consume less alcohol have lower rates of cardiovascular disease suggesting that alcohol itself may not be protective. Excessive alcohol intake increases the risk of cardiovascular disease and consumption of alcohol is associated with increased risk of a cardiovascular event in the day following consumption.
 * Decrease non-HDL cholesterol. Statin treatment reduces cardiovascular mortality by about 31%.
 * Stopping smoking and avoidance of second-hand smoke. Stopping smoking reduces risk by about 35%.
 * At least 150 minutes (2 hours and 30 minutes) of moderate exercise per week.
 * Lower blood pressure, if elevated. A 10 mmHg reduction in blood pressure reduces risk by about 20%. Lowering blood pressure appears to be effective even at normal blood pressure ranges.
 * Decrease psychosocial stress. This measure may be complicated by imprecise definitions of what constitute psychosocial interventions. Mental stress–induced myocardial ischemia is associated with an increased risk of heart problems in those with previous heart disease. Severe emotional and physical stress leads to a form of heart dysfunction known as Takotsubo syndrome in some people. Stress, however, plays a relatively minor role in hypertension. Specific relaxation therapies are of unclear benefit.
 * Not enough sleep also raises the risk of high blood pressure. Adults need about 7–9 hours of sleep. Sleep apnea is also a major risk as it causes breathing to stop briefly, which can put stress on the body which can raise the risk of heart disease.

Most guidelines recommend combining preventive strategies. There is some evidence that interventions aiming to reduce more than one cardiovascular risk factor may have beneficial effects on blood pressure, body mass index and waist circumference; however, evidence was limited and the authors were unable to draw firm conclusions on the effects on cardiovascular events and mortality.

There is additional evidence to suggest that providing people with a cardiovascular disease risk score may reduce risk factors by a small amount compared to usual care. However, there was some uncertainty as to whether providing these scores had any effect on cardiovascular disease events. It is unclear whether or not dental care in those with periodontitis affects their risk of cardiovascular disease. According to a 2021 WHO study, working 55+ hours a week raises the risk of stroke by 35% and the risk of dying from heart conditions by 17%, when compared to a 35-40 hours week.

Diet
A diet high in fruits and vegetables decreases the risk of cardiovascular disease and death.

A 2021 review found that plant-based diets can provide a risk reduction for CVD if a healthy plant-based diet is consumed. Unhealthy plant-based diets do not provide benefits over diets including meat. A similar meta-analysis and systematic review also looked into dietary patterns and found "that diets lower in animal foods and unhealthy plant foods, and higher in healthy plant foods are beneficial for CVD prevention". A 2018 meta-analysis of observational studies concluded that "In most countries, a vegan diet is associated with a more favourable cardio-metabolic profile compared to an omnivorous diet."

Evidence suggests that the Mediterranean diet may improve cardiovascular outcomes. There is also evidence that a Mediterranean diet may be more effective than a low-fat diet in bringing about long-term changes to cardiovascular risk factors (e.g., lower cholesterol level and blood pressure).

The DASH diet (high in nuts, fish, fruits and vegetables, and low in sweets, red meat and fat) has been shown to reduce blood pressure, lower total and low density lipoprotein cholesterol and improve metabolic syndrome; but the long-term benefits have been questioned. A high-fiber diet is associated with lower risks of cardiovascular disease.

Worldwide, dietary guidelines recommend a reduction in saturated fat, and although the role of dietary fat in cardiovascular disease is complex and controversial there is a long-standing consensus that replacing saturated fat with unsaturated fat in the diet is sound medical advice. Total fat intake has not been found to be associated with cardiovascular risk. A 2020 systematic review found moderate quality evidence that reducing saturated fat intake for at least 2 years caused a reduction in cardiovascular events. A 2015 meta-analysis of observational studies however did not find a convincing association between saturated fat intake and cardiovascular disease. Variation in what is used as a substitute for saturated fat may explain some differences in findings. The benefit from replacement with polyunsaturated fats appears greatest, while replacement of saturated fats with carbohydrates does not appear to have a beneficial effect. A diet high in trans fatty acids is associated with higher rates of cardiovascular disease, and in 2015 the Food and Drug Administration (FDA) determined that there was 'no longer a consensus among qualified experts that partially hydrogenated oils (PHOs), which are the primary dietary source of industrially produced trans fatty acids (IP-TFA), are generally recognized as safe (GRAS) for any use in human food'. There is conflicting evidence concerning whether dietary supplements of omega-3 fatty acids (a type of polyunsaturated essential fatty acid) added to diet improve cardiovascular risk.

The benefits of recommending a low-salt diet in people with high or normal blood pressure are not clear. In those with heart failure, after one study was left out, the rest of the trials show a trend to benefit. Another review of dietary salt concluded that there is strong evidence that high dietary salt intake increases blood pressure and worsens hypertension, and that it increases the number of cardiovascular disease events; both as a result of the increased blood pressure and probably through other mechanisms. Moderate evidence was found that high salt intake increases cardiovascular mortality; and some evidence was found for an increase in overall mortality, strokes, and left ventricular hypertrophy.

Intermittent fasting
Overall, the current body of scientific evidence is uncertain on whether intermittent fasting could prevent cardiovascular disease. Intermittent fasting may help people lose more weight than regular eating patterns, but was not different from energy restriction diets.

Medication
Blood pressure medication reduces cardiovascular disease in people at risk, irrespective of age, the baseline level of cardiovascular risk, or baseline blood pressure. The commonly-used drug regimens have similar efficacy in reducing the risk of all major cardiovascular events, although there may be differences between drugs in their ability to prevent specific outcomes. Larger reductions in blood pressure produce larger reductions in risk, and most people with high blood pressure require more than one drug to achieve adequate reduction in blood pressure. Adherence to medications is often poor, and while mobile phone text messaging has been tried to improve adherence, there is insufficient evidence that it alters secondary prevention of cardiovascular disease.

Statins are effective in preventing further cardiovascular disease in people with a history of cardiovascular disease. As the event rate is higher in men than in women, the decrease in events is more easily seen in men than women. In those at risk, but without a history of cardiovascular disease (primary prevention), statins decrease the risk of death and combined fatal and non-fatal cardiovascular disease. The benefit, however, is small. A United States guideline recommends statins in those who have a 12% or greater risk of cardiovascular disease over the next ten years. Niacin, fibrates and CETP Inhibitors, while they may increase HDL cholesterol do not affect the risk of cardiovascular disease in those who are already on statins. Fibrates lower the risk of cardiovascular and coronary events, but there is no evidence to suggest that they reduce all-cause mortality.

Anti-diabetic medication may reduce cardiovascular risk in people with Type 2 diabetes, although evidence is not conclusive. A meta-analysis in 2009 including 27,049 participants and 2,370 major vascular events showed a 15% relative risk reduction in cardiovascular disease with more-intensive glucose lowering over an average follow-up period of 4.4 years, but an increased risk of major hypoglycemia.

Aspirin has been found to be of only modest benefit in those at low risk of heart disease, as the risk of serious bleeding is almost equal to the protection against cardiovascular problems. In those at very low risk, including those over the age of 70, it is not recommended. The United States Preventive Services Task Force recommends against use of aspirin for prevention in women less than 55 and men less than 45 years old; however, it is recommended for some older people.

The use of vasoactive agents for people with pulmonary hypertension with left heart disease or hypoxemic lung diseases may cause harm and unnecessary expense.

Antibiotics for secondary prevention of coronary heart disease

Antibiotics may help patients with coronary disease to reduce the risk of heart attacks and strokes. However, evidence in 2021 suggests that antibiotics for secondary prevention of coronary heart disease are harmful, with increased mortality and occurrence of stroke; the use of antibiotics is not supported for preventing secondary coronary heart disease.

Physical activity
Exercise-based cardiac rehabilitation following a heart attack reduces the risk of death from cardiovascular disease and leads to less hospitalizations. There have been few high-quality studies of the benefits of exercise training in people with increased cardiovascular risk but no history of cardiovascular disease.

A systematic review estimated that inactivity is responsible for 6% of the burden of disease from coronary heart disease worldwide. The authors estimated that 121,000 deaths from coronary heart disease could have been averted in Europe in 2008 if people had not been physically inactive. Low-quality evidence from a limited number of studies suggest that yoga has beneficial effects on blood pressure and cholesterol. Tentative evidence suggests that home-based exercise programs may be more efficient at improving exercise adherence.

Dietary supplements
While a healthy diet is beneficial, the effect of antioxidant supplementation (vitamin E, vitamin C, etc.) or vitamins has not been shown to protect against cardiovascular disease and in some cases may possibly result in harm. Mineral supplements have also not been found to be useful. Niacin, a type of vitamin B3, may be an exception with a modest decrease in the risk of cardiovascular events in those at high risk. Magnesium supplementation lowers high blood pressure in a dose-dependent manner. Magnesium therapy is recommended for people with ventricular arrhythmia associated with torsades de pointes who present with long QT syndrome, and for the treatment of people with digoxin intoxication-induced arrhythmias. There is no evidence that omega-3 fatty acid supplementation is beneficial. A 2022 review found that some dietary supplements, including micronutrients, may reduce risk factors for cardiovascular disease.

Management
Cardiovascular disease is treatable with initial treatment primarily focused on diet and lifestyle interventions. Influenza may make heart attacks and strokes more likely and therefore influenza vaccination may decrease the chance of cardiovascular events and death in people with heart disease.

Proper CVD management necessitates a focus on MI and stroke cases due to their combined high mortality rate, keeping in mind the cost-effectiveness of any intervention, especially in developing countries with low or middle-income levels. Regarding MI, strategies using aspirin, atenolol, streptokinase or tissue plasminogen activator have been compared for quality-adjusted life-year (QALY) in regions of low and middle income. The costs for a single QALY for aspirin and atenolol were less than US$25, streptokinase was about $680, and t-PA was $16,000. Aspirin, ACE inhibitors, beta-blockers, and statins used together for secondary CVD prevention in the same regions showed single QALY costs of $350.

There are also surgical or procedural interventions that can save someone's life or prolong it. For heart valve problems, a person could have surgery to replace the valve. For arrhythmias, a pacemaker can be put in place to help reduce abnormal heart rhythms and for a heart attack, there are multiple options two of these are a coronary angioplasty and a coronary artery bypass surgery.

There is probably no additional benefit in terms of mortality and serious adverse events when blood pressure targets were lowered to ≤ 135/85 mmHg from ≤ 140 to 160/90 to 100 mmHg.

Epidemiology

Cardiovascular diseases are the leading cause of death worldwide and in all regions except Africa. In 2008, 30% of all global death was attributed to cardiovascular diseases. Death caused by cardiovascular diseases are also higher in low- and middle-income countries as over 80% of all global deaths caused by cardiovascular diseases occurred in those countries. It is also estimated that by 2030, over 23 million people will die from cardiovascular diseases each year.

It is estimated that 60% of the world's cardiovascular disease burden will occur in the South Asian subcontinent despite only accounting for 20% of the world's population. This may be secondary to a combination of genetic predisposition and environmental factors. Organizations such as the Indian Heart Association are working with the World Heart Federation to raise awareness about this issue.

Research
There is evidence that cardiovascular disease existed in pre-history, and research into cardiovascular disease dates from at least the 18th century. The causes, prevention, and/or treatment of all forms of cardiovascular disease remain active fields of biomedical research, with hundreds of scientific studies being published on a weekly basis.

Recent areas of research include the link between inflammation and atherosclerosis the potential for novel therapeutic interventions, and the genetics of coronary heart disease.

title: Cardiovascular disease


text:
Chita, Zabaykalsky Krai

Chita (Чита, ) is a city and the administrative center of Zabaykalsky Krai, Russia, located on the Trans-Siberian Railway route, roughly 900 km east of Irkutsk. Population:

History
Pyotr Beketov's Cossacks founded Chita in 1653. The name of the settlement came from the local River Chita.

Following the Decembrist revolt of 1825, from 1827 several of the Decembrists suffered exile to Chita. According to George Kennan, who visited the area in the 1880s, "Among the exiles in Chita were some of the brightest, most cultivated, most sympathetic men and women that we had met in Eastern Siberia."

When Richard Maack visited the city in 1855, he saw a wooden town, with one church, also wooden. He estimated Chita's population at under 1,000, but predicted that the city would soon experience fast growth, due to the upcoming annexation of the Amur valley by Russia.

By 1885, Chita's population had reached 5,728, and by 1897 it increased to 11,500. In 1897 the Trans-Siberian Railway reached Chita; rail traffic from 1899 rapidly made Chita the transport hub and industrial centre of the Transbaikal.

During the Russian Revolution of 1905, revolutionary socialists declared the Chita Republic. Tsarist government forces took control again in January 1906.

The Bolsheviks took power in Chita in February 1918. The Imperial Japanese Army occupied Chita from September 1918 to 1920 in the course of the Siberian intervention. On behalf of the White movement, Ataman Grigory Semyonov's Eastern Okraina ruled from Chita for some few months in early 1920 with Japanese support. From October 1920 to November 1922 the city served as the capital of the Far Eastern Republic, which became part of the RSFSR in November 1922.

In 1945, the Soviet authorities held Puyi, who had reigned (1908–1912, 1917) as the last Emperor of China, and some of his associates as prisoners in the city, in a former sanatorium for officers.

Geography
Chita lies at the confluence of the Chita and Ingoda Rivers, between the Yablonoi Mountains to the west and the Chersky Range to the east. Lake Kenon is located to the west, within the city limits, and the Ivan-Arakhley Lake System is a group of lakes lying about 50 km west of Chita.

Climate
Chita experiences a dry-winter borderline humid continental climate/subarctic climate (Köppen climate classification: Dwb/Dwc) with very cold, very dry winters and warm, relatively wet summers. The coldest temperature to have ever been recorded in Chita was -49.6 C.

Administrative and municipal status
Chita is the administrative center of Zabaykalsky Krai, and, within the framework of administrative divisions, it also serves as the administrative center of Chitinsky District, to which it is also subordinated. As a municipal division, the city of Chita together with one rural locality in Chitinsky District is incorporated as Chita Urban Okrug.

City districts
The city is subdivided into four administrative districts: Chernovsky (named after the Chernovskiye coal mines and colloquially known as "Chernovskiye" ), Ingodinsky (named after the Ingoda River), Tsentralny, and Zheleznodorozhny.

Chernovsky Administrative District used to be a mining settlement, which was incorporated into Chita in 1941. Chernovskiye mines themselves are a geological nature monument of international status.

Transportation
Chita is served by Kadala Airport, situated 15 km to the west.

Education
Chita is home to several facilities of higher education:
 * Transbaikal State University (formerly Chita State University)
 * Chita State Academy of Medicine

Military
Chita Northwest air base is located nearby, as well as the 101st (Hub) Communications Brigade and the 53rd Material Support Regiment.

Sports
FC Chita is Chita's association football club.

An indoor arena for speed skating is planned.

Twin towns – sister cities
Chita is twinned with:
 * 🇨🇳 Hailar District, China (1992)
 * 🇲🇳 Choibalsan, Mongolia (1994)
 * 🇨🇳 Manzhouli, China (1999)
 * 🇨🇳 Hulunbuir, China (2001)
 * 🇷🇺 Ulan-Ude, Russia (2011)

Notable people

 * Yevgeni Alkhimov (born 1977), Russian professional footballer
 * Nataliya Kuznetsova (born 1991), Russian professional female bodybuilder who holds the world armlifting, bench press, and deadlift titles
 * Oleg Lundstrem (1916–2005), Soviet and Russian jazz composer
 * Igor Mirnov (born 1984), Russian professional ice hockey player
 * Ivan Nagibin (born 1986), Russian professional football player
 * Lev Okhotin (1911–1948), member of the Supreme Council of the Russian Fascist Party
 * Aleksandr Perfilyev (1895–1973), Russian journalist, poet and writer
 * Anastasia Pivovarova (born 1990), Russian professional tennis player
 * Boris Polevoy (1918–2002), Russian historian
 * Aleksandra Samusenko (1922–1945), Soviet Tank Captain, Sole female tank commander in 1st Guards Tank Army
 * Volodymyr Shkidchenko (born 1948), Ukrainian military, General of Army of Ukraine
 * Sergei Smirnov (born 1950), Russian security services official
 * Anatoly Sobchak (1937–2000), Russian politician
 * Vitaly Solomin (1941–2002), Soviet and Russian actor, director and screenwriter
 * Yury Solomin (born 1935), Soviet and Russian actor and director
 * Alina Stadnik (born 1991), Ukrainian female wrestler
 * Alexander Stranichkin (born 1955), Abkhazian politician
 * Lyudmila Titova (born 1946), Russian speed skater
 * Dmytro Tymchuk (born 1972), Ukrainian military expert and blogger
 * Yemelyan Yaroslavsky (1878–1943), Russian revolutionary, Soviet politician, communist party organizer
 * Oksana Zhnikrup (1931-1993), Ukrainian ceramicist, whose works inspired Jeff Koons
 * Stanislav Drobyshevsky (born 1978), Russian anthropologist and science popularizer

title: Chita, Zabaykalsky Krai


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Islamic Party of Britain

The Islamic Party of Britain is a defunct political party in the United Kingdom that was active from its formation in 1989 until 2006. The IPB was opposed to both capitalism and communism. David Musa Pidcock, a Sheffield man who converted from Roman Catholicism to Islam while working as an engineer in Saudi Arabia, founded and led the party. The IPB published a quarterly magazine entitled Common Sense.

The party entered the 1992 general election, standing three unsuccessful candidates in the constituencies of Bradford, a city with a large Muslim minority, and one in a London constituency, Streatham.

Founding
The Islamic Party of Britain was founded in September 1989 by Muslims who had grown dissatisfied with the Labour Party, a party that has traditionally gained the support of Muslims in Britain. Many Muslims were unhappy with the atheism of Neil Kinnock, the Labour leader, and wanted a party that would cater specifically for the needs of Muslims. Many also felt that both Labour and the Conservatives had not done enough to help Muslims in the controversy over Salman Rushdie's book The Satanic Verses.

Performance
The Islamic Party never achieved a seat in either house of Parliament. Pidcock represented the party in the 1990 Bradford North by-election, earning 800 votes (2.2%), finishing fourth from ten candidates.

At the 1992 general election, the party stood candidates in each of the three constituencies in the City of Bradford. All finished in last place, with leader Pidcock in Bradford West performing best, on 471 votes (0.96%). It also stood a candidate in Streatham, coming fifth of seven candidates.

Relations with other parties
In its first year, Pidcock claimed that his party was planning co-operation with the Green Party.

Members of the party have supported the Respect Party; one of their leading members, home affairs spokesman Mohammad Naseem, stood for and funded the party.

Policies
The party believed in equal treatment under the law regardless of an individual's status, income or ethnicity. The IPB argued that religion is the most important thing in life. It called for reform of the British banking system to make it interest-free and Islamic, and for increased trade with the Islamic world. At one time, the party answered questions sent in by readers of its website. When answering one question, the party argued that homosexuality needed treatment, was not to be tolerated and that homosexuals should be put to death for a "public display of lewdness", a policy that was condemned by gay activist Peter Tatchell.

title: Islamic Party of Britain


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Gyrocar

A gyrocar is a two-wheeled automobile. The difference between a bicycle or motorcycle and a gyrocar is that in a bike, dynamic balance is provided by the rider, and in some cases by the geometry and mass distribution of the bike itself, and the gyroscopic effects from the wheels. Steering a motorcycle is done by precessing the front wheel. In a gyrocar, balance was provided by one or more gyroscopes, and in one example, connected to two pendulums by a rack and pinion.

The concept was originally described in fiction in 1911 "Two Boys in a Gyrocar: The story of a New York to Paris Motor Race" by Kenneth Brown, (Houghton Mifflin Co). However the first prototype Gyrocar, The Shilovski Gyrocar, was commissioned in 1912 by the Russian Count Pyotr Shilovsky, a lawyer and member of the Russian royal family. It was manufactured to his design by the Wolseley Tool and Motorcar Company in England in 1914 and demonstrated in London the same year. The gyrocar was powered by a modified Wolseley C5 engine of 16 –, with a bore of 90 mm and a stroke of 121 mm. It was mounted ahead of the radiator, driving the rear wheel through a conventional clutch and gear box. A transmission brake was fitted after the gearbox – there were no brakes on the wheels themselves. The weight of the vehicle was 2.75 tons and it had a very large turning radius.

In 1927, Louis Brennan, funded to the tune of £12,000 (plus a £2000 per year) by John Cortauld, built a rather more successful gyrocar. Two contra-rotating gyros were housed under the front seats, spun in a horizontal plane at 3500 rpm by 24V electric motors powered from standard car batteries. This was the greatest speed obtainable with the electric motors available, and meant that each rotor had to weigh 200 lb to generate sufficient forces. Precession was in the vertical fore-aft plane. The car had a Morris Oxford engine, engine mountings, and gearbox. Two sidewheels (light aircraft tailwheels were used) were manually lowered on stopping; if the driver forgot and switched off the gyros and walked away, the car would continue to balance itself using the gyro momentum for a few minutes, and then the wheels would automatically be dropped to stop tipping.

title: Gyrocar


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The Ugly Little Boy

"The Ugly Little Boy" is a science fiction short story by American writer Isaac Asimov. The story first appeared in the September 1958 issue of Galaxy Science Fiction under the title "Lastborn", and was reprinted under its current title in the 1959 collection Nine Tomorrows. The story deals with a Homo neanderthalensis child which is brought to the future by means of time travel. Robert Silverberg later expanded it into a novel with the same title published in 1992 (also published as Child of Time in the UK).

Asimov has said that this was his second or third favorite of his own stories.

Plot summary
A Neanderthal child is brought to the present day as a result of time travel experiments by Stasis Inc, a research organization. He cannot be removed from his immediate area because of the vast energy loss and time paradoxes that would result, and is kept in the present by way of a Stasis module. In order to care for the boy the organization hires Edith Fellowes, a children's nurse.

Initially repelled by the boy's appearance, Edith soon begins to regard him as her own child, learning to love him and realizing that he is far more intelligent than she first imagined. She dubs him 'Timmie' and attempts to ensure that he has the best possible childhood despite his circumstance. She is enraged when the newspapers refer to him as an "ape-boy." Edith's love for Timmie brings her into conflict with her employer, for whom he is more of an experimental animal than a human being.

Eventually, her employer comes to the conclusion that his organization has exacted all the knowledge and publicity it can from Timmie and that the time has come to move on to the next project. This involves bringing a medieval peasant into the present, which necessitates the return of Timmie to his own time. Edith fights the decision, knowing the boy cannot survive if returned to his own time due to his acquisition of modern dependencies and speech. She attempts to smuggle the boy out of the facility, but when that plan fails she disrupts the integrity of the Stasis module and returns to the ancient past with Timmie.

Television adaptation
In 1977, "The Ugly Little Boy" was made into a 26-minute telefilm in Canada. The film was directed by and stars Barry Morse. London-born actress Kate Reid played the role of Nurse Fellowes. Guy Big, in his last role, played the boy. The film is noteworthy for its fidelity to the short story, as well as the pathos between Timmy and Nurse Fellowes which garnered praise from both fans and reviewers. The film was named to the ALA Notable Children's Films list in 1977.

Novelization
The 1991 novelization of the same title (published as Child of Time in the UK) expands on the short story by introducing Timmie's original Neanderthal tribe as well as a children's advocacy group that seeks to liberate Timmie. The Neanderthals are shown sympathetically as a highly articulate people whose tribal society and culture is complex and sophisticated, a far cry from the "primitive brutes" which the future scientists consider them to have been, having only the fragmentary information derived from a little Neanderthal child. This Neanderthal society—shown mainly from the point of view of an assertive tribal woman determined to prove herself the equal of the male hunters/warriors—is suddenly faced with the appearance of a completely different, competing kind of human being: the Cro-Magnons. While the Cro-Magnons try to negotiate with the Neanderthals, they cannot communicate and understand each other due to their differing languages. The Neanderthal characters are filled with a sense of foreboding.

The two story lines merge when Edith Fellowes makes the irrevocable decision to go back to the past with Timmie. Her appearance coincides with the crisis point in the confrontation between Neanderthal and Cro-Magnon; both groups regard her as a goddess to be worshiped. As she is clearly akin to the Cro-Magnon but has adopted a Neanderthal child, her appearance deflects the two groups from a would-be inevitable conflict.

The ending suggests that in the modified past Neanderthals and Cro-Magnon would cooperate and come closer to each other in the common worship of the "Goddess" - with Timmie growing up to be her acolyte and a "demigod" himself. It also suggests that the Neanderthals may not become extinct but could coexist with the Cro-Magnon, possibly interbreeding with them, which would change the whole of subsequent human history (or, according to a different theory of the implications of time travel, could have no effect at all due to the "convergent series").

Critical view
Margaret Woods wrote about the novel: "Well, 'Ugly Little Boy' draws you right in and does not let go. An enthralling plot, credible characters which make you feel great empathy - all of which serves to hide a very fundamental flaw: the basic premise of the plot just does not make any sense. What the hell is the use of spending a lot of money and effort in order to bring a Neanderthal child into the here-and-now - and then proceeding to give him an English name, teach him English, and place him in a modern environment with modern toys to play with? How is that supposed to help you learn about the Neanderthals?"

Original ending
In the first draft of the story, the story had ended very differently. Timmie was not returned to his own time, and it transpired that, due to his abduction, he was no longer the inventor of the technique for artificially creating fire, as he would have been. The course of history was therefore set back by 2,500 years, wiping out modern civilization - a clear Butterfly effect. This assumes, however, that a child snatched at complete random from prehistoric times would turn out to be exactly the unique inventor of making fire, and also that with him absent no one else would have invented it - both quite unlikely.

Galaxy editor Horace Gold insisted that Asimov change the ending. Asimov agreed, and once he had written the new ending the story became one of Asimov's own favourites.

title: The Ugly Little Boy


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Heald Green Ratepayers

Heald Green and Long Lane Ratepayers Association is a Ratepayers' Association in the Heald Green ward of the Metropolitan Borough of Stockport.

In every local election since its creation in 1927, independents sponsored by the association have held the council seats in the ward. The association has also supplied three mayors and two deputy mayors since the ward became a part of Stockport in 1974.

The association states that it does not have a manifesto or party policies, instead sponsoring councillors who live in the area to represent the community.

History
The association was formed in 1927 following the creation of the Heald Green electoral ward.

In 1962, the ratepayers' launched a community magazine named CONTACT.

The ratepayers' association would become entangled with the construction and development of runways at Manchester Airport several times through its history. As far back as April 1960, the association joined forces with the Hale Barns and Handforth ratepayer associations to spearhead opposition against the development of the new runways, due to noise pollution concerns. During a meeting of the Manchester Airport Consultative Committee, founded by the airport in 1969, the chair stated "we are watching the airport consultative committee like hawks and we shall not hesitate to give it a kick in the right place." In 1997, the group began campaigning alongside local groups such as the Manchester Airport Joint Action Group and the Stockport Campaign Against Runway Extension against the construction of Runway 2. Councillor Peter Burns made a statement on the runway in 2005, nearly four years following its construction amid local complaints: "I feel that Manchester Airport has already broken an undertaking given to residents under the flight path of this runway - and it had only been open for 102 hours." A spokesperson for Manchester Airport stated that due to debris, planes were forced to land on the second runway from the Stockport direction.

title: Heald Green Ratepayers