The International Epidemiological Association (IEA)  is a worldwide association with more than 2000 members in over 100 different countries, who follow the aims of the association to facilitate communication amongst those engaged in research and teaching of epidemiology throughout the world, and to encourage its use in all fields of health including social, community and preventative medicine. These aims are achieved by holding scientific meetings and seminars, by publication of journals, reports, translations of books, by contact amongst members and by other activities consistent with these aims. Members are accepted without regard to race, religion, sex, political affiliation or country of origin.

The association publishes its own Journal, the International Journal of Epidemiology (IJE) International Journal of Epidemiology, which is published bi-monthly, a complimentary copy of which is included in the membership dues.  It also sponsors a number of highly reputable publications such as A Dictionary of Epidemiology, and The Development of Modern Epidemiology The Development of Modern Epidemiology: Personal reports from those who were there. In addition, the association organizes The World Congress of Epidemiology (WCE) Chơi Cờ Đô Mi Nô - Chơi cờ tướng, cờ úp online which is held triennially in different parts of the world. The 19th WCE World Congress of Epidemiology 7-11th August 2011. EICC, Edinburgh, Scotland. was held in Edinburgh, Scotland, August 2011, while the 20th WCE will be held in Anchorage, Alaska, August 2014 Chơi Cờ Đô Mi Nô - Chơi cờ tướng, cờ úp online. Regional Scientific Meetings are also held in the IEA regions during three-year periods between WCEs.

The IEA is in official relations with the World Health Organization (WHO) and is run by a council including executive and regional councilors for its 7 regions in addition to the ex-officio members.

Aims

The objectives of the IEA are to:
 Promote the use of epidemiology and its application to the solution of health problems.
 Encourage the development of epidemiological methods and improvement in these methods.
 Promote the communication of epidemiological methods and findings amongst epidemiologists throughout the world as well as amongst all others concerned with health.
 Co-operate with both national and international organisations which are concerned with the promotion of health in the application of epidemiological methods in the solution of problems.
 Improve the dissemination of epidemiological findings nationally and internationally.
 Improve the recruitment, education and training of epidemiologists.

These objectives are achieved through networking professionals working in the field of epidemiology through different means, including its website: www.IEAweb.org Home; holding national, regional and international scientific meetings and congresses, as well as individual contacts between professional members. These have guided IEA's activities over the years.

A determined effort was made in this decade to develop regional activities and to strengthen IEA links and co-operation with the WHO.

How it started

The International Corresponding Club, as the IEA was first called, was started in 1954 by John Pemberton of Great Britain and Harold N Willard of the United States with the advice and help of Robert Cruickshank. They had found, as traveling Research Fellows each in the other's country, that they were handicapped by not being sufficiently well informed about the research and teaching in the field of social and preventive medicine in the various medical schools and research institutes. Initially it was to try and remedy this defect, that the Club was established on a small and informal basis. At first it was just a corresponding club whose object was 'to facilitate the communication between physicians working for the most part in university departments of preventive and social medicine, or in research institutes devoted to these aspects of medicine, throughout the world'. This was to be achieved by the publication of a Bulletin twice a year and by members endeavouring to 'ensure a friendly and hospitable welcome for visitors' from other countries. The first issue of the Bulletin appeared in January 1955 and contained contributions from 26 correspondents from nine countries.

Correspondents soon felt the need to meet to discuss research and teaching and the first formal meeting took place at the Ciba Foundation in London at the end of June 1956. By this time there were 49 correspondents from 18 countries, and one of them, A. Querido of Amsterdam invited the Club to hold its First International Scientific Meeting in the Netherlands. As a consequence a 'Study Group on Current Epidemiological Research', supported by a grant from the Rockefeller Foundation, took place at Noordwijk in September 1957. There were 58 participants representing 44 university departments from 20 countries at this meeting. A constitution was formulated and the first executive committee was elected. The Noordwijk meeting was the first of the nineteenth international scientific meetings which have been held to date. The second was held in the Universidad del Valle in Cali, Colombia in 1959 when the present title of the association was adopted.

The World Congress of Epidemiology (WCE)

With few exceptions, the scientific meetings of the association have been held every three years since 1957 in different locations around the world. At the first Council Meeting held in Montreal 17–18 August 2002, it was agreed that all meetings formerly entitled International Scientific Meeting would henceforth be called World Congress of Epidemiology (WCE), with a continued sequence of numbering. Here is a list of the WCE held since 1957:
 I Noordwijk, Netherlands, September 1957
 II Cali, Colombia, August 1959
 III Korčula, Yugoslavia, August 1961
 IV Princeton, USA, August 1964
 V Primosten, Yugoslavia, August 1968
 VI Primosten, Yugoslavia, August 1971
 VII Brighton, England, August 1974
 VIII San Juan, Puerto Rico, September 1977
 IX Edinburgh, Scotland, August 1981
 X Vancouver, Canada, August 1984
 XI Helsinki, Finland, August 1987
 XII Los Angeles, USA, August 1990
 XIII Sydney, Australia, September 1993
 XIV Nagoya, Japan, August 1996
 XV Florence, Italy, August 1999
 XVI Montreal, Canada, August 2002
 XVII Bangkok, Thailand, August 2005
 XVIII Porto Alegre, Brazil, September 2008
 XIX Edinburgh, Scotland, August 2011
 XX Anchorage, USA, August 2014
 XXI Saitama, Japan, August 2017

The Educational work of the association

The IEA has always attached great importance to the educational aspects of its work and its first Chairman, Robert Cruikshank, often used the phrase 'spreading the gospel' to describe these aims.

The meeting in Cali in 1959 stimulated great interest in epidemiology in Colombia and as a result three seminars on epidemiology were later organized by the IEA in that country. This marked the beginning of a series of seminars in the South American continent and the Caribbean area.

The Milbank Memorial Fund helped to make this extensive series of seminars possible and the WHO, through the Pan American Health Organization, also cooperated in these seminars. By 1977 the IEA had organized, or played a prominent part in, 23 Seminars or Workshops on epidemiology in 19 different countries. These were often conducted in association with the WHO. The association only undertakes to organize or participate in seminars at the invitation of the national or local educational or governmental bodies concerned.

In 1969 a decision was taken to produce a guide on the teaching of epidemiology which would be suitable for use throughout the world. The WHO agreed to cooperate in this project and Dr Ronald Lowe and Jan  Kostrzewski were asked to edit the guide. It was published first in English as Epidemiology: A guide to Teaching Methods Teaching Epidemiology: A guide for teachers in epidemiology, public health and clinical medicine and also published in French, German, Polish, Serbo-Croat Slovak, and Spanish editions; and editions in Russian and Slovakare in preparation.

Other of the classic texts sponsored by the IEA in collaboration with Oxford University Press is 'A Dictionary of Epidemiology' Oxford University Press: A Dictionary of Epidemiology: Miquel Porta which remains the definitive dictionary in epidemiology worldwide. In fact, with contributions from over 220 epidemiologists and other users of epidemiology from around the globe, it is more than a dictionary: it includes explanations and comments on both core epidemiologic terms and on other scientific terms relevant to all professionals in clinical medicine and public health, as well as to professionals in the other health, life, and social sciences. The aim of the IEA in cosponsoring this dictionary in its more than 20 years' history has been to facilitate communication among epidemiologist to develop a "common language" to the extent that this is possible. The first fourth editions of the dictionary were edited by John Last and the fifth edition was edited by Miquel Porta. In addition, the IEA has produced a publication to commemorate its 50th anniversary called "History of Modern Epidemiology" in addition to supporting 3 editions of the important publication Teaching Epidemiology Teaching Epidemiology: A guide for teachers in epidemiology, public health and clinical medicine.  The IEA offers a free copy of one of the first two publications as an incentive for life-time (10-years) or 3-year membership.

The IEA also comments on current topical issues in epidemiology through a series of online "rapid response" commentaries EpiBlog « IEA.

The International Journal of Epidemiology (IJE)

An important decision was taken at the Sixth International Meeting in 1971 to found an international quarterly journal of epidemiology. The council believed that the journal could replace the old Bulletin in providing a link between members in intervals between international meetings by publishing association news, and serve a valuable purpose by publishing original articles in the field of epidemiology. Walter W. Holland was appointed the first editor in 1972.  The IJE continues to go from strength to strength.  Between 2001 - 2016 under the editorship of George Davey Smith and Shah Ebrahim, the journal expanded. They introduced a number of new features and the positive effects of these changes are reflected in its improved impact factor (7.2 in 2015), which places it first among the international epidemiology journals.  Six issues of the journal are published every year. Stephen Leeder took over as editor in 2017.

Affiliations with international organizations

The association has a long tradition of collaboration with other organizations, particularly with the WHO and the Council for International Organizations of Medical Sciences (CIOMS)  and International Clinical Epidemiologic Network (INCLEN) Inclen.

The IEA became affiliated with the CIOMS in 1955 and was represented on its executive committee. This affiliation led the association to the participation in preparing the international ethical guidelines for epidemiological studies, recognized by WHO as a key reference.

In 1966 the association was recognized by the WHO as a Non-Governmental Organization.  In addition to representation at the World Health Assembly and regional committees, this affiliation contributed to excellent working relationships with WHO in the planning and execution of educational programmes of the IEA and in the production of the "Guide to Teaching Epidemiology".

The IEA is also an active member of the Countdown initiative, and provides oversight on data quality, analyses and interpretation. The Countdown to 2015: Maternal, Newborn and Child Health is a global initiative that includes academics and representatives of multilateral and bilateral agencies, professional organizations and civil society who share the common goal of increasing accountability for progress towards the Millennium Development Goals for improving the health of mothers and children.

The membership

In the earlier years of the IEA, British and North American members were in the majority, mainly because the association had its origins in the UK and US. The council of the association has always been very conscious of this tendency and made active efforts to broaden the representativeness of the association by encouraging members to nominate epidemiologists from other countries. Nowadays, membership is growing in the association, with over 2,000 current members from around the world. Current membership categories include:

 Ordinary members (fully paid up members)
 Senior members (eligible for 50% discount of annual membership)
 Student members (eligible for 50% discount of annual membership)
 Joint members (with national epidemiological associations)
 Sponsored members
 Honorary members

The IEA has recently introduced a scheme of joint membership with various national epidemiological societies. Members of participating national societies join IEA at 30% of the usual rate and have all of the benefits of regular IEA membership, except that they receive the e-version of the IJE only. Joint membership have established with the following associations:

Regional activities

The development and strengthening of regional activities is manifested by the record of the regional meetings.  These have been stimulating affairs as shown by the publications which resulted.  There have been regular meetings in most IEA Regions, including: Africa, South-East Asia, Eastern Mediterranean, Europe, Latin America & Caribbean, North America and Western Pacific and occasional ones in the remainder. Of particular note have been those which marked the foundation and strength of national epidemiological associations as in Japan, China and Holland.  The growth and interest in epidemiology and the enormous improvement in the quality, as well as the quantity of epidemiological research has been particularly notable in some IEA regions as South East Asia. For example, the Australian Regional IEA meeting in 1973 was attended by 9 Japanese - at that time the only such practicing scientists in that country. There was, by 1995, a flourishing national association with more than 900 members and its own Journal published in English. It was the host for the 1996 International Scientific Meeting (ISM). The number of participants, at Regional Meetings in this area e.g. from China, Indonesia, Malaysia, Philippines, Singapore and Thailand illustrate the increasing penetration of Epidemiology discipline.

The growth and strengthening of Epidemiology discipline outside Western Europe and North America has also led to increase in bids to act as hosts for ISMs, now known as WCEs.

International Training

In effort of enforcing the capacity building role of IEA and moving the 20-year-old Florence course to the south, IEA has started an annual short-course in epidemiological methods. Indeed, the course is allied to the IEA-sponsored European Educational Programme in Epidemiology Programmes EEPE, annually held in Florence for three weeks every June/July, under the directorship of Rodolfo Saracci, for more than 2 decades. Thus, such course is intended as a "Florence South" course, run annually on a five-year cycle of the IEA regions outside of Europe and North America (South East Asia, Eastern Mediterranean, Africa, Latin America and Western Pacific). Introductory, intermediate and advance level courses are offered to provide epidemiologists and public health professionals an opportunity to become acquainted with the advances in epidemiologic methods that can enhance the role of epidemiology in clinical medicine and public health.  These courses are addressed to epidemiologists, public health professionals, statisticians, and clinicians and include lectures, computer based analyses, exercises, discussion sessions, and practical experience in the design of a research proposal. The first course was held in Jaipur, India, in April 2009, the second in Riyadh, Saudi Arabia in April, 2010, the third in Malawi in April 2011, while the latest was held in Lima, Peru during May 2012.  It is planned to have the upcoming course in Hangzhou, China, 2013 .

The IEA also sponsors pre-conference courses prior to the WCE.

Sir Richard Doll Prize

In commemoration of Sir Richard Doll, IEA established in 2007 the "Richard Doll Prize in Epidemiology" to be awarded on triennial basis. The prize is awarded to an epidemiologist of the highest scientific standard. The recipient is honored for his/her scientific achievements that have advanced our understanding of the determinants of a disease of importance for health in populations through a body of research that may involve a series of studies, rather than a single publication. The prize winner is selected by a committee which includes current IEA president, president-elect, past-president in addition to two members appointed by the IEA Council. The prize is presented at the triennial WCE as $30,000 and a special plaque. The first prize has been conferred in 2008 to Prof Nubia Muñoz, while the second was awarded to Prof David Barker in 2011. Subsequent winners included Sir Richard Peto in 2014 George Davey Smith in 2017 and Cesar Victora in 2021.

Early Career Epidemiologists (ECE)

The IEA Executive Committee recently decided to create an International (worldwide) Early Career Epidemiologists group (ECE) within the IEA structure. A successful first meeting of ECE was held during the XIX IEA World Congress of Epidemiology (WCE) in Edinburgh (Scotland). The aims of this group are similar to those of the IEA, with a focus on identifying tools and opportunities to develop knowledge and careers for emerging professionals engaged in the field of epidemiology throughout the world. The IEA has decided to invest effort and resources in ensuring the connectivity among ECE and thus facilitate the promulgation of opportunities for IEA training events, a mentoring scheme, and other activities which promote the advance and appropriate use of the epidemiological methods and its development in all regions.

The future

The educational work of the IEA has always been regarded as one of its most important functions. This will continue through the media of the International Journal of Epidemiology and the International and Regional Scientific meetings. It is hoped that the IEA will be able to continue to play a part in the organization of seminars particularly in those parts of the world where epidemiology is not well developed. Owing to the lack of funds for this purpose such activities may have to be confined, for the present, to co-operation with national or international organizations, in particular the WHO, by providing faculty members and resource material rather than funds.

There was general support for continued regional development at the Seventh International Meeting and the first steps were taken towards the organization of further regional meetings. The previous council recommended that regional IEA councils covering the WHO regions should be established in order to stimulate recruitment of members and the organization of international meetings within regions. The present council consists of members from all the WHO regions and it is now considering the whole question of regional development.

See also
 Environmental epidemiology
 Epidemiology
 E-epidemiology
 Epidemic model
 Epidemiological methods
 Epidemiological Transition
 European Epidemiology Federation (IEA EEF)

References

External links

Epidemiology organizations
Health care-related professional associations
International medical and health organizations
Scientific organizations established in 1954


Sinewave é uma netlabel fundada em 2008, na cidade de São Paulo, pelos músicos Elson Barbosa e o Luiz Freitas.

Ao todo, o selo lançou mais de 200 projetos para download gratuito de mais de 90 artistas brasileiros e também é organizador do Sinewave Festival, que já foi realizado em cidades como São Paulo, Campinas, Rio de Janeiro, Curitiba e Porto Alegre.

História
No ano de 2008, Elson Barbosa e Luiz Freitas faziam parte de bandas diferentes, com o primeiro sendo da Herod Layne e o outro da Gray Strawberries. Após se conhecerem, ambos sempre comentavam sobre o cenário do rock independente e frequentemente encontravam um monte de bandas boas no MySpace ou no Trama Virtual, com divulgação zero. Eles se questionaram como poderiam fazer para ajudar essas bandas e então resolveram montar um selo virtual que disponibilizasse projetos gratuitos, baseado em outros selos como Lost Children e a Pisces Records, e fundaram a Sinewave no mesmo ano, com o nome sendo retirado do B-Side "Sine Wave" da banda britânica Slowdive.

Nesse período de atividade, a Sinewave ajudou a mapear e a formar novos talentos e apoiar pequenos cenários antes desconexos em lugares como Curitiba, Porto Alegre e Recife. O selo também começou a organizar o Sinewave Festival, a fim de promover suas bandas. A primeira edição ocorreu em 2009 e aconteceram mais edições, com três delas sendo em parceria com os selos Howlin' Records, Bichano Records, The Blog That Celebrates Itself Records e Midsummer Madness. Em 2012, o selo criou um grupo no Facebook e os participantes tiveram a ideia de organizar celebrações na sede da Sinewave como uma forma de aproximar a interação entre os artistas e fãs. Nesses eventos, ocorriam vários churrascos feito pela equipe da Sinewave, que acabaram ficando famosos entre esse público.

No dia 15 de fevereiro de 2013, o selo ganhou reconhecimento ao entrar na lista dos "Dez Melhores Selos Brasileiros de Música", feito pelo portal Botequim de Ideias.

A Sinewave lançou em 2016 a "Sinewave Essentials – The Best Of 2016", uma super coletânea que tem uma música de cada trabalho lançado durante esse ano pelo selo e o álbum de compilação "The Best Of/ The Rest Of 2006-2016", em comemoração aos 10 anos de atividade da banda Herod!.

No ano de 2017, a Sinewave se destacou em duas matérias sobre selos independentes importantes, uma feita pelo site de música Tenho Mais Discos Que Amigos! e a outra feita pela Red Bull Brasil, indicando sua importância no mercado fonográfico brasileiro.. Em julho do mesmo ano, a Sinewave participou da Feira de Selos e Publicações Independentes, realizado pelo selo Balaclava Records em parceria com o Sesc São Paulo.

Em 13 de agosto de 2019, a netlabel participou da matéria "Selos independentes brasileiros comentam sobre seu papel em nossos tempos", realizada pelo site Hits Perdidos.

Referências

Gravadoras do Brasil
Gravadoras fundadas em 2008

Sinewave


Marin Ljubičić (nogometaš, rođen 1988.)
 Marin Ljubičić (nogometaš, rođen 2002.)

Marin Ljubičić


Immortal kan henvise til:

Musik
 Immortal (band) – et norsk heavy metal band
 Immortal (ep) – en EP med Immortal
 Immortal (Michael Jackson-album) – et album med Michael Jackson
 Immortal (wrestling) – en gruppe wrestlere
 Immortal (Pyramaze-album) – et album med Pyramaze
 Immortal (Beth Hart-album) – et album med Beth Hart
 Immortal Songs 2 - et koreansk talentshow
 Immortal Records - et uafhængig pladeselskab fra Los Angeles i Californien

Film
 Immortal (film fra 2004) – en film fra 2004

Immortal


L'île Baudisson est une île de Papouasie-Nouvelle-Guinée, située au sud de l'île de la Nouvelle-Hanovre et à l'ouest de la partie nord de la Nouvelle-Irlande. Elle est située entre l'île Selapiu et l'île Manne.

Géographie

Histoire

Politique

Économie

Une plantation est implantée sur l'île.

Référence

Voir aussi

Bibliographie

Articles connexes

Île en Papouasie-Nouvelle-Guinée

Baudisson Island


Sole may refer to:
 Sole (foot), the bottom of the foot
 Sole (shoe), the bottom supporting member of the shoe

Business
 Sole proprietorship, a business which legally has no separate existence from its owner
 Corporation sole, in English law, a legal entity consisting of a single person ("sole")
 Sole Technology, an American footwear company specializing in skateboarding shoes

Fish
 Sole (fish), one of several species and groups of flatfishes:
 Soleidae, the family of the "true soles"
 Solea solea, the common or Dover sole, used in European cooking
 American sole, the family Achiridae
 Tonguefish, or tongue sole, in the family Cynoglossidae
 Several species of righteye flounder in the family Pleuronectidae:
 Lemon sole
 Microstomus pacificus (Pacific Dover sole)

People
 Solé (surname), a French and Spanish surname
 Sole (hip hop artist) (born 1977), hip-hop emcee and co-founder of the Anticon record label
 Solé (born 1973), American rapper and former wife of R&B singer Ginuwine
 Alfred Sole (1943–2022), American production designer, film director, producer, and writer
 Anil Sole (born 1959), Indian politician
 Catherine Sole (born 1978), South African entomologist
 Chris Sole (born 1994), Scottish cricketer
 Christian Sole (1896–1980), Norwegian politician
 David Sole (born 1962), Scottish rugby union player
 Fabio Sole (born 2001), English footballer
 Jonathan Sole (born 1987), New Zealand cricketer
 Josh Sole (born 1980), New Zealand born rugby union player
 William Sole (1739–1802), British apothecary and botanist
 Caro Soles, Canadian author
 Henry Soles Jr. (1935–2018), American minister
 Linden Soles (born 1956), Canadian journalist
 Michael Soles (1966–2021), Canadian football player
 P. J. Soles, American actress
 Paul Soles (1930–2021), Canadian voice actor
 R. C. Soles Jr. (1934–2021), American politician
 Steven Soles, American musician

Other uses
 Sole (currency), a 19th-century Argentine and Bolivian currency
 European Liberal Social Democracy (), a defunct political party in Italy
 Sole Bank, a sand bank in the Atlantic Ocean to the southwest of Cornwall, England, giving its name to the Sole sea area in the Shipping Forecast
 Sun (film) (), a 1929 silent Italian film directed
 Sole, the flat bottom part of plane that slides along the workpiece
 Sole, a part of a tool such as a spokeshave

See also
 Sol (disambiguation)
 Sola (disambiguation)
 Soul (disambiguation)
 Soules, a surname

Sole


Die SpVgg Deggendorf war ein Sportverein aus der niederbayerischen Kreisstadt Deggendorf.

Geschichte
Die SpVgg Deggendorf wurde im Februar 1920 gegründet. 1946 wurde der Verein zum ersten Mal Niederbayerischer Pokalmeister. Nachdem Max Thoma 1949 die Vereinsführung übernommen hatte, stellten sich die größten Vereinserfolge ein. 1952/53 wurde die Mannschaft unter Trainer Ludwig Stiglbauer Meister der II. Amateurliga Niederbayern und stieg in die 1. Amateurliga Südbayern auf, der man – unterbrochen durch einen Abstieg – insgesamt acht Saisonen lang angehörte. In der Saison 1958/59 spielte sich der Verein im DFB-Pokal unter die letzten 16 Mannschaften Süddeutschlands, unterlag dann aber im Februar 1959 auf eigenem Platz dem FC Bayern München mit 2:3. Im gleichen Jahr wurde die SpVgg zum zweiten Mal Niederbayerischer Pokalsieger.

1963 qualifizierte sich der Verein für die neu geschaffene Landesliga. Mit dem sportlichen Niveau konnte er aber nicht mithalten und stieg gleich im ersten Jahr wieder ab. Erst nach dem Wiederaufstieg 1972 gelang es, sich in der Landesliga zu etablieren. Bis 1983 spielte man elf Jahre ununterbrochen viertklassig. Nach zwei weiteren Aufstiegen in die Landesliga 1988 und 1993, die jeweils nur eine Saison währten, setzte der sportliche Niedergang ein, der die SpVgg bis in die B-Klasse abrutschen ließ.

Eine neue Vereinsführung stellte unterstützt von der Deggendorfer Firma Stangl eine konkurrenzfähige Mannschaft zusammen. Kontinuierlich führten sie die Mannschaft wieder in die oberen Ligen Niederbayerns, 2003 gelang sogar die Rückkehr in die Landesliga.

Anfang 2003 hatten die Vorstände der SpVgg Deggendorf und des SV Grün-Weiß Deggendorf Verhandlungen zur Fusion aufgenommen. Nach Zustimmung der Mitglieder der beiden Vereine wurde am 30. April 2003 die SpVgg Grün-Weiß Deggendorf gegründet.

Erfolge
 Aufstieg in die I. Amateurliga Südbayern (3. Liga): 1953, 1959
 Aufstieg in die Landesliga (4. Liga) 1963, 1972, 1988, 1993
 Aufstieg in die Landesliga 2003
 Niederbayerischer Pokalsieger: 1946, 1959, 1960, 1974
 Niederbayerischer Meister 2003

Siehe auch
 SpVgg Grün-Weiß Deggendorf

Weblinks
 Vereinsgeschichte der SpVgg Grün-Weiß Deggendorf 03

Einzelnachweise

Ehemaliger Fußballverein aus Bayern
Sport (Deggendorf)
Organisation (Deggendorf)
SpVgg Deggendorf
Aufgelöst 2003
Sportverein (Landkreis Deggendorf)
Geschichte (Landkreis Deggendorf)

SpVgg Deggendorf


Perşembe, Ordu ilinin bir ilçesi ve bu ilçenin merkezi kasabadır. Vona Yarımadasında yer alır. Dünyanın sayılı sakin şehirleri arasında gösterilmektedir.

Tarihçe

Perşembe ilçesinin eski adı Vona'dır. Nitekim 1914 yılına ait bir Osmanlı haritasında yarımadadaki burun ve limanın adı Vona (وونا) olarak geçer. Bugünkü Perşembe kasabasının çekirdeğini oluşturan yerleşim ise, Babalı (بابالی) adını taşıyordu.

Perşembe, uzun zaman Roma ve Bizans hakimiyetinde kalmıştır. 1461 yılında Fatih Sultan Mehmet'in Trabzon İmparatorluğu'nu ortadan kaldırmasından sonra Vona Osmanlı İmparatorluğu'nun hakimiyetine girmiştir. Osmanlı Devleti eyalet sisteminden vilayet sistemine geçince, 1867 yılında Trabzon Vilayeti kuruldu. Perşembe, "Perşenbe" (پرشنبە) adıyla bu vilayetin Trabzon sancağına bağlı ordu kazsının bir nahiyesiydi.

Perşembe, 1928 tarihli Osmanlıca köy listesinde yine "Perşenbe" (پرشنبە) adıyla Ordu vilayetinin merkez kazasına bağlı nahiyelerden biriydi ve 36 köyü kapsıyordu. Bu nahiyenin merkezi Babalı köyüdü. 1940 genel nüfus sayımında 33 köyü kapsayan Perşembe nahiyesinin nüfusu 23.937 kişiden oluşuyordu. Nahiye merkezi Babalı köyünde ise, 1.705 kişi yaşıyordu. 25 Haziran 1945 tarihinde ilçe olan Perşembe, sadece merkez bucağa bağlı 34 köyden oluşuyordu. 1950 genel nüfus sayımında Babalı köyünün adının geçmemsi, bu yerleşimin adının da Perşembe olarak değiştirilmiş olduğunu göstermektedir. Bu tarihte Perşembe kasabasının nüfusu 2.182 kişiden oluşuyordu. 1965 gelen nüfus sayımımda Perşembe ilçesinin nüfusu 37.053 kişiden oluşuyor ve bu nüfus içinde 12.428 kişi okuma yazma biliyordu. Perşembe kasabasında ise, 4.390 kişi yaşıyordu ve 2.666 kişi okuryazardı.

Yason Burnu'nda yer alan Yason Kilisesi Perşembe ilçesindeki en önemli tarihsel yapılardan biridir. Eski zamanlarda gemiciler tarafından depo ve sığınma alanı olarak kullanılmış olan Hoynat Adası da Perşembe ilçesi sınırları içindedir.

Coğrafya

Ordu-Samsun eski devlet karayolu üzerinde Vona tabii liman koyunda kordon tepesi eteğinde kurulmuştur. Kuzeyinde Karadeniz, doğusunda Ordu, batısında Fatsa, güneyinde Ordu-Ulubey ve Fatsa İlçeleri ile sınırlıdır. İl Merkezine 13 km uzaklıktadır.

Nüfus

Kaynakça

Cittaslow

Perşembe, Ordu


Wound healing refers to a living organism's replacement of destroyed or damaged tissue by newly produced tissue.

In undamaged skin, the epidermis (surface, epithelial layer) and dermis (deeper, connective layer) form a protective barrier against the external environment. When the barrier is broken, a regulated sequence of biochemical events is set into motion to repair the damage. This process is divided into predictable phases: blood clotting (hemostasis), inflammation, tissue growth (cell proliferation), and tissue remodeling (maturation and cell differentiation). Blood clotting may be considered to be part of the inflammation stage instead of a separate stage.

The wound-healing process is not only complex but fragile, and it is susceptible to interruption or failure leading to the formation of non-healing chronic wounds. Factors that contribute to non-healing chronic wounds are diabetes, venous or arterial disease, infection, and metabolic deficiencies of old age.

Wound care encourages and speeds wound healing via cleaning and protection from reinjury or infection. Depending on each patient's needs, it can range from the simplest first aid to entire nursing specialties such as wound, ostomy, and continence nursing and burn center care.

Stages
 Hemostasis (blood clotting): Within the first few minutes of injury, platelets in the blood begin to stick to the injured site. They change into an amorphous shape, more suitable for clotting, and they release chemical signals to promote clotting. This results in the activation of fibrin, which forms a mesh and acts as "glue" to bind platelets to each other. This makes a clot that serves to plug the break in the blood vessel, slowing/preventing further bleeding.
 Inflammation: During this phase, damaged and dead cells are cleared out, along with bacteria and other pathogens or debris. This happens through the process of phagocytosis, where white blood cells engulf debris and destroy it. Platelet-derived growth factors are released into the wound that cause the migration and division of cells during the proliferative phase.
 Proliferation (growth of new tissue): In this phase, angiogenesis, collagen deposition, granulation tissue formation, epithelialization, and wound contraction occur. In angiogenesis, vascular endothelial cells form new blood vessels. In fibroplasia and granulation tissue formation, fibroblasts grow and form a new, provisional extracellular matrix (ECM) by excreting collagen and fibronectin.  Concurrently, re-epithelialization of the epidermis occurs, in which epithelial cells proliferate and 'crawl' atop the wound bed, providing cover for the new tissue. In wound contraction, myofibroblasts decrease the size of the wound by gripping the wound edges and contracting using a mechanism that resembles that in smooth muscle cells. When the cells' roles are close to complete, unneeded cells undergo apoptosis.
 Maturation (remodeling): During maturation and remodeling, collagen is realigned along tension lines, and cells that are no longer needed are removed by programmed cell death, or apoptosis.

Timing and re-epithelialization
Timing is important to wound healing. Critically, the timing of wound re-epithelialization can decide the outcome of the healing. If the epithelization of tissue over a denuded area is slow, a scar will form over many weeks, or months; If the epithelization of a wounded area is fast, the healing will result in regeneration.

Early vs cellular phase

Wound healing is classically divided into hemostasis, inflammation, proliferation, and remodeling. Although a useful construct, this model employs considerable overlapping among individual phases. A complementary model has recently been described where the many elements of wound healing are more clearly delineated. The importance of this new model becomes more apparent through its utility in the fields of regenerative medicine and tissue engineering (see Research and development section below). In this construct, the process of wound healing is divided into two major phases: the early phase and the cellular phase:

The early phase, which begins immediately following skin injury, involves cascading molecular and cellular events leading to hemostasis and formation of an early, makeshift extracellular matrix that provides structural staging for cellular attachment and subsequent cellular proliferation.

The cellular phase involves several types of cells working together to mount an inflammatory response, synthesize granulation tissue, and restore the epithelial layer. Subdivisions of the cellular phase are:
 Macrophages and inflammatory components (within 1–2 days)
 Epithelial-mesenchymal interaction: re-epithelialization (phenotype change within hours, migration begins on day 1 or 2)
 Fibroblasts and myofibroblasts: progressive alignment, collagen production, and matrix contraction (between day 4 and day 14)
 Endothelial cells and angiogenesis (begins on day 4)
 Dermal matrix: elements of fabrication (begins on day 4, lasting 2 weeks) and alteration/remodeling (begins after week 2, lasting weeks to months—depending on wound size).

Inflammatory phase
Just before the inflammatory phase is initiated, the clotting cascade occurs in order to achieve hemostasis, or the stopping of blood loss by way of a fibrin clot. Thereafter, various soluble factors (including chemokines and cytokines) are released to attract cells that phagocytise debris, bacteria, and damaged tissue, in addition to releasing signaling molecules that initiate the proliferative phase of wound healing.

Clotting cascade

When tissue is first wounded, blood comes in contact with collagen, triggering blood platelets to begin secreting inflammatory factors. Platelets also express sticky glycoproteins on their cell membranes that allow them to aggregate, forming a mass.

Fibrin and fibronectin cross-link together and form a plug that traps proteins and particles and prevents further blood loss.  This fibrin-fibronectin plug is also the main structural support for the wound until collagen is deposited. Migratory cells use this plug as a matrix to crawl across, and platelets adhere to it and secrete factors. The clot is eventually lysed and replaced with granulation tissue and then later with collagen.

Platelets, the cells present in the highest numbers shortly after a wound occurs, release mediators into the blood, including cytokines and growth factors. Growth factors stimulate cells to speed their rate of division. Platelets release other proinflammatory factors like serotonin, bradykinin, prostaglandins, prostacyclins, thromboxane, and histamine, which serve several purposes, including increasing cell proliferation and migration to the area and causing blood vessels to become dilated and porous. In many ways, extravasated platelets in trauma perform a similar function to tissue macrophages and mast cells exposed to microbial molecular signatures in infection: they become activated, and secrete molecular mediators – vasoactive amines, eicosanoids, and cytokines  – that initiate the inflammatory process.

Vasoconstriction and vasodilation
Immediately after a blood vessel is breached, ruptured cell membranes release inflammatory factors like thromboxanes and prostaglandins that cause the vessel to spasm to prevent blood loss and to collect inflammatory cells and factors in the area. This vasoconstriction lasts five to ten minutes and is followed by vasodilation, a widening of blood vessels, which peaks at about 20 minutes post-wounding. Vasodilation is the result of factors released by platelets and other cells. The main factor involved in causing vasodilation is histamine. Histamine also causes blood vessels to become porous, allowing the tissue to become edematous because proteins from the bloodstream leak into the extravascular space, which increases its osmolar load and draws water into the area. Increased porosity of blood vessels also facilitates the entry of inflammatory cells like leukocytes into the wound site from the bloodstream.

Polymorphonuclear neutrophils
Within an hour of wounding, polymorphonuclear neutrophils (PMNs) arrive at the wound site and become the predominant cells in the wound for the first two days after the injury occurs, with especially high numbers on the second day. They are attracted to the site by fibronectin, growth factors, and substances such as kinins. Neutrophils phagocytise debris and kill bacteria by releasing free radicals in what is called a respiratory burst. They also cleanse the wound by secreting proteases that break down damaged tissue. Functional neutrophils at the wound site only have life-spans of around two days, so they usually undergo apoptosis once they have completed their tasks and are engulfed and degraded by macrophages.

Other leukocytes to enter the area include helper T cells, which secrete cytokines to cause more T cells to divide and to increase inflammation and enhance vasodilation and vessel permeability. T cells also increase the activity of macrophages.

Macrophages
One of the roles of macrophages is to phagocytize other expended phagocytes, bacteria and damaged tissue, and they also debride damaged tissue by releasing proteases.

Macrophages function in regeneration and are essential for wound healing. They are stimulated by the low oxygen content of their surroundings to produce factors that induce and speed angiogenesis and they also stimulate cells that reepithelialize the wound, create granulation tissue, and lay down a new extracellular matrix. By secreting these factors, macrophages contribute to pushing the wound healing process into the next phase. They replace PMNs as the predominant cells in the wound by two days after injury.

The spleen contains half the body's monocytes in reserve ready to be deployed to injured tissue. Attracted to the wound site by growth factors released by platelets and other cells, monocytes from the bloodstream enter the area through blood vessel walls. Numbers of monocytes in the wound peak one to one and a half days after the injury occurs. Once they are in the wound site, monocytes mature into macrophages. Macrophages also secrete a number of factors such as growth factors and other cytokines, especially during the third and fourth post-wounding days. These factors attract cells involved in the proliferation stage of healing to the area.

In wound healing that result in incomplete repair, scar contraction occurs, bringing varying gradations of structural imperfections, deformities and problems with flexibility. Macrophages may restrain the contraction phase. Scientists have reported that removing the macrophages from a salamander resulted in failure of a typical regeneration response (limb regeneration), instead bringing on a repair (scarring) response.

Decline of inflammatory phase
As inflammation dies down, fewer inflammatory factors are secreted, existing ones are broken down, and numbers of neutrophils and macrophages are reduced at the wound site. These changes indicate that the inflammatory phase is ending and the proliferative phase is underway. In vitro evidence, obtained using the dermal equivalent model, suggests that the presence of macrophages actually delays wound contraction and thus the disappearance of macrophages from the wound may be essential for subsequent phases to occur.

Because inflammation plays roles in fighting infection, clearing debris and inducing the proliferation phase, it is a necessary part of healing. However, inflammation can lead to tissue damage if it lasts too long. Thus the reduction of inflammation is frequently a goal in therapeutic settings. Inflammation lasts as long as there is debris in the wound. Thus, if the individual's immune system is compromised and is unable to clear the debris from the wound and/or if excessive detritus, devitalized tissue, or microbial biofilm is present in the wound, these factors may cause a prolonged inflammatory phase and prevent the wound from properly commencing the proliferation phase of healing. This can lead to a chronic wound.

Proliferative phase

About two or three days after the wound occurs, fibroblasts begin to enter the wound site, marking the onset of the proliferative phase even before the inflammatory phase has ended. As in the other phases of wound healing, steps in the proliferative phase do not occur in a series but rather partially overlap in time.

Angiogenesis

Also called neovascularization, the process of angiogenesis occurs concurrently with fibroblast proliferation when endothelial cells migrate to the area of the wound. Because the activity of fibroblasts and epithelial cells requires oxygen and nutrients, angiogenesis is imperative for other stages in wound healing, like epidermal and fibroblast migration. The tissue in which angiogenesis has occurred typically looks red (is erythematous) due to the presence of capillaries.

Angiogenesis occurs in overlapping phases in response to inflammation:
 Latent period: During the haemostatic and inflammatory phase of the wound healing process, vasodilation and permeabilisation allow leukocyte extravasation and phagocytic debridement and decontamination of the wound area. Tissue swelling aids later angiogenesis by expanding and loosening the existing collagenous extracellular matrix.
 Endothelial activation: As the wound macrophages switches from inflammatory to healing mode, it begins to secrete endothelial chemotactic and growth factors to attract adjacent endothelial cells. Activated endothelial cells respond by retracting and reducing cell junctions, loosening themselves from their embedded endothelium. Characteristically the activated endothelial cells show enlarged nucleoli.
 Degradation of endothelial basement membrane: The wound macrophages, mast cells and the endothelial cells themselves secrete proteases to break down existing vascular basal lamina.
 Vascular sprouting: With the breakdown of endothelial basement membrane, detached endothelial cells from pre-existing capillaries and post-capillary venules can divide and migrate chemotactically towards the wound, laying down new vessels in the process. Vascular sprouting can be aided by ambient hypoxia and acidosis in the wound environment, as hypoxia stimulates the endothelial transcription factor, hypoxia inducible factor (HIF) to transactivate angiogenic genes such as VEGF and GLUT1. Sprouted vessels can self-organise into luminal morphologies, and fusion of blind channels give rise to new capillary networks.
 Vascular maturation: the endothelium of vessels mature by laying down new endothelial extracellular matrix, followed by basal lamina formation. Lastly the vessel establishes a pericyte layer.

Stem cells of endothelial cells, originating from parts of uninjured blood vessels, develop pseudopodia and push through the ECM into the wound site to establish new blood vessels.

Endothelial cells are attracted to the wound area by fibronectin found on the fibrin scab and chemotactically by angiogenic factors released by other cells, e.g. from macrophages and platelets when in a low-oxygen environment. Endothelial growth and proliferation is also directly stimulated by hypoxia, and presence of lactic acid in the wound. For example, hypoxia stimulates the endothelial transcription factor, hypoxia-inducible factor (HIF) to transactivate a set of proliferative genes including vascular endothelial growth factor (VEGF) and glucose transporter 1 (GLUT1).

To migrate, endothelial cells need collagenases and plasminogen activator to degrade the clot and part of the ECM. Zinc-dependent metalloproteinases digest basement membrane and ECM to allow cell migration, proliferation and angiogenesis.

When macrophages and other growth factor-producing cells are no longer in a hypoxic, lactic acid-filled environment, they stop producing angiogenic factors. Thus, when tissue is adequately perfused, migration and proliferation of endothelial cells is reduced. Eventually blood vessels that are no longer needed die by apoptosis.

Fibroplasia and granulation tissue formation
Simultaneously with angiogenesis, fibroblasts begin accumulating in the wound site. Fibroblasts begin entering the wound site two to five days after wounding as the inflammatory phase is ending, and their numbers peak at one to two weeks post-wounding. By the end of the first week, fibroblasts are the main cells in the wound. Fibroplasia ends two to four weeks after wounding.

As a model the mechanism of fibroplasia may be conceptualised as an analogous process to angiogenesis (see above) - only the cell type involved is fibroblasts rather than endothelial cells. Initially there is a latent phase where the wound undergoes plasma exudation, inflammatory decontamination and debridement. Oedema increases the wound histologic accessibility for later fibroplastic migration. Second, as inflammation nears completion, macrophage and mast cells release fibroblast growth and chemotactic factors to activate fibroblasts from adjacent tissue. Fibroblasts at this stage loosen themselves from surrounding cells and ECM. Phagocytes further release proteases that break down the ECM of neighbouring tissue, freeing the activated fibroblasts to proliferate and migrate towards the wound. The difference between vascular sprouting and fibroblast proliferation is that the former is enhanced by hypoxia, whilst the latter is inhibited by hypoxia. The deposited fibroblastic connective tissue matures by secreting ECM into the extracellular space, forming granulation tissue (see below). Lastly collagen is deposited into the ECM.

In the first two or three days after injury, fibroblasts mainly migrate and proliferate, while later, they are the main cells that lay down the collagen matrix in the wound site. Origins of these fibroblasts are thought to be from the adjacent uninjured cutaneous tissue (although new evidence suggests that some are derived from blood-borne, circulating adult stem cells/precursors). Initially fibroblasts utilize the fibrin cross-linking fibers (well-formed by the end of the inflammatory phase) to migrate across the wound, subsequently adhering to fibronectin.   Fibroblasts then deposit ground substance into the wound bed, and later collagen, which they can adhere to for migration.

Granulation tissue functions as rudimentary tissue, and begins to appear in the wound already during the inflammatory phase, two to five days post wounding, and continues growing until the wound bed is covered.  Granulation tissue consists of new blood vessels, fibroblasts, inflammatory cells, endothelial cells, myofibroblasts, and the components of a new, provisional extracellular matrix (ECM). The provisional ECM is different in composition from the ECM in normal tissue and its components originate from fibroblasts. Such components include fibronectin, collagen, glycosaminoglycans, elastin, glycoproteins and proteoglycans. Its main components are fibronectin and hyaluronan, which create a very hydrated matrix and facilitate cell migration. Later this provisional matrix is replaced with an ECM that more closely resembles that found in non-injured tissue.

Growth factors (PDGF, TGF-β) and fibronectin encourage proliferation, migration to the wound bed, and production of ECM molecules by fibroblasts. Fibroblasts also secrete growth factors that attract epithelial cells to the wound site.  Hypoxia also contributes to fibroblast proliferation and excretion of growth factors, though too little oxygen will inhibit their growth and deposition of ECM components, and can lead to excessive, fibrotic scarring.

Collagen deposition
One of fibroblasts' most important duties is the production of collagen.

Collagen deposition is important because it increases the strength of the wound; before it is laid down, the only thing holding the wound closed is the fibrin-fibronectin clot, which does not provide much resistance to traumatic injury. Also, cells involved in inflammation, angiogenesis, and connective tissue construction attach to, grow and differentiate on the collagen matrix laid down by fibroblasts.

Type III collagen and fibronectin generally begin to be produced in appreciable amounts at somewhere between approximately 10 hours and 3 days, depending mainly on wound size. Their deposition peaks at one to three weeks. They are the predominating tensile substances until the later phase of maturation, in which they are replaced by the stronger type I collagen.

Even as fibroblasts are producing new collagen, collagenases and other factors degrade it. Shortly after wounding, synthesis exceeds degradation so collagen levels in the wound rise, but later production and degradation become equal so there is no net collagen gain. This homeostasis signals the onset of the later maturation phase. Granulation gradually ceases and fibroblasts decrease in number in the wound once their work is done. At the end of the granulation phase, fibroblasts begin to commit apoptosis, converting granulation tissue from an environment rich in cells to one that consists mainly of collagen.

Epithelialization
The formation of granulation tissue into an open wound allows the reepithelialization phase to take place, as epithelial cells migrate across the new tissue to form a barrier between the wound and the environment. Basal keratinocytes from the wound edges and dermal appendages such as hair follicles, sweat glands and sebaceous (oil) glands are the main cells responsible for the epithelialization phase of wound healing. They advance in a sheet across the wound site and proliferate at its edges, ceasing movement when they meet in the middle. In healing that results in a scar, sweat glands, hair follicles and nerves do not form. With the lack of hair follicles, nerves and sweat glands, the wound, and the resulting healing scar, provide a challenge to the body with regards to temperature control.

Keratinocytes migrate without first proliferating. Migration can begin as early as a few hours after wounding. However, epithelial cells require viable tissue to migrate across, so if the wound is deep it must first be filled with granulation tissue. Thus the time of onset of migration is variable and may occur about one day after wounding. Cells on the wound margins proliferate on the second and third day post-wounding in order to provide more cells for migration.

If the basement membrane is not breached, epithelial cells are replaced within three days by division and upward migration of cells in the stratum basale in the same fashion that occurs in uninjured skin. However, if the basement membrane is ruined at the wound site, reepithelization must occur from the wound margins and from skin appendages such as hair follicles and sweat and oil glands that enter the dermis that are lined with viable keratinocytes. If the wound is very deep, skin appendages may also be ruined and migration can only occur from wound edges.

Migration of keratinocytes over the wound site is stimulated by lack of contact inhibition and by chemicals such as nitric oxide. Before they begin to migrate, cells must dissolve their desmosomes and hemidesmosomes, which normally anchor the cells by intermediate filaments in their cytoskeleton to other cells and to the ECM. Transmembrane  receptor proteins called integrins, which are made of glycoproteins and normally anchor the cell to the basement membrane by its cytoskeleton, are released from the cell's intermediate filaments and relocate to actin filaments to serve as attachments to the ECM for pseudopodia during migration. Thus keratinocytes detach from the basement membrane and are able to enter the wound bed.

Before they begin migrating, keratinocytes change shape, becoming longer and flatter and extending cellular processes like lamellipodia and wide processes that look like ruffles. Actin filaments and pseudopodia form. During migration, integrins on the pseudopod attach to the ECM, and the actin filaments in the projection pull the cell along. The interaction with molecules in the ECM through integrins further promotes the formation of actin filaments, lamellipodia, and filopodia.

Epithelial cells climb over one another in order to migrate. This growing sheet of epithelial cells is often called the epithelial tongue. The first cells to attach to the basement membrane form the stratum basale. These basal cells continue to migrate across the wound bed, and epithelial cells above them slide along as well. The more quickly this migration occurs, the less of a scar there will be.

Fibrin, collagen, and fibronectin in the ECM may further signal cells to divide and migrate.  Like fibroblasts, migrating keratinocytes use the fibronectin cross-linked with fibrin that was deposited in inflammation as an attachment site to crawl across.

As keratinocytes migrate, they move over granulation tissue but stay underneath the scab, thereby separating the scab from the underlying tissue. Epithelial cells have the ability to phagocytize debris such as dead tissue and bacterial matter that would otherwise obstruct their path.  Because they must dissolve any scab that forms, keratinocyte migration is best enhanced by a moist environment, since a dry one leads to formation of a bigger, tougher scab. To make their way along the tissue, keratinocytes must dissolve the clot, debris, and parts of the ECM in order to get through. They secrete plasminogen activator, which activates plasminogen, turning it into plasmin to dissolve the scab.  Cells can only migrate over living tissue, so they must excrete collagenases and proteases like matrix metalloproteinases (MMPs) to dissolve damaged parts of the ECM in their way, particularly at the front of the migrating sheet. Keratinocytes also dissolve the basement membrane, using instead the new ECM laid down by fibroblasts to crawl across.

As keratinocytes continue migrating, new epithelial cells must be formed at the wound edges to replace them and to provide more cells for the advancing sheet. Proliferation behind migrating keratinocytes normally begins a few days after wounding and occurs at a rate that is 17 times higher in this stage of epithelialization than in normal tissues. Until the entire wound area is resurfaced, the only epithelial cells to proliferate are at the wound edges.

Growth factors, stimulated by integrins and MMPs, cause cells to proliferate at the wound edges.  Keratinocytes themselves also produce and secrete factors, including growth factors and basement membrane proteins, which aid both in epithelialization and in other phases of healing. Growth factors are also important for the innate immune defense of skin wounds by stimulation of the production of antimicrobial peptides and neutrophil chemotactic cytokines in keratinocytes.

Keratinocytes continue migrating across the wound bed until cells from either side meet in the middle, at which point contact inhibition causes them to stop migrating.  When they have finished migrating, the keratinocytes secrete the proteins that form the new basement membrane.  Cells reverse the morphological changes they underwent in order to begin migrating; they reestablish desmosomes and hemidesmosomes and become anchored once again to the basement membrane. Basal cells begin to divide and differentiate in the same manner as they do in normal skin to reestablish the strata found in reepithelialized skin.

Contraction
Contraction is a key phase of wound healing with repair. If contraction continues for too long, it can lead to disfigurement and loss of function. Thus there is a great interest in understanding the biology of wound contraction, which can be modelled in vitro using the collagen gel contraction assay or the dermal equivalent model.

Contraction commences approximately a week after wounding, when fibroblasts have differentiated into myofibroblasts.  In full thickness wounds, contraction peaks at 5 to 15 days post wounding. Contraction can last for several weeks and continues even after the wound is completely reepithelialized. A large wound can become 40 to 80% smaller after contraction.  Wounds can contract at a speed of up to 0.75 mm per day, depending on how loose the tissue in the wounded area is.  Contraction usually does not occur symmetrically; rather most wounds have an 'axis of contraction' which allows for greater organization and alignment of cells with collagen.

At first, contraction occurs without myofibroblast involvement.  Later, fibroblasts, stimulated by growth factors, differentiate into myofibroblasts.  Myofibroblasts, which are similar to smooth muscle cells, are responsible for contraction.  Myofibroblasts contain the same kind of actin as that found in smooth muscle cells.

Myofibroblasts are attracted by fibronectin and growth factors and they move along fibronectin linked to fibrin in the provisional ECM in order to reach the wound edges.  They form connections to the ECM at the wound edges, and they attach to each other and to the wound edges by desmosomes.  Also, at an adhesion called the fibronexus, actin in the myofibroblast is linked across the cell membrane to molecules in the extracellular matrix like fibronectin and collagen.  Myofibroblasts have many such adhesions, which allow them to pull the ECM when they contract, reducing the wound size.  In this part of contraction, closure occurs more quickly than in the first, myofibroblast-independent part.

As the actin in myofibroblasts contracts, the wound edges are pulled together.  Fibroblasts lay down collagen to reinforce the wound as myofibroblasts contract. The contraction stage in proliferation ends as myofibroblasts stop contracting and commit apoptosis.  The breakdown of the provisional matrix leads to a decrease in hyaluronic acid and an increase in chondroitin sulfate, which gradually triggers fibroblasts to stop migrating and proliferating.  These events signal the onset of the maturation stage of wound healing.

Maturation and remodeling
When the levels of collagen production and degradation equalize, the maturation phase of tissue repair is said to have begun. During maturation, type III collagen, which is prevalent during proliferation, is replaced by type I collagen. Originally disorganized collagen fibers are rearranged, cross-linked, and aligned along tension lines. The onset of the maturation phase may vary extensively, depending on the size of the wound and whether it was initially closed or left open, ranging from approximately three days to three weeks. The maturation phase can last for a year or longer, similarly depending on wound type.

As the phase progresses, the tensile strength of the wound increases. Collagen will reach approximately 20% of its tensile strength after three weeks, increasing to 80% after 12 months. The maximum scar strength is 80% of that of unwounded skin. Since activity at the wound site is reduced, the scar loses its red appearance as blood vessels that are no longer needed are removed by apoptosis.

The phases of wound healing normally progress in a predictable, timely manner; if they do not, healing may progress inappropriately to either a chronic wound such as a venous ulcer or pathological scarring such as a keloid scar.

Factors affecting wound healing
Many factors controlling the efficacy, speed, and manner of wound healing fall under two types: local and systemic factors.

Local factors
 Moisture; keeping a wound moist rather than dry makes wound healing more rapid and with less pain and less scarring
 Mechanical factors
 Oedema
 Ionizing radiation
 Faulty technique of wound closure
 Ischemia and necrosis
 Foreign bodies. Sharp, small foreign bodies can penetrate the skin leaving little surface wound but causing internal injury and internal bleeding. For a glass foreign body, "frequently, an innocent skin wound disguises the extensive nature of the injuries beneath". First-degree nerve injury requires a few hours to a few weeks to recover. If a foreign body passes by a nerve and causes first-degree nerve injury during entry, then the sensation of the foreign body or pain due to internal wounding may be delayed by a few hours to a few weeks after entry. A sudden increase in pain during the first few weeks of wound healing could be a sign of a recovered nerve reporting internal injuries rather than a newly developed infection.
 Low oxygen tension
 Perfusion

Systemic factors
 Inflammation
 Diabetes – Individuals with diabetes demonstrate reduced capability in the healing of acute wounds. Additionally, diabetic individuals are susceptible to developing chronic diabetic foot ulcers, a serious complication of diabetes which affects 15% of people with diabetes and accounts for 84% of all diabetes-related lower leg amputations. The impaired healing abilities of diabetics with diabetic foot ulcers and/or acute wounds involves multiple pathophysiological mechanisms. This impaired healing involves hypoxia, fibroblast and epidermal cell dysfunction, impaired angiogenesis and neovascularization, high levels of metalloproteases, damage from reactive oxygen species and AGEs (advanced glycation end-products), decreased host immune resistance, and neuropathy.
 Nutrients – Malnutrition or nutritional deficiencies have a recognizable impact on wound healing post trauma or surgical intervention. Nutrients including proteins, carbohydrates, arginine, glutamine, polyunsaturated fatty acids, vitamin A, vitamin C, vitamin E, magnesium, copper, zinc and iron all play significant roles in wound healing. Fats and carbohydrates provide the majority of energy required for wound healing.  Glucose is the most prominent source of fuel and it is used to create cellular ATP, providing energy for angiogenesis and the deposition of new tissues. As the nutritional needs of each patient and their associated wound are complex, it is suggested that tailored nutritional support would benefit both acute and chronic wound healing.
 Metabolic diseases
 Immunosuppression
 Connective tissue disorders
 Smoking – Smoking causes a delay in the speed of wound repair notably in the proliferative and inflammatory phases. It also increases the likelihood of certain complications such as wound rupture, wound and flap necrosis, decrease in wound tensile strength and infection. Passive smoking also impairs a proper wound healing process.
 Age – Increased age (over 60 years) is a risk factor for impaired wound healing. It is recognized that, in older adults of otherwise overall good health, the effects of aging causes a temporal delay in healing, but no major impairment with regard to the quality of healing. Delayed wound healing in patients of increasing age is associated with altered inflammatory response; for example delayed T-cell infiltration of the wound with alterations in the production of chemokines, and reduced macrophage phagocytic capacity.
 Alcohol – Alcohol consumption impairs wound healing and also increases the chances of infection. Alcohol affects the proliferative phase of healing. A single unit of alcohol causes a negative effect on re-epithelialization, wound closure, collagen production and angiogenesis.

In the 2000s there arose the first Mathematical models of the healing process, based on simplified assumptions and on a system of differential equations solved through MATLAB. The models show that the "rate of the healing process" appears to be "highly influenced by the activity and size of the injury itself as well as the activity of the healing agent."

Research and development
Up until about 2000, the classic paradigm of wound healing, involving stem cells restricted to organ-specific lineages, had never been seriously challenged. Since then, the notion of adult stem cells having cellular plasticity or the ability to differentiate into non-lineage cells has emerged as an alternative explanation. To be more specific, hematopoietic progenitor cells (that give rise to mature cells in the blood) may have the ability de-differentiate  back into hematopoietic stem cells and/or transdifferentiate into non-lineage cells, such as fibroblasts.

Stem cells and cellular plasticity
Multipotent adult stem cells have the capacity to be self-renewing and give rise to different cell types. Stem cells give rise to progenitor cells, which are cells that are not self-renewing, but can generate several types of cells. The extent of stem cell involvement in cutaneous (skin) wound healing is complex and not fully understood. Stem cell injection leads to wound healing primarily through stimulation of angiogenesis.

It is thought that the epidermis and dermis are reconstituted by mitotically active stem cells that reside at the apex of rete ridges (basal stem cells or BSC), the bulge of hair follicles (hair follicular stem cell or HFSC), and the papillary dermis (dermal stem cells). Moreover, bone marrow may also contain stem cells that play a major role in cutaneous wound healing.

In rare circumstances, such as extensive cutaneous injury, self-renewal subpopulations in the bone marrow are induced to participate in the healing process, whereby they give rise to collagen-secreting cells that seem to play a role during wound repair. These two self-renewal subpopulations are (1) bone marrow-derived mesenchymal stem cells (MSC) and (2) hematopoietic stem cells (HSC). Bone marrow also harbors a progenitor subpopulation (endothelial progenitor cells or EPC) that, in the same type of setting, are mobilized to aid in the reconstruction of blood vessels. Moreover, it is thought that extensive injury to skin also promotes the early trafficking of a unique subclass of leukocytes (circulating fibrocytes) to the injured region, where they perform various functions related to wound healing.

Wound repair versus regeneration
An injury is an interruption of morphology and/or functionality of a given tissue. After injury, structural tissue heals with incomplete or complete regeneration. Tissue without an interruption to the morphology almost always completely regenerates. An example of complete regeneration without an interruption of the morphology is non-injured tissue, such as skin. Non-injured skin has a continued replacement and regeneration of cells which always results in complete regeneration.

There is a subtle distinction between 'repair' and 'regeneration'. Repair means incomplete regeneration. Repair or incomplete regeneration, refers to the physiologic adaptation of an organ after injury in an effort to re-establish continuity without regards to exact replacement of lost/damaged tissue.
True tissue regeneration or complete regeneration, refers to the replacement of lost/damaged tissue with an 'exact' copy, such that both morphology and functionality are completely restored.  Though after injury mammals can completely regenerate spontaneously, they usually do not completely regenerate. An example of a tissue regenerating completely after an interruption of morphology is the endometrium; the endometrium after the process of breakdown via the menstruation cycle heals with complete regeneration.

In some instances, after a tissue breakdown, such as in skin, a regeneration closer to complete regeneration may be induced by the use of biodegradable (collagen-glycoaminoglycan) scaffolds. These scaffolds are structurally analogous to extracellular matrix (ECM) found in normal/un-injured dermis. Fundamental conditions required for tissue regeneration often oppose conditions that favor efficient wound repair, including inhibition of (1) platelet activation, (2) inflammatory response, and (3) wound contraction. In addition to providing support for fibroblast and endothelial cell attachment, biodegradable scaffolds inhibit wound contraction, thereby allowing the healing process to proceed towards a more-regenerative/less-scarring pathway. Pharmaceutical agents have been investigated which may be able to turn off myofibroblast differentiation.

A new way of thinking derived from the notion that heparan sulfates are key player in tissue homeostasis:  the process that makes the tissue replace dead cells by identical cells. In wound areas, tissue homeostasis is lost as the heparan sulfates are degraded preventing the replacement of dead cells by identical cells. Heparan sulfate analogues cannot be degraded by all known heparanases and glycanases and bind to the free heparin sulfate binding spots on the ECM, therefore preserving the normal tissue homeostasis and preventing scarring.

Repair or regeneration with regards to hypoxia-inducible factor 1-alpha (HIF-1a). In normal circumstances after injury HIF-1a is degraded by prolyl hydroxylases (PHDs). Scientists found that the simple up-regulation of HIF-1a via PHD inhibitors regenerates lost or damaged tissue in mammals that have a repair response; and the continued down-regulation of Hif-1a results in healing with a scarring response in mammals with a previous regenerative response to the loss of tissue. The act of regulating HIF-1a can either turn off, or turn on the key process of mammalian regeneration.

Scarless wound healing
Scarless wound healing is a concept based on the healing or repair of the skin (or other tissue/organs) after injury with the aim of healing with subjectively and relatively less scar tissue than normally expected. Scarless healing is sometimes mixed up with the concept of scar free healing, which is wound healing which results in absolutely no scar (free of scarring). However they are different concepts.

A reverse to scarless wound healing is scarification (wound healing to scar more). Historically, certain cultures consider scarification attractive; however, this is generally not the case in the modern western society, in which many patients are turning to plastic surgery clinics with unrealistic expectations. Depending on scar type, treatment may be invasive (intralesional steroid injections, surgery) and/or conservative (compression therapy, topical silicone gel, brachytherapy, photodynamic therapy). Clinical judgment is necessary to successfully balance the potential benefits of the various treatments available against the likelihood of a poor response and possible complications resulting from these treatments. Many of these treatments may only have a placebo effect, and the evidence base for the use of many current treatments is poor.

Since the 1960s, comprehension of the basic biologic processes involved in wound repair and tissue regeneration have expanded due to advances in cellular and molecular biology. Currently, the principal goals in wound management are to achieve rapid wound closure with a functional tissue that has minimal aesthetic scarring. However, the ultimate goal of wound healing biology is to induce a more perfect reconstruction of the wound area. Scarless wound healing only occurs in mammalian foetal tissues and complete regeneration is limited to lower vertebrates, such as salamanders, and invertebrates. In adult humans, injured tissue are repaired by collagen deposition, collagen remodelling and eventual scar formation, where fetal wound healing is believed to be more of a regenerative process with minimal or no scar formation. Therefore, foetal wound healing can be used to provide an accessible mammalian model of an optimal healing response in adult human tissues. Clues as to how this might be achieved come from studies of wound healing in embryos, where repair is fast and efficient and results in essentially perfect regeneration of any lost tissue.

The etymology of the term scarless wound healing has a long history. In print the antiquated concept of scarless healing was brought up the early 20th century and appeared in a paper published in the London Lancet. This process involved cutting in a surgical slant, instead of a right angle...; it was described in various Newspapers.

Cancer
After inflammation, restoration of normal tissue integrity and function is preserved by feedback interactions between diverse cell types mediated by adhesion molecules and secreted cytokines. Disruption of normal feedback mechanisms in cancer threatens tissue integrity and enables a malignant tumor to escape the immune system. An example of the importance of the wound healing response within tumors is illustrated in work by Howard Chang and colleagues at Stanford University studying Breast cancers.

Oral collagen supplements
Preliminary results are promising for the short and long-term use of oral collagen supplements for wound healing and skin aging. Oral collagen supplements also increase skin elasticity, hydration, and dermal collagen density. Collagen supplementation is generally safe with no reported adverse events. Further studies are needed to elucidate medical use in skin barrier diseases such as atopic dermatitis and to determine optimal dosing regimens.

Wound dressings
Modern wound dressing to aid in wound repair have undergone considerable research and development in recent years. Scientists aim to develop wound dressings which have the following characteristics:
 Provide wound protection
 Remove excess exudate
 Antimicrobial properties
 Maintain a humid environment
 Have high permeability to oxygen
 Easily removed from a wound site
 Non-anaphylactic characteristics

Cotton gauze dressings have been the standard of care, despite their dry properties that can adhere to wound surfaces and cause discomfort upon removal. Recent research has set out to improve cotton gauze dressings to bring them closer in line to achieve modern wound dressing properties, by coating cotton gauze wound dressing with a chitosan/Ag/ZnO nanocomposite. These updated dressing provide increase water absorbency and improved antibacterial efficacy.

Wound cleansing
Dirt or dust on the surface of the wound, bacteria, tissue that has died, and fluid from the wound may be cleaned. The evidence supporting the most effective technique is not clear and there is insufficient evidence to conclude whether cleaning wounds is beneficial for promoting healing or whether wound cleaning solutions (polyhexamethylene biguanide, aqueous oxygen peroxide, etc.) are better than sterile water or saline solutions to help venous leg ulcers heal. It is uncertain whether the choice of cleaning solution or method of application makes any difference to venous leg ulcer healing.

Simulating wound healing from a growth perspective
Considerable effort has been devoted to understanding the physical relationships governing wound healing and subsequent scarring, with mathematical models and simulations developed to elucidate these relationships.  The growth of tissue around the wound site is a result of the migration of cells and collagen deposition by these cells.  The alignment of collagen describes the degree of scarring; basket-weave orientation of collagen is characteristic of normal skin, whereas aligned collagen fibers lead to significant scarring.  It has been shown that the growth of tissue and extent of scar formation can be controlled by modulating the stress at a wound site.

The growth of tissue can be simulated using the aforementioned relationships from a biochemical and biomechanical point of view.  The biologically active chemicals that play an important role in wound healing are modeled with Fickian diffusion to generate concentration profiles.  The balance equation for open systems when modeling wound healing incorporates mass growth due to cell migration and proliferation.  Here the following equation is used:

Dtρ0 = Div (R) + R0,

where ρ represents mass density, R represents a mass flux (from cell migration), and R0 represents a mass source (from cell proliferation, division, or enlargement). Relationships like these can be incorporated into an agent-based models, where the sensitivity to single parameters such as initial collagen alignment, cytokine properties, and cell proliferation rates can be tested.

Wound closure intentions
Successful wound healing is dependent on various cell types, molecular mediators and structural elements.

Primary intention
Primary intention is the healing of a clean wound without tissue loss. In this process, wound edges are brought together, so that they are adjacent to each other (re-approximated). Wound closure is performed with sutures (stitches), staples, or adhesive tape or glue.

Primary intention can only be implemented when the wound is precise and there is minimal disruption to the local tissue and the epithelial basement membrane, e.g. surgical incisions.

This process is faster than healing by secondary intention. There is also less scarring associated with primary intention, as there are no large tissue losses to be filled with granulation tissue, though some granulation tissue will form.
 Examples of primary intention include: well-repaired lacerations, well reduced bone fractures, healing after flap surgery.
 Early removal of dressings from clean or clean-contaminated wounds does affect primary healing of wounds.

Secondary intention
 Secondary intention is implemented when primary intention is not possible because of significant tissue damage or loss, usually due to the wound having been created by major trauma.
 The wound is allowed to granulate.
 Surgeon may pack the wound with a gauze or use a drainage system.
 Granulation results in a broader scar.
 Healing process can be slow due to presence of drainage from infection.
 Wound care must be performed daily to encourage wound debris removal to allow for granulation tissue formation.
 Using antibiotics or antiseptics for the surgical wound healing by secondary intention is controversial.
 Examples: gingivectomy, gingivoplasty, tooth extraction sockets, poorly reduced fractures, burns, severe lacerations, pressure ulcers.
 There is insufficient evidence that the choice of dressings or topical agents affects the secondary healing of wounds.
 There is lack of evidence for the effectiveness of negative pressure wound therapy in wound healing by secondary intention.

Tertiary intention
(Delayed primary closure):
 The wound is initially cleaned, debrided and observed, typically 4 or 5 days before closure.
 The wound is purposely left open.
 Examples: healing of wounds by use of tissue grafts.

If the wound edges are not reapproximated immediately, delayed primary wound healing transpires. This type of healing may be desired in the case of contaminated wounds. By the fourth day, phagocytosis of contaminated tissues is well underway, and the processes of epithelization, collagen deposition, and maturation are occurring. Foreign materials are walled off by macrophages that may metamorphose into epithelioid cells, which are encircled by mononuclear leukocytes, forming granulomas. Usually the wound is closed surgically at this juncture, or the scab is eaten, and if the "cleansing" of the wound is incomplete, chronic inflammation can ensue, resulting in prominent scarring.

Overview of involved growth factors
Following are the main growth factors involved in wound healing:

Complications of wound healing

The major complications are many:

 Deficient scar formation: Results in wound dehiscence or rupture of the wound due to inadequate formation of granulation tissue.
 Excessive scar formation: Hypertrophic scar, keloid, desmoid.
 Exuberant granulation (proud flesh).
 Deficient contraction (in skin grafts) or excessive contraction (in burns).
 Others: Dystrophic calcification, pigmentary changes, painful scars, incisional hernia

Other complications can include infection and Marjolin's ulcer.

Biologics, skin substitutes, biomembranes and scaffolds
Advancements in the clinical understanding of wounds and their pathophysiology have commanded significant biomedical innovations in the treatment of acute, chronic, and other types of wounds. Many biologics, skin substitutes, biomembranes and scaffolds have been developed to facilitate wound healing through various mechanisms. This includes a number of products under the trade names such as Epicel, Laserskin, Transcyte, Dermagraft, AlloDerm/Strattice, Biobrane, Integra, Apligraf, OrCel, GraftJacket and PermaDerm.

See also

 Wound response in plants
 Collective cell migration
 Dressing (medical)
 History of wound care
 Regeneration in humans
 Scar free healing
 Wound bed preparation
 Wound licking

Notes and references

External links

Healing
Skin physiology
Physiology
Trauma surgery

Wound healing


Eğirdir, Isparta iline bağlı  Eğirdir Gölü kıyısında bir ilçe. Isparta'ya 34 km uzaklıktadır.

Tarihçe
Eğirdir ve çevresinin Arvaza Krallığı (M.Ö.2000-1200) döneminden beri meskun olduğu kayıtlardan anlaşılmaktadır.Eğirdir Gölü güney ucu merkez olmak üzere Burdur Gölü'ne kadar olan bölgeye İlkçağ'da Askania adının verildiği sanılmaktadır.

Bu yöreye Luwi uygarlığı çağında Askawana,yani 'Ada Ülkesi' adı verilmiştir.Yöre,Arzava Krallığından sonra M.Ö. 1200 yıllarında Friglerin egemenliğini girmiştir.Daha sonra M.Ö. 687-547 yılları arasında Lidyalılar tarafından işgal edilmiştir.

'Eğirdir kentinin Lidya'nın son hükümdarı Kroisos (MÖ 560-MÖ 547) tarafından kurulduğu ve ilk adının da "Krozos" olduğu sanılmaktadır. Şehrin iç kalesi de Lidyalılar tarafından yaptırılmıştır. M.Ö. 540 yılında Pers İmparatorluğu tarafından işgal edilmiş,yaklaşık 200 sene Pers imparatorluğu egemenliğinde kalmış,daha sonra Seleukos egemenliği altına girmiştir.Yöre   Seleukoslar tarafından M.Ö. 188 yılında Apamea (Dinar) antlaşmasıyla Romalılara bırakılmıştır.Romalılar döneminde ilçe Prostanna diye anılmıştır.

Eğirdir ve çevresi 395 tarihinde Bizans egemenliğine girilmesinden sonra Akritur olarak isimlendirilmiştir.

Yörede ilk Türk yerleşiminin 1071'den birkaç yıl sonra gerçekleştiği sanılmaktadır. Anadolu Selçuklu hükümdarı III. Kılıçaslan 1204 yılında çevredeki şehirler ile birlikte, Eğirdir'i de Selçuklu egemenliği altına almıştır. Selçuklular, sayfiye yeri olarak kullandıkları Eğirdir'e doğal güzelliklerinden dolayı Cennetâbad ismini vermişlerdir. Anadolu Selçuklu Devleti yıkılınca 1280 yılında günümüz Isparta, Burdur ve Antalya illerini hakimiyetine alan Hamitoğulları Beyliği kurulmuştur. Eğirdir uzun yıllar boyunca bu beyliğe başkentlik yapmıştır. Bu süre zarfı içerisinde Eğirdir gelişmiş ve bayındır hale gelmiştir. Bu gelişmelerden dolayı Eğirdir'e "Felekâbât", Isparta'ya ise "Hamit Eli" denmeye ve farklı iki merkez olarak ele alınmaya başlanmıştır. Eğirdir'in beylik başkenti olması sebebiyle; Hamitoğulları Beyliği'nin ikinci beyi olan Dündar Bey tarafından yaptırılan "Dündar Bey Medresesi" bu beyliğin en önemli mimari eserlerindendir. Eğirdir'in merkezinde yer alan bu tarihi taş medrese günümüzde kapalı çarşı olarak kullanılmaya devam etmektedir. 1391'de Eğirdir ve yöresi Osmanlı Devleti egemenliğine girmiştir.Osmanlıların ilk egemenlik dönemi çok kısa sürmüş,Timur Ankara Savaşından sonra Anadolu'yu istilası sırasında Eğirdir'de kendisine boyun eğmeyen şehri ve halkın sığındığı Nis Adası'nı kuşatarak zapt etmiş ve bölgeyi 1402 yılında ve Karamanoğlu 2. Mehmet Bey  idaresine bırakmıştır. Eğirdir, Sultan II. Murat zamanında 1423'te tam olarak Osmanlı topraklarına katılmıştır. Osmanlı egemenliği döneminde yörenin devlet sınırlarından uzak kalması savunma ihtiyacını ortadan kaldırmıştır.Bu yüzden şehrin surları onarım görmemiş,beylik dönemindeki canlı hayat sönmeye başlamıştır." Bu dönemde Eğirdir,Hamid Sancağının kazaları arasında görülmektedir.

Bu dönemde Eğirdir, Hamit ilinin kalesinde 'Hisar Erleri' bulunan,surlarla çevrili tek şehirdi.Bu surlar, 17. yüzyılda Fransız seyyah Paul Lucas'ın belirttiğine göre hala sağlamdı. Osmanlı İmparatorluğunda Hamideli Sancağı'nın merkezi olan Eğirdir, Tanzimat'tan sonra ise Konya Vilayeti Hamit Sancağına bağlı bir kaza olmuştur. Cumhuriyetin kurulmasından sonra da Eğirdir, ilçe statüsünü korumuştur.

Eğirdir, Sevr Antlaşmasıyla İtilaf Devletleri tarafından bölüşülen Anadolu'da işgale uğramamış bölgelerimizden birisidir. Eğirdir halkı işgale karşı protestolara yeni bir boyut getirerek, 22 Mayıs 1915 tarihinde Yunanlara karşı Talayzade Salih Bey önderliğinde 700 kişilik bir silahlı kuvvet oluşturmuş, bu sayede Isparta Sancağında Milli Mücadele için ilk milis kuvvet kurulmuştur. İşgalci Yunan ve İtalyan kuvvetlerine karşı caydırıcı güç teşvik etmiştir. Bu milis güç, Isparta'da işgallere karşı Hafız İbrahim Demiralay önderliğinde kurulan daha sonra "Demir Alay" ismiyle anılan Kuvâ-yi Milliye birliğinin öncülü ve katılımcısı olmuştur. Böylece işgalci İtalyan kuvvetleri Antalya'dan yukarı iç kesimlere rahatça ilerleyememiştir. Yunan işgal kuvvetlerine karşı ise Denizli dolaylarında başarılı savunmalar yapılmıştır. Böylece Isparta ve Eğirdir'in işgal görmesi engellenmiştir.

Eğirdir Kalesi
M.Ö. 4. yüzyılın başında Lidya Kralı Krezus tarafından yaptırılmıştır.Yapı tarzı bakımından Lidya mimarisinin özelliklerini yansıtan kalenin yapımında taşlar arasında boydan boya ardıç ağacından hatıllar atılmıştır.Duvar yapımında taş bloklar kullanılmış,iç kısmında ise moloztaş dolgu maddesinden yararlanılmıştır.

İlçede göle doğru uzanan yarımada üzerinde iç ve dış kale bulunmaktadır.Yarımadayı ve bugünkü Kale Mahallesini kuzey-güney doğrultusunda kesen ve günümüze kadar varlığını koruyan İç Kale özellikle gölden ve karadan (Sivri Dağı'ndan) gelebilecek saldırılara karşı korunmak amacıyla üç tarafı su ile çevrili yarımadanın en güvenli bir yerinde yapılmıştır.

Dış kale ise,temel kalıntıları bulunan Demir Kapı Mahallesine kadar ulaşmaktadır.

Hızırbey Camii
Eğirdir'de bulunan camilerin en büyüğü olup,duvarları kâgir ve üstü toprak dam olarak Hızır Bey tarafından yaptırılmıştır.Kesin tarihi bilinmemekle birlikte 13. yüzyılda  2.Gıyasettin Keyhüsrev tarafından yaptırılmış olabileceği belirtilmektedir.1327'de Hızır Bey tarafından geniş çaplı onarım ve tamir görerek genişletilmiş olan bu eser in ismi Hızırbey Camii olagelmiştir. Camii'nin doğu cephesinde sur duvarlarından iç kaleye açılan bir kapı ve yol bulunmaktadır.İç Kaleye açılan kapı kemerinin 4,5–5 m üzerine Camii'nin zarif mimarisi inşa edilmiştir.

Kemerli minare Anadolu Türk'lerinin sanat anlayışını yansıtmakta ve Türk-İslam Dünyası'nın ender yapıtlarından biri olarak kabul edilir.

Dündarbey Medresesi
İlçenin en merkezi yerinde bulunan ve taş medrese adıyla da anılan bina,1237 yılında Gıyaseddin Keyhüsrev zamanında han olarak yapılmıştır.Daha sonra 1301 yılında Hamidoğlu Dündar Bey tarafından medrese haline getirilmiştir.Medrese 2 katlı olup,ortada avlu yer alır ve 30 hücresi vardır.

Medresenin girişinde büyük bir taç kapı vardır.Kapının etrafında Selçuklu karakterinde geometrik şekille süslenmiştir.Yapının malzemeleri yakındaki Kervansaray'dan sökülerek getirilmiştir.Medrese bugün kapalıçarşı olarak kullanılmaktadır.

İklim
İlçe iklim bakımından Akdeniz ve İç Anadolu iklimleri arasında bir geçiş alanında yer almaktadır.
İlçede, ne Akdeniz'in yağışlı ne de İç Anadolu'nun kurak iklimi söz konusudur. Yağışlar genelde kış ve ilkbahar aylarında olup yıllık yağış ortalaması 705 mm civarındadır. Hakim rüzgarların lodos ve poyrazdan estiği ilçede, ortalama sıcaklık 11,9 °C dereceyi bulmaktadır..

Nüfus
İlçeye bağlı 1 belde ve 28 köy vardır.

Ekonomi
Eğirdir'in yerli halk arasında "Bağlar" olarak anılan bölgesinde tarım önemli yer tutmaktadır. Başlıca üretilen tarım ürünleri şunlardır: Elma, üzüm, ayva, muşmula ve az da olsa ceviz. Ancak en önemli bölgesel çaptaki tarımsal üretimi elmadır. Elması ile meşhurdur. Birçok çeşit elma üretimi yapılmaktadır. Fujı, Golden, Starking, Gala, Topaz, Pink Lady, Braeburn ve Grany Smith bunlardan bazılarıdır. Elmaları renk açısından genelde sarı, yeşil, pembe ve kırmızı renkte olmaktadır. Ayrıca tat ve şeker miktarı bakımından çoklu seçeneğe sahiptir. Örnek: Mayhoş, tatlı, ekşi.

En çok Akdeniz Bölgesi'nde beslenen keçi olan Kıl Keçisi; Eğirdir'in başlıca küçükbaş hayvancılığını oluşturur. Hayvancılık yaygın olmamakla birlikte dağlık kesimlerde rastlanmaktadır. Eğirdir'de balıkçılık faaliyeti önemlidir. Kılçıksız göl levreği, siraz, eğrez ve kerevit avı önemli balıkçılık faaliyetleridir. Eğirdir Gölü 1980 öncesinde 10 çeşitten fazla balık türü (bazıları endemik tür) barındırırken göl ekolojisine yanlış beşeri müdahaleler ve bazı balık hastalıkları yüzünden günümüzde bu sayı giderek azalmaktadır. Ayrıca ihracatta önemli bir ekonomik değere sahip olan kerevitten (su ıstakozu) 2005-2013 yılları arası popülasyonu önemli ölçüde azaldığı için faydalanılamamıştır. Son ekolojik sayım ve raporlarda 2014 yılından itibaren kerevit popülasyonun toparlanıp yeniden ekonomik değer kazanacağı öngörülmektedir.

İlçe, turizm potansiyeli açısından oldukça zengin bir içeriğe sahiptir. Özellikle "Altınkum Mahallesi"nde ve "Bedre Koyu"nda yaz turizmi önemli yer tutar. Buralarda yer alan plajlar; gölde yüzme aktivitesi ve kamping imkânı vermektedir. "Altınkum Plajı" ve Bedre Plajı" orta ölçekte yerli ve yabancı turist misafir etmektedir. Bu çok amaçlı plajlardan Altınkum'un içerisinde yer alan bungalovlarda veya bireysel çadır kurma imkânıyla konaklama yapılabilmektedir. "Bedre Plajı" ise Çadır kurma ve karavan park alanıyla konaklama imkânı sunarken içerisinde bulunan su kaydırakları ile çocukların vakit geçirebilecekleri alanlara sahiptir. Bunların dışında plaja yakın  oteller ve pansiyonlar da yer almaktadır. Yaz turizminin yanında kültür, tarih ve doğa turizmi potansiyelleri fazladır.

Kültür
Isparta Uygulamalı Bilimler Üniversitesi'ne bağlı Turizm Fakültesi, Sağlık Hizmetleri Meslek Yüksek Okulu ve Eğirdir Meslek Yüksek Okulu burada bulunmaktadır.

Eğirdir halkı tarafından Atatürk'e verilen Can Adası, Türk Silahlı Kuvvetlerinin Dağ Komando Okulu, ender rastlanan Kasnak Meşesi ve Sığla Ormanları, Türkiye'nin en önde gelen Kemik Hastalıkları Hastanesi, elması ve sadece Eğirdir'de görülen Apollon Kelebeği ile tarih ve doğa zengini bir ilçedir.

Yerli halk arasında adı "Sivri Dağ" olarak geçen dağı, Türkiye'nin en büyük 2. (ikinci) tatlı su gölü olan Eğirdir Gölü ve iki yarımadası (Can Ada ve Yeşil Ada) önemli doğal güzellikleridir.

İlçe merkezinde yer alan, Lidyalılar döneminden kalan "Eğirdir Kalesi" ve Hamitoğulları Beyliği'nden kalan "Dündar Bey Taş Medresesi" önemli tarihi yapılarıdır. Ayrıca "Poyraz Mahallesi" ve civarında yer alan çoğunda hâlâ ikamet edilen taş ve ahşap yapılı evleri ilçenin tarihi ve mimari özelliği yansıtmaktadır.

Adalarının yer aldığı bölüm yerli halk tarafından "Nis" adıyla anılmaktadır. "Can Ada" (Küçük Ada) ve Yeşil Ada (Büyük Ada) ; Eğirdir Gölü üzerinde yer alan, doğal oluşumlu, yan yana iki adadır. Adalar, merkez karaya yakın olması dolayısıyla doldurma yol ile hem birbirine hem de merkez karaya bağlanmıştır. Böylece her iki ada da yarımada özelliği kazanmıştır. Yeşil Ada ya da diğer adıyla Büyük Ada üzerinde restore edilmiş ancak kullanılmayan tarihi bir Rum kilisesi yer almaktadır. Ayrıca bu ada deniz mahsulleri restoranları ve konaklama tesisleri açısından oldukça gelişmiştir.

Kaynakça

Dış bağlantılar

 Kültür Bakanlığı
 Eğirdir Kaymakamlığı
 Yerelnet: Eğirdir

Cittaslow

Eğirdir


දුරකතනය යනු ශබ්දය (බහුලව මිනිස් කටහඬ) සම්ප්‍රේෂණයට හා ලබා ගැනීමට භාවිතා වන විදුලි සංදේශ උපකරණයකි. සාමාන්‍යයෙන් මෙය භාවිතා කරන්නේ පුද්ගලයන් දෙදෙනෙකු අතර සාකච්ඡාවකට වුවත් සමහරක් විට එය තිදෙනෙකු හෝ ඊට වඩා වැඩි ගණනක් විය හැක.
වර්තමානයේ ලෝකයේ වඩාත් බහුලම ගෘහස්ත උපකරණවලින් එකක් බවට එය පත්ව ඇත. බොහෝමයක් දුරකතන ක්‍රියාත්මක වන්නේ සංකීර්ණ දුරකතන ජාලයක් හරහා විද්‍යුත් සංඥා සම්ප්‍රේෂණය කිරීමෙනි. මෙමඟින් ඕනෑම දුරකතන පරිශීලකයෙකුට ඕනෑම කෙනෙකු සමඟ පාහේ සන්නිවේදනය කිරීමට ඉඩ ප්‍රස්ථාව ලැබේ.

මූලික සිද්ධාන්ත

දුරකතන වර්ග දෙකක තොරතුරු හසුරවයි. ඒවා නම් සංඥා හා කටහඬයි. මෙය විවිධ අවස්ථාවලදී එකම ඇඹරුණු රැහැන් යුගලයක් මත සිදු වේ. සංඥා ලබා දීමේ උපකරණය ලැබෙන ඇමතුම් පිළිබඳ පරිශීලකයා දැනුවත් කිරීමට සීනුවකින් ද ගන්නා ඇමතුම්වල දුරකතන අංක ඇතුල් කිරීම සඳහා වූ ඩයලයකින් ද යුක්ත වේ. වෙනත් දුරකතනයකට කතා කිරීමට බලාපොරොත්තු වන පරිශීලකයෙක් රිසීවරය ඔසවයි. එමනිසා ස්විචයක් ක්‍රියාත්මක වේ. එමඟින් දුරකතනය ක්‍රියාකාරී තත්වයට පත් කරන අතර රැහැන් හරහා ප්‍රතිරෝධී ලුහුවත් වීමක් ද ඇති වේ. එමනිසා රැහැන් හරහා ධාරාවක් ගලා යයි. දුරකතන හුවමාරුව මෙම DC ධාරාව අනාවරණය කර ගෙන සංඛ්‍යාංක ආදායකයක් අමුණා සූදානම් බව ඇඟවීම සඳහා අක්වට තානය (dial tone) යවයි. පරිශීලකයා ඉලක්කම්  බොත්තම් ඔබන අතර ඒවා ඩයලය තුළ වූ නාද උත්පාදකයකට සම්බන්ධය. එමඟින් DTMF නාද නිපදවේ. ඉන්පසු හුවමාරුව අදාල දුරකතනය සම්බන්ධ කරන අතර එයට දැනුම් දීමක් සිදු කරයි.

දුරකතනය ක්‍රියා විරහිතව ඇති විට (රිසීවරය තබා) එහි සීනුව, බීපරය හෝ අනෙක් දැනුම් දීමේ උපකරණ ධාරිත්‍රක හරහා දුරකතන මාර්ගයට සම්බන්ධ කර ඇත. අක්‍රීය දුරකතනය දුරකතන මාර්ගය ලුහුවත් නොකරන අතර එමනිසා හුවමාරුව එහි රිසීවරය තබා තිබෙන බව හා සීනුව පමණක් විද්‍යුත් වශයෙන් සම්බන්ධ බව දැන ගනී. එම දුරකතනයට කිසිවෙකු ඇමතූ විට දුරකතන හුවමාරුව දුරකතන මාර්ගයට අධි වෝල්ටීයතා ස්පන්ද සංඥාවක් යොදයි. මෙමඟින් ඇමතුම් ලබන පාර්ශවයට සීනුව නාද වීම බීපරය ක්‍රියාත්මක වීම හෝ වෙනත් දැනුම් දීමේ උපකරණයක් ක්‍රියාත්මක වීම සිදු වේ. පරිශීලකයා රිසීවරය එසවූ විට එසවුම් ස්විචය සීනුව අක්‍රිය කර දුරකතනයේ හඬ කොටස ක්‍රියාත්මක කරයි. ඉන්පසු දුරකතන මාර්ගයට ප්‍රතිරෝධී ලුහුවත් කිරීමක් ලබා දෙන අතර එමඟින් දුරකතනය පිළිතුරු ලබා දුන් බව හා ක්‍රියාත්මක බව දැනුම් දේ. සම්බන්ධ වූ පාර්ශවයන් දුරකතනයේ හඬ කොටස භාවිතයෙන් සාකච්ඡා කරයි.

දුරකතනයේ හඬ කොටස රිසීවරයේ ඇති අතර එය සම්ප්‍රේෂකයකින් (බහුලව මයික්‍රොෆෝනය ලෙස හඳුන්වන) හා ආදායකයකින් සමන්විත වේ. සම්ප්‍රේෂකය දුරකතන මාර්ගයේ ජවය ලබා ගන්නා අතර කටහඬ මඟින් ඇති කරන ධ්වනි පීඩන තරංගවලට අනුරූපව විද්‍යුත් ධාරාවක් නිකුත් කරයි. මෙම විද්‍යුත් ධාරා විචලනය දුරකතන මාර්ගය ඔස්සේ අනෙක් දුරකතනය වෙත සම්ප්‍රේෂණය වී එහි වූ ආදායකයේ කුඩා ශබ්ද විකාශකයක් කම්බි දඟරය තුළට ඇතුල් වේ. විද්‍යුත් ධාරාවේ විචලනය දඟරය ඉදිරියට සහ පසු පසට චලනය වීමට හේතු වන අතර එමඟින් සම්ප්‍රේශකයෙහි වූ ධ්වනි පීඩන තරංග ප්‍රතිනිර්මාණය වේ. එක් පාර්ශවයක් රිසීවරය තැබූ විට මාර්ගයේ DC ධාරා ගලනය නවතින අතර එමඟින් හුවමාරු වන දුරකතන ඇමතුම විසන්ධි කරන ලෙස සංඥා කෙරේ.

ලින් මෑන්ගේ රිසීවරය දුරකතන ජාල පරීක්ෂා කිරීම සඳහා නිර්මාණය කරන ලද දුරකතනයකි.

References

http://en.wikipedia.org/wiki/Telephone

දුරකතනය


Grenadajorddue (Leptotila wellsi) er en kritisk truet dueart, der lever på Grenada.

Noter
 Avibase - the world bird database

Eksterne henvisninger

Duefugle
Fugle fra Caribien

Grenadajorddue