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Unbibium

Unbibium, also known as element 122 or eka-thorium, is a hypothetical chemical element; it has placeholder symbol Ubb and atomic number 122. Unbibium and Ubb are the temporary systematic IUPAC name and symbol respectively, which are used until the element is discovered, confirmed, and a permanent name is decided upon. In the periodic table of the elements, it is expected to follow unbiunium as the second element of the superactinides and the fourth element of the 8th period. Similarly to unbiunium, it is expected to fall within the range of the island of stability, potentially conferring additional stability on some isotopes, especially 306Ubb which is expected to have a magic number of neutrons (184).

Despite several attempts, unbibium has not yet been synthesized, nor have any naturally occurring isotopes been found to exist. There are currently no plans to attempt to synthesize unbibium. In 2008, it was claimed to have been discovered in natural thorium samples, but that claim has now been dismissed by recent repetitions of the experiment using more accurate techniques.

Chemically, unbibium is expected to show some resemblance to cerium and thorium. However, relativistic effects may cause some of its properties to differ; for example, it is expected to have a ground state electron configuration of [Og] 7d1 8s2 8p1 or [Og] 8s2 8p2, despite its predicted position in the g-block superactinide series.

Fusion-evaporation
Two attempts were made to synthesize unbibium in the 1970s, both propelled by early predictions on the island of stability at N = 184 and Z > 120, and in particular whether superheavy elements could potentially be naturally occurring. The first attempts to synthesize unbibium were performed in 1972 by Flerov et al. at the Joint Institute for Nuclear Research (JINR), using the heavy-ion induced hot fusion reactions:

 * + → * → no atoms

Another unsuccessful attempt to synthesize unbibium was carried out in 1978 at the GSI Helmholtz Center, where a natural erbium target was bombarded with xenon-136 ions:

 * + → 298,300,302,303,304,306unbibium* → no atoms

No atoms were detected and a yield limit of 5 nb (5,000 pb) was measured. Current results (see flerovium) have shown that the sensitivity of these experiments were too low by at least 3 orders of magnitude. In particular, the reaction between 170Er and 136Xe was expected to yield alpha emitters with half-lives of microseconds that would decay down to isotopes of flerovium with half-lives perhaps increasing up to several hours, as flerovium is predicted to lie near the center of the island of stability. After twelve hours of irradiation, nothing was found in this reaction. Following a similar unsuccessful attempt to synthesize unbiunium from 238U and 65Cu, it was concluded that half-lives of superheavy nuclei must be less than one microsecond or the cross sections are very small. More recent research into synthesis of superheavy elements suggests that both conclusions are true.

In 2000, the Gesellschaft für Schwerionenforschung (GSI) Helmholtz Center for Heavy Ion Research performed a very similar experiment with much higher sensitivity:

 * + → * → no atoms

These results indicate that the synthesis of such heavier elements remains a significant challenge and further improvements of beam intensity and experimental efficiency is required. The sensitivity should be increased to 1 fb in the future for more quality results.

Compound nucleus fission
Several experiments studying the fission characteristics of various superheavy compound nuclei such as 306Ubb were performed between 2000 and 2004 at the Flerov Laboratory of Nuclear Reactions. Two nuclear reactions were used, namely 248Cm + 58Fe and 242Pu + 64Ni. The results reveal how superheavy nuclei fission predominantly by expelling closed shell nuclei such as 132Sn (Z = 50, N = 82). It was also found that the yield for the fusion-fission pathway was similar between 48Ca and 58Fe projectiles, suggesting a possible future use of 58Fe projectiles in superheavy element formation.

Claimed discovery as a naturally occurring element
In 2008, a group led by Israeli physicist Amnon Marinov at the Hebrew University of Jerusalem claimed to have found single atoms of unbibium-292 in naturally occurring thorium deposits at an abundance of between 10−11 and 10−12 relative to thorium. This was the first time in 69 years that a new element had been claimed to be discovered in nature, after Marguerite Perey's 1939 discovery of francium. The claim of Marinov et al. was criticized by the scientific community, and Marinov says he has submitted the article to the journals Nature and Nature Physics but both turned it down without sending it for peer review. The unbibium-292 atoms were claimed to be superdeformed or hyperdeformed isomers, with a half-life of at least 100 million years.

A criticism of the technique, previously used in purportedly identifying lighter thorium isotopes by mass spectrometry, was published in Physical Review C in 2008. A rebuttal by the Marinov group was published in Physical Review C after the published comment.

A repeat of the thorium experiment using the superior method of accelerator mass spectrometry (AMS) failed to confirm the results, despite a 100-fold better sensitivity. This result throws considerable doubt on the results of the Marinov collaboration with regards to their claims of long-lived isotopes of thorium, roentgenium, and unbibium. Current understanding of superheavy elements indicates that it is very unlikely for any traces of unbibium to persist in natural thorium samples.

Naming
Using Mendeleev's nomenclature for unnamed and undiscovered elements, unbibium should instead be known as eka-thorium. After the recommendations of the IUPAC in 1979, the element has since been largely referred to as unbibium with the atomic symbol of (Ubb), as its temporary name until the element is officially discovered and synthesized, and a permanent name is decided on. Scientists largely ignore this naming convention, and instead simply refer to unbibium as "element 122" with the symbol of (122), or sometimes even E122 or 122.

Prospects for future synthesis

Every element from mendelevium onward was produced in fusion-evaporation reactions, culminating in the discovery of the heaviest known element oganesson in 2002 and most recently tennessine in 2010. These reactions approached the limit of current technology; for example, the synthesis of tennessine required 22 milligrams of 249Bk and an intense 48Ca beam for six months. The intensity of beams in superheavy element research cannot exceed 1012 projectiles per second without damaging the target and detector, and producing larger quantities of increasingly rare and unstable actinide targets is impractical. Consequently, future experiments must be done at facilities such as the superheavy element factory (SHE-factory) at the Joint Institute for Nuclear Research (JINR) or RIKEN, which will allow experiments to run for longer stretches of time with increased detection capabilities and enable otherwise inaccessible reactions.

It is possible that fusion-evaporation reactions will not be suitable for the discovery of unbibium or heavier elements. Various models predict increasingly short alpha and spontaneous fission half-lives for isotopes with Z = 122 and N ~ 180 on the order of microseconds or less, rendering detection nearly impossible with current equipment. The increasing dominance of spontaneous fission also may sever possible ties to known nuclei of livermorium or oganesson and make identification and confirmation more difficult; a similar problem occurred in the road to confirmation of the decay chain of 294Og which has no anchor to known nuclei. For these reasons, other methods of production may need to be researched such as multi-nucleon transfer reactions capable of populating longer-lived nuclei. A similar switch in experimental technique occurred when hot fusion using 48Ca projectiles was used instead of cold fusion (in which cross sections decrease rapidly with increasing atomic number) to populate elements with Z > 113.

Nevertheless, several fusion-evaporation reactions leading to unbibium have been proposed in addition to those already tried unsuccessfully, though no institution has immediate plans to make synthesis attempts, instead focusing first on elements 119, 120, and possibly 121. Because cross sections increase with asymmetry of the reaction, a chromium beam would be most favorable in combination with a californium target, especially if the predicted closed neutron shell at N = 184 could be reached in more neutron-rich products and confer additional stability. In particular, the reaction between and  would generate the compound nucleus  and reach the shell at N = 184, though the analogous reaction with a  target is believed to be more feasible because of the presence of unwanted fission products from  and difficulty in accumulating the required amount of target material. One possible synthesis of unbibium could occur as follows:

 * + →  + 3 $1 0$

Should this reaction be successful and alpha decay remain dominant over spontaneous fission, the resultant 300Ubb would decay through 296Ubn which may be populated in cross-bombardment between 249Cf and 50Ti. Although this reaction is one of the most promising options for the synthesis of unbibium in the near future, the maximum cross section is predicted to be 3 fb, one order of magnitude lower than the lowest measured cross section in a successful reaction. The more symmetrical reactions 244Pu + 64Ni and 248Cm + 58Fe have also been proposed and may produce more neutron-rich isotopes. With increasing atomic number, one must also be aware of decreasing fission barrier heights, resulting in lower survival probability of compound nuclei, especially above the predicted magic numbers at Z = 126 and N = 184.

Nuclear stability and isotopes

The stability of nuclei decreases greatly with the increase in atomic number after plutonium, the heaviest primordial element, so that all isotopes with an atomic number above 101 decay radioactively with a half-life under a day. No elements with atomic numbers above 82 (after lead) have stable isotopes. Nevertheless, because of reasons not very well understood yet, there is a slight increased nuclear stability around atomic numbers 110–114, which leads to the appearance of what is known in nuclear physics as the "island of stability". This concept, proposed by University of California professor Glenn Seaborg, explains why superheavy elements last longer than predicted.

In this region of the periodic table, N = 184 has been suggested as a closed neutron shell, and various atomic numbers have been proposed as closed proton shells, such as Z = 114, 120, 122, 124, and 126. The island of stability would be characterized by longer half-lives of nuclei located near these magic numbers, though the extent of stabilizing effects is uncertain due to predictions of weakening of the proton shell closures and possible loss of double magicity. More recent research predicts the island of stability to instead be centered at beta-stable copernicium isotopes 291Cn and 293Cn, which would place unbibium well above the island and result in short half-lives regardless of shell effects. The increased stability of elements 112–118 has also been attributed to the oblate shape of such nuclei and resistance to spontaneous fission. The same model also proposes 306Ubb as the next spherical doubly magic nucleus, thus defining the true island of stability for spherical nuclei.

A quantum tunneling model predicts the alpha-decay half-lives of unbibium isotopes 284–322Ubb to be on the order of microseconds or less for all isotopes lighter than 315Ubb, highlighting a significant challenge in experimental observation of this element. This is consistent with many predictions, though the exact location of the 1 microsecond border varies by model. Additionally, spontaneous fission is expected to become a major decay mode in this region, with half-lives on the order of femtoseconds predicted for some even–even isotopes due to minimal hindrance resulting from nucleon pairing and loss of stabilizing effects farther away from magic numbers. A 2016 calculation on the half-lives and probable decay chains of isotopes 280–339Ubb yields corroborating results: 280–297Ubb will be proton unbound and possibly decay by proton emission, 298–314Ubb will have alpha half-lives on the order of microseconds, and those heavier than 314Ubb will predominantly decay by spontaneous fission with short half-lives. For the lighter alpha emitters that may be populated in fusion-evaporation reactions, some long decay chains leading down to known or reachable isotopes of lighter elements are predicted. Additionally, the isotopes 308–310Ubb are predicted to have half-lives under 1 microsecond, too short for detection as a result of significantly lower binding energy for neutron numbers immediately above the N = 184 shell closure. Alternatively, a second island of stability with total half-lives of approximately 1 second may exist around Z ~ 124 and N ~ 198, though these nuclei will be difficult or impossible to reach using current experimental techniques. However, these predictions are strongly dependent on the chosen nuclear mass models, and it is unknown which isotopes of unbibium will be most stable. Regardless, these nuclei will be hard to synthesize as no combination of obtainable target and projectile can provide enough neutrons in the compound nucleus. Even for nuclei reachable in fusion reactions, spontaneous fission and possibly also cluster decay might have significant branches, posing another hurdle to identification of superheavy elements as they are normally identified by their successive alpha decays.

Chemical
Unbibium is predicted to be similar in chemistry to cerium and thorium, which likewise have four valence electrons above a noble gas core, although it may be more reactive. Additionally, unbibium is predicted to belong to a new block of valence g-electron atoms, although the 5g orbital is not expected to start filling until about element 125. The predicted ground-state electron configuration of unbibium is either [Og] 7d1 8s2 8p1 or 8s2 8p2, in contrast to the expected [Og] 5g2 8s2 in which the 5g orbital starts filling at element 121. (The ds2p and s2p2 configurations are expected to be only separated by about 0.02 eV.) In the superactinides, relativistic effects might cause a breakdown of the Aufbau principle and create overlapping of the 5g, 6f, 7d and 8p orbitals; experiments on the chemistry of copernicium and flerovium provide strong indications of the increasing role of relativistic effects. As such, the chemistry of elements following unbibium becomes more difficult to predict.

Unbibium would most likely form a dioxide, UbbO2, and tetrahalides, such as UbbF4 and UbbCl4. The main oxidation state is predicted to be +4, similar to cerium and thorium. A first ionization energy of 5.651 eV and second ionization energy of 11.332 eV are predicted for unbibium; this and other calculated ionization energies are lower than the analogous values for thorium, suggesting that unbibium will be more reactive than thorium.

title: Unbibium


text: Category:Dukes of Bohemia

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title: Category:Dukes of Bohemia


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Mary Shelley's Frankenstein (film)

Mary Shelley's Frankenstein is a 1994 science fiction horror film directed by Kenneth Branagh who also stars as Victor Frankenstein, with Robert De Niro portraying Frankenstein's monster (called The Creation in the film), and co-stars Tom Hulce, Helena Bonham Carter, Ian Holm, John Cleese, Richard Briers and Aidan Quinn. Considered the most faithful film adaptation of Mary Shelley's 1818 novel, Frankenstein; or, The Modern Prometheus, despite several differences and additions in plot from the novel, the film follows a medical student named Victor Frankenstein who creates new life in the form of a monster composed of various corpses' body parts.

Mary Shelley's Frankenstein premiered at the London Film Festival, and was released theatrically on November 4, 1994, by TriStar Pictures. The film received mixed reviews from critics, grossing $112 million worldwide on a budget of $45 million, making it less successful than the previous Francis Ford Coppola-produced horror adaptation, Bram Stoker's Dracula (1992).

Plot
In 1794, Captain Walton leads a troubled expedition to reach the North Pole. While their ship is trapped in the ice of the Arctic Sea, the crew hears a frightening noise and witnesses a mysterious figure killing their sled dogs before vanishing. The crew rescues a man, Victor Frankenstein, who had fallen in the Arctic waters. When Walton tells Victor of his determination to continue the expedition, Victor replies, "Do you share my madness?" He proceeds to tell Walton and the crew his life story, presented in flashback.

Victor grows up in Geneva with his adopted sister, Elizabeth Lavenza, the love of his life. Before he leaves for the University of Ingolstadt, Victor's mother dies giving birth to his brother William. Devastated by her loss, Victor vows on his mother's grave that he will find a way to conquer death. Victor and his friend Henry Clerval study under Shmael Augustus Waldman, a professor whose notes contain information on how to create life; Waldman warns Victor not to use them, lest he create an "abomination".

While performing vaccinations, Waldman is murdered by a patient, who is later hanged in the village square. Using the killer's body, a leg from a fellow student who died of cholera, and Waldman's brain, Victor builds a creature based on the professor's notes. He is so obsessed with his work that he drives Elizabeth away when she comes to take him away from Ingolstadt, which is being quarantined amid a cholera epidemic. Victor finally gives his creation life, but he is horrified by the creature's hideous appearance and tries to kill him. Frightened and confused, the creature steals Victor's coat and flees the laboratory, and is later driven away by the townspeople when he tries to steal food.

The creature finds shelter in a family's barn and stays there for months without their knowledge, gradually learning to read and speak by watching them. He attempts to earn their trust by anonymously bringing them food, and eventually converses with the elderly, blind patriarch after murdering an abusive debt collector. When the blind man's family returns, however, they are terrified of the creature and chase him away. The creature finds Victor's journal in his coat and learns of the circumstances of his creation. Upon returning to the farmhouse, he discovers the family has abandoned it, leaving him all alone once again. He burns down the farm and vows revenge on Victor for bringing him into a world that hates him.

Victor returns to Geneva to marry Elizabeth, only to find that his younger brother William has been murdered. The Frankensteins' servant Justine is blamed for the crime and hanged, but Victor knows the creature is responsible. The creature abducts Victor and demands that he make a female companion for him, promising to leave his creator in peace in return. Victor begins gathering the tools he used to create life, but when the creature insists that he use Justine's body to make the companion, a disgusted Victor breaks his promise. The creature exacts his revenge on Victor's wedding night by breaking into Elizabeth's bridal suite and ripping her heart out.

Desperate with grief, Victor races home to bring Elizabeth back to life. He stitches Elizabeth's head onto Justine's body and reanimates her as a disfigured, mindless shadow of her former self. The creature appears, demanding Elizabeth as his bride. Victor and the creature fight for Elizabeth's affections, but Elizabeth, horrified by her own reflection, commits suicide by setting herself on fire. Both Victor and the creature escape as the mansion burns down.

The story returns to the Arctic. Victor tells Walton that he has been pursuing his creation for months to kill him. Soon after recalling his story, Victor dies of pneumonia. Walton discovers the creature weeping over Victor's body, having lost the only family he has ever known. The crew prepares a funeral pyre, but the ceremony is interrupted when the ice around the ship cracks. Walton invites the creature to stay with the ship, but the creature insists on remaining with the pyre. He takes the torch and burns himself alive with Victor's body. Walton, having seen the consequences of Victor's obsession, orders the ship to return home.

Cast

 * Robert De Niro as The Creation, a reanimated corpse who is rejected by all of humanity and swears revenge on the entire world as a result.
 * De Niro also portrays Professor Waldman's killer, whose body was used for the creature.
 * Kenneth Branagh as Victor Frankenstein, a scientist obsessed with conquering death, an obsession that ultimately destroys his life.
 * Rory Jennings as young Victor Frankenstein.
 * Tom Hulce as Henry Clerval, Frankenstein's best friend and fellow medical student, and later, his trusted partner when he inherits his father's practice.
 * Helena Bonham Carter as Elizabeth Lavenza Frankenstein, Frankenstein's fiancée and adoptive sister. She is murdered by the Creation, but Frankenstein brings her back to life before she commits suicide, horrified by her own appearance.
 * Hannah Taylor Gordon as young Elizabeth Lavenza.
 * Ian Holm as Baron Alphonse Frankenstein, Victor Frankenstein's elderly father, and one of the Creation's victims.
 * John Cleese as Professor Waldman, Frankenstein's tutor and colleague who shares his interest in creating life but fears the consequences of doing so. His brain is later used for the creature following his death at the hands of a patient.
 * Aidan Quinn as Captain Robert Walton, the commander of the ship which picks up Frankenstein in the Arctic Circle.
 * Richard Briers as Grandfather, an elderly blind man who is kind to the Creation.
 * Robert Hardy as Professor Krempe, a university tutor of medical sciences who condemns Frankenstein's theories of life beyond death.
 * Trevyn McDowell as Justine Moritz, Mrs. Moritz's daughter, a nursemaid in the Frankenstein household who is close friends with Elizabeth and harbors an unrequited love for Victor. She is executed for murdering William, a crime actually committed by the Creation.
 * Christina Cuttall as young Justine Moritz.
 * Celia Imrie as Mrs. Moritz, the head of the household staff at Frankenstein Manor who often fights with her daughter, Justine.
 * Cherie Lunghi as Caroline Frankenstein, Victor's mother who dies during the birth of his younger brother, William.
 * Ryan Smith as William Frankenstein, Victor's younger brother.
 * Charles Wyn-Davies as young William Frankenstein.
 * Hugh Bonneville as Schiller.
 * Jenny Galloway as Vendor's wife.
 * Alex Lowe as Crewman.
 * George Asprey as Policeman.
 * Patrick Doyle (uncredited) as Ballroom orchestra conductor.
 * Stuart Hazeldine (uncredited) as Man in crowd scene.
 * Fay Ripley (deleted scenes) as Whore.

Release
The film had its world premiere on November 3, 1994 at the London Film Festival before opening in the United Kingdom and United States on November 4.

Frank Darabont
Original screenwriter Steph Lady, who sold the script to Francis Ford Coppola's American Zoetrope, said "the film was a shocking disappointment; a misshapen monster born of Kenneth Branagh's runaway ego. He took a poignant, thought-provoking tragedy and turned it into a heavy metal monster movie. The casting of Robert De Niro as the monster was beyond inexplicable." Frank Darabont, who did a second draft, later called the film "the best script I ever wrote and the worst movie I've ever seen". He elaborated: "There's a weird doppelgänger effect when I watch the movie. It's kind of like the movie I wrote, but not at all like the movie I wrote. It has no patience for subtlety. It has no patience for quiet moments. It has no patience period. It's big and loud and blunt and rephrased by the director at every possible turn. Cumulatively, the effect was a totally different movie. I don't know why Branagh needed to make this big, loud film ... the material was subtle. Shelley's book was way out there in a lot of ways, but it's also very subtle. I don't know why it had to be this operatic attempt at filmmaking. Shelley's book is not operatic, it whispers at you a lot. The movie was a bad one. That was my Waterloo. That's where I really got my ass kicked most as a screenwriter ... [Branagh] really took the brunt of the blame for that film, which was appropriate. That movie was his vision entirely. If you love that movie you can throw all your roses at Ken Branagh's feet. If you hated it, throw your spears there too, because that was his movie."

Critical response
Roger Ebert gave the film two and a half stars out of four, writing: "I admired the scenes with De Niro [as the Creature] so much I'm tempted to give Mary Shelley's Frankenstein a favorable verdict. But it's a near miss. The Creature is on target, but the rest of the film is so frantic, so manic, it doesn't pause to be sure its effects are registered".

Janet Maslin wrote: "Branagh is in over his head. He displays neither the technical finesse to handle a big, visually ambitious film nor the insight to develop a stirring new version of this story. Instead, this is a bland, no-fault Frankenstein for the '90s, short on villainy but loaded with the tragically misunderstood. Even the Creature (Robert De Niro), an aesthetically challenged loner with a father who rejected him, would make a dandy guest on any daytime television talk show".

Conversely, James Berardinelli of Reelviews.net gave the film three out of four stars: "Mary Shelley's Frankenstein may not be the definitive version of the 1818 novel, and the director likely attempted more than is practical for a two-hour film, but overambition is preferable to the alternative, especially if it results—as in this case—in something more substantial than Hollywood's typical, fitfully entertaining fluff".

Audiences polled by CinemaScore gave the film an average grade of "B−" on an A+ to F scale.

Box office
Mary Shelley's Frankenstein collected $11,212,889 during its opening weekend, ranking in second place at the box office below Stargate. In the U.S. and Canada, the film grossed $22,006,296, with the opening weekend making up more than half of its total. The film opened the same day in the United Kingdom and Ireland and grossed £2 million in its opening week from 320 screens. Outside the U.S., it grossed $90 million, bringing the worldwide gross to $112 million.

Year-end lists

 * 3rd worst – Peter Travers, Rolling Stone
 * 9th worst – Janet Maslin, The New York Times

Video game
A video game adaptation based on the film was released on numerous home video game consoles in 1994. A themed pinball machine was released in early 1995 by Sega Pinball; it is one of the machines included in the video pinball simulator The Pinball Arcade.

title: Mary Shelley's Frankenstein (film)


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Vesicular monoamine transporter

The vesicular monoamine transporter (VMAT) is a transport protein integrated into the membranes of synaptic vesicles of presynaptic neurons. It transports monoamine neurotransmitters – such as dopamine, serotonin, norepinephrine, epinephrine, and histamine – into the vesicles, which release the neurotransmitters into synapses, as chemical messages to postsynaptic neurons. VMATs utilize a proton gradient generated by V-ATPases in vesicle membranes to power monoamine import.

Pharmaceutical drugs that target VMATs have possible applications for many conditions, leading to a plethora of biological research, including hypertension, drug addiction, psychiatric disorders, Parkinson's disease, and other neurological disorders. Many drugs that target VMATs act as inhibitors and alter the kinetics of the protein. Much research regarding the effects of altered VMATs on biological systems is still ongoing.

Monoamines
Monoamines transported by VMATs are mainly noradrenaline, adrenaline, dopamine, serotonin, histamine, and trace amines. Exogenous substrates include guanethidine and MPP+.

Discovery
VMAT research began in 1958 when Nils-Åke Hillarp discovered secretory vesicles. In the 1970s, scientists like Arvid Carlsson recognized the need to understand how transport systems and ion gradients work in different organisms in order to explore new treatment options such as reserpine (RES). Researchers discovered inhibitors that blocked the uptake of neurotransmitters into vesicles, suggesting the existence of VMATs. A decade later, molecular genetic tools have improved methods for protein identification. Scientists have used these tools to analyze DNA and amino acid sequences, and discovered that transporters in bacteria and humans were very similar, which emphasized the importance and universality of transporters. The transporters were first structurally identified by cloning VMATs in rats. The VMAT were first isolated and purified in bovine chromaffin granules, in both its native and denatured forms.

Location
There are two types of VMATs expressed in humans: VMAT1 and VMAT2. VMAT1 is expressed mainly in large dense-core vesicles (LDCVs) of the peripheral nervous system. VMAT1 may be found in neuroendocrine cells, particularly chromaffin and enterochromaffin granules, which are primarily found in the medulla of the adrenal glands.

VMAT2 favors expression in a variety of monoaminergic cells of the central nervous system, such as the brain, sympathetic nervous system, mast cells, It is prevalent in β-cells, expressed in blood platelets,  and co-expressed in chromaffin cells. Expression of the two transporters in internal organs seems to differ between species: only VMAT1 is expressed in rat adrenal medulla cells, whereas VMAT2 is the major transporter in bovine adrenal medulla cells.

Structure and function

VMAT1 and VMAT2 are acidic glycoproteins with a molecular weight of approximately 70 kDa. Both isoforms are transmembrane proteins with 12 transmembrane domains (TMDs).

VMATs function by loading monoamines—dopamine, serotonin, histamine, norepinephrine, and epinephrine—into transport vesicles. VMATs use the same transport mechanism for all types of monoamines, and transport them from the cytosol into high-concentration storage vesicles. Transport vesicles are released into the space between neurons, called the synaptic cleft, where they convey a chemical message to the next neuron. VMATs also function in sorting, storing, and releasing neurotransmitters, and are believed to participate in protecting these neurotransmitters from autoxidation. The transporters are also known to continue biochemical modification after loading certain neurotransmitters.

Vesicle packing requires a large energy source to store large quantities of neurotransmitters into a small vesicular space at high concentrations. VMAT transport relies on the pH and electrochemical gradient generated by a vesicular H+-ATPase. The current model of VMAT function proposes that the efflux of two protons (H+) against the H+ gradient is coupled with influx of one monoamine. The first H+ efflux generates a transporter conformation associated with a high-affinity amine-binding site in the cytosolic phase, and the second H+ efflux is coupled with a second large conformational change that leads to amine transport from the cytosolic side into the vesicle, reducing amine-binding affinity.

Studies indicate that the amino acid residue His419, located on the domain between TMDs X and XI of rat VMAT1, plays a role in energy coupling to the amine transport by assisting the first proton-dependent conformational change. It has been proposed that RES inhibits VMAT by interacting with this conformation.

VMAT gene sequence analysis demonstrates that four aspartic acid residues in the middle region of TMDs I, VI, X, and XI and one lysine residue in TMD II have highly conserved gene sequences, suggesting these residues play a critical role in transporter structure and function. Specifically, the residues Lys139 and Asp427 are thought to compose an ion pair that promotes high-affinity interaction with VMAT substrates and inhibitors. The Asp431 residue located in TMD XI is believed to be critical for amine transport, but does not interact with RES binding; it is thought to complete the substrate transport cycle.

Kinetics
VMATs have a relatively low Vmax, with an estimated rate of 5–20/sec depending on the substrate. Vesicle filling may limit monoamine release from neurons with high rates of firing.

Specific amine-binding affinity varies by VMAT isoform; studies indicate that catecholamines dopamine, norepinephrine, and epinephrine have a threefold higher affinity for VMAT2 than VMAT1 binding and uptake. The imidazoleamine histamine has a thirtyfold higher affinity for VMAT2 compared to VMAT1, and is thought to bind to a different site than other monoamines. Unlike catecholamines and histamine, the indoleamine serotonin binds to VMAT1 and VMAT2 with a similar affinity for both transporter isoforms.

VMAT1 has a lower turnover number and a lower affinity for most monoamine substrates than VMAT2, which may be because of VMAT2's location in the central nervous system, which demands fast recovery from neurotransmitter release in order to prepare for subsequent releases. The uptake efficiencies of each VMAT substrate can be ranked in order of efficiency as: serotonin, dopamine, epinephrine, and norepinephrine.

Methamphetamines decrease Vmax, while cocaine increases Vmax reversibly in rat brain.

Inhibition
The effects of VMAT inhibition have been studied in-depth in animal models. Mutant homozygous VMAT(-/-) mice move little, feed poorly, and die within a few days of birth.

More specifically, inhibition of VMAT2 may cause an increase in cytosolic catecholamine levels, which can result in an increase in efflux of catecholamines through the cell membrane, depleting catecholamine concentrations and causing increased oxidative stress and oxidative damage to the neuron.

Heterozygous VMAT mutants display hypersensitivity to amphetamine, cocaine, and MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine), the latter being a substance causally linked to Parkinson's disease (PD) in rodents. This suggests a protective role of VMATs against oxidative stress through removal of such substances from the cytosol.

VMAT inhibitors include:
 * Reserpine (RES), bietaserpine, and ketanserin (KET) (potent inhibitors of VMAT2 mediated serotonin transport)
 * Tetrabenazine (TBZ) (specific to VMAT2)
 * Phenylethylamine
 * Amphetamine
 * MDMA
 * N-Methyl-4-phenylpyridinium (MPP+) (very potent inhibitors of VMAT2 mediated serotonin transport)
 * Fenfluramine (specific to VMAT1 )
 * Non-hydrolysable GTP-analogue guanylyllimidodiphosphate GMP-P(NH)P (VMAT2 only)

Ligand-binding affinities and structures
Two known binding sites for VMAT inhibitors include the RES binding site and the TBZ binding site. Some evidence suggests these two sites may overlap or exist as two separate conformations of the same binding site. VMAT inhibitors tend to fall into two classes: those that interact with the RES binding site and those that interact with the TBZ binding site.

RES, methoxytetrabenazine (MTBZ), and the drug amiodarone bind to the RES binding site. TBZ (also called Nitoman and Xenazine), dihydrotetrabenazine (DTBZOH), ketanserin (KET), and the drug lobeline bind to the TBZ binding site. Amphetamine, methamphetamine and GZ-7931 are also known to interact with VMAT2.

Inhibitor affinity varies among VMAT isoforms. RES and KET have higher inhibitory affinity for VMAT2–mediated 5HT transport than for that of VMAT1; TBZ seems to inhibit VMAT2 exclusively.

The residues asp33 and ser180, 181, and 182 are believed to be involved in substrate recognition, and interact with the protonated amino group and hydroxyl group on the catechol or indole rings.

Cocaine and methylphenidate (MPD, also known as Ritalin and Concerta) are believed to interact with VMAT2 to cause a shift in VMAT2 "from a plasmalemmal membrane-associated fraction to a vesicle-enriched, nonmembrane-associated fraction."

RES binding site
Consistent with catecholamine-binding affinity, RES has a threefold higher affinity for VMAT2 than for VMAT1. The RES binding site is known to be hydrophobic, which is thought to contribute to ligand binding affinity. Methamphetamine binds to the RES site on VMATs.

The current working model proposes that RES and the substrate bind to a single site in a pH-gradient modulated conformational structure of the transporter. The conformation occurs after the transport of one H+ across the membrane and into the vesicle; proton transport drives the substrate recognition site from the lumen to the cytoplasmic surface of the vesicle for RES and substrate binding. Methoxytetrabenazine (MTBZ) may bind to the RES binding site, based on studies indicating that RES significantly inhibited MTBZ-binding. Amiodarone is also believed to inhibit monoamine vesicular uptake by binding to the RES binding site.

TBZ binding site
TBZ and dihydrotetrabenazine (DTBZOH) are believed to bind to a different binding site from the RES/substrate binding site, or to a different conformation of the RES/substrate binding site. This site is believed to be located at the N-terminus, based on studies done in bovine VMAT2. Tyr434 and asp461 are identified as being responsible for the high-affinity interaction of TBZ, serotonin, and histamine in VMAT2. Unlike methamphetamine, amphetamine binds to the TBZ site on hVMAT2.

Unlike RES inhibition, TBZ inhibition is only affected by very high concentrations of monoamines; however, single injections of RES can inhibit TBZ binding. ketanserin (KET) and lobeline also bind to the TBZ binding site conformation.

Glycosylation sites: N- and C-linked terminals
Three to four glycosylation sites exist in the vesicular matrix on a loop between TMD I and TMD II. In biology, the vesicle matrix refers to the material or tissue between cells in which more specialized structures are embedded. Two of the glycosylation sites, the N-linked glycosylation terminal and C-linked terminal, are located in the cytosolic portion of the vesicle.

The highest amount of genetic variance between VMAT1 and VMAT2 exists near the N- and C- terminals in the cytosolic phase, and in the glycosylated loop between TMDs I and II.

C-terminus and VMAT trafficking cycle
Several motifs involved in the VMAT trafficking cycle are believed to be encoded in the C-terminus. A dileucine motif in the C-terminus is required for VMAT2 endocytosis. Studies suggest the acidic residues in the dileucine motif sort VMAT2 away from constitutive secretory vesicles and into the regulated secretory pathway. The hydrophobic residues in the dileucine motif are thought to couple with the acidic residues as a single unit to help sort VMAT2 to large dense course vesicles. Acidic glutamate residues located upstream of the dileucine motif are known to be important for localization of VMAT2 to large dense core vesicles; these residues are also conserved in VMAT1.

Genetic expression and transporter regulation
Although both VMAT1 and VMAT2 are encoded by two different genes, the individual genetic sequences demonstrate high homology. Polymorphisms in VMAT2 that affect regulation and quantitative expression may pose genetic risk factors for PD. A specific VMAT1 gene (SLC18A1) has several associated polymorphisms, which have a locus 8p21.3 that has been strongly connected to schizophrenia susceptibility.

Over-expression of VMAT2 results in increased secretion of neurotransmitter upon cell stimulation. Data suggests that deletion of the VMAT2 genes does not affect the size of small clear-core vesicles.

VMATs may be regulated by changes in transcription, post-transcriptional modifications such as phosphorylation and mRNA splicing of exons, and vesicular transport inactivation facilitated by heterotrimeric G-proteins, which are thought to be possessed by chromaffin granules, and have shown to regulate small clear-core vesicles.

Specific heterotrimeric G-protein type regulation is tissue-dependent for VMAT2; it is not known whether this is the case for VMAT1. Heterotrimeric G-protein Gαo2 decreases VMAT1 activity in pancreatic and adrenal medulla cells, and activates heterotrimeric G-proteins to inhibit VMAT2 activity in the brain, regardless of whether they are localized on small clear-core or large-dense-core vesicles. The activated heterotrimeric G-protein Gαq downregulates VMAT2-mediated serotonin transport in blood platelets, but not in the brain, where Gαq completely inhibits VMAT2 activity. Although the exact signalling pathway for G-protein mediated regulation of VMATs is not known, it has recently been described that implicated G-proteins act directly on the VMATs.

Clinical significance
VMAT2 has been shown to contribute to many clinical neurological disorders including drug addiction, mood disorders, and stress, as well as Parkinson's disease and Alzheimer's disease.

Parkinson's disease
Studies indicate VMAT2 mRNA is present in all cell groups damaged by Parkinson's disease (PD); these findings have identified VMAT2 as a target for preventing Parkinson's. VMAT2 presence does not independently protect neurons from PD, but a decrease in VMAT2 expression has been shown to correlate with susceptibility to the disease, which may be due to a ratio between the dopamine transporter and VMAT2.

Based on the understanding the increased cytosolic dopamine levels lead to dopaminergic cell death in PD, it has been proposed that regulatory polymorphisms in VMAT2 affect VMAT2 quantitative expression, and may serve as a genetic risk factor for PD. Specifically, the SLC18A2 promoter region for the VMAT2 gene has been identified as an area where several polymorphisms form discrete haplotypes.

Mood disorders
Studies using a genetic rodent model to understand clinical depression in humans suggest that VMAT2 genetic or functional alterations may be involved in depression. Reduced VMAT2 levels were identified in specific subregions of the striatum involved in clinical depression, including the nucleus accumbens shell but not the core, the ventral tegmental area, and the substantia nigra's pars compacta. The reduced VMAT2 protein levels were not accompanied by similar levels of VMAT2 mRNA alterations. Based on these findings, it has been proposed that VMAT2 activity is not altered at the level of genetic expression, but may be altered at the functional level in ways that may correlate with clinical depression.

Drug addiction
Many psychostimulant drugs are known to interact with VMAT, including amphetamine analogs such as methamphetamine, cocaine, and ecstasy (MDMA).

Pharmacology
VMAT inhibitors tend to fall into two classes; those that interact with the RES binding site and those that interact with the TBZ binding site.

RES, methoxytetrabenazine, and amiodarone bind to the RES binding site.

TBZ, DTBZOH, ketanserin, and lobeline bind to the TBZ binding site.

Many psychostimulants, including substituted amphetamines and cocaine, are known to interact with VMAT2. Studies indicate that both amphetamines and cocaine act to increase non-exocytotic release of dopamine in specific regions of the brain by interacting directly with VMAT2 function.

Methamphetamine
VMAT is a main target of methamphetamine. Studies indicate that substituted amphetamines including methamphetamine interact with VMAT2 at the TBZ/DTBZOH binding site. By acting as a competitive antagonist, methamphetamine blocks the presynaptic cell's ability to use VMAT for vesicular packaging.

Methamphetamine alters the subcellular location of VMAT2, which affects the distribution of dopamine in the cell. Treatment with methamphetamine relocates VMAT2 from a vesicle-enriched fraction to a location that is not continuous with synaptosomal preparations.

Repeated amphetamine exposure may increase VMAT2 mRNA in certain brain regions with little or no decline upon withdrawal from the drug.

A study performed by Sonsalla et al. demonstrated that methamphetamine treatment decreases DHTBZ binding and vesicular dopamine uptake. Another study demonstrated that multiple high doses of methamphetamine removed DTBZ binding sites from the vesicles.

In addition to an interaction with the TBZ/DTBZOH binding site, some researchers propose that substituted amphetamines like methamphetamine decrease dopamine uptake because of the weak base properties of substituted amphetamines. This “Weak Base Hypothesis” proposes that amphetamine analogs enter the cell through transport and lipophilic diffusion, then diffuses through the vesicular membrane where they accumulate in synaptic vesicles and offset the proton electrochemical gradient in the vesicle that drives monoamine transport through VMAT. Amphetamine administration would prevent vesicular dopamine uptake through VMAT, and explain the finding that amphetamine administration correlates with decreased dopamine release from vesicles and a neurotoxic increase in intracellular dopamine.

Cocaine
Unlike methamphetamine, cocaine interacts with VMAT2 by mobilizing VMAT2-expressing vesicles, causing a shift in VMAT2 proteins from a plasmalemmal (synaptosomal) membrane fraction to a vesicle-enriched fraction that is not associated with the synaptosomal membrane and not retained in synaptosomal preparations. Methylphenidate is believed to interact with VMAT2 in a similar fashion.

In addition to mobilizing VMAT2-expressing vesicles, cocaine has been shown to increase the Vmax of VMAT2 for dopamine and increase the number of DTBZ binding sites. It has also mobilized a synapsin-dependent reserve pool of dopamine-containing synaptic vesicles, which interacts with the vesicular trafficking cycle to increase dopamine release.

Short-term exposure to cocaine increases VMAT2 density in the prefrontal cortex and striatum of mammalian brains. This is theorized to be a defensive mechanism against the depletive effects cocaine has on cytosolic dopamine through increasing monoamine storage capacity. Chronic cocaine use has been implicated with a reduction in VMAT2 immunoreactivity as well as a decrease in DTBZOH binding in humans.

Research suggests a decline in VMAT2 protein through prolonged cocaine use could play an important role in the development of cocaine-induced mood disorders.

MDMA
MDMA is known to affect serotonergic neurons, but has been shown to inhibit synaptosomal and vesicular uptake of serotonin and dopamine to roughly the same extent in vitro. In vivo studies indicate short-term MDMA exposure causes short-term reduction in VMAT2 activity, which is reversed after 24 hours.

Clinical research
Genetic research models have shown that polymorphisms in SLC18A1 and SLC18A2, the genes that encode for VMAT1 and 2 proteins, respectively, may confer risk for some neuropsychiatric disorders; however, no specific diseases have been identified yet as directly resulting from a genetic mutation in an SLC18 gene, which codes for VMAT proteins.

Much of the current research related to VMAT explores the genetic underpinnings of neuropsychiatric disorders as they may be affected by SLC18A family mutations.

The dopaminergic neuron is known to play a central role in drug addiction and abuse and the potential role of the dopamine transporter has been well-explored as a target for amphetamine and cocaine. Current research looks toward VMAT2 as a target for such psychostimulants. A combination of imaging, neurochemical, biochemical, cell biological, genetic, and immunohistochemical evidence has been compiled to provide the most current comprehensive understanding of the role the VMAT2 plays in amphetamine and cocaine abuse and addiction through aminergic neurotransmission.

As VMATs are membrane proteins, structural information is limited and researchers have yet to completely understand the structure of both isoforms. Further studies are needed in order to determine the structure and therefore complete function of these proteins. There is preliminary evidence that the gene for VMAT1 may be linked to susceptibility to schizophrenia, bipolar disorder, and various anxiety disorders. Further studies are needed in order to confirm these findings and to gain a better understanding of the role of VMATs in the central nervous system.

Multiple single-nucleotide polymorphisms (SNPs) have been identified in the coding region of VMATs. The effects of some of these SNPs have been alteration of VMAT function, structure and regulation. Further investigation of these SNPs is required in order to distinguish whether they may be attributable to certain diseases with suspected SNP-mutation origins.

α-synuclein, a cytosolic protein found mainly in pre-synaptic nerve terminals, has been found to have regulatory interactions with the trafficking of VMATs; mutations involving α-synuclein have been linked to familial PD. Further research is needed to clarify the extent to which these proteins modulate the trafficking of VMATs, and whether they may be exploited in order to gather more information about the exact mechanism of how disorders such as PD occurs, and how they may potentially be treated.

Studies have shown that at the synaptic membrane, enzymes responsible for the synthesis of dopamine, tyrosine hydroxylase and amino acid aromatic decarboxylase are physically and functionally coupled with VMAT2. It was initially thought that the synthesis of these substances and the subsequent packaging of them into vesicles were two entirely separate processes.

Animal research
Current research related to VMAT uses VMAT2 knockout mice to explore the behavioral genetics of this transporter in an animal model. VMAT2 knockouts are known to be lethal as homozygotes, but heterozygote knockouts are not lethal and are used in many studies as a durable animal model.

From knockout and knockdown mice, researchers have discovered that it is good to have over-expression or under-expression of the VMAT genes in some circumstances. Mice are also used in drug studies, particularity studies involving the effect cocaine and methamphetamine have on VMATs. Studies involving animals have prompted scientists to work on developing drugs that inhibit or enhance the function of VMATs. Drugs that inhibit VMATs may have use in addiction but further studies are needed. Enhancing the function of VMATs may also have therapeutic value.

title: Vesicular monoamine transporter


text:
Talk:Doctor Who season 23

older entries
We should talk about what exactly are the proper titles for each of the segments of Trial of a Time Lord and/or which ones should be given priority. The pages also need a rewrite, as they are very confusing. -khaosworks 20:46, 5 Dec 2004 (UTC)

 * Well, Parts 1 to 4 are called The Mysterious Planet, 5 to 8 are called Mindwarp, 9 to 12 are Terror of the Vervoids and 13 and 14 are officially called The Ultimate Foe or Time Inc. Also, in Notes, number 2 is off-colour as the BBC actually agrees with that! Jashank 03:00, 3 January 2006 (UTC)

 * Yeah, a lot of editing between that note and now. :) --khaosworks (talk • contribs) 03:33, 3 January 2006 (UTC)

mel
is it worth noting that mel came from the future to the trail but leaves with the doctor. she would be living the same things over and over again. —The preceding unsigned comment was added by Billy turner (talk • contribs) 14:18, January 8, 2006 (UTC)

 * Probably worth a note, yes. We can also mention that the spin-offs have generally assumed that after the events of the trial the Doctor took Mel back to her regular timeline (his own future), and then waited until he would meet her for the "first" time.  I'm heading out now, but will see if I can add something later tonight. —Josiah Rowe (talk • contribs) 01:07, 9 January 2006 (UTC)

 * The note probably better belongs in The Ultimate Foe. Terror of the Vervoids already notes that Mel comes from the future. --khaosworks (talk • contribs) 01:32, 9 January 2006 (UTC)

 * Done. But it's pretty long-winded.  If anyone wants to tighten it up, please feel free to do so — I was having trouble with the wording of the various "first meetings".  What is it that Douglas Adams said about the trouble with time travel being the verb tenses? —Josiah Rowe (talk • contribs) 07:04, 9 January 2006 (UTC)

Example of parodies of frequent close-up of Doctor's face?
I'm intrigued to read in this article that the frequent close-ups of the Doctor's face in Trial of a Timelord were often parodied; do you have any examples of this, as I've not encountered this information before.

In Joke
The article states that "A frequently used in-joke throughout this serial is that, during the showing of the evidence, the Doctor interjects with protests about the overly violent nature of the scenes. " I watched the serial recently, and I can only remember one instance of this - and that was by the Inqusitor. StuartDD ( t  •   c ) 19:47, 17 September 2007 (UTC)

"Righting" the wrongs
I have replaced the use of "segment" with "part" as I feel that it answers the reviewers problem and perhaps simplifies the meaning. Please feel free to revert if this does not work. The dates have been de-linked as well. Glubbdrubb (talk) 21:12, 2 January 2009 (UTC)

You can visit my talk page if you want to help bring the out the best from this article. Glubbdrubb (talk) 21:29, 7 January 2009 (UTC)

Copyedit
I've given the prose something of a facelift on behalf of the guild of Copyeditors. Not having seen the serial, I couldn't do much but rephrase, but hopefully it flows a little better now. Please review the changes to ensure any factual errors which may have crept in are fixed. Regards, Skomorokh  03:37, 14 February 2009 (UTC)

Jargon?
The term "Gallifreyan law" is flagged as jargon. Is the term "Gallifreyan," meaning "of or by the principal language, people or government of the planet Gallifrey" really that difficult to understand? I mean, there is a link to the Wiki article on the planet and everything. Must it be spelled out as, for instance, "the law of the planet Gallifrey," when the vast majority of the people reading this article will either know that the Doctor is from there or will just click the link? I think this is an excellent example of why people joke that Wikipedians will flag things like "there are five fingers on the human hand" with the tag. Boomshadow 23:13, 20 February 2009 (UTC)
 * I added the tag. Speaking as someone who is unfamiliar with the topic, I had no idea what "Gallifreyan law" was, beyond that it was law that had something to do with something named "Gallifrey". It is not obvious that Gallifrey is a planet or even a jurisdiction; compare the phrase Draconian law for example. I copyedited this article in response to a request to the Guild of Copyeditors from an editor looking to take this through FAC. The lead section of an article is an introduction to the topic, and must summarize the most important points without relying on either the body of the article or on linked articles. For more on this, see Writing_better_articles and Lead_section. Ciao, Skomorokh  04:45, 21 February 2009 (UTC)
 * Well, the other way to say it would be "Laws of Gallifrey". You'd still need to find out what Gallifrey was (i.e. a fictional planet), but it won't be confused with something like "Draconian". DonQuixote (talk) 05:19, 21 February 2009 (UTC)
 * I tried to fix it. --Syzygy (talk) 14:56, 25 March 2009 (UTC)

Real Episodes?
Sorry, I don't know what to title this as, but I was wondering if these episodes (without the trial interrupting them) were ever made by themselves, then added the trial around them. In the same way Star Trek showed The Cage (first pilot episode) through a court case with Captain Pike since the original episode wasn't released until the '80s. Nemmex (talk) 06:28, 12 May 2013 (UTC)
 * From the outset it was intended by JNT (producer) and Eric Saward (script editor) that there would be a linking theme of a trial (with the linking scenes written by Saward), the evidence at the trial to consist of three sub-plots, which would be written by others (such as Robert Holmes) and then linked into the main story by Saward. No pre-existing material was used: it was all commissioned fresh. -- Red rose64 (talk) 08:42, 12 May 2013 (UTC)

Colour contrast problems
It seems that this article is using colours in the infobox which don't satisfy Wikipedia's accessibility guidelines. The contrast between the foreground colour and the background colour is low, which means that it may be difficult or impossible for people with visual impairments to read it.

To correct this problem, a group of editors have decided to remove support for invalid colours from Template:Infobox television season and other television season templates after 1 September 2015. If you would still like to use custom colours for the infobox and episode list in this article after that date, please ensure that the colours meet the WCAG AAA standard.

To test whether a colour combination is AAA-compliant you can use Snook's colour contrast tool. If your background colour is dark, then please test it against a foreground colour of "FFFFFF" (white). If it is light, please test it against a foreground colour of "000000" (black). The tool needs to say "YES" in the box for "WCAG 2 AAA Compliant" when you input the foreground and the background colour. You can generally make your colour compliant by adjusting the "Value (%)" fader in the middle box.

Please be sure to change the invalid colour in every place that it appears, including the infobox, the episode list, and the series overview table. If you have any questions about this, please ask on Template talk:Infobox television season. MediaWiki message delivery (talk) 05:31, 2 August 2015 (UTC)

Infoboxes Headings
While I was making some changes across the different series infoboxes today, The Trial of a Time Lord and The Key to Time stood out as the season number is not displayed anywhere in the infobox and it does seem like something that should be there. I'm not sure the best way to achieve that, I did make an attempt which did feel a little misguided and I wasn't surprised when it was reverted. I'm not sure of others thoughts if it needs to be there and how to do it if so. Cheers, Dresken (talk) 10:21, 4 July 2016 (UTC)
 * It didn't appear to be necessary while the article has existed for as long as it has, before the implementation of the granularity edits. The article explicitly starts with The Trial of a Time Lord is a 14-part science fiction serial, and the lead also contains The serial, produced as the show's twenty-third season. Same with the latter article. Alex|The|Whovian ? 10:23, 4 July 2016 (UTC)
 * I'm sorry if it came across as if I was criticising your actions, it was a good revert as I wasn't quite sure of what I had done though in the first place - I just gave it a go. Although, I felt I had to at least pose the question as the season number seemed to me to be so obviously missing - and I thought the purpose of infoboxes was to summarise the most pertinent information. While I do agree that the info is in the article, so is most of the information in the infobox so I'm not sure that alone justifies it's absence. Most of the series articles of Doctor Who do contain the season/series number. And the next/prev links to these articles from other infoboxes list the season number for the linked season (eg on Doctor Who (season 22)). Cheers, Dresken (talk) 11:39, 4 July 2016 (UTC)

Colin Baker - pushed or jumped inconsistencies & BLP fail
Currently the article says this: So two problems:
 * This was the last serial to star Colin Baker after he was dismissed from the role when it ended. (my emphasis)
 * Colin Baker makes his final appearance as the Doctor in this longest running serial before being fired by the BBC. (my emphasis)
 * ^a Although the following serial Time and the Rani was the Sixth Doctor's final appearance, Baker declined an offer to return either for the entire story (as originally offered) or solely for a regeneration scene... (my emphasis)
 * 1) that last nugget, found under the Notes heading, seems to contradict the first two assertions.
 * 2) Asserting someone has been fired/dismissed, without referring to a source, seems like a BLP failure to me. --Tagishsimon (talk) 01:33, 5 July 2016 (UTC)
 * He was fired between seasons and then asked to come back for one more story, a concession JNT managed to wrangle from Grade, but Colin declined so he could focus on his career post Who.   Etron81 (talk) 23:34, 6 July 2016 (UTC)

Rename for consistency?
Hi

I'd like to suggest that this article is renamed to "Doctor Who (Season 23)" in order to be consistent with the other seasons of the classic era of Doctor Who. Having the article titled by its "story arc name" makes it difficult when browsing seasons of the show as it is unnecessarily different. In the past I thought it was okay since this is what it's commonly known as, but even the BBC have called it 'Season 23' for their upcoming Blu-Ray release and I think it'd be much easier if this article was also called that.

Any thoughts?

HTS126 (talk) 10:10, 3 September 2019 (UTC)
 * Disagree. Per WP:NCTV, the article should be titled by its distinctive name if it has one. Same as The Key to Time. -- / Alex /21  11:25, 3 September 2019 (UTC)
 * In any case, the link Doctor Who (season 23) works perfectly well. -- Red rose64 🌹 (talk) 18:13, 3 September 2019 (UTC)

Move discussion in progress
There is a move discussion in progress on Talk:The Key to Time which affects this page. Please participate on that page and not in this talk page section. Thank you. —RMCD bot 11:17, 18 February 2020 (UTC)

Move discussion in progress
There is a move discussion in progress on Talk:Doctor Who series 14 which affects this page. Please participate on that page and not in this talk page section. Thank you. —RMCD bot 05:24, 3 May 2024 (UTC)

title: Talk:Doctor Who season 23


text:
Reading for special needs

Reading for special needs has become an area of interest as the understanding of reading has improved. Teaching children with special needs how to read was not historically pursued due to perspectives of a Reading Readiness model. This model assumes that a reader must learn to read in a hierarchical manner such that one skill must be mastered before learning the next skill (e.g., a child might be expected to learn the names of the letters in the alphabet in the correct order before being taught how to read his or her name). This approach often led to teaching sub-skills of reading in a decontextualized manner. This style of teaching made it difficult for children to master these early skills, and as a result, did not advance to more advanced literacy instruction and often continued to receive age-inappropriate instruction (e.g., singing the alphabet song).

During the mid-to-late 1970s, the education system shifted to targeting functional skills that were age appropriate for people with special needs. This led to teaching sight words that were viewed as necessary for participation in the school and community (e.g., "exit", "danger", "poison", "go"). This approach was an improvement to previous practices, but it limited the range of literacy skills that people with special needs developed.

A newer model for reading development, specifically with regard to early reading development, is emergent literacy, sometimes referred to as early literacy, model. This model purports that children begin reading from birth, and that learning to read is an interactive process based on children's exposure to literate activities. It is under this new model that children with developmental disabilities and special needs have been considered to be able to learn to read. Note that there is limited research regarding reading in special needs, but this article attempts to represent the most current evidence on this topic.

Literacy
Literacy refers to both reading and writing skills, writing being the symbolic representation of language, and reading the cognitive process of decoding and understanding the written symbol system. These are very broad and basic definitions as the definitions of these terms often vary based on the model or approach.

Approaches and models of reading
There are multiple models and approaches of reading. A few are discussed below.

The Simple View of Reading
The Simple View of Reading was originally described by Gough and Tunmer in 1986 and modified by Hoover and Gough in 1990. The Simple View suggests that the ultimate goal of reading comprehension, and in order to have good reading comprehension, one needs to have good decoding ability (e.g., ability to interpret the symbols) and good listening comprehension (e.g., one's ability to understand oral language). This model predicts four categories of readers. Readers with poor decoding skills but relatively preserved listening comprehension skills would be considered readers who are poor decoders, or dyslexic. Readers with poor listening comprehension skills are referred to as readers who are poor comprehenders. Readers with poor decoding skills and poor listening comprehension skills are considered poor readers, or sometimes referred to as garden-variety poor readers. Readers who have good decoding and listening comprehension skills are considered typical readers.

The connectionist model of reading development
Connectionist models have emphasized an interconnected and interactive system of mappings between printed words (orthography), spoken sounds/words (phonology), and word meanings (semantics). The computation of these three codes (orthographic, phonologic, and semantic) is required for reading. According to Seidenberg and McClelland, one mechanism is involved in reading (including reading regular words, exception words, and nonwords). Through development, experience with meaningful words and spelling-sound correspondences allow one's representation of semantics, orthography, and phonology to be modified. Developing representations of orthography, phonology, and semantics is an interactive process where development of one component influences and is influenced by the other components.

Dual-route approach
The dual-route approach suggests that two separate mechanisms, or routes, can be used in word reading. Words that follow spelling-sound rules (including regular words and nonwords that follow letter-to-sound rules) are processed through the nonlexical route. The nonlexical route follows a system of rules specifying the relationship between letters and sounds to process words. Conversely, exception words, or irregular words, that do not follow the spelling-sound rules are processed through the lexical route. The lexical route can be thought of as a dictionary lookup procedure.

Whole language
Reading is a linguistic act. With this, some have applied the whole language philosophy to reading instruction. In the early 1990s, a movement for whole language encouraged educators to view learning to read as being similar to learning to talk. This philosophy emphasizes learning language and reading skills through meaningful experiences instead of through decontextualized rule teaching. Some other terms for this approach of reading instruction include literature-based instruction and guided reading.

Balanced literacy instruction
To meet the recommendations of breadth and depth of literacy instruction set by the National Reading Panel (2000), many literacy programs incorporate four main components: guided reading, which focuses on comprehension skills though exposure to a wide range of literature experiences; word study, which incorporates phonics, phonemic awareness, and vocabulary instruction; self-selected reading, which provides children daily experiences in independent reading time; and writing, which focuses on both the mechanics of composition and on communicating effectively for multiple purposes (Foley & Stables, 2007).

Populations at increased risk
Children with language difficulties are at increased risk for reading disorders or difficulties that can occur early on in preschool and continue on throughout development. This population includes children with language abilities that fall below expectations for their chronological age, at a clinical level or with weaknesses in language that are not severe enough to meet criteria for a clinical diagnosis of a language disorder. Children with other disabilities can also have language impairments that can cause an increase risk of developing reading problems. Such disabilities include (but are not restricted to) specific language impairment, phonological disorder, language disorder, developmental disability, autism spectrum disorder, Down syndrome, fragile X syndrome, and cerebral palsy.

People with severe speech difficulties can use augmentative and alternative communication (AAC) devices. The importance and positive outcomes of literacy for people with language difficulties and AAC users are endless. As with everyone literacy opens doors to education, employment, and allows "individuals to exchange information, maintain interpersonal communication, to convey needs and wants and to develop channels of personal expression". However, for the AAC user literacy skills may be of even greater importance as reading and writing "allows individuals with severe speech impairments the opportunity to initiate topics, to develop ideas, to provide clarification, to communicate independently, to interact with a diverse audience, and to express ideas, thoughts, and feelings." Unfortunately, even given the importance of literacy skills people who use AAC are often not given "authentic learning opportunities" to learn literacy skills. More research is needed on how to increase literacy instruction to people with severe speech difficulties and users of AAC.

Intervention team
Classroom teachers are expected to provide the primary source of reading instruction for most students. Special education teachers may supplement the classroom instruction in reading and writing skills based on the independent performance of their students. Other professionals including a reading specialist, a speech-language pathologist, an educational or school psychologist, and an occupational therapist may also provide reading and writing support to individuals with reading and writing difficulties.

Difficulties with decoding
In general terms, individuals who have challenges in decoding are referred to as poor decoders. Dyslexia is a more specific disability where individuals demonstrate difficulty with decoding. Poor decoders have not acquired the basic knowledge of sound-letter correspondence rules, specifically phonological skills (skills that include identifying and manipulation of words, syllables, onsets, rimes, and phonemes – individual sounds). In addition, language abilities often evidence poor morphological and syntactic knowledge. Interventions that target decoding abilities may include instruction in phonics, phonological awareness, and phonemic awareness (see also Dyslexia intervention).

Difficulties with reading rate
Some individuals may have difficulty with reading rate, where they have accurate word recognition and often normal comprehension abilities, but reading speed that is typically one and a half years below grade level. Strategies that may improve reading rate include: shared/partner reading, guided reading, repeated reading, and silent reading, listening to another person fluently read (National Reading Panel, 2000 ).

Difficulties with reading fluency
Individuals may also have trouble with reading fluency, or accurate, smooth, and appropriately paced reading with accurate expression. Strategies: shared/partner reading, guided reading, repeated reading, and silent reading, listening to another person fluently read (National Reading Panel, 2000 ).

Difficulties with reading comprehension
Some individuals may have skills within the normal range on the above factors but may still have trouble with reading comprehension. These individuals are often referred to as poor comprehenders, or individuals with a specific comprehension deficit. Strategies that can be used to improve reading comprehension include: building oral and auditory language skills, including skills in: vocabulary knowledge, narratives, listening comprehension, and figurative language. Additionally, when working toward increasing reading comprehension for specific texts, one can preteach vocabulary words and discuss prior knowledge on a topic related to the text before reading. (For more strategies and information, see reading comprehension.)

Mixed reading difficulties
Children can have difficulties in more than one of the areas previously listed.

Reading in special populations
Reading difficulties in special populations such as Downs syndrome, autism, and cerebral palsy follow similar patterns of reading development and reading difficulty as described in the subgroups of reading problems section.

Down syndrome
It has been found true for children with intellectual disabilities, such as children with Down syndrome, that phonological awareness skills are often deficient and require targeted teaching. For example, studies have found that children with Down syndrome show deficits in phonological awareness, and though they can develop such skills, often rely on sight word vocabulary knowledge rather than phonological awareness skills to decode words. Given this, it is recommended that phonological awareness skills be taught in a systematic manner with explicit instruction of how to use these skills when reading.

Autism
Children with autism spectrum disorder (ASD) have been identified as having particular difficulties with reading comprehension despite normal decoding abilities,. Historically, those individuals who are especially good at decoding but have poor comprehension are considered to have hyperlexia. Not all individuals with autism, however, are poor comprehenders as there is a wide range of abilities in children on the spectrum. Despite the type of reader an individual with autism might be, individuals should be given the opportunity to learn to read. Very few studies have examined the effectiveness of interventions for reading for individuals with ASD. Using computer-assisted instruction to implement programs for individuals with ASD that target skills in decoding could be an effective way to help improve these skills in these individuals. Procedural facilitation tasks such as prereading questions, anaphoric cuing, or a cloze task helped to improve reading comprehension with the anaphoric cuing task being the most effective task.

Cerebral palsy
Children with cerebral palsy (CP) may or may not have motor speech impairments and/or language impairments, which can lead to reading difficulties. Often children with CP can be classified as having severe speech and physical impairments (SSPI), but children with other disorders can fall into this category as well. Children with SSPI can be at increased risk for reading difficulties not only because they may have language impairments, but also because they can have limited literary experiences and limited reading instruction. Additionally, parents and teachers may have low expectations of the child's ability to become a reader, which may influence experiences with text and impact literacy instruction. Assistive technology (also Alternative and Augmentative Communication devices; AAC) can be used to overcome physical barriers to manipulating books, and to augment speech motor and language difficulties (e.g., type, or select symbols to identify rhyming words), and cognitive impairments (to provide needed support required for target skill acquisition) (Copeland & Keef, 2007, see chapter 9). Of course, access to assistive devices is not sufficient for reading development. Appropriate reading instruction is required (e.g., instruction in phonological awareness skills, phonemic awareness skills, phonics, fluency, vocabulary, text comprehension, and book conventions), regularly conducted story reading sessions, constructive AT/AAC use to target literacy skills, high expectations of student literacy achievement, and text-rich environments have been found to be important for developing literacy skills in children with CP.

title: Reading for special needs


text:
Donald M. Fraser

Donald MacKay Fraser (February 20, 1924 – June 2, 2019) was an American politician from Minnesota who served as U.S. Representative from Minnesota's 5th congressional district from 1963 to 1979 and as mayor of Minneapolis from 1980 to 1994.

Early life
Fraser was born in Minneapolis, Minnesota, to Everett and Lois (McKay) Fraser, immigrants from Canada. His father studied law at Harvard University, began teaching at George Washington University and became dean of the University of Minnesota Law School in 1920. Fraser graduated from University High School in 1941 and that year, he entered the University of Minnesota. During college, he was a member of the varsity swimming team.

Having joined the US Navy ROTC, he was placed on active duty in July 1942 and continued his naval studies on campus until February 1944, when he was commissioned an officer and sent to the Pacific Theater during World War II. Fraser worked as a radar officer into the peacetime that followed, ending in 1946. In June 1946 Fraser returned to Minneapolis to study law at the University of Minnesota Law School.

Fraser served as a member of the Minnesota Law Review and wrote a law review article on the illegality of racial covenants for land, a position supported by the United States Supreme Court in 1948. Fraser earned his law degree and was admitted to the bar, the same year. He joined the politically active firm of Larson, Loevinger, Lindquist, Freeman, and Fraser. Fraser engaged in general law practice and served as municipal attorney for the suburban community of Brooklyn Center, Minnesota. He married Arvonne Skelton in 1950 and the following year, they had the first of their six children: Thomas, Mary, John, Lois, Anne, and Jean.

Political career
In 1954, Fraser was elected to the Minnesota Senate and served for eight years. In 1962, he was elected to the U.S. House of Representatives from Minnesota's Fifth District. He served there in the 88th through the 95th Congresses, from January 3, 1963 until January 3, 1979. Fraser is now best known for his work as the chair of the International Organizations and Movements subcommittee, a post he used to hold hearings on human rights violations in U.S. allies. As the historian Barbara Keys has shown, from 1973 to 1976, Fraser was a key leader in Congress in drafting legislation to reduce U.S. aid to countries whose governments engaged in a pattern of "gross violations of human rights." His efforts laid the foundations for much of Jimmy Carter's human rights agenda and transformed the way the U.S. Department of State operates, mandating that it write annual country reports on human rights and ensuring that diplomatic posts take note of human rights issues. He gave up his seat to run for the U.S. Senate. He narrowly lost the 1978 Senate primary election to Bob Short, who then lost in the general election to David Durenberger.

Fraser served as president of Americans for Democratic Action from 1974 to 1976. He was elected mayor of Minneapolis in 1979, taking office on January 2, 1980. His first mayoral term was two years; he was re-elected to three four-year terms. He was the oldest, longest-lived and longest-serving mayor in Minneapolis history. He left office on January 3, 1994, and was succeeded by the city's first female and first African-American mayor, Sharon Sayles Belton.

Fraser died on June 2, 2019, at age 95.

Papers
His papers are available for research. The collection is particularly strong in its documentation of international relations, Democratic Party policy and reform, human rights issues, environmental conservation, and women's issues, in the 1960s and 1970s.

Endorsement of United Nations Parliamentary Assembly (UNPA)
On April 23, 2014, Fraser endorsed the proposal for the United Nations Parliamentary Assembly. He is one of only six people who served in Congress to do so.

title: Donald M. Fraser


text:
Wikipedia:Articles for deletion/Topeka Constitution

Topeka Constitution
Can this be expanded, or is it a hoax? Topeka is only a city as far as I know, and unlikely to have its own constitution. And regarding the Topeka convention referred to in the article, what, is this supposed to be like the Geneva convention? I don't know of any other Topekas, and couldn't find anything on a Google search. — [[User:Knowledge Seeker|Knowledge Seeker দ (talk)]] 20:49, 5 Dec 2004 (UTC) Update: Based on the efforts of the users below, I withdraw my nomination. — [[User:Knowledge Seeker|Knowledge Seeker দ (talk)]] 23:22, 5 Dec 2004 (UTC)
 * Keep. Appears to be a Bleeding Kansas event and notable as a submitted territorial constitution.  I expanded this into a stub based on a quick Google search. --Goobergunch|? 20:55, 5 Dec 2004 (UTC)
 * Comment. I should note that the article was a 5-word substub when this VfD was submitted. --Goobergunch|? 21:32, 5 Dec 2004 (UTC)
 * Keep and please withdraw this nomination Kappa 21:24, 5 Dec 2004 (UTC)
 * since it's been verified and no longer a substub Kappa 22:25, 5 Dec 2004 (UTC)
 * Keep and agree with Kappa. -- Scott $e^{i \pi} \,\!$ 21:44, Dec 5, 2004 (UTC)
 * Thanks guys, and especially Goobergunch for expanding the article. Although perhaps it should be moved to "Topeka Convention"? Anyway, now that it has been expanded beyond the "The Topeka Convention forbade slavery" stage and looks like a proper stub, yes, I am willing to withdraw my nomination. I am uncertain how to do that, but I will remove the VfD tag from the article and remove the entry from the VfD page. — [[User:Knowledge Seeker|Knowledge Seeker দ (talk)]] 23:22, 5 Dec 2004 (UTC)


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Return to the 36 Chambers: The Dirty Version

Return to the 36 Chambers: The Dirty Version is the debut studio album by American rapper and Wu-Tang Clan member Ol' Dirty Bastard, released March 28, 1995, by Elektra Records in the United States. Intent on creating a solo album away from Wu-Tang, he signed to Elektra in January of 1993 and began a two year recording process that started that same year.

Background
It was the second solo album, after Method Man's Tical, to be released from the nine-member Wu-Tang Clan following the release of their debut album. Return to the 36 Chambers was primarily produced by RZA, with additional production from Ol' Dirty Bastard, and affiliates True Master and 4th Disciple. The album features guest appearances from Wu-Tang Clan members GZA, RZA, Method Man, Raekwon, Ghostface Killah and Masta Killa as well as Wu-Tang Killa Beez.

Return to the 36 Chambers: The Dirty Version peaked at number seven on the Billboard 200 and number two on the Top R&B/Hip-Hop Albums chart. The album sold 81,000 copies in its first week, and was certified Platinum in sales by the Recording Industry Association of America (RIAA) on March 26, 2019. Upon its release, the album received positive reviews from most music critics, with many complimenting Ol' Dirty Bastard's bizarre lyrical delivery and RZA's eerie production. The album was nominated for Best Rap Album at the 1996 Grammy Awards.

Critical reception
Upon its release, Return to the 36 Chambers received general acclaim, including award nominations and inclusions on year-end publications. In his review for Rolling Stone magazine, Touré commented: "With his raspy, lisp-punctuated voice and half-sung, half-rapped style, Ol' Dirty Bastard may well be the most original vocalist in hip-hop history." Entertainment Weekly Tiarra Mukherjee thought the album showed the "raw, innovative talent of their illest member ... The RZA's signature dissonant piano loops [sparkle] behind Dirty's delirious, reverberating delivery." Michael Bonner of Melody Maker wrote, "... an hour of cruel hard and frighteningly funny hip hop; the perfect companion piece to Wu-Tang's 36 Chambers ... the songs are driven by a vicious, unstable urgency."

By contrast, Select magazine's Matt Hall was more critical of the album. His review found the album inferior to Method Man's album Tical, stating that "From the extremely long and unfunny – intro skit, its obvious ideas are spread wafer thin across the 15 tracks."

The Dirty Version was nominated for the 1996 Grammy Award for Best Rap Album, but lost to Naughty by Nature's Poverty's Paradise.

Retrospectively, the album has continually seen positive coverage. Pitchfork contributor Sheldon Pearce lauded the album in a classic review as "a work of orchestrated negligence and a makeshift classic."

Track listing
Track listing information is taken from the official liner notes and AllMusic.

Musicians

 * Ol' Dirty Bastard – assistant engineer, mixing, producer, vocals
 * RZA – producer, mixing, vocals
 * Ghostface Killah, GZA, Masta Killa, Method Man, Raekwon, Killah Priest, Sunz Of Man, Brooklyn Zu – vocals
 * Buddha Monk – vocals, mixing
 * Big Dore – producer vocals

Additional

 * Big Dore – producer
 * True Master – producer
 * Ethan Ryman – producer, engineer
 * John Wydrycs, Tim Latham – engineer, mixing
 * Jimmie Lee, Jack Hersca – engineer, assistant engineer
 * Deden Sumandani – mixing
 * Martin Czembor – assistant engineer, mixing
 * David Sealy, Jay Nicholas – assistant engineer
 * Alli – art direction
 * Danny Clinch – photography

Accolades

 * (*) signifies unordered lists


text: Talk:Return to the 36 Chambers: The Dirty Version


text:
BASIC 8

BASIC 8 (or BASIC 8.0) – "The Enhanced Graphics System For The C128" –  was an American-designed graphics system developed by Walrusoft of Gainesville, Florida and published in 1986 by Patech Software of Somerset, New Jersey. The system was an extension of Commodore's BASIC 7.0 for the Commodore 128 computer. BASIC 8.0 provided commands lacking in BASIC 7.0 to generate (color) graphics in the C128's high-resolution 80-column mode (640×200 pixels) for RGB monitors.

The BASIC 8 package was developed by Walrusoft's Louis Wallace and David Darus, with contributions from Ken French (printer drivers) and indirectly from Richard Rylander (who allowed his 3D solids commands for the Commodore 64, originally published in Dr. Dobb's Journal, to be converted to the C128's hi-res mode).

The problem
Unlike its competitors, such as the Apple II and Atari 8-bit computers, previous iterations of BASIC in Commodore's computers lack commands for handling sound, graphics, and input devices. Instead they require awkward PEEK and POKE sequences, or machine language routines, in order to read from joysticks and paddles, and generate high-resolution graphics, sounds, and music.

The lack of sound and graphics commands in BASIC 2.0, used for the Commodore 64, led to the development of many third-party language extensions, such as Simons' BASIC, which were more accessible to non-expert users.

The Commodore 128 (C128) launched with BASIC 7.0 which contained several sound and graphics commands. However, these only worked in the "40-column" video mode, a TV or composite monitor mode with a resolution equal to the C64's. Programming graphics for the C128's new high-resolution "80-column mode", primarily intended for RGBI monitors, was more challenging than it had been with the C64, due to the C128's 8563 VDC graphics chip being more difficult to work with than the VIC-II.

A solution
BASIC 8.0, available via floppy disk or ROM, provided many graphics commands that were competitive with the C128's competitors in the high-end 8-bit microcomputer market. BASIC 8.0 was fully compatible with the various first-party RAM and video RAM expansion chips and cartridges, as well as mice and joysticks. It also provided basic 3D graphics commands. Along with a 188-page manual, the software package included an example of a GUI, and a high-res paint program, Basic Paint, both developed using BASIC 8.0.

Source code and copy protection
Source code of some of the BASIC 8 package was provided, and the BASIC 8.0 disk lacked any sort of copy protection, but this was before the Open Source Initiative; it was done as a courtesy. Instead of threatening legal action, Walrusoft simply asked users not to copy the software in the documentation. It worked; BASIC 8.0 became one of the best selling expansions for the C128.

Sample commands
In BASIC 8.0, all added commands were prefaced with the @ mark, which was not normally used in Commodore BASIC, to distinguish between the original and the new keywords. The use of this character would allow the developer to extend BASIC 7.0 without having to re-tokenize the commands as it was done on the C64. It was accomplished by trapping the syntax error generated by the command.
 * – Displays a text string on a bitmap field (similar to the BASIC 7.0's low-res  command)
 * – Switch between one of up to 32 high-res screens
 * – Fill a closed area with a color or a pattern
 * – Returns the color value of a pixel
 * – Copies part or all of a screen for later usage
 * – Displays the Walrusoft logo and the type/size of video RAM used (16K or 64K)
 * – Define part of the screen as a 'window' for purposes of drawing

title: BASIC 8


text:
Donald Fraser

Donald or Don Fraser may refer to:

Law and politics

 * Donald F. Fraser (1872–1946), Canadian politician
 * Donald M. Fraser (British politician) (born 1904), British politician, chair of the Common Wealth Party
 * Donald J. Fraser (1908–1982), Canadian politician in Nova Scotia
 * Donald M. Fraser (1924–2019), U.S. congressman from Minnesota
 * Donald Fraser (Ohio politician) (1927–2010), American politician; member of the Ohio House of Representatives

Religion

 * Donald Allan Fraser (1793–1843), Scottish Presbyterian minister in Nova Scotia and Newfoundland
 * Donald B. Fraser (1868–1952), British religious minister and political activist
 * Donald Fraser (missionary) (1870–1933), Scottish missionary in Africa

Sports

 * Donald Fraser (footballer) (fl. 1889–1890), Scottish footballer
 * Don Fraser (footballer, born 1882) (1882–1963), Australian rules footballer for Collingwood
 * Don Fraser Sr. (1901–1978), Australian rules footballer for Oakleigh and Richmond
 * Don Fraser Jr. (1922–1987), Australian rules footballer for Richmond, Port Melbourne and Prahran
 * Don Fraser (figure skater) (born 1955), Canadian pair skater

Others

 * Donald A. S. Fraser (1925–2020), Canadian statistician
 * Donald Hamilton Fraser (1929–2009), British landscape painter
 * Donald Fraser (geologist) (born 1949), English geologist

title: Donald Fraser


text: Category:Monarchs of Bohemia

title: Category:Monarchs of Bohemia


text:
HMS Hurst Castle

HMS Hurst Castle (K416) was one of 44 Castle-class corvettes built for the Royal Navy during World War II. Completed in June 1944, she began escorting convoys in August and was sunk by a German U-boat the following month.

Design and description
The Castle-class corvette was a stretched version of the preceding Flower class, enlarged to improve seakeeping and to accommodate modern weapons. The ships displaced 1010 LT at standard load and 1510 LT at deep load. They had an overall length of 252 ft, a beam of 36 ft and a deep draught of 14 ft. They were powered by a pair of triple-expansion steam engines, each driving one propeller shaft using steam provided by two Admiralty three-drum boilers. The engines developed a total of 2880 ihp and gave a maximum speed of 16.5 kn. The Castles carried enough fuel oil to give them a range of 6500 nmi at 15 kn. The ships' complement was 99 officers and ratings.

The Castle-class ships were equipped with a single QF 4 in Mk XVI gun forward, but their primary weapon was their single three-barrel Squid anti-submarine mortar. This was backed up by one depth charge rail and two throwers for 15 depth charges. The ships were fitted with two twin and a pair of single mounts for 20 mm Oerlikon light AA guns. Provision was made for a further four single mounts if needed. They were equipped with Type 145Q and Type 147B ASDIC sets to detect submarines by reflections from sound waves beamed into the water. A Type 277 search radar and a HF/DF radio direction finder rounded out the Castles' sensor suite.

Construction and career
Hurst Castle, the only ship of her name to serve in the Royal Navy, was ordered on 2 February 1943 from Caledon Shipbuilding & Engineering Company and was laid down at their shipyard in Dundee on 6 August. She was launched on 23 February 1944 and was completed on 9 June. The ship sailed to the anti-submarine training base in Tobermory, Mull, HMS Western Isles, for working up. Hurst Castle was assigned to Escort Group B3 on 3 July and escorted Convoy OS 85/KMS 59 from Britain to Gibraltar on 2 August. The group escorted Convoy SL 167/MKS 58 from Gibraltar to the UK later that month.

On 30 August Hurst Castle and her sister ship HMS Oxford Castle (K692) departed Derry, Northern Ireland, to rendezvous with Force 33 the following day. After meeting up with the other ships, they were tasked to search for the GS U-482 which had been spotted by a Royal Air Force Consolidated B-24 Liberator patrol aircraft on the morning of 1 September. At 08:25, Hurst Castle was struck port side aft by a torpedo fired by the submarine; the ship sank in six minutes at 55.58333°N, -8.18333°W with the loss of 17 ratings. The escort destroyer HMS Ambuscade (D38) rescued all 102 survivors.

title: HMS Hurst Castle