Merry Christmas (Mariah Carey album)

juli 29th, 2016

Merry Christmas is the first Christmas album, and the fourth studio album, by American singer and songwriter Mariah Carey. Released by Columbia Records on November 1, 1994, the album features cover versions of popular Christmas tunes and original material. Carey worked with Walter Afanasieff, with whom she wrote all of the original tracks, as well as producing Carey’s interpretations of the covered material. The album contains a contemporary holiday theme, and featured ”authentic, gospel flavored background vocals”. The album received generally positive reviews and became a worldwide success. Critics praised Carey’s uplifting and flavored vocals, as well as her skilled songwriting alongside Afanasieff. Three singles were released from the album, of which All I Want for Christmas Is You went on to become one of the best-selling singles of all time.
Merry Christmas was released at the peak of the initial stretch of Carey’s career, between Music Box (1993) and Daydream (1995). The album produced the worldwide classic single, ”All I Want for Christmas Is You”, which became the best-selling holiday ringtone in the US. The album has sold 5,500,000 copies in the United States as of December 2015 according to Nielsen SoundScan, and has been certified five-times Platinum by the Recording Industry Association of America (RIAA) for shipment of five million copies in the United States. In Japan, Merry Christmas has sold 2,500,000 copies and is the fourth best-selling album of all time by a non-Asian solo artist, behind Carey’s other release #1’s (1998) bottega taschen, Whitney Houston’s The Bodyguard and Carey’s Daydream. Merry Christmas has sold 15 million copies worldwide and is the best-selling Christmas album of all time.
A Deluxe Anniversary Edition was released on October 23, 2015.

Carey has expressed her belief in God and her connection between music and spirituality, and felt the album was finally a way to portray her mysticism into music. After the success of Carey’s previous effort, Music Box, there was speculation of a new project in the works; however it was not until October 1994, only one month before the album’s release, that Billboard announced Carey would be releasing a holiday album for the Christmas season. Initially, critics were shocked; they did not know how Carey would fare as an entertainer, as she had previously only been viewed as a pop star. Nevertheless, Carey, unaffected by the speculation, continued working on, and promoting the album in high spirits, confident in her work. The idea proved to be wise, earning Carey recognition in various markets including Christian radio and contemporary R&B stations, as well as extended her fame in Japan, where the album experienced much of its success.
Throughout the album’s development, Carey worked extensively with Walter Afanasieff, with whom she collaborated extensively on Emotions (1991) and Music Box (1993). Together, they wrote all three of the album’s original songs, as well as producing most of the traditional tracks. ”All I Want for Christmas Is You”, the album’s debut single, was written by Carey and Afanasieff, which was sent to top-forty and adult contemporary stations, with the video having been filmed the year before. Another track they wrote, ”Miss You Most (At Christmas Time)”, was sent to R&B stations, with ”Jesus Born on This Day”, another original song, being sent to Christian and gospel radio stations around the world.
Additionally, Carey recorded a cover of ”Christmas (Baby Please Come Home)” by Darlene Love, as well as classics such as ”Silent Night”, ”O Holy Night” and ”Joy to the World”. The latter song, which was used as a promotional single, was remixed several times and sent to various clubs; adding to the album’s range of listeners. Record producer and composer, Loris Holland, co-produced some of the albums gospel flavored tracks, including ”Silent Night”, where he arranged the backing vocals and synthesizers. Carey’s rendition of ”Santa Claus Is Coming to Town”, was deemed as ”one of the more playful tracks on the album”, alongside ”Christmas (Baby Please Come Home)”.
Merry Christmas boasted a variety of musical arrangements, sounds and genres. Carey’s goal was to provide an album that would have a ”Christmas feel”, providing a mixture of soulful tracks, as well as fun and joyous holiday treats. The song ”Jesus, Oh What a Wonderful Child”, was described as an original track that ”really took flight”. The song was recorded in a church, with many live back-up singers and children playing tambourines and other melodious instruments. The goal was to produce a ”real church flavored song”, in which Afanasieff played the keyboards and allowed Carey’s voice to ”cut loose”. According to Chris Nickson, Carey’s love of gospel music came through on the track, writing, ”[she] led the band without pushing herself forward, letting the song develop and work out, trading lines with the chorus until, after the crescendo, the musicians moved into a fast double time to the end.”
”You have to have a nice balance between standard Christian hymns and fun songs. It was definitely a priority for me to write at least a few new songs, but for the most part people really want to hear the standards at Christmas, no matter how good a new song is.”
The album’s lead track, ”All I Want for Christmas Is You”, was described as an ”up-tempo love song, one that could have easily been written for Tommy Mottola.” Another one of the album’s original tracks was, ”Miss You Most (At Christmas Time)”, which was very different from its whimsical predecessor. The song was described as a ”sad ballad”, in line with many of Carey’s previous hit singles. The song featured a synthesized orchestra, including keyboard notes courtesy of Afanasieff, during which Carey would sing to her ”long-gone lover, crystallizing the way that Christmas brought memories of the past into focus.” According to Nickson, it was ”Jesus Born on This Day”, that was the most impressive original track on the album. It was described as a ”full-blown production number”, which again featured synthesized orchestra, as well as a live children’s choir. The song’s tune was described as ”solemn and hymn-like, but the arrangement, oddly, made it less religious and rather more glitzy, behind the lyrics that overtly praised Jesus.”
The album garnered generally positive reviews from music critics. Barry Schwartz, editor of Stylus Magazine, gave the album a very positive review, praising Carey’s vocals, the album’s authenticity and songwriting. Aside from the album, Schwartz lauded ”All I Want for Christmas Is You”: ”To say this song is an instant classic somehow doesn’t capture its amazingicity; it’s a modern standard: joyous, exhilarating, and loud jimmy choo bags, with even a hint of longing (ooh longing!). She sings, ‘I don’t want a lot for Christmas / I won’t even wish for snow,’ such a beautiful phrase delivered with full sincerity over rolling pianos, spine-squashing tympanis, philharmonic strings, and a quasi-wall of sound—and Mariah’s gorgeous voice bursts through it all. Rats, why haven’t I been celebrating Christmas?!” J.D. Considine from The Baltimore Sun said that the album ”may look like just another attempt to cash in on Christmas cheer, but is actually the work of someone who genuinely loves this music. Granted, Carey’s gospel inclinations come through a lot stronger than might be expected on traditional tunes like ‘Silent Night’, but that hardly diminishes the effect of her performance; in fact, her soulful ornamentation adds oomph to the reading of ‘O Holy Night’. But the album’s real strength is the conviction she brings to otherwise corny fare like ‘Santa Claus Is Comin’ to Town’, while the way she augments ‘Joy to the World’ with a bit of the Three Dog Night hit is pure genius.”
The album received a less enthusiastic review from Roch Parisien of AllMusic, who praised ”All I Want for Christmas Is You”, writing, ”On the positive side, her co-penned (one of three) ‘All I Want for Christmas Is You’ is a well-crafted Phil Spector tribute, with Beach Boys-style harmonies, jangling bells, and a sleigh-ride pace, injecting one of the few bits of exuberant fun in this otherwise vanilla set.” However, he was more critical of Carey’s take on ”O Holy Night” and ”Joy to the World”, writing, ”Pretensions to high opera on ‘O Holy Night’ and a horrid dance club take on ‘Joy to the World’.” Steve Morse from The Boston Globe commented ”Her early albums were often polished to a fault, but she cuts loose with unbridled soul on the new Christmas disc. Oddly enough, it may be her best album. She blends original songs (such as ‘All I Want for Christmas Is You’, which debuted in video form on MTV [at the time]) with traditional carols (‘Silent Night’ and ‘Joy to the World’) and even Phil Spector’s Yuletide classic, ‘Christmas (Baby Please Come Home)’.” Jon Pareles of The New York Times wrote ”There are gospelly versions of familiar carols like ‘Silent Night’, dramatic ballads like her own ‘Miss You Most (At Christmas Time)’, and uptempo imitations, with chimes, of Phil Spector’s 1963 Christmas album, like ‘Santa Claus Is Comin’ to Town’. Regardless of backup, Ms. Carey oversings, glutting songs with her vocal tics—like sliding down from the note above the melody note—and turning expressions of devotion into narcissistic displays.”
Merry Christmas debuted at number thirty on the US Billboard 200 with 45,000 copies sold in its first week. In its fifth week, the album peaked at number three, with sales of 208,000 copies, but experienced its highest sales in its sixth week (when it was at number six), with another 500,000 copies sold. The album was the second best-selling holiday album that year with a total of 1 giuseppe zanotti shoes,859,000 copies sold. It remained in the top twenty for eight weeks and on the Billboard 200 for thirteen weeks, re-entering the chart three times; peaking at number 149 the first time, 115 the second and at 61 the third (it has spent a total of fifty-five weeks on the chart). On January 30, 2003, Merry Christmas was certified five-times Platinum by the Recording Industry Association of America (RIAA) for shipment of five million copies in the US. As of December 2015

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, the album has sold 5,500,000 copies in the US and is one of the best-selling holiday albums in the United States. In Europe, Merry Christmas experienced success, being certified gold in Austria, Germany, Switzerland and United Kingdom. In Australia, the album was certified six-times platinum, denoting shipments of 420,000 copies and finishing 11th on the Australian Recording Industry Association (ARIA) 1994 End of Year Chart.
Outside the United States, the album experienced its highest sales in Japan, where it sold 2.5 million copies and became the fourth best-selling album by a non-Asian solo artist. Additionally, the album’s lead single ”All I Want for Christmas Is You” was certified the ”Million” award, The single achieved similar success around the world, where it reached the top-five position in most countries, as well as re-entering many times throughout the years. In the US, ”All I Want for Christmas Is You” is one of the few songs in recent years to be considered a classic and is the only holiday song and ringtone to reach multi-platinum status in the US. Merry Christmas has sold 15 million copies worldwide, and is the best-selling Christmas album of all time.
Carey is currently developing a musical film based on Merry Christmas. The plot revolves around a small town—perhaps not unlike Carey’s hometown of Huntington, New York—where a ruthless developer wants to turn the land into a large shopping plaza. ”Mariah doesn’t want to let that happen,” says her producing partner Benny Medina. ”Her character uses song and love to keep the Christmas spirit alive.”
According to Carey, the script will be written by High School Musical writer Peter Barsocchini, but is still in its early stages of production. However, Carey gave Daily News a few more details regarding the project, saying, ”Since I recorded the Christmas album, I’ve always wanted to make a movie to go with it, something that people could watch and hear and enjoy every year. I’m into it. I’m all about the holiday season.”
Credits adapted from AllMusic.
*sales figures based on certification alone ^shipments figures based on certification alone xunspecified figures based on certification alone

Adrian Feint

juli 28th, 2016

Adrian Feint (28 June 1894 – 25 April 1971) was an Australian artist born in Narrandera, New South Wales. He worked in various media, but is noted for his bookplate designs.

Feint studied at Sydney Art School from 1911 under Julian Ashton and Elioth Gruner. In 1916, Feint enlisted with the Australian Imperial Forces, and was sent to France with the 15th Field Ambulance paul frank t shirts. Before being demobbed in 1919, he was granted three months leave to study at the Académie Julien in Paris. He studied plate etching from 1922 to 1926; woodblock-engraving from 1926 to 1928, with assistance from Thea Proctor in 1927; and oil painting beginning in 1938, with Margaret Preston.
He was co-director (with bookbinder Wal Taylor) and manager of Grosvenor Gallery, Sydney, from 1924–28. Exhibitors included the now-famous Thea Proctor, Elioth Gruner, Margaret Preston, Roland Wakelin, Roy de Maistre and G W Lambert.
He was employed as assistant editor (to Sydney Ure Smith) of Art in Australia from 1928–40, contributing many cover illustrations to this and filling many commissions for his advertising agency Smith and Julius Karen Millen Online. Between 1927 and 1939, Feint made 18 covers for Ure Smith’s magazine The Home, including the famous illustration on the October 1928 issue in collaboration with Hera Roberts.
He abandoned graphic arts around 1939 (he reworked one bookplate in 1944) to work as a bookbinder with Benjamin Waite and to illustrate limited edition books. After World War II he took up flower painting in watercolours, then oil-painting, but without critical acclaim in this last medium under armour shoes us.
Feint’s bookplates are his greatest legacy. Thea Proctor, Dorothea Mackellar, Ethel Turner, Ethel Curlewis, John Lane Mullins, Frank Clune, Peter Tansey and the Duke and Duchess of York were among those who commissioned personal ex libris plates. In 1930 his bookplate designs were recognised by an exhibition at the Division of Fine Arts, Library of Congress, Washington US (organised by the American Society of Bookplate Collectors and Designers), and in 1933 were highlights of the first International Exhibition of Bookplates held in Sydney. They are prized by collectors such as members of the American Society of Bookplate Collectors and Designers and the New Australian Bookplate Collectors Society. According to the checklist compiled by Thelma Clune, he produced 221 commissioned bookplates. Apart from Norman Lindsay, the only other Australian artist whose bookplates command anywhere the same interest is G D Perrottet.
”Tony’s Book”
David Robertson
Bertram Norris
M. I. Humphries
Dorothea MacKellar
Feint was elected to the Society of Artists, and was a member of the Australian Painter-Etchers Society.

National Rail

juli 20th, 2016

National Rail ist ein unternehmensübergreifender Markenname der in der Association of Train Operating Companies vertretenen britischen Eisenbahngesellschaften. Der Markenname und die Verwertungsgesellschaft sind im gemeinsamen Besitz dieser Gesellschaften, die nach der Privatisierung der Staatsbahn British Rail entstanden sind. Der Begriff wird üblicherweise verwendet, um sich von jenen Bahnangeboten abzuheben, die ihren Ursprung nicht bei British Rail haben. Diese Unterscheidung ist wichtig, da die Mitgliedsgesellschaften von National Rail ein gemeinsames Tarifsystem besitzen und ihre Fahrscheine untereinander anerkennen (deren Gültigkeit erstreckt sich normalerweise zwar nicht auf die Angebote von Nichtmitgliedern, vereinzelt werden aber auch auf den eigentlich nicht durch das Angebot abgedeckten Strecken geltende, durchgehende Tickets angeboten).

Der Begriff National Rail ist nicht zu verwechseln mit dem Begriff Network Rail. National Rail ist ein Markenname für die Bezeichnung der Gesamtheit aller Personenverkehrsangebote der meisten Bahngesellschaften. Network Rail hingegen ist als Eisenbahninfrastrukturunternehmen eine juristische Person, welche die festen Anlagen auf dem britischen Eisenbahnnetz besitzt.
Die Netze von National Rail und Network Rail sind in geographischer Hinsicht sehr ähnlich, jedoch nicht ganz deckungsgleich. Auf den meisten Strecken von Network Rail gibt es Güterverkehr, auf einigen gibt es ausschließlich Güterverkehr. Einige Strecken werden nicht durch das Angebot von National Rail abgedeckt, dazu zählen insbesondere der Channel Tunnel Rail Link, der Heathrow Express, die Tyne and Wear Metro und die London Underground. Umgekehrt wiederum gibt es Angebote von National Rail, die nicht auf dem Streckennetz von Network Rail verkehren (z.B. die East London Line von London Overground).
Siehe auch: Liste von Eisenbahngesellschaften im Vereinigten Königreich
Züge mit Personenverkehr auf dem Streckennetz von National Rail werden durch 25 privatwirtschaftlich organisierte Bahngesellschaften betrieben. Die Association of Train Operating Companies (ATOC) vertritt die gemeinsamen Interessen der Bahngesellschaften und führt einige zentralisierte Funktionen aus, wie z. B. die Herausgabe eines landesweiten Fahrplans. National Rail verwendet als Erkennungszeichen auf Gebäuden sowie Dokumenten wie Fahrkarten das alte Doppelpfeil-Logo von British Rail weiter.
Der Betrieb von British Rail erstreckte sich nie auf Nordirland. Dieser Landesteil besitzt eine eigene Bahngesellschaft, die Northern Ireland Railways (NIR). Als Konsequenz davon gehört NIR nicht zum Verbund von National Rail.
Mehrere britische Städte besitzen eigene U-Bahnen, Stadtbahnen oder Straßenbahnen, die ebenfalls nicht zum Netz von National Rail gehören. Dies sind Docklands Light Railway, Glasgow Subway, London Underground, Manchester Metrolink, Midland Metro, Nottingham Express Transit, Sheffield Supertram, Tramlink und Tyne and Wear Metro.
Ebenfalls nicht zum Verbund von National Rail gehören Eurostar und Heathrow Express, der schnelle Zubringer zum Flughafen London-Heathrow. Darüber hinaus gibt es eine große Anzahl privat betriebener Bahnen oder Museumsbahnen, deren Tarifsysteme ebenfalls unabhängig sind.
Die Mitglieder von National Rail verwenden ein einheitliches Tarifsystem, das von British Rail übernommen wurde. Fahrscheine sind zwischen allen Bahnhöfen auf dem Netz von Network Rail erhältlich und können an jedem beliebigen Bahnhof gekauft werden. Die Fahrscheine sind im Allgemeinen bei allen Bahngesellschaften gültig, die auf der gewählten Strecke verkehren. Abweichungen von dieser Regel sind auf dem Fahrschein unter dem Feld „Route“ vermerkt. Statt „ANY PERMITTED“ wird dann etwa „NXEA TRAINS ONLY“ oder „GRAND CTRL ONLY“ vermerkt.
Dies ist etwa der Fall auf der Strecke zwischen London und dem Flughafen London-Gatwick. Hier geben seit März 2006 drei verschiedene Gesellschaften (First Capital Connect, Southern, Gatwick Express) Fahrscheine heraus, die jeweils nur in ihren eigenen Zügen gültig sind (es gibt jedoch eine Variante, die für alle drei Gesellschaften gilt). Auch für Strecken, auf denen Open-Access-TOCs verkehren (etwa Grand Central Trains), können vergünstigte TOC-gebundene Fahrscheine gekauft werden.
Da die Bahnunternehmen den Kunden gegenüber einheitlich auftreten, erfolgt die Ausschüttung der Erlöse über die Association of Train Operating Companies. Sitzplatzreservierungen sind im Allgemeinen kostenfrei.
Zurzeit wird die sogenannte Integrated Transport Smartcard Organisation (ITSO)-Smartcard eingeführt, mit der im Eisenbahnverkehr bargeldlos bezahlt werden kann. Im Großraum London kann im National Rail-Netz die Oyster Card bereits jetzt sowohl als Zeitkarte (Travelcard) als auch als Einzelfahrschein (Pay As You Go) genutzt werden. Lesegeräte dafür sind an jedem Bahnhof in den Londoner Tarifzonen 1-9 installiert. Dies gilt jedoch nur für den Nahverkehr; Strecken des Fernverkehrs auch innerhalb Londons, wie von Southeastern auf der High Speed 1 zwischen St. Pancras International und Stratford International, unterliegen einem gesonderten Tarif.

Yde et Olive

juli 20th, 2016

Yde et Olive is a thirteenth-century Old French chanson de geste. It is a sequel to Huon de Bordeaux and follows the Chanson d’Esclarmonde, the story of Huon’s wife, and Clarisse et Florent, the story of Yde’s parents, in the cycle. The poem is punctuated by a poem titled Croissant, which some scholars have named a separate chanson and which tells the story of Yde and Olive’s son, after which the main story of Yde et Olive picks up again. It is perhaps the earliest Old French adaptation of the myth of Iphis. This myth is found in Ovid’s Metamorphoses (Ipthis and Ianthe) but other ancient Indian sources and no sources at all have also been suggested for the chanson. Yde et Olive is a relatively unstudied chanson, with only one critically edited published text, Max Schweigel’s from 1889, one unpublished edition from a 1977 dissertation by Barbara Anne Brewka at Vanderbilt University, a recent unpublished edition and translation into modern English from a 2015 MA thesis by Mounawar Abbouchi at The University of Georgia.
The story of Yde and Olive was worked into dramatic form in the Miracle de la fille d’un roy (1454). It does not significantly deviate from the chanson except in its finale. In the early sixteenth century it was printed as part of Les prouesses et faictz merveilleux du noble huon de bordeaulx, which was translated into English and printed as The Boke of Duke Huon of Burdeux by John Bourchier, Lord Berners, for Francis Hastings, Earl of Huntingdon, early in the century, to be printed twice more, c. 1570 and in 1601.
There are two extant manuscripts: Paris, Bibliothèque nationale de France, français, 1451, f. 225r |N| (short resumé of the text); Turin, Biblioteca nazionale universitaria, L. II. 14, f. 389va-395va et 397rb-399va |N|
The marriage of Florent to Clarisse is briefly recounted. A triumphant Florent returns to Aragon and is crowned king after the death of his father, Garin. Shortly after, Clarisse finds herself with child, but fears her pregnancy, and with good reason as the queen dies giving birth to a daughter named Yde. Florent goes into prolongued mourning, ignoring his king and fatherly duties, and refusing to remarry in order to produce a male heir. However, as Yde grows into a young woman much like her mother, her father falls in love with her and plans to marry her. Horrified by the prospect, Yde disguises herself as a man, steals her father’s horse, and flees the country. She embarks on a series of chivalric adventures that eventually land her in Rome, where she begins to serve the king, Oton. Impressed by her valour, Oton decides to marry Yde to his one and only daughter, Olive, and make her his heir. Though she initially opposes the idea, Yde surrenders to wed Olive. The couple practice abstinence for fifteen days after their wedding, but Yde finally finds herself unable to resist her wife’s urging that they consummate the marriage and confesses her secret to Olive. The latter reassures her that her secret is safe, but their conversation is overheard and reported to the king, who vows to have them both burned if the story is true. In order to learn the truth, Oton summons Yde to bathe with him. The two girls believe that all is lost and pray for salvation, and at the last minute, an angel descends from heaven to appeal to the king not to test such a tried and true vassal. The angel then announces that Yde is now a man, that Oton will die eight days hence, and that Yde and Olive will conceive a child who will be named Croissant that very night.
The episode some scholars have called Croissant follows telling of the deeds of Yde and Olive’s son. The Yde et Olvie narrative then picks up with Florent dead and Yde returning to Aragon as the rightful heir to claim his throne.
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Miracle Play

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Jon MacLellan

juli 20th, 2016

Jon MacLellan is an English computer game level designer. He is best known for his time while working in England for Epic Games’ sales, webmaster and technical support office where he was an active part of the game communities surrounding the game studio’s games Jazz Jackrabbit 2, and Unreal. He is also credited as a level designer for the titles Jazz Jackrabbit 2, Jazz Jackrabbit 2: The Secret Files, and Jazz Jackrabbit 2: Holiday Hare ’98.
Even after his time at Epic Games, Jon continued to be a part of the Jazz Jackrabbit 2 online community, releasing several unofficial custom-made levels to the community. He was also a founder of the level design group concept within the Jazz 2 community, forming the level design group Mystic Legends; a Jazz 2 community level design group where all members would release their levels under this group-name.
When Epic Games decided to shift its focus away from the shareware model and concentrate solely on game design, Jon moved to the United States and for a time worked with MPath Interactive’s Xtreme Network and GameSpy Industries on some of their high profile gaming news websites.
Jon currently resides with his family in Sacramento, CA.

Neurodegeneration

juli 20th, 2016

Neurodegeneration is the umbrella term for the progressive loss of structure or function of neurons, including death of neurons. Many neurodegenerative diseases including amyotrophic lateral sclerosis, Parkinson’s, Alzheimer’s, and Huntington’s occur as a result of neurodegenerative processes. Such diseases are incurable, resulting in progressive degeneration and/or death of neuron cells. As research progresses, many similarities appear that relate these diseases to one another on a sub-cellular level. Discovering these similarities offers hope for therapeutic advances that could ameliorate many diseases simultaneously. There are many parallels between different neurodegenerative disorders including atypical protein assemblies as well as induced cell death. Neurodegeneration can be found in many different levels of neuronal circuitry ranging from molecular to systemic.

Many neurodegenerative diseases are caused by genetic mutations, most of which are located in completely unrelated genes. In many of the different diseases, the mutated gene has a common feature: a repeat of the CAG nucleotide triplet. CAG encodes for the amino acid glutamine. A repeat of CAG results in a polyglutamine (polyQ) tract. Diseases showing this are known as polyglutamine diseases.
Several neurodegenerative diseases are classified as proteopathies as they are associated with the aggregation of misfolded proteins.
Parkinson’s disease and Huntington’s disease are both late-onset and associated with the accumulation of intracellular toxic proteins. Diseases caused by the aggregation of proteins are known as proteinopathies, and they are primarily caused by aggregates in the following structures:
There are two main avenues eukaryotic cells use to remove troublesome proteins or organelles:
Damage to the membranes of organelles by monomeric or oligomeric proteins could also contribute to these diseases. Alpha-synuclein can damage membranes by inducing membrane curvature, and extensive tubulation and vesiculation were observed when these proteins were incubated with artificial phospholipid vesicles.
The most common form of cell death in neurodegeneration is through the intrinsic mitochondrial apoptotic pathway. This pathway controls the activation of caspase-9 by regulating the release of cytochrome c from the mitochondrial intermembrane space (IMS). Reactive oxygen species (ROS) are normal byproducts of mitochondrial respiratory chain activity. ROS concentration is mediated by mitochondrial antioxidants such as manganese superoxide dismutase (SOD2) and glutathione peroxidase. Over production of ROS (oxidative stress) is a central feature of all neurodegenerative disorders. In addition to the generation of ROS, mitochondria are also involved with life-sustaining functions including calcium homeostasis, PCD, mitochondrial fission and fusion, lipid concentration of the mitochondrial membranes, and the mitochondrial permeability transition. Mitochondrial disease leading to neurodegeneration is likely, at least on some level, to involve all of these functions.
There is strong evidence that mitochondrial dysfunction and oxidative stress play a causal role in neurodegenerative disease pathogenesis, including in four of the more well known diseases Alzheimer’s, Parkinson’s, Huntington’s, and Amyotrophic lateral sclerosis.
Axonal swelling and spheroids have been observed in many different neurodegenerative diseases. This suggests that defective axons are not only present in diseased neurons, but also that they may cause certain pathological insult due to accumulation of organelles. Axonal transport can be disrupted by a variety of mechanisms including damage to: kinesin and cytoplasmic dynein, microtubules, cargoes, and mitochondria. When axonal transport is severely disrupted a degenerative pathway known as Wallerian-like degeneration is often triggered.
Programmed cell death (PCD) is death of a cell in any form, mediated by an intracellular program. This process can be activated in neurodegenerative diseases including Parkinson’s disease, amytrophic lateral sclerosis, Alzheimer’s disease and Huntington’s disease. There are, however, situations in which these mediated pathways are artificially stimulated due to injury or disease.
Apoptosis is a form of programmed cell death in multicellular organisms. It is one of the main types of programmed cell death (PCD) and involves a series of biochemical events leading to a characteristic cell morphology and death.
Caspases (cysteine-aspartic acid proteases) cleave at very specific amino acid residues. There are two types of caspases: initiators and effectors. Initiator caspases cleave inactive forms of effector caspases. This activates the effectors that in turn cleave other proteins resulting in apoptotic initiation.
Autophagy is essentially a form of intracellular phagocytosis in which a cell actively consumes damaged organelles or misfolded proteins by encapsulating them into an autophagosome, which fuses with a lysosome to destroy the contents of the autophagosome. Many neurodegenerative diseases show unusual protein aggregates. This could potentially be a result of underlying autophagic defect common to multiple neurodegenerative diseases. It is important to note that this is a hypothesis, and more research must be done.
The final and least understood PCD mechanism is through non-apoptotic processes. These fall under Type III, or cytoplasmic cell death. Many other forms of PCD are observed but not fully understood or accepted by the scientific community. For example, PCD might be caused by trophotoxicity, or hyperactivation of trophic factor receptors. In addition to this, other cytotoxins that induce PCD at low concentrations act to cause necrosis, or aponecrosis – the combination of apoptosis and necrosis, when in higher concentrations. It is still unclear exactly what combination of apoptosis, non-apoptosis, and necrosis causes different kinds of aponecrosis.
In the above mentioned neurodegenerative diseases, PCD may be pathogenic. In order to identify the potential of neuroprotective targets in PCD machinery, there were experimental models conducted on these neurodegenerative diseases. These studies showed that the expression of certain components have been altered by genetic and pharmacological means. Expression of PCD molecular components are said to be controlled by gene and antisense therapy, but this needs further research. Pharmacological approaches involve inhibitors of caspase activity, and caspase inhibition might delay cell death in the different experimental models.
Alzheimer’s disease is characterised by loss of neurons and synapses in the cerebral cortex and certain subcortical regions. This loss results in gross atrophy of the affected regions, including degeneration in the temporal lobe and parietal lobe, and parts of the frontal cortex and cingulate gyrus.
Alzheimer’s disease has been hypothesized to be a protein misfolding disease (proteopathy), caused by accumulation of abnormally folded A-beta and tau proteins in the brain. Plaques are made up of small peptides, 39–43 amino acids in length, called beta-amyloid (also written as A-beta or Aβ). Beta-amyloid is a fragment from a larger protein called amyloid precursor protein (APP), a transmembrane protein that penetrates through the neuron’s membrane. APP is critical to neuron growth, survival and post-injury repair. In Alzheimer’s disease, an unknown process causes APP to be divided into smaller fragments by enzymes through proteolysis. One of these fragments gives rise to fibrils of beta-amyloid, which form clumps that deposit outside neurons in dense formations known as senile plaques.
Parkinson’s disease is the second most common neurodegenerative disorder and manifests as bradykinesia, rigidity, resting tremor and posture instability. The crude prevalence rate of PD has been reported to range from 15 per 100,000 to 12,500 per 100,000, and the incidence of PD from 15 per 100,000 to 328 per 100,000, with the disease being less common in Asian countries. Parkinson’s disease is a degenerative disorder of the central nervous system. It results from the death of dopamine-generating cells in the substantia nigra, a region of the midbrain; the cause of cell-death is unknown. The following paragraph is an excerpt from the Pathophysiology section of the article Parkinson’s disease.
The mechanism by which the brain cells in Parkinson’s are lost may consist of an abnormal accumulation of the protein alpha-synuclein bound to ubiquitin in the damaged cells. The alpha-synuclein-ubiquitin complex cannot be directed to the proteosome. This protein accumulation forms proteinaceous cytoplasmic inclusions called Lewy bodies. The latest research on pathogenesis of disease has shown that the death of dopaminergic neurons by alpha-synuclein is due to a defect in the machinery that transports proteins between two major cellular organelles — the endoplasmic reticulum (ER) and the Golgi apparatus. Certain proteins like Rab1 may reverse this defect caused by alpha-synuclein in animal models.
Recent research suggests that impaired axonal transport of alpha-synuclein leads to its accumulation in the Lewy bodies. Experiments have revealed reduced transport rates of both wild-type and two familial Parkinson’s disease-associated mutant alpha-synucleins through axons of cultured neurons. Membrane damage by alpha-synuclein could be another Parkinson’s disease mechanism.
The main known risk factor is age. Susceptibility genes including α-synuclein, leucine-rich repeat kinase 2 (LRRK-2), and glucocerebrosidase (GBA) have shown that genetic predisposition is another important causal factor.
The following paragraph is an excerpt from the Mechanism section of the article Huntington’s disease.
HD causes astrogliosis and loss of medium spiny neurons. Areas of the brain are affected according to their structure and the types of neurons they contain, reducing in size as they cumulatively lose cells. The areas affected are mainly in the striatum, but also the frontal and temporal cortices. The striatum’s subthalamic nuclei send control signals to the globus pallidus, which initiates and modulates motion. The weaker signals from subthalamic nuclei thus cause reduced initiation and modulation of movement, resulting in the characteristic movements of the disorder.
Mutant Huntingtin is an aggregate-prone protein. During the cells’ natural clearance process, these proteins are retrogradely transported to the cell body for destruction by lysosomes. It is a possibility that these mutant protein aggregates damage the retrograde transport of important cargoes such as BDNF by damaging molecular motors as well as microtubules.
Amyotrophic lateral sclerosis (ALS or Lou Gehrig’s Disease) is a disease in which motor neurons are selectively targeted for degeneration. In 1993, missense mutations in the gene encoding the antioxidant enzyme Cu/Zn superoxide dismutase 1 (SOD1) were discovered in subsets of patients with familial ALS. This discovery led researchers to focus on unlocking the mechanisms for SOD1-mediated diseases. However, the pathogenic mechanism underlying SOD1 mutant toxicity has yet to be resolved. More recently, TDP-43 and FUS protein aggregates have been implicated in some cases of the disease, and a mutation in chromosome 9 (C9orf72) is thought to be the most common known cause of sporadic ALS.
Recent independent research by Nagai et al. and Di Giorgio et al. provide in vitro evidence that the primary cellular sites where SOD1 mutations act are located on astrocytes. Astrocytes then cause the toxic effects on the motor neurons. The specific mechanism of toxicity still needs to be investigated, but the findings are significant because they implicate cells other than neuron cells in neurodegeneration.
The greatest risk factor for neurodegenerative diseases is aging. Mitochondrial DNA mutations as well as oxidative stress both contribute to aging. Many of these diseases are late-onset, meaning there is some factor that changes as a person ages for each disease. One constant factor is that in each disease, neurons gradually lose function as the disease progresses with age.
The process of neurodegeneration is not well-understood so the diseases that stem from it have, as yet, no cures. In the search for effective treatments (as opposed to palliative care), investigators employ animal models of disease to test potential therapeutic agents. Model organisms provide an inexpensive and relatively quick means to perform two main functions: target identification and target validation. Together, these help show the value of any specific therapeutic strategies and drugs when attempting to ameliorate disease severity. An example is the drug Dimebon (Medivation). This drug is in phase III clinical trials for use in Alzheimer’s disease, and also recently finished phase II clinical trials for use in Huntington’s disease. In March 2010, the results of a clinical trial phase III were released; the investigational Alzheimer’s disease drug Dimebon failed in the pivotal CONNECTION trial of patients with mild-to-moderate disease. With CONCERT, the remaining Pfizer and Medivation Phase III trial for Dimebon (latrepirdine) in Alzheimer’s disease failed in 2012, effectively ending the development in this indication.
In another experiment using a rat model of Alzheimer’s disease, it was demonstrated that systemic administration of hypothalamic proline-rich peptide (PRP)-1 offers neuroprotective effects and can prevent neurodegeneration in hippocampus amyloid-beta 25–35. This suggests that there could be therapeutic value to PRP-1.
Protein degradation offers therapeutic options both in preventing the synthesis and degradation of irregular proteins. There is also interest in upregulating autophagy to help clear protein aggregates implicated in neurodegeneration. Both of these options involve very complex pathways that we are only beginning to understand.
The goal of immunotherapy is to enhance aspects of the immune system. Both active and passive vaccinations have been proposed for Alzheimer’s disease and other conditions, however more research must be done to prove safety and efficacy in humans.

Hirschberg (Kaufunger Wald)

juli 20th, 2016

Blick aus Richtung Osten vom Heiligenberg (am Hohen Meißner) zum Hirschberg
Der Hirschberg ist mit 643,4 m ü. NHN der höchste Berg im Kaufunger Wald im nordhessischen Werra-Meißner-Kreis (Deutschland). Im Fulda-Werra-Bergland liegt er im Osten der sich an die eigentliche Hochfläche des Kaufunger Waldes nach Süden anschließenden Söhre.

Im Nordosten von Nordhessen erhebt sich der Hirschberg im Werra-Meißner-Kreis etwa 20 km südöstlich der Innenstadt von Kassel; unterhalb von etwa 560 m ü. NHN gehören seine Nord- und Nordwestflanken zum Landkreis Kassel. Er liegt zwar im eingangs genannten Kaufunger Wald, jedoch nur etwas außerhalb der verwinkelten Grenzen vom Naturpark Meißner-Kaufunger Wald, knapp 2,5 km südwestlich der Kernstadt von Großalmerode, knapp 2 km nordwestlich von Rommerode (südlicher Stadtteil von Großalmerode) und etwa 2 km (Entfernungen jeweils Luftlinie) südöstlich von Wickenrode (östlicher Gemeindeteil von Helsa).
Zu den Nachbarbergen des Hirschbergs gehören der Giesenberg (526,8 m ü. NHN) im Nordnordwesten, der Steinberg (ca. 585 m) im Nordnordosten mit den Steinbergseen und dem jenseits davon befindlichen Bilstein (641,2 m), der Exberg (505,5 m) im Südosten mit den beiden Exbergseen und der Rohrberg (535,6 m) im Südwesten.
Auf der Nordwestflanke des Hirschbergs entspringt die Wedemann, die in die Losse mündet, unweit südöstlich des Bergs entspringt die Wehre und am Pfaffenberg – dem Nordausläufer des Bergs – die Gelster, die jeweils Zuflüsse der Werra sind.
Die Basaltkuppe des Hirschbergs ist ein fast kreisrundes Plateau, das oberhalb der 600-m-Höhenlinie etwa 1 km Durchmesser hat. Darauf befinden sich zwei etwa 450 m voneinander entfernte und sanft ansteigende Kuppen:
Der Hirschberg (Nr. 357.700) gehört in der naturräumlichen Haupteinheitengruppe Osthessisches Bergland (35), in der Haupteinheit Fulda-Werra-Bergland (357) und in der Untereinheit Kaufunger Wald und Söhre (357.7) überwiegend zum Naturraum Söhre (357.70), und seine Ost- und Südostflanke zählt in der Witzenhausen-Altmorschener Talung (357.5) zum Naturraum Rommeroder Hügelland (357.53).
Die Hochlagen des Hirschbergs sind stark bewaldet. Es gibt aber abgesehen von den durch Braunkohleabbau an seinen Flanken entstandenen Tagebaugruben im südwestlichen Plateaubereich eine Lichtung mit etwa 140 bis 165 m Durchmesser und an anderen Stellen ein paar kleinere. Auf der Ostflanke des Bergs liegt eine etwa 550 mal 250 m große Lichtung.
Seit (mindestens?) 1690 wurde am Hirschberg ein intensiver Braunkohle-Tagebau betrieben, was an den Abbaugebieten zu erkennen ist, die sich an den nördlichen Flanken des Bergs befinden. Am 3. Oktober 2003 wurde die Zeche Hirschberg geschlossen; dies war das Ende des nordhessischen Kohlebergbaus.
Nördlich vorbei am Hirschberg verläuft zwischen Wickenrode und Großalmerode die Bundesstraße 451 (Wickenrode–Großalmerode), östlich und südlich die Landesstraße 3225 (Großalmerode–Rommerode–Friedrichsbrück) und südwestlich die L 3400 (Friedrichsbrück–Helsa). Zu erreichen ist das Bergplateau, auf das keine Straßen führen, zum Beispiel von den vorgenannten Ortschaften kommend auf durch meistens bewaldete Landschaft verlaufenden Wanderwegen.

Charles Ragon de Bange

juli 20th, 2016

Charles Ragon de Bange, né le 17 octobre 1833 à Balignicourt et décédé le 9 juillet 1914 à Le Chesnay, était un Polytechnicien et colonel d’artillerie français, directeur de l’Atelier-de-précision du dépôt central de Paris. Il est le concepteur d’un système d’arme (obturateur de Bange) qui accroît la vitesse de chargement des canons, procédé si efficace qu’il est toujours en utilisation de nos jours.

Il entra à École polytechnique en 1853 d’où il sortit pour servir dans l’artillerie. Lieutenant il combattit à la Bataille de Solférino et, lorsqu’il rentra en France, il choisit de servir dans les services techniques. Il fut capitaine en 1862, servit au 9e régiment de Besançon (1867-1869), puis entra à l’Atelier de précision au Dépôt Central de Paris (1869-1882). Il passa chef d’escadron en 1874, lieutenant-colonel en 1878 et colonel en 1880. Il reçut la Légion d’honneur en 1876 et en devint Commandeur en 1889.
De rapides progrès se firent jour après les années 1870 et rapidement acceptés par l’armée pour relever le défi de la défaite face aux Prussiens. Les canons Gribeauval (en bronze) avaient été modernisés par de Reffye (modèle 1870 avec mise en en place d’une culasse) et par Lahitolle (modèle 1875) avec l’utilisation de l’acier pour le tube du canon.
L’apparition de la mélinite et de la « poudre B » augmentèrent les performances des munitions mais en même temps les contraintes sur les systèmes d’armes. Les fusils connaissaient parallèlement une évolution majeure avec la mise en service du Chassepot modèle 1866.
En 1872, de Bange dessine le système de Bange, un type d’obturateur pour les canons qui permit une étanchéité plus importante de la culasse des éléments d’artillerie,..
Jusque là, les systèmes en service ne rendaient pas la culasse étanche et subissaient des retours de flammes, dangereux pour les artilleurs, ainsi qu’une perte de puissance, ce qui faisait qu’ils n’étaient pas satisfaisant. La culasse coulissante à vis interrompue en forme de champignon était complètement étanche. et son système est toujours celui qui est utilisé de nos jours. Le système s’ouvrait vers l’arrière avec une partie mobile qui laissait entrer la douille permettant un usage rapide et efficace du canon ; cette partie pouvait ensuite effectuer une rotation qui assurait la fermeture de la culasse. Cette partie rayée s’emboitait dans les mêmes rayures sur le canon, lisse en face de rayé pour ouvrir, rayé dans rayé pour maintenir fermé et donc tirer, le tout se réalisait en quelques secondes, à la main et par un seul homme.
Une fois fermée, la culasse devait son étanchéité à la présence d’un champignon central qui sous la pression de l’explosion reculait en appuyant sur la chambre, l’ensemble était facilité par une graisse à l’amiante.
Le système de Bange fut rapidement adopté par les forces armées française mais aussi dans la Royal Navy et l’United States Navy en raison de leurs gros canons de marine ne pouvant être chargés que par une culasse.
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Mais le recul non maitrisé empêchait un tir réellement rapide, il fallait remettre à la culée après chaque tir ou avoir un canon sur un affût fixe comme pour les navires.
En 1873, il devint le directeur des Ateliers de précision au Dépôt Central de Paris avec pour tâche de redessiner tous les canons de l’armée. Il mena cette tâche à bien en concevant :
Ce système d’arme connut ses heures de gloires lors des guerres coloniales mais a aussi massivement servi lors de la Première Guerre mondiale; le grand besoin de canon fit qu’ils furent utilisés sur tous les fronts, et il restait encore certains de ces canons en service pendant la Seconde guerre mondiale.
De 1882 à 1889, de Bange fut le directeur de la Société anonyme des anciens établissements Cail; il y travailla comme concepteur d’armes mais aussi à leur commercialisation comme par exemple en Serbie.
un de Bange donné aux finlandais pour la Deuxième guerre mondiale qui en firent un canon de forteresse.
un mortier de 200 de Bange à la garnison de Toul vers 1880.
Un 155 L en action en 1915.
155L présenté devant le mémorial de Verdun.
une culasse de 155 ouverte.
Outre la renommée de son système et les canons associés à son nom, une rue de Versailles à Le Chesnay porte son nom, ainsi qu’une école en la même ville.
Sur les autres projets Wikimedia :

Charles Hobhouse

juli 20th, 2016

Sir Charles Edward Henry Hobhouse, 4. baronet (ur. 30 czerwca 1862, zm. 26 czerwca 1941) – brytyjski polityk, członek Partii Liberalnej, minister w pierwszym rządzie Herberta Henry’ego Asquitha.
Był najstarszym synem sir Charlesa Hobhouse’a, 3. baroneta. Wykształcenie odebrał w Eton College oraz w Christ Church na Uniwersytecie Oksfordzkim. W latach 1884-1890 był porucznikiem w King’s Royal Rifle Corps.
W 1892 r. został wybrany do Izby Gmin jako reprezentant okręgu Devizes. W latach 1892-1895 był prywatnym sekretarzem w Ministerstwie Kolonii. W 1895 r. Hobhouse przegrał wybory parlamentarne w swoim okręgu. Do Izby Gmin powrócił w 1900 r. jako reprezentant okręgu Bristol East. W 1906 r. został komisarzem posiadłości kościelnych. W latach 1907-1908 był podsekretarzem stanu w Ministerstwie ds. Indii. Następnie został finansowym sekretarzem skarbu. W 1911 r. został członkiem gabinetu jako Kanclerz Księstwa Lancaster. W latach 1914-1915 był poczmistrzem generalnym. W 1918 r. Zrezygnował z miejsca w parlamencie.
Hobhouse był ponadto aldermanem hrabstwa Wiltshire w latach 1893-1924 oraz honorowym pułkownikiem Royal Tank Regiment. W 1909 r. został członkiem Tajnej Rady. W 1916 r., po śmierci ojca, odziedziczył tytuł baroneta.
Henry Bishop • Daniel O’Neill • Lady Chesterfield • Lord Arlington • Lord Rochester • John Wildman • John Evelyn • Lord Cornwallis • Lord Lovel • Everard Fawkener • Lord Trevor • Lord Egmont • Lord Hyde • Lord Grantham • Lord Hillsborough • Lord Sandwich • Lord le Despencer • Lord Carteret • Lord Foley • Lord Westmorland • Lord Chesterfield • Lord Leicester • Lord Auckland • Lord Buckinghamshire • Lord Chichester • Frederick Montagu • Książę Manchester • Książę Richmond • Lord Conyngham • Lord Maryborough • Lord Conyngham • Lord Lichfield • Lord Lowther • Lord St Germans • Lord Clanricarde • Lord Harwicke • Lord Canning • Książę Argyll • Lord Colchester • Lord Elgin • Lord Stanley of Alderley • Książę Montrose • Lord Hartington • William Monsell • Lyon Payfair • John Manners • Henry Fawcett • George Shaw-Lefevre • John Manners • Lord Wolverton • Henry Raikes • James Fergusson • Arnold Morley • Książę Norfolk • Lord Londonderry • Austen Chamberlain • Lord Stanley • Sydney Buxton • Herbert Samuel • Charles Hobhouse • Herbert Samuel • Joseph Pease • Albert Illingworth • Frederick Kellaway • Neville Chamberlain • William Joynson-Hicks • Laming Worthington-Evans • Vernon Hartshorn • William Mitchell-Thomson • Hastings Lees-Smith • Clement Attlee • William Ormsby-Gore • Kingsley Wood • George Tryon • William Morrison • Harry Crookshank • Lord Listowel • Wilfred Paling • Ness Edwards • Lord De La Warr • Charles Hill • Ernest Marples • Reginald Bevins • Tony Benn • Edward Short • Roy Mason • John Stonehouse
Herbert Henry Asquith • Augustine Birrell • John Burns • Sydney Buxton • Lord Carrington • Winston Churchill • Lord Crewe • Herbert Gladstone • Edward Grey • Richard Haldane • Lewis Harcourt • David Lloyd George • Lord Loreburn • Reginald McKenna • Lord Morley • Lord Pentland • Lord Ripon • Walter Runciman • Lord Tweedmouth • Lord Wolverhampton
Lord Beauchamp • Lord Emmott • Lord Fitzmaurice • Charles Hobhouse • Rufus Isaacs • Lord Kitchener • Lord Lucas • Charles Masterman • Edwin Samuel Montagu • Joseph Pease • Herbert Samuel • John Simon • John Seely • Thomas McKinnon Wood

Vocational secondary education in Denmark

juli 20th, 2016

Vocational secondary education in Denmark (Danish: erhvervsuddannelse) takes place at special state-funded vocational schools (erhvervsskoler), most of which are either technical schools (tekniske skoler) or business colleges (handelsskoler). Through a combination of teaching in vocational schools and apprenticeship, mostly in private companies, students are trained for work as tradesmen, clerks, farmers etc.
Vocational education takes 2-5 years and can be commenced after the completion of the compulsory primary folkeskole (‘public school’), i.e. at age 15-16.
Contrary to academically oriented types of secondary education such as the Gymnasium, vocational secondary education aims directly at jobs rather than higher education, although it is possible, with certain requirements, to enter a university to study for instance engineering upon completing vocational education.
Students train for work in a specific profession (e.g. as an electrician or a chef), but the different education programmes are organized in eight main groups that share certain subjects:
In addition, it is also possible to pursue vocational secondary education aimed at work in social and health institutions such as nursing homes: Basic Social and Health Education (Social- og Sundhedsuddannelse or SoSu).
Furthermore, there are programmes combining vocational elements with more adacemically oriented elements: Higher Technical Examination Programme (HTX) and Higher Commercial Examination Programme. These aim at higher education and are comparable to the more general and theoretical Gymnasium and Higher Preparatory Examination (HF).


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