where was the original hawaii 5 0 filmed

The CBS television network produced Hawaii Five-O, which aired from September 20, 1968, to April 5, 1980. The program continues to be broadcast in syndication worldwide. Created by Leonard Freeman, Hawaii Five-O was shot on location in Honolulu, Hawaii, and throughout the island of Oahu and other Hawaiian islands with occasional filming in locales such as Los Angeles, Singapore, and Hong Kong.

Hawaii Five-O (1968 TV series)

Hawaii Five-O is an American police procedural drama series produced by CBS Productions and Leonard Freeman. Set in Hawaii, the show originally aired for 12 seasons from 1968 to 1980, and continues in reruns.  At the airing of its last episode it was the longest-running police drama in American television history.

Jack Lord portrayed Detective Captain Steve McGarrett, the head of a special state police task force which was based on an actual unit that existed under martial law in the 1940s.[3]  The theme music composed by Morton Stevens became especially popular.  Many episodes would end with McGarrett instructing his subordinate to "Book 'em, Danno!", sometimes specifying a charge such as "murder one".

Hawaii Five-O was named in honor of Hawaii's being the 50th state.  Although the show's name has always ended with the numeral "0", the soundtrack album, released in the late 1960s, used the letter "O" instead of the numeral zero.[4][unreliable source?] The letter "O" is sometimes used to differentiate the original series and the remake, which premiered in 2010 and always uses the numeral zero.[citation needed] The show centers on a fictional state police force led by former US naval officer Steve McGarrett (played by Jack Lord), a detective captain, who is appointed by the Governor, Paul Jameson. In the show, McGarrett oversees state police officers â€“ the young Danny Williams, veteran Chin Ho Kelly, and streetwise Kono Kalakaua for seasons one through four. Honolulu Police Department Officer Duke Lukela joined the team as a regular, as did Ben Kokua, who replaced Kono beginning with season five. Occasionally, McGarrett's Five-O team is assisted by other officers as needed: Douglas Mossman as Det. Frank Kamana, P.O. Sandi Wells (Amanda McBroom), medical examiner Doc Bergman (Al Eben), forensic specialist Che Fong (Harry Endo), and a secretary. The first secretary was May, then Jenny, and later Malia, Lani and Luana.[5]

For 12 seasons, McGarrett and his team hounded international secret agents, criminals, and organized crime syndicates plaguing the Hawaiian Islands. With the aid of District Attorney and later Hawaii's Attorney General John Manicote, McGarrett is successful in sending most of his enemies to prison. One such crime syndicate was led by crime family patriarch Honore Vashon, a character introduced in the fifth season. Most episodes of Hawaii Five-O ended with the arrest of criminals and McGarrett snapping, "Book 'em." The offense occasionally was added after this phrase, for example, "Book 'em, murder one." In many episodes, this was directed to Danny Williams and became McGarrett's catchphrase: "Book 'em, Danno." [6]

Other criminals and organized crime bosses on the islands were played by actors such as Ricardo Montalbán, Gavin MacLeod, and Ross Martin as Tony Alika.  By the 12th and final season, series regular James MacArthur had left the show (in 1996, he admitted that he had become tired of the role and wanted to do other things), as had Kam Fong. Unlike other characters before him, Fong's character, Chin Ho, at Fong's request, was killed off, murdered while working undercover to expose a protection ring in Chinatown in the last episode of season 10. New characters Jim 'Kimo' Carew (William Smith), Lori Wilson (Sharon Farrell), and Truck (Moe Keale) were introduced in season 12 alongside returning regular character Duke Lukela.[5]

The Five-O team consists of three to five members (small for a real state police unit), and is portrayed as occupying a suite of offices in the Iolani Palace.[7] Five-O lacks its own radio network, necessitating frequent requests by McGarrett to the Honolulu Police Department dispatchers. McGarrett's tousled yet immaculate hairstyle, as well as his proclivity for wearing a dark suit and tie on all possible occasions (uncommon in the islands), rapidly entered popular culture. While the other members of Five-O "dressed mainland" much of the time, they also often wore local styles, such as the ubiquitous Aloha shirt.

In many episodes (including the pilot), McGarrett is drawn into the world of international espionage and national intelligence. McGarrett's nemesis is a rogue intelligence officer of the People's Republic of China named Wo Fat.  The communist rogue agent was played by veteran actor Khigh Dheigh. In the show's final episode in 1980, titled "Woe to Wo Fat", McGarrett finally sees his foe go to jail.[7]

Unlike the reboot the show's action and straightforward storytelling left little time for personal stories involving wives or girlfriends,[6] though a two-part story in the first season dealt with the loss of McGarrett's sister's baby. Occasionally, a show would flash back to McGarrett's younger years or to a romantic figure.

In the episode "Number One with a Bullet, Part 2", McGarrett tells a criminal, "It was a bastard like you who killed my father." His 42-year-old father had been run down and killed by someone who had just held up a supermarket. Because Steve McGarrett is also a commander in the Naval Reserve, he sometimes uses their resources to help investigate and solve crimes. Hence the closing credits of some episodes mentioned the Naval Reserve.[8]  A 1975 episode involving Danno's aunt, played by MacArthur's adoptive mother Helen Hayes, provided a bit of Williams' back story.

Sources differ on how the show came to be.  Producer Leonard Freeman moved to Hawaii to recuperate after suffering a heart attack.  One source states the idea for the show may have come from a conversation Freeman had with Hawaii's then-Governor John A. Burns.[4][9]  Another source instead claims that Freeman wanted to set a show in San Pedro, Los Angeles, California until his friend Richard Boone convinced him to shoot it entirely in Hawaii.[10] A third source claims Freeman discussed the show with Governor Burns only after pitching the idea to CBS.[11]  Before settling on the name "Hawaii Five-O", Freeman considered titling the show "The Man".[4]

Freeman offered Richard Boone the part of McGarrett, but Boone turned it down;[10] Gregory Peck[11] and Robert Brown[12] were also considered.  Ultimately, Jack Lord – then living in Beverly Hills – was asked at the last moment. Lord read for the part on a Wednesday, was cast, and flew to Hawaii two days later. On the following Monday, Lord was in front of the cameras. Freeman and Lord had worked together previously on an unsold TV pilot called Grand Hotel.[11]

Tim O'Kelly originated the role of Danny Williams in the pilot episode, "Cocoon." Test audiences apparently weren't positive on O'Kelly, however, and the producers replaced him with James MacArthur.

Kam Fong Chun, an 18-year veteran of the Honolulu Police Department, auditioned for the part of the lead villain Wo Fat, but Freeman cast him in the part of Chin Ho Kelly instead. Freeman took the name Wo Fat from a restaurant in downtown Honolulu. The name Chin Ho came from Chinn Ho, the owner of the Ilikai Hotel where the penthouse shot of Steve McGarrett in the opening title sequence was taken.[13] Richard Denning, who played the governor, had retired to Hawaii and came out of retirement for the show. Zulu was a Waikiki beach boy and local DJ when he was cast for the part of Kono, which he played for the next four years.

The first season was shot in a rusty military Quonset hut in Pearl City, which the various cast members quickly nicknamed "Mongoose Manor".[14] The roof tended to leak, and rats would often gnaw at the cables. The show then moved to a Fort Ruger location for seasons two to eight. A third studio was built at Diamond Head, and was used during the last four seasons.

A problem from the beginning was the lack of a movie industry in Hawaii. Much of the crew and cast, including many locals who ended up participating in the show, had to learn their respective jobs as they went along. Jack Lord was known as a perfectionist who insisted on the best from everyone.[15] His temper flared when he felt that others did not give their best, but in later reunions they admitted that Lord's hard-driving force had made them better actors and made Hawaii Five-O a better show. Lord's high standards helped the show last another six years after Leonard Freeman's death from heart trouble during the sixth season.[15]

To critics and viewers, there was no question that Jack Lord was the center of the show, and that the other actors frequently served as little more than props, standing and watching while McGarrett emoted and paced around his office, analyzing the crime. But occasionally episodes would focus on the other actors, and let them showcase their own talents, such as Danno defusing bombs in "The Clock Struck Twelve". Since Jack Lord had a financial interest in the show, he referred to other regular cast actors in the program as a "with", as in "With James MacArthur"; they were never called "co-stars".[16]

Very few episodes were shot outside of Hawaii. At least two episodes were shot in Los Angeles, one in Hong Kong, and one in Singapore. Episodes shot in these locations were the only ones not to bear the "Filmed entirely on location in Hawaii" legend.

The opening title sequence was created by television director Reza S. Badiyi. Early shows began with a cold open suggesting the sinister plot for that episode, then cut to a shot of a big ocean wave and the start of the theme song.[6][17][18] A fast zoom-in to the top balcony of the Ilikai Hotel followed,[13] showing McGarrett turning to face the camera, followed by many quick-cuts and freeze-frames of Hawaiian scenery, and Hawaiian-Chinese-Caucasian model Elizabeth Malamalamaokalani Logue turning to face the camera.[19]  A grass-skirted hula dancer from the pilot episode was also included, played by Helen Kuoha-Torco, who later became a professor of business technology at Windward Community College.[20]  The opening scene ended with shots of the supporting players, and the flashing blue light of a police motorcycle racing through a Honolulu street.

At the conclusion of each episode, Jack Lord narrated a promo for the next episode, often emphasizing the "guest villain", especially if the villain is a recurring character, such as that played by actor Hume Cronyn.  The line he spoke was, "This is Jack Lord inviting you to be with us next week for <name of episode>" and then, "Be here. Aloha." The promos were removed from the syndicated episodes but most have been restored in DVD releases from the second season through the ninth. Most of the promos are slightly edited to remove references to "next week".

This tradition has been continued in the 2010 version of Hawaii Five-0, but is not limited to Alex O'Loughlin.  All of the primary cast members take turns with the iconic "Be here. Aloha" line at the end of the preview segment.

There were two versions of the closing credits portion of the show. During the first season, the theme music was played over a short film of a flashing blue light attached to the rear of a police motorcycle in Waikiki heading west (the film is shown at twice the normal speed, as can be seen from people crossing a street behind the police motorcycle).[21] In later seasons, the same music was played over film of outrigger canoeists battling the surf.

In a 2010 issue of TV Guide, the show's opening title sequence ranked No. 4 on a list of TV's top 10 credits sequences, as selected by readers.[22]

The show was the longest-running crime show on American television until Law & Order surpassed it in 2003, and was the first to enjoy an uninterrupted run that exceeded a decade (it has since been joined in that distinction by several other series including Law & Order: Special Victims Unit, CSI: Crime Scene Investigation and NCIS).

When the show premiered in 1968 Hawaii had been a state for only 9 years and was relatively obscure to Americans who had never served in the Pacific Theater, but as a geographic part of Polynesia it had an exotic image.

Known for the location, theme song, and ensemble cast, Hawaii Five-O contains a heavy use of exterior location shooting throughout the entire 12 seasons.  A typical episode, on average, would have at least two-thirds of all footage shot on location, as opposed to a "typical" show of the time which would be shot largely on sound stages and backlots. It is also remembered for its unusual setting during an era when most crime dramas of the era were set in or around the Los Angeles or New York City areas.

The Hawaii-based television show Magnum, P.I. was created after Hawaii Five-O ended its run, in order to make further use of the expensive production facilities created there for Five-O. The first few Magnum P.I. episodes made direct references to Five-O, suggesting that it takes place in the same fictional setting. Magnum's producers made a few attempts to coax Jack Lord out of retirement for a cameo appearance, but he refused.[7]

Many local people were cast in the show, which was ethnically diverse by the standards of the late 1960s.[6] The first run and syndication were seen by an estimated 400 million people around the world.

A one-hour pilot for a new series was made in 1996 but never aired. Produced and written by Stephen J. Cannell, it starred Gary Busey and Russell Wong as the new Five-O team. James MacArthur returned as Dan Williams, having become governor of Hawaii.[23] Several cameos were made by other Five-O regulars, including Kam Fong as Chin Ho Kelly[24] (even though the character had been killed off at the end of Season 10).[citation needed]

The one-hour pilot for a revived show, called Hawaii Five-0 (the last character is a zero instead of the letter "O", which is the true title of the original series as well), aired September 20, 2010, on CBS, and as of October 2013, the series now airs Friday nights at 9 PM Eastern, 8 PM Central time.[citation needed] The remake version Hawaii Five-0 uses the same principal character names as the original, and the new Steve McGarrett's late father's vintage 1974 Mercury Marquis is the actual specimen driven by Lord in the original series's final seasons.  The new series opening credit sequence is an homage to the original; the theme song is cut in half, from 60 to 30 seconds, but is an otherwise identical instrumentation. Most of the iconic shots are replicated, beginning with the helicopter approach and close-up turn of McGarrett at the Ilikai Hotel penthouse, the jet engine nacelle, a hula dancer's hips, the quickly stepped zoom-in to the face of the Lady Columbia statue at Punchbowl, the close-up of the Kamehameha Statue's face, and the ending with a police motorcycle's flashing blue light. Starting with the Season 7 many of the clips that were part of the original opening were removed and more action shots of the cast were included. On the March 19, 2012 episode, Ed Asner reprised his role as "August March", a character he first played in a 1975 episode. Clips from the 1975 episode were included in the new one, even though the 2010 series is intended to be in a different narrative universe than the Jack Lord series.

Another legacy of the show is the popularity of the Hawaii Five-O theme music. The tune was composed by Morton Stevens, who also composed numerous episode scores performed by the CBS Orchestra. The theme was later recorded by the Ventures, whose version reached No. 4 on the Billboard Hot 100 pop chart,[6] and is particularly popular with college and high school marching bands, especially at the University of Hawaii where it has become the unofficial fight song. The tune has also been heard at Robertson Stadium after Houston Dynamo goals scored by Brian Ching, a native of Hawaii.  Because of the tempo of the music, the theme gained popularity in the UK with followers of Northern soul and was popular on dance floors in the 1970s.[25]

Although the theme is most widely known as an instrumental, it has been released with at least two similar but different sets of lyrics. The first, "You Can Come with Me" by Don Ho, opens with an instrumental in the familiar tempo, then settles into a ballad style for the sung portion.[26]  The second, by Sammy Davis, Jr., titled "You Can Count on Me (Theme from Hawaii Five-O)", maintains the driving style of the original instrumental throughout.[27]

Australian proto-punk band Radio Birdman borrowed heavily from the program and its theme for their 1977 single "Aloha, Steve & Danno", later included on selected versions of the album Radios Appear.  Band leader Deniz Tek, who grew up in Ann Arbor, Michigan during the heyday of MC5 and The Stooges, commented that he found Sydney of the early 1970s to be a rather quiet and staid place in comparison, and that airings of the program were a weekly highlight.  The song was written after the band members realized they were spending a lot of evenings watching the program.  The lyrics of the song's verses consist entirely of references to story lines of the early episodes.  The chorus alludes to the boredom which band members experienced when the program wasn't on.  The song's guitar solos and other elements of the music were directly derivative of the program's theme; Stevens received a writing credit on the song as a result.

In the Australian movie The Dish, the theme was mistaken for the national anthem of the US by a local band upon the visit of the US Ambassador to Parkes, NSW, to commemorate the 1969 Moon landing.

Bill Murray sang his own made-up lyrics to the song on one of his "Nick the Lounge Singer" skits on Saturday Night Live.

On the 1997 Bill Nye the Science Guy episode "Volcanoes", the MIDI version of "Hawaii Five-O" was used during the "Pahoehoe Five-O" segments.

The song  was also featured in the film 50 First Dates (2004), and the Sammy Davis Jr. version of the theme song was re-recorded by Los Straitjackets with Deke Dickerson and released in 2014.

Darts player Wayne Mardle used the song as his walk-on song in 2013.[28]

The phrase "Five-O" (or any variation, such as "5â€“0", "5-o", and "five O", all usually pronounced "five oh") has come to refer to the police in the United States.[29]

"Bored, She Hung Herself", the 16th episode of the second season, depicted a Five-O investigation into the apparent suicide of a woman by hanging, which she was supposedly practicing as part of a health regimen.[31] A viewer reportedly died trying the same technique, and as a result, the episode was not rebroadcast, was never included in any syndication packages, and has not been included on any DVD release of the show to date.[32][33]

Hawaii Five-O survived long enough to overlap with reruns of early episodes, which were broadcast by CBS in their late night schedule while new episodes were still being produced. Once the program entered syndication after the original run of the series, CBS broadcast reruns of season 12 in late night under the title McGarrett to avoid confusion with the episodes in syndication broadcast under the title Hawaii Five-O. MeTV began airing this series with episode 1, on August 21, 2017, in a 6 PM EDT time slot daily.

In the United Kingdom, the series first aired on ITV on July 19, 1970 in a Saturday evening timeslot.

CBS Interactive had presented the entire first season of the show online via Adobe Flash streaming media.[34]
As of July 2017, almost every episode is available at CBS.com.[35]
The first 10 episodes of season 1 are available free of charge. All other episodes require a CBS All Access subscription to view.

CBS DVD (distributed by Paramount) has released all twelve seasons on DVD in Region 1. The first eight seasons have been released in region 2 and region 4.

Note: The episode "Bored, She Hung Herself" is not included in The Second Season set. The omission is mentioned on the back of the box.  Only some Australian bootlegs have had the episode. Seasons 2â€“8 contain episode promos by Jack Lord.

On December 3, 2013, Paramount released Hawaii Five-O â€“ The Complete Series on DVD in Region 1.[36]

On April 18, 2017, the complete series set was reissued.

A soundtrack album featuring Morton Stevens' theme and incidental music from the pilot and the first two seasons was issued by Capitol Records in 1970. Unlike many albums of television music of the time, the music was taken directly from the scoring sessions rather than being specially re-recorded for album release. One of the instrumental pieces on the album, "Call to Danger", was originally recorded for the unsold 1967 pilot of the same name and also excerpted as background music accompanying a "Special Presentation" logo that CBS used to introduce its prime time television specials throughout the 1970s and 1980s. The album was re-issued on compact disc by Film Score Monthly in 2010.

Hawaii Five-O was the subject of six novelizations. Each one had a plot line written for the book and was not based on a television episode. The first two books were published by Signet Paperbacks in 1968 and 1969. After that were two juvenile hard covers published by Whitman publishing in 1969 and 1971 and finally two more books were published in England.[37]


what is the first step in the major events of the inflammatory process

Redness and heat are due to increased blood flow at body core temperature to the inflamed site; swelling is caused by accumulation of fluid; pain is due to the release of chemicals such as bradykinin and histamine that stimulate nerve endings. Loss of function has multiple causes.[10]

Inflammation

Inflammation (from Latin inflammatio) is part of the complex biological response of body tissues to harmful stimuli, such as pathogens, damaged cells, or irritants,[1] and is a protective response involving immune cells, blood vessels, and molecular mediators. The function of inflammation is to eliminate the initial cause of cell injury, clear out necrotic cells and tissues damaged from the original insult and the inflammatory process, and initiate tissue repair.

The classical signs of inflammation are heat, pain, redness, swelling, and loss of function. Inflammation is a generic response, and therefore it is considered as a mechanism of innate immunity, as compared to adaptive immunity, which is specific for each pathogen.[2] Too little inflammation could lead to progressive tissue destruction by the harmful stimulus (e.g. bacteria) and compromise the survival of the organism. In contrast, chronic inflammation may lead to a host of diseases, such as hay fever, periodontitis, atherosclerosis, rheumatoid arthritis, and even cancer (e.g., gallbladder carcinoma). Inflammation is therefore normally closely regulated by the body.

Inflammation can be classified as either acute or chronic. Acute inflammation is the initial response of the body to harmful stimuli and is achieved by the increased movement of plasma and leukocytes (especially granulocytes) from the blood into the injured tissues. A series of biochemical events propagates and matures the inflammatory response, involving the local vascular system, the immune system, and various cells within the injured tissue. Prolonged inflammation, known as chronic inflammation, leads to a progressive shift in the type of cells present at the site of inflammation, such as mononuclear cells, and is characterized by simultaneous destruction and healing of the tissue from the inflammatory process.

Inflammation is not a synonym for infection. Infection describes the interaction between the action of microbial invasion and the reaction of the body's inflammatory response â€” the two components are considered together when discussing an infection, and the word is used to imply a microbial invasive cause for the observed inflammatory reaction. Inflammation on the other hand describes purely the body's immunovascular response, whatever the cause may be. But because of how often the two are correlated, words ending in the suffix -itis (which refers to inflammation) are sometimes informally described as referring to infection. For example, the word urethritis strictly means only "urethral inflammation", but clinical health care providers usually discuss urethritis as a urethral infection because urethral microbial invasion is the most common cause of urethritis.

It is useful to differentiate inflammation and infection as there are many pathological situations where inflammation is not driven by microbial invasion – for example, atherosclerosis, type III hypersensitivity, trauma, ischaemia. There are also pathological situations where microbial invasion does not result in classic inflammatory response—for example, parasitosis, eosinophilia.

Acute inflammation is a short-term process, usually appearing within a few minutes or hours and begins to cease upon the removal of the injurious stimulus.[8] It involves a coordinated and systemic mobilization response locally of various immune, endocrine and neurological mediators of acute inflammation. In a normal healthy response, it becomes activated, clears the pathogen and begins a repair process and then ceases.[9] It is characterized by five cardinal signs:[10]

An acronym that may be used to remember the key symptoms is "PRISH", for pain, redness, immobility (loss of function), swelling and heat.

The traditional names for signs of inflammation come from Latin:

The first four (classical signs) were described by Celsus (ca. 30 BCâ€“38 AD),[12] while loss of function was added later by Galen[13] even though the attribution is disputed and the origination of the fifth sign has also been ascribed to Thomas Sydenham[14] and Virchow.[8][10]

Acute inflammation of the lung (usually caused in response to pneumonia) does not cause pain unless the inflammation involves the parietal pleura, which does have pain-sensitive nerve endings.[10]

The process of acute inflammation is initiated by resident immune cells already present in the involved tissue, mainly resident macrophages, dendritic cells, histiocytes, Kupffer cells and mast cells. These cells possess surface receptors known as pattern recognition receptors (PRRs), which recognize (i.e., bind) two subclasses of molecules: pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs). PAMPs are compounds that are associated with various pathogens, but which are distinguishable from host molecules. DAMPs are compounds that are associated with host-related injury and cell damage.

At the onset of an infection, burn, or other injuries, these cells undergo activation (one of the PRRs recognize a PAMP or DAMP) and release inflammatory mediators responsible for the clinical signs of inflammation. Vasodilation and its resulting increased blood flow causes the redness (rubor) and increased heat (calor). Increased permeability of the blood vessels results in an exudation (leakage) of plasma proteins and fluid into the tissue (edema), which manifests itself as swelling (tumor). Some of the released mediators such as bradykinin increase the sensitivity to pain (hyperalgesia, dolor). The mediator molecules also alter the blood vessels to permit the migration of leukocytes, mainly neutrophils and macrophages, outside of the blood vessels (extravasation) into the tissue. The neutrophils migrate along a chemotactic gradient created by the local cells to reach the site of injury.[8] The loss of function (functio laesa) is probably the result of a neurological reflex in response to pain.

In addition to cell-derived mediators, several acellular biochemical cascade systems consisting of preformed plasma proteins act in parallel to initiate and propagate the inflammatory response. These include the complement system activated by bacteria and the coagulation and fibrinolysis systems activated by necrosis, e.g. a burn or a trauma.[8]

Acute inflammation may be regarded as the first line of defense against injury. Acute inflammatory response requires constant stimulation to be sustained. Inflammatory mediators are short-lived and are quickly degraded in the tissue. Hence, acute inflammation begins to cease once the stimulus has been removed.[8]

As defined, acute inflammation is an immunovascular response to an inflammatory stimulus. This means acute inflammation can be broadly divided into a vascular phase that occurs first, followed by a cellular phase involving immune cells (more specifically myeloid granulocytes in the acute setting). The vascular component of acute inflammation involves the movement of plasma fluid, containing important proteins such as fibrin and immunoglobulins (antibodies), into inflamed tissue.

Upon contact with PAMPs, tissue macrophages and mastocytes release vasoactive amines such as histamine and serotonin, as well as eicosanoids such as prostaglandin E2 and leukotriene B4 to remodel the local vasculature. Macrophages and endothelial cells release nitric oxide. These mediators vasodilate and permeabilize the blood vessels, which results in the net distribution of blood plasma from the vessel into the tissue space. The increased collection of fluid into the tissue causes it to swell (edema). This exuded tissue fluid contain various antimicrobial mediators from the plasma such as complement, lysozyme, antibodies, which can immediately deal damage to microbes, and opsonise the microbes in preparation for the cellular phase. If the inflammatory stimulus is a lacerating wound, exuded platelets, coagulants, plasmin and kinins can clot the wounded area and provide haemostasis in the first instance. These clotting mediators also provide a structural staging framework at the inflammatory tissue site in the form of a fibrin lattice – as would construction scaffolding at a construction site – for the purpose of aiding phagocytic debridement and wound repair later on. Some of the exuded tissue fluid is also funnelled by lymphatics to the regional lymph nodes, flushing bacteria along to start the recognition and attack phase of the adaptive immune system.

Acute inflammation is characterized by marked vascular changes, including vasodilation, increased permeability and increased blood flow, which are induced by the actions of various inflammatory mediators. Vasodilation occurs first at the arteriole level, progressing to the capillary level, and brings about a net increase in the amount of blood present, causing the redness and heat of inflammation. Increased permeability of the vessels results in the movement of plasma into the tissues, with resultant stasis due to the increase in the concentration of the cells within blood â€“ a condition characterized by enlarged vessels packed with cells. Stasis allows leukocytes to marginate (move) along the endothelium, a process critical to their recruitment into the tissues. Normal flowing blood prevents this, as the shearing force along the periphery of the vessels moves cells in the blood into the middle of the vessel.

* non-exhaustive list

The cellular component involves leukocytes, which normally reside in blood and must move into the inflamed tissue via extravasation to aid in inflammation. Some act as phagocytes, ingesting bacteria, viruses, and cellular debris. Others release enzymatic granules that damage pathogenic invaders. Leukocytes also release inflammatory mediators that develop and maintain the inflammatory response. In general, acute inflammation is mediated by granulocytes, whereas chronic inflammation is mediated by mononuclear cells such as monocytes and lymphocytes.

Various leukocytes, particularly neutrophils, are critically involved in the initiation and maintenance of inflammation. These cells must be able to move to the site of injury from their usual location in the blood, therefore mechanisms exist to recruit and direct leukocytes to the appropriate place. The process of leukocyte movement from the blood to the tissues through the blood vessels is known as extravasation, and can be broadly divided up into a number of steps:

Extravasated neutrophils in the cellular phase come into contact with microbes at the inflamed tissue. Phagocytes express cell-surface endocytic pattern recognition receptors (PRRs) that have affinity and efficacy against non-specific microbe-associated molecular patterns (PAMPs). Most PAMPs that bind to endocytic PRRs and initiate phagocytosis are cell wall components, including complex carbohydrates such as mannans and β-glucans, lipopolysaccharides (LPS), peptidoglycans, and surface proteins. Endocytic PRRs on phagocytes reflect these molecular patterns, with C-type lectin receptors binding to mannans and β-glucans, and scavenger receptors binding to LPS.

Upon endocytic PRR binding, actin-myosin cytoskeletal rearrangement adjacent to the plasma membrane occurs in a way that endocytoses the plasma membrane containing the PRR-PAMP complex, and the microbe. Phosphatidylinositol and Vps34-Vps15-Beclin1 signalling pathways have been implicated to traffic the endocytosed phagosome to intracellular lysosomes, where fusion of the phagosome and the lysosome produces a phagolysosome. The reactive oxygen species, superoxides and hypochlorite bleach within the phagolysosomes then kill microbes inside the phagocyte.

Phagocytic efficacy can be enhanced by opsonization. Plasma derived complement C3b and antibodies that exude into the inflamed tissue during the vascular phase bind to and coat the microbial antigens. As well as endocytic PRRs, phagocytes also express opsonin receptors Fc receptor and complement receptor 1 (CR1), which bind to antibodies and C3b, respectively. The co-stimulation of endocytic PRR and opsonin receptor increases the efficacy of the phagocytic process, enhancing the lysosomal elimination of the infective agent.

* non-exhaustive list

Specific patterns of acute and chronic inflammation are seen during particular situations that arise in the body, such as when inflammation occurs on an epithelial surface, or pyogenic bacteria are involved.

Inflammatory abnormalities are a large group of disorders that underlie a vast variety of human diseases. The immune system is often involved with inflammatory disorders, demonstrated in both allergic reactions and some myopathies, with many immune system disorders resulting in abnormal inflammation. Non-immune diseases with causal origins in inflammatory processes include cancer, atherosclerosis, and ischemic heart disease.[8]

Examples of disorders associated with inflammation include:

Atherosclerosis, formerly considered a bland lipid storage disease, actually involves an ongoing inflammatory response. Recent advances in basic science have established a fundamental role for inflammation in mediating all stages of this disease from initiation through progression and, ultimately, the thrombotic complications of atherosclerosis. These new findings provide important links between risk factors and the mechanisms of atherogenesis. Clinical studies have shown that this emerging biology of inflammation in atherosclerosis applies directly to human patients. Elevation in markers of inflammation predicts outcomes of patients with acute coronary syndromes, independently of myocardial damage. In addition, low-grade chronic inflammation, as indicated by levels of the inflammatory marker C-reactive protein, prospectively defines risk of atherosclerotic complications, thus adding to prognostic information provided by traditional risk factors. Moreover, certain treatments that reduce coronary risk also limit inflammation. In the case of lipid lowering with statins, this anti-inflammatory effect does not appear to correlate with reduction in low-density lipoprotein levels. These new insights into inflammation in atherosclerosis not only increase our understanding of this disease but also have practical clinical applications in risk stratification and targeting of therapy for this scourge of growing worldwide importance.[19]

An allergic reaction, formally known as type 1 hypersensitivity, is the result of an inappropriate immune response triggering inflammation, vasodilation, and nerve irritation. A common example is hay fever, which is caused by a hypersensitive response by mast cells to allergens. Pre-sensitised mast cells respond by degranulating, releasing vasoactive chemicals such as histamine. These chemicals propagate an excessive inflammatory response characterised by blood vessel dilation, production of pro-inflammatory molecules, cytokine release, and recruitment of leukocytes.[8] Severe inflammatory response may mature into a systemic response known as anaphylaxis.

Inflammatory myopathies are caused by the immune system inappropriately attacking components of muscle, leading to signs of muscle inflammation. They may occur in conjunction with other immune disorders, such as systemic sclerosis, and include dermatomyositis, polymyositis, and inclusion body myositis.[8]

Due to the central role of leukocytes in the development and propagation of inflammation, defects in leukocyte functionality often result in a decreased capacity for inflammatory defense with subsequent vulnerability to infection.[8] Dysfunctional leukocytes may be unable to correctly bind to blood vessels due to surface receptor mutations, digest bacteria (Chédiak–Higashi syndrome), or produce microbicides (chronic granulomatous disease). In addition, diseases affecting the bone marrow may result in abnormal or few leukocytes.

Certain drugs or exogenous chemical compounds are known to affect inflammation. Vitamin A deficiency causes an increase in inflammatory responses,[20] and anti-inflammatory drugs work specifically by inhibiting the enzymes that produce inflammatory eicosanoids. Certain illicit drugs such as cocaine and ecstasy may exert some of their detrimental effects by activating transcription factors intimately involved with inflammation (e.g. NF-κB).[21][22]

Inflammation orchestrates the microenvironment around tumours, contributing to proliferation, survival and migration.[23] Cancer cells use selectins, chemokines and their receptors for invasion, migration and metastasis.[24] On the other hand, many cells of the immune system contribute to cancer immunology, suppressing cancer.[25] Molecular intersection between receptors of steroid hormones, which have important effects on cellular development, and transcription factors that play key roles in inflammation, such as NF-κB, may mediate some of the most critical effects of inflammatory stimuli on cancer cells.[26] This capacity of a mediator of inflammation to influence the effects of steroid hormones in cells, is very likely to affect carcinogenesis on the one hand; on the other hand, due to the modular nature of many steroid hormone receptors, this interaction may offer ways to interfere with cancer progression, through targeting of a specific protein domain in a specific cell type. Such an approach may limit side effects that are unrelated to the tumor of interest, and may help preserve vital homeostatic functions and developmental processes in the organism.

According to a review of 2009, recent data suggests that cancer-related inflammation (CRI) may lead to accumulation of random genetic alterations in cancer cells.[27]

It has long been recognized that infection with HIV is characterized not only by development of profound immunodeficiency but also by sustained inflammation and immune activation.[28][29][30] A substantial body of evidence implicates chronic inflammation as a critical driver of immune dysfunction, premature appearance of aging-related diseases, and immune deficiency.[28][31] Many now regard HIV infection not only as an evolving virus-induced immunodeficiency but also as chronic inflammatory disease.[32] Even after the introduction of effective antiretroviral therapy (ART) and effective suppression of viremia in HIV-infected individuals, chronic inflammation persists. Animal studies also support the relationship between immune activation and progressive cellular immune deficiency: SIVsm infection of its natural nonhuman primate hosts, the sooty mangabey, causes high-level viral replication but limited evidence of disease.[33][34] This lack of pathogenicity is accompanied by a lack of inflammation, immune activation and cellular proliferation. In sharp contrast, experimental SIVsm infection of rhesus macaque produces immune activation and AIDS-like disease with many parallels to human HIV infection.[35]

Delineating how CD4 T cells are depleted and how chronic inflammation and immune activation are induced lies at the heart of understanding HIV pathogenesis––one of the top priorities for HIV research by the Office of AIDS Research, National Institutes of Health. Recent studies demonstrated that caspase-1-mediated pyroptosis, a highly inflammatory form of programmed cell death, drives CD4 T-cell depletion and inflammation by HIV.[36][37][38] These are the two signature events that propel HIV disease progression to AIDS. Pyroptosis appears to create a pathogenic vicious cycle in which dying CD4 T cells and other immune cells (including macrophages and neutrophils) release inflammatory signals that recruit more cells into the infected lymphoid tissues to die. The feed-forward nature of this inflammatory response produces chronic inflammation and tissue injury.[39] Identifying pyroptosis as the predominant mechanism that causes CD4 T-cell depletion and chronic inflammation, provides novel therapeutic opportunities, namely caspase-1 which controls the pyroptotic pathway. In this regard, pyroptosis of CD4 T cells and secretion of pro-inflmammatory cytokines such as IL-1β and IL-18 can be blocked in HIV-infected human lymphoid tissues by addition of the caspase-1 inhibitor VX-765,[36] which has already proven to be safe and well tolerated in phase II human clinical trials.[40] These findings could propel development of an entirely new class of “anti-AIDS” therapies that act by targeting the host rather than the virus. Such agents would almost certainly be used in combination with ART. By promoting “tolerance” of the virus instead of suppressing its replication, VX-765 or related drugs may mimic the evolutionary solutions occurring in multiple monkey hosts (e.g. the sooty mangabey) infected with species-specific lentiviruses that have led to a lack of disease, no decline in CD4 T-cell counts, and no chronic inflammation.

The inflammatory response must be actively terminated when no longer needed to prevent unnecessary "bystander" damage to tissues.[8] Failure to do so results in chronic inflammation, and cellular destruction. Resolution of inflammation occurs by different mechanisms in different tissues. Mechanisms that serve to terminate inflammation include:[8][41]

There is evidence for a link between inflammation and depression.[53] Inflammatory processes can be triggered by negative cognitions or their consequences, such as stress, violence, or deprivation. Thus, negative cognitions can cause inflammation that can, in turn, lead to depression.[54][55][dubious â€“ discuss] In addition there is increasing evidence that inflammation can cause depression because of the increase of cytokines, setting the brain into a "sickness mode".[56] Classical symptoms of being physically sick like lethargy show a large overlap in behaviors that characterize depression. Levels of cytokines tend to increase sharply during depressive episodes in manics and drop off during remission.[57] Furthermore, it has been shown in clinical trials that anti-inflammatory medicines taken in addition to antidepressants not only significantly improves symptoms but also increases the proportion of subjects positively responding to treatment.[58] Inflammations that lead to serious depression could be caused by common infections such as those caused by a virus, bacteria or even parasites.[59]

An infectious organism can escape the confines of the immediate tissue via the circulatory system or lymphatic system, where it may spread to other parts of the body. If an organism is not contained by the actions of acute inflammation it may gain access to the lymphatic system via nearby lymph vessels. An infection of the lymph vessels is known as lymphangitis, and infection of a lymph node is known as lymphadenitis. When lymph nodes cannot destroy all pathogens, the infection spreads further. A pathogen can gain access to the bloodstream through lymphatic drainage into the circulatory system.

When inflammation overwhelms the host, systemic inflammatory response syndrome is diagnosed. When it is due to infection, the term sepsis is applied, with the terms bacteremia being applied specifically for bacterial sepsis and viremia specifically to viral sepsis. Vasodilation and organ dysfunction are serious problems associated with widespread infection that may lead to septic shock and death.

Inflammation also induces high systemic levels of acute-phase proteins. In acute inflammation, these proteins prove beneficial; however, in chronic inflammation they can contribute to amyloidosis.[8] These proteins include C-reactive protein, serum amyloid A, and serum amyloid P, which cause a range of systemic effects including:[8]

Inflammation often affects the numbers of leukocytes present in the body:

With the discovery of interleukins (IL), the concept of systemic inflammation developed. Although the processes involved are identical to tissue inflammation, systemic inflammation is not confined to a particular tissue but involves the endothelium and other organ systems.

Chronic inflammation is widely observed in obesity.[60][61] The obese commonly have many elevated markers of inflammation, including:[62][63]

Low-grade chronic inflammation is characterized by a two- to threefold increase in the systemic concentrations of cytokines such as TNF-α, IL-6, and CRP.[66] Waist circumference correlates significantly with systemic inflammatory response.[67] A predominant factor in this correlation is due to the autoimmune response triggered by adiposity, whereby immune cells may mistake fatty deposits for intruders. The body attacks fat similar to bacteria and fungi. When expanded fat cells leak or break open, macrophages mobilize to clean up and embed into the adipose tissue. Then macrophages release inflammatory chemicals, including TNF-α and IL-6. TNF's primary role is to regulate the immune cells and induce inflammation. White blood cells then assist by releasing more cytokines. This link between adiposity and inflammation has been shown to produce 10–35% of IL-6 in a resting individual, and this production increases with increasing adiposity.[68]

Loss of white adipose tissue reduces levels of inflammation markers.[60] The association of systemic inflammation with insulin resistance and atherosclerosis is the subject of intense research.[69]

In the obese mouse models, inflammation and macrophage-specific genes are upregulated in white adipose tissue (WAT). There were also signs of dramatic increase in circulating insulin level, adipocyte lipolysis and formation of multinucleate giant cells.[70] The fat-derived protein called angiopoietin-like protein 2 (Angptl2) elevates in fat tissues. Higher than normal Angptl2 level in fat tissues develop inflammation as well as insulin and leptin resistance. Stored fat secretes Leptin to signal satiety. Leptin resistance plays a role in the process where appetite overrules the message of satiety. Angptl2 then starts an inflammatory cascade causing blood vessels to remodel and attract macrophages. Angptl2 is an adipocyte-derived inflammatory mediator linking obesity to systemic insulin resistance.[71] It is possible that, as an inflammatory marker, leptin responds specifically to adipose-derived inflammatory cytokines.

C-reactive protein (CRP) is generated at a higher level in obese people. It raises when there is inflammation throughout the body. Mild elevation in CRP increase risk of heart attacks, strokes, high blood pressure, muscle weakness and fragility.[72][citation needed]

Hyperglycemia induces IL-6 production from endothelial cells and macrophages.[73] Meals high in saturated fat, as well as meals high in calories have been associated with increases in inflammatory markers.[74][75] In addition, interstitial abdominal adiposity (also referred to as accumulated intra-abdominal fat) may be a factor in increasing systemic risk for multiple inflammatory diseases. Although the exact mechanisms are still being investigated, a review published in 2010 suggested that significant growth of adipose tissue in response to overeating can evoke a chronic inflammatory response.[76]

The outcome in a particular circumstance will be determined by the tissue in which the injury has occurred and the injurious agent that is causing it. Here are the possible outcomes to inflammation:[8]

Inflammation is usually indicated by adding the suffix "itis", as shown below. However, some conditions such as asthma and pneumonia do not follow this convention. More examples are available at list of types of inflammation.

Acute infective meningitis

The Dietary Inflammatory Index (DII) is a score (number) that describes the potential of diet to modulate systemic inflammation within the body. As stated chronic inflammation is linked to most chronic diseases including arthritis, many types of cancer, cardiovascular diseases, inflammatory bowel diseases, and diabetes.

Acute inflammation of the muscle cells, as understood in exercise physiology,[77] can result after induced eccentric and concentric muscle training. Participation in eccentric training and conditioning, including resistance training and activities that emphasize eccentric lengthening of the muscle including downhill running on a moderate to high incline can result in considerable soreness within 24 to 48 hours, even though blood lactate levels, previously thought to cause muscle soreness, were much higher with level running. This delayed onset muscle soreness (DOMS) results from structural damage to the contractile filaments and z-disks, which has been noted especially in marathon runners whose muscle fibers revealed remarkable damage to the muscle fibers after both training and marathon competition [78][citation needed]. The onset and timing of this gradient damage to the muscle parallels the degree of muscle soreness experienced by the runners.

Z-disks are the point of contact for the contractile proteins. They provide structural support for transmission of force when muscle fibers are activated to shorten. However, in marathon runners and those who subscribe to the overload principle to enhance their muscles, show moderate Z-disk streaming and major disruption of thick and thin filaments in parallel groups of sarcomeres as a result of the force of eccentric actions or stretching of tightened muscle fibers.

This disruption of muscle fibers triggers white blood cells to increase following induced muscle soreness, leading to the inflammatory response observation from induced muscle soreness. Elevations in plasma enzymes, myoglobinemia, and abnormal muscle histology and ultrastructure are concluded to be associated with inflammatory response. High tension in the contractile-elastic system of muscle results in structural damage to the muscle fiber and plasmalemma and its epimysium, perimysium, and/or endomysium. The mysium damage disrupts calcium homeostasis in injured fibers and fiber bundles, resulting in necrosis that peaks about 48 hours after exercise. The products of macrophage activity and intracellular contents (such as histamines, kinins, and K+) accumulate outside cells. These substances then stimulate free nerve endings in the muscle; a process that appears accentuated by eccentric exercise, in which large forces are distributed over a relatively small cross-sectional area of the muscle[78][citation needed].

There is a known relationship between inflammation and muscle growth.[79] For instance, high doses of anti-inflammatory medicines (e.g., NSAIDs) are able to blunt muscle growth.[80][81][original research?] Cold therapy has been shown to negatively affect muscle growth as well. Reducing inflammation results in decreased macrophage activity and lower levels of IGF-1[82] Acute effects of cold therapy on training adaptations show reduced satellite cell proliferation.[83] Long term effects include less muscular hypertrophy and an altered cell structure of muscle fibers.[84]

It has been further theorized that the acute localized inflammatory responses to muscular contraction during exercise, as described above, are a necessary precursor to muscle growth.[85] As a response to muscular contractions, the acute inflammatory response initiates the breakdown and removal of damaged muscle tissue.[86] Muscles can synthesize cytokines in response to contractions,[87][88][89] such that the cytokines interleukin-1 beta (IL-1β), TNF-α, and IL-6 are expressed in skeletal muscle up to 5 days after exercise.[86]

In particular, the increase in levels of IL-6 (interleukin 6), a myokine, can reach up to one hundred times that of resting levels.[89] Depending on volume, intensity, and other training factors, the IL-6 increase associated with training initiates about 4 hours after resistance training and remains elevated for up to 24 hours.[90][91][92]

These acute increases in cytokines, as a response to muscle contractions, help initiate the process of muscle repair and growth by activating satellite cells within the inflamed muscle. Satellite cells are crucial for skeletal muscle adaptation to exercise.[93] They contribute to hypertrophy by providing new myonuclei and repair damaged segments of mature myofibers for successful regeneration following injury- or exercise-induced muscle damage;[94][95][96] high-level powerlifters can have up to 100% more satellite cells than untrained controls.[97][98]

A rapid and transient localization of the IL-6 receptor and increased IL-6 expression occurs in satellite cells following contractions.[90] IL-6 has been shown to mediate hypertrophic muscle growth both in vitro and in vivo.[93] Unaccustomed exercise can increase IL-6 by up to sixfold at 5 hours post-exercise and threefold 8 days after exercise.[99] Also telling is the fact that NSAIDs can decrease satellite cell response to exercise,[80] thereby reducing exercise-induced protein synthesis.[81]

The increase in cytokines (myokines) after resistance exercise coincides with the decrease in levels of myostatin, a protein that inhibits muscle differentiation and growth.[92] The cytokine response to resistance exercise and moderate-intensity running occur differently, with the latter causing a more prolonged response, especially at the 12â€“24 hour mark.[92]

Developing research has demonstrated that many of the benefits of exercise are mediated through the role of skeletal muscle as an endocrine organ. That is, contracting muscles release multiple substances known as myokines, including but not limited to those cited in the above description, which promote the growth of new tissue, tissue repair, and various anti-inflammatory functions, which in turn reduce the risk of developing various inflammatory diseases. The new view that muscle is an endocrine organ is transforming our understanding of exercise physiology and with it, of the role of inflammation in adaptation to stress.[100]

Both chronic and extreme inflammation are associated with disruptions of anabolic signals initiating muscle growth. Chronic inflammation has been implicated as part of the cause of the muscle loss that occurs with aging.[79][101] Increased protein levels of myostatin have been described in patients with diseases characterized by chronic low-grade inflammation.[102] Increased levels of TNF-Î± can suppress the AKT/mTOR pathway, a crucial pathway for regulating skeletal muscle hypertrophy,[103] thereby increasing muscle catabolism.[104][105][106] Cytokines may antagonize the anabolic effects of insulin-like growth factor 1 (IGF-1).[107][108] In the case of sepsis, an extreme whole body inflammatory state, the synthesis of both myofibrillar and sarcoplasmic proteins are inhibited, with the inhibition taking place preferentially in fast-twitch muscle fibers.[107][109] Sepsis is also able to prevent leucine from stimulating muscle protein synthesis.[87] In animal models, when inflammation is created, mTOR loses its ability to be stimulated by muscle growth.[110]

Regular physical activity is reported to decrease markers of inflammation,[111][112][113] although the correlation is imperfect and seems to reveal differing results contingent upon training intensity. For instance, while baseline measurements of circulating inflammatory markers do not seem to differ greatly between healthy trained and untrained adults,[114][115] long-term training may help reduce chronic low-grade inflammation.[116] On the other hand, levels of the anti-inflammatory myokine IL-6 (interleukin 6) remained elevated longer into the recovery period following an acute bout of exercise in patients with inflammatory diseases, relative to the recovery of healthy controls.[116] It may well be that low-intensity training can reduce resting pro-inflammatory markers (CRP, IL-6), while moderate-intensity training has milder and less-established anti-inflammatory benefits.[114][117][118][119] There is a strong relationship between exhaustive exercise and chronic low-grade inflammation.[120] Marathon running may enhance IL-6 levels as much as 100 times over normal and increases total leuckocyte count and neturophil mobilization.[120]

Regarding the above, IL-6 had previously been classified as a proinflammatory cytokine. Therefore, it was first thought that the exercise-induced IL-6 response was related to muscle damage.[121] However, it has become evident that eccentric exercise is not associated with a larger increase in plasma IL-6 than exercise involving concentric “nondamaging” muscle contractions. This finding clearly demonstrates that muscle damage is not required to provoke an increase in plasma IL-6 during exercise. As a matter of fact, eccentric exercise may result in a delayed peak and a much slower decrease of plasma IL-6 during recovery.[122]

Recent work has shown that both upstream and downstream signalling pathways for IL-6 differ markedly between myocytes and macrophages. It appears that unlike IL-6 signalling in macrophages, which is dependent upon activation of the NFκB signalling pathway, intramuscular IL-6 expression is regulated by a network of signalling cascades, including the Ca2+/NFAT and glycogen/p38 MAPK pathways. Thus, when IL-6 is signalling in monocytes or macrophages, it creates a pro-inflammatory response, whereas IL-6 activation and signalling in muscle is totally independent of a preceding TNF-response or NFκB activation, and is anti-inflammatory.[123]

Several studies show that markers of inflammation are reduced following longer-term behavioural changes involving both reduced energy intake and a regular program of increased physical activity, and that, in particular, IL-6 was miscast as an inflammatory marker. For example, the anti-inflammatory effects of IL-6 have been demonstrated by IL-6 stimulating the production of the classical anti-inflammatory cytokines IL-1ra and IL-10.[123] As such, individuals pursuing exercise as a means to treat the causal factors underlying chronic inflammation are pursuing a course of action strongly supported by current research, as an inactive lifestyle is strongly associated with the development and progression of multiple inflammatory diseases. Note that cautions regarding over-exertion may apply in certain cases, as discussed above, though this concern rarely applies to the general population.

Given that localized acute inflammation is a necessary component for muscle growth, and that chronic low-grade inflammation is associated with a disruption of anabolic signals initiating muscle growth, it has been theorized that a signal-to-noise model may best describe the relationship between inflammation and muscle growth.[124] By keeping the "noise" of chronic inflammation to a minimum, the localized acute inflammatory response signals a stronger anabolic response than could be achieved with higher levels of chronic inflammation.


when did venda become part of south africa

The first President of Venda, Patrick Mphephu, was also a Paramount Chief of the Vhavenda people; he was born and lived in Dzanani in Limpopo. His successor, Orifuna Ndou, was overthrown in a military coup by the Venda Defence Force in 1990, after which the territory was ruled by the Council of National Unity. Venda was re-absorbed into South Africa on 27 April 1994.[4]

Venda

Venda (/ˈvɛndə/) was a Bantustan in northern South Africa, close to the South African border with Zimbabwe to the north, while to the south and east, it shared a long border with another black homeland, Gazankulu. It is now part of the Limpopo province. Venda was founded as a homeland by the South African government for the Venda people, speakers of the Venda language.[3] The United Nations and international community refused to recognize Venda (or any other Bantustan) as an independent state.

Venda was declared self-governing on 1 February 1973,[4] with elections held later in the year.[5] Further elections were held in July 1978.[5] The territory was declared independent by the South African government on 13 September 1979 and its residents lost their South African citizenship.[6][7] In common with other Bantustans, its independence was not recognized by the international community.

Venda was initially a series of non-contiguous territories in the Transvaal, with one main part and one main exclave. Its capital, formerly at Sibasa, was moved to Thohoyandou (which included the old Sibasa administrative district) when Venda was declared independent in 1979. Prior to independence it was expanded to form one contiguous territory, with a total land area of 6,807 km².[3] In the 1984 elections the ruling Venda Independence People's Party (VIPP) lost to the Venda National Party (VNP).[5]

At independence in 1979, the population of Vhavenda stood at about 200,000 people. The state was cut off from neighboring Zimbabwe by the Madimbo corridor, patrolled by South African troops, to the North, and from nearby Mozambique by the Kruger National Park.[3]

In 1982, the University of Venda known as Univen was established as an institution of higher learning for the Vhavenda people.[8] Being nominally independent it was able to set up a casino in the early 1980s, staffed mainly by British workers. This would not have been legally possible in South Africa proper.[citation needed]

Districts of the province and population at the 1991 census.[2]


purified extract of the female tropical cochineal insect

Carminic acid is extracted from the female cochineal insects and is treated to produce carmine, which can yield shades of red such as crimson and scarlet. The body of the insect is 19â€“22% carminic acid.[9] The insects are processed by immersion in hot water or exposure to sunlight, steam, or the heat of an oven. Each method produces a different colour that results in the varied appearance of commercial cochineal. The insects must be dried to about 30% of their original body weight before they can be stored without decaying.[21] It takes about 80,000 to 100,000 insects to make one kilogram of cochineal dye.[25]

Cochineal

Coccus cacti Linnaeus, 1758
Pseudococcus cacti Burmeister, 1839

The cochineal (/kɒtʃɪˈniːl/ kotch-ih-NEEL, /ˈkɒtʃɪniːl/ KOTCH-ih-neel; Dactylopius coccus) is a scale insect in the suborder Sternorrhyncha, from which the natural dye carmine is derived. A primarily sessile parasite native to tropical and subtropical South America as well as Mexico and Arizona, this insect lives on cacti in the genus Opuntia, feeding on plant moisture and nutrients. These insects are found on the pads of prickly pear cacti, then are brushed off and dried.

The insect produces carminic acid that deters predation by other insects. Carminic acid, typically 17-24% of dried insects' weight, can be extracted from the body and eggs, then mixed with aluminium or calcium salts to make carmine dye, also known as cochineal. Today, carmine is primarily used as a colorant in food and in lipstick (E120 or Natural Red 4).

The carmine dye was used in Central America in the 15th century for coloring fabrics and became an important export good during the colonial period. After synthetic pigments and dyes such as alizarin were invented in the late 19th century, natural-dye production gradually diminished. Health fears over artificial food additives, however, have renewed the popularity of cochineal dyes, and the increased demand has made cultivation of the insect profitable again,[1] with Peru being the largest exporter. Some towns in the Mexican state of Oaxaca are still working in handmade textiles using this cochineal.[2]

Other species in the genus Dactylopius can be used to produce cochineal extract, but they are extremely difficult to distinguish from D. coccus, even for expert taxonomists, and the latter scientific name (and the vernacular "cochineal insect") is therefore commonly used when one is actually referring to other biological species. The primary biological distinctions between species are minor differences in host plant preferences, in addition to very different geographic distributions.

Cochineal is probably from French cochenille, Spanish cochinilla, Latin coccinus, meaning'scarlet-colored', and Latin coccum, meaning 'berry (actually an insect) yielding scarlet dye'. See also the related word kermes which is the source of a similar but weaker Mediterranean dye also called crimson, which was used to color cloth red before discovery of cochineal in the New World. Some sources identify the Spanish source word for cochineal as cochinilla "wood louse" (a diminutive form of Spanish cochino, cognate with French cochon, meaning "pig")."[3]

Cochineal dye was used by the Aztec and Maya peoples of Central and North America. Eleven cities conquered by Montezuma in the 15th century paid a yearly tribute of 2000 decorated cotton blankets and 40 bags of cochineal dye each.[4] Production of cochineal is depicted in Codex Osuna. During the colonial period, the production of cochineal (grana fina) grew rapidly. Produced almost exclusively in Oaxaca by indigenous producers, cochineal became Mexico's second-most valued export after silver.[5] Soon after the Spanish conquest of the Aztec Empire, it began to be exported to Spain, and by the 17th century was a commodity traded as far away as India.[6] The dyestuff was consumed throughout Europe and was so highly prized, its price was regularly quoted on the London and Amsterdam Commodity Exchanges. In 1777, French botanist Nicolas-Joseph Thiéry de Menonville, presenting himself as a botanizing physician, smuggled the insects and pads of the Opuntia cactus to Saint Domingue. This particular collection failed to thrive and ultimately died out, leaving the Mexican monopoly intact.[7] After the Mexican War of Independence in 1810–1821, the Mexican monopoly on cochineal came to an end. Large-scale production of cochineal emerged, especially in Guatemala and the Canary Islands; it was also cultivated in Spain and North Africa.[6]

The demand for cochineal fell sharply with the appearance on the market of alizarin crimson and many other artificial dyes discovered in Europe in the middle of the 19th century, causing a significant financial shock in Spain as a major industry almost ceased to exist.[5] The delicate manual labour required for the breeding of the insect could not compete with the modern methods of the new industry, and even less so with the lowering of production costs. The "tuna blood" dye (from the Mexican name for the Opuntia fruit) stopped being used and trade in cochineal almost totally disappeared in the course of the 20th century. The breeding of the cochineal insect has been done mainly for the purposes of maintaining the tradition rather than to satisfy any sort of demand.[8]

It has become commercially valuable again.[9] One reason for its popularity is that many commercial synthetic red dyes were found to be carcinogenic.[10]

The carmine of antiquity also contains carminic acid, and was extracted from a similar insect, Kermes vermilio, which lives on Quercus coccifera oaks native to the Near East and the European side of the Mediterranean Basin. Kermes carmine was used as a dye and a laked pigment in ancient Egypt, Greece, and the Near East and is one of the oldest organic pigments.[11] Recipes for artists' use of carmine appear in many early painting and alchemical handbooks throughout the Middle Ages; the laking process for both pigments was improved in the 19th century. Carmine was not light-fast and was largely abandoned in art.[12]

Spanish influence changed the way in which Aztecs used pigments, particularly in their manuscripts. For example, Cochineal was replaced by Spanish dyes like minium and alizarin crimson.[13] The image of Moctezuma's death (seen to the right) uses both indigenous and Spanish pigments, and is therefore representative of the transition and influence between cultures.

Cochineal insects are soft-bodied, flat, oval-shaped scale insects. The females, wingless and about 5 mm (0.20 in) long, cluster on cactus pads. They penetrate the cactus with their beak-like mouthparts and feed on its juices, remaining immobile unless alarmed. After mating, the fertilised female increases in size and gives birth to tiny nymphs. The nymphs secrete a waxy white substance over their bodies for protection from water loss and excessive sun. This substance makes the cochineal insect appear white or grey from the outside, though the body of the insect and its nymphs produces the red pigment, which makes the insides of the insect look dark purple. Adult males can be distinguished from females in that males have wings, and are much smaller.[14]

The cochineal disperses in the first nymph stage, called the "crawler" stage. The juveniles move to a feeding spot and produce long wax filaments. Later, they move to the edge of the cactus pad, where the wind catches the wax filaments and carries the insects to a new host. These individuals establish feeding sites on the new host and produce a new generation of cochineals.[15] Male nymphs feed on the cactus until they reach sexual maturity. At this time, they can no longer feed at all and live only long enough to fertilise the eggs.[16] They are, therefore, seldom observed.[15] In addition, females typically outnumber males due to environmental factors.[17]

Dactylopius coccus is native to tropical and subtropical South America and Mexico, where their host cacti grow natively. They have been widely introduced to many regions where their host cacti also grow. About 200 species of Opuntia cacti are known, and while it is possible to cultivate cochineal on almost all of them, the most common is Opuntia ficus-indica.[18] D. coccus has only been noted on Opuntia species, including O. amyclaea, O. atropes, O. cantabrigiensis, O. brasilienis, O. ficus-indica, O. fuliginosa, O. jaliscana, O. leucotricha, O. lindheimeri, O. microdasys, O. megacantha, O. pilifera, O. robusta, O. sarca, O. schikendantzii, O. stricta, O. streptacantha, and O. tomentosa.[1] Feeding cochineals can damage and kill the plant. Other cochineal species feed on many of the same Opuntia, and the wide range of hosts reported for D. coccus likely is because of the difficulty in distinguishing it from other Dactylopius species.[19]

A nopal cactus farm for the production of cochineal is traditionally known as a nopalry.[20] The two methods of farming cochineal are traditional and controlled. Cochineals are farmed in the traditional method by planting infected cactus pads or infesting existing cacti with cochineals and harvesting the insects by hand. The controlled method uses small baskets called Zapotec nests placed on host cacti. The baskets contain clean, fertile females that leave the nests and settle on the cactus to await fertilization by the males. In both cases, the cochineals must be protected from predation, cold, and rain. The complete cycle lasts three months, during which time the cacti are kept at a constant temperature of 27 °C (81 °F). At the end of the cycle, the new cochineals are left to reproduce or are collected and dried for dye production.[18]

To produce dye from cochineals, the insects are collected when they are around 90 days old. Harvesting the insects is labour-intensive, as they must be individually knocked, brushed, or picked from the cacti and placed into bags. The insects are gathered by small groups of collectors who sell them to local processors or exporters.[21]

Several natural enemies can reduce the population of the insects on hosts. Of all the predators, insects seem to be the most important group. Insects and their larvae such as pyralid moths (order Lepidoptera), which destroy the cactus, and predators such as lady bugs (Coleoptera), various Diptera (such as Syrphidae and Chamaemyiidae), lacewings (Neuroptera), and ants (Hymenoptera) have been identified, as well as numerous parasitic wasps. Many birds, human-commensal rodents (especially rats) and reptiles also prey on cochineal insects. In regions dependent on cochineal production, pest control measures are taken seriously. For small-scale cultivation, manual methods of control have proved to be the safest and most effective. For large-scale cultivation, advanced pest control methods have to be developed, including alternative bioinsecticides or traps with pheromones.[1]

Opuntia species, known commonly as prickly pears, were first brought to Australia in an attempt to start a cochineal dye industry in 1788. Captain Arthur Phillip collected a number of cochineal-infested plants from Brazil on his way to establish the first European settlement at Botany Bay, part of which is now Sydney, New South Wales. At that time, Spain and Portugal had a worldwide cochineal dye monopoly via their New World colonial sources, and the British desired a source under their own control, as the dye was important to their clothing and garment industries; it was used to colour the British soldiers' red coats, for example.[22] The attempt was a failure in two ways: the Brazilian cochineal insects soon died off, but the cactus thrived, eventually overrunning about 100,000 sq mi (259,000 km2) of eastern Australia.[23] The cacti were eventually brought under control in the 1920s by the deliberate introduction of a South American moth, Cactoblastis cactorum, the larvae of which feed on the cactus.[23]

The nopal pear has been traditionally eaten in parts of northern Ethiopia, where it is utilized more than cultivated. Carmine cochineal was introduced into northern Ethiopia early in the 2000s to be cultivated among farming communities. Foodsafe exported 2000 tons of dried carmine cochineal over 3 years.

A conflict of interest among communities led to closure of the cochineal business in Ethiopia, but the insect spread and became a pest. Cochineal infestation continued to expand after the cochineal business had ended. Control measures were unsuccessful and by 2014 about 16,000 hectares (62 sq mi) of cactus land had become infested with cochineal.[24]

The two principal forms of cochineal dye are cochineal extract, a colouring made from the raw dried and pulverised bodies of insects, and carmine, a more purified colouring made from the cochineal. To prepare carmine, the powdered insect bodies are boiled in ammonia or a sodium carbonate solution, the insoluble matter is removed by filtering, and alum is added to the clear salt solution of carminic acid to precipitate the red aluminium salt. Purity of colour is ensured by the absence of iron. Stannous chloride, citric acid, borax, or gelatin may be added to regulate the formation of the precipitate. For shades of purple, lime is added to the alum.[4]

As of 2005,[needs update] Peru produced 200 tons of cochineal dye per year and the Canary Islands produced 20 tons per year.[9][21] Chile and Mexico also export cochineal.[1] In Mexico, production and exportation of the dye has been found to lower poverty and improve female literacy.[26] France is believed to be the world's largest importer, and Japan and Italy also import the insect. Much of these imports are processed and re-exported to other developed economies.[21] As of 2005,[needs update] the market price of cochineal was between US$50 and 80 per kilogram,[needs update][18] while synthetic raw food dyes are available at prices as low as $10â€“20 per kilogram.[27]

Traditionally, cochineal was used for colouring fabrics. During the colonial period, with the introduction of sheep to Latin America, the use of cochineal increased, as it provided the most intense colour and it set more firmly on woolen garments than on clothes made of materials of pre-Hispanic origin such as cotton or agave and yucca fibers. In general, cochineal is more successful on protein-based animal fibres (including silk) than plant-based material. Once the European market discovered the qualities of this product, the demand for it increased dramatically. By the beginning of the 17th century, it was traded internationally.[6] Carmine became strong competition for other colourants such as madder root, kermes, Polish cochineal, Armenian cochineal, brazilwood, and Tyrian purple,[28] as they were used for dyeing the clothes of kings, nobles, and the clergy. For the past several centuries, it was the most important insect dye used in the production of hand-woven oriental rugs, almost completely displacing lac.[6] It was also used for painting, handicrafts, and tapestries.[8] Cochineal-coloured wool and cotton are important materials for Mexican folk art and crafts.[29][30]

Cochineal is used as a fabric and cosmetics dye and as a natural food colouring. It is also used in histology as a preparatory stain for the examination of tissues and carbohydrates.[31] In artists' paints, it has been replaced by synthetic reds and is largely unavailable for purchase due to poor lightfastness. Natural carmine dye used in food and cosmetics can render the product unacceptable to vegetarian or vegan consumers. Many Muslims consider carmine-containing food forbidden (haraam) because the dye is extracted from insects and all insects except the locust are haraam in Islam.[32] Jews also avoid food containing this additive, though it is not treif, and some authorities allow its use because the insect is dried and reduced to powder.[33]

Cochineal is one of the few water-soluble colourants to resist degradation with time. It is one of the most light- and heat-stable and oxidation-resistant of all the natural organic colourants and is even more stable than many synthetic food colours.[34] The water-soluble form is used in alcoholic drinks with calcium carmine; the insoluble form is used in a wide variety of products. Together with ammonium carmine, they can be found in meat, sausages, processed poultry products (meat products cannot be coloured in the United States unless they are labeled as such), surimi, marinades, alcoholic drinks, bakery products and toppings, cookies, desserts, icings, pie fillings, jams, preserves, gelatin desserts, juice beverages, varieties of cheddar cheese and other dairy products, sauces, and sweets.[34]

Carmine is considered safe enough for cosmetic use in the eye area.[35] A significant proportion of the insoluble carmine pigment produced is used in the cosmetics industry for hair- and skin-care products, lipsticks, face powders, rouges, and blushes.[34] A bright red dye and the stain carmine used in microbiology is often made from the carmine extract, too.[16] The pharmaceutical industry uses cochineal to colour pills and ointments.[21]

In spite of the widespread use of carmine-based dyes in food and cosmetic products, a small number of people have been found to experience occupational asthma, food and cosmetic allergies (such as allergic rhinitis and cheilitis), IgE-mediated respiratory hypersensitivity, and in rare cases anaphylactic shock.[36][37][38] In 2009 the FDA ruled that labels of cosmetics and food that include cochineal extract must include that information on their labels (under the name "cochineal extract" or "carmine").[39][40] In 2006 the FDA stated it found no evidence of a "significant hazard" to the general population.[41] In the EU authorities list carmine as additive E 120 in the list of EU-approved food additives.[42] An artificial, non-allergenic cochineal dye is labeled E 124.[36] The directive governing food dyes approves the use of carmine for certain groups of foods only, but is still found in several products particularly alcoholic beverages.[citation needed]