document_title: DNA replication

question_text: dna polymerase assembles new strands in what direction

text: DNA replication

text: DNA structures[edit]

text: DNA usually exists as a double-stranded structure, with both strands coiled together to form the characteristic double-helix. Each single strand of DNA is a chain of four types of nucleotides. Nucleotides in DNA contain a deoxyribose sugar, a phosphate, and a nucleobase. The four types of nucleotide correspond to the four nucleobases adenine, cytosine, guanine, and thymine, commonly abbreviated as A, C, G and T. Adenine and guanine are purine bases, while cytosine and thymine are pyrimidines. These nucleotides form phosphodiester bonds, creating the phosphate-deoxyribose backbone of the DNA double helix with the nuclei bases pointing inward (i.e., toward the opposing strand). Nucleotides (bases) are matched between strands through hydrogen bonds to form base pairs. Adenine pairs with thymine (two hydrogen bonds), and guanine pairs with cytosine (stronger: three hydrogen bonds).

text: DNA strands have a directionality, and the different ends of a single strand are called the "3' (three-prime) end" and the "5' (five-prime) end". By convention, if the base sequence of a single strand of DNA is given, the left end of the sequence is the 5' end, while the right end of the sequence is the 3' end. The strands of the double helix are anti-parallel with one being 5' to 3', and the opposite strand 3' to 5'. These terms refer to the carbon atom in deoxyribose to which the next phosphate in the chain attaches. Directionality has consequences in DNA synthesis, because DNA polymerase can synthesize DNA in only one direction by adding nucleotides to the 3' end of a DNA strand.

text: The pairing of complementary bases in DNA (through hydrogen bonding) means that the information contained within each strand is redundant. Phosphodiester (intra-strand) bonds are stronger than hydrogen (inter-strand) bonds. This allows the strands to be separated from one another. The nucleotides on a single strand can therefore be used to reconstruct nucleotides on a newly synthesized partner strand.[4]

text: DNA polymerase[edit]

text: DNA polymerases are a family of enzymes that carry out all forms of DNA replication.[6] DNA polymerases in general cannot initiate synthesis of new strands, but can only extend an existing DNA or RNA strand paired with a template strand. To begin synthesis, a short fragment of RNA, called a primer, must be created and paired with the template DNA strand.

text: DNA polymerase adds a new strand of DNA by extending the 3' end of an existing nucleotide chain, adding new nucleotides matched to the template strand one at a time via the creation of phosphodiester bonds. The energy for this process of DNA polymerization comes from hydrolysis of the high-energy phosphate (phosphoanhydride) bonds between the three phosphates attached to each unincorporated base. Free bases with their attached phosphate groups are called nucleotides; in particular, bases with three attached phosphate groups are called nucleoside triphosphates. When a nucleotide is being added to a growing DNA strand, the formation of a phosphodiester bond between the proximal phosphate of the nucleotide to the growing chain is accompanied by hydrolysis of a high-energy phosphate bond with release of the two distal phosphates as a pyrophosphate. Enzymatic hydrolysis of the resulting pyrophosphate into inorganic phosphate consumes a second high-energy phosphate bond and renders the reaction effectively irreversible.[Note 1]

text: In general, DNA polymerases are highly accurate, with an intrinsic error rate of less than one mistake for every 107 nucleotides added.[7] In addition, some DNA polymerases also have proofreading ability; they can remove nucleotides from the end of a growing strand in order to correct mismatched bases. Finally, post-replication mismatch repair mechanisms monitor the DNA for errors, being capable of distinguishing mismatches in the newly synthesized DNA strand from the original strand sequence. Together, these three discrimination steps enable replication fidelity of less than one mistake for every 109 nucleotides added.[7]

text: The rate of DNA replication in a living cell was first measured as the rate of phage T4 DNA elongation in phage-infected E. coli.[8] During the period of exponential DNA increase at 37 °C, the rate was 749 nucleotides per second. The mutation rate per base pair per replication during phage T4 DNA synthesis is 1.7 per 108.[9]

text: Replication process[edit]

text: DNA replication, like all biological polymerization processes, proceeds in three enzymatically catalyzed and coordinated steps: initiation, elongation and termination.

text: Initiation[edit]

text: For a cell to divide, it must first replicate its DNA.[10] This process is initiated at particular points in the DNA, known as "origins", which are targeted by initiator proteins.[3] In E. coli this protein is DnaA; in yeast, this is the origin recognition complex.[11] Sequences used by initiator proteins tend to be "AT-rich" (rich in adenine and thymine bases), because A-T base pairs have two hydrogen bonds (rather than the three formed in a C-G pair) and thus are easier to strand separate.[12] Once the origin has been located, these initiators recruit other proteins and form the pre-replication complex, which unzips the double-stranded DNA.

text: Elongation[edit]

text: DNA polymerase has 5'-3' activity. All known DNA replication systems require a free 3' hydroxyl group before synthesis can be initiated (note: the DNA template is read in 3' to 5' direction whereas a new strand is synthesized in the 5' to 3' direction—this is often confused). Four distinct mechanisms for DNA synthesis are recognized:

text:
All cellular life forms and many DNA viruses, phages and plasmids use a primase to synthesize a short RNA primer with a free 3' OH group which is subsequently elongated by a DNA polymerase.
The retroelements (including retroviruses) employ a transfer RNA that primes DNA replication by providing a free 3′ OH that is used for elongation by the reverse transcriptase.
In the adenoviruses and the φ29 family of bacteriophages, the 3' OH group is provided by the side chain of an amino acid of the genome attached protein (the terminal protein) to which nucleotides are added by the DNA polymerase to form a new strand.
In the single stranded DNA viruses — a group that includes the circoviruses, the geminiviruses, the parvoviruses and others — and also the many phages and plasmids that use the rolling circle replication (RCR) mechanism, the RCR endonuclease creates a nick in the genome strand (single stranded viruses) or one of the DNA strands (plasmids). The 5′ end of the nicked strand is transferred to a tyrosine residue on the nuclease and the free 3′ OH group is then used by the DNA polymerase to synthesize the new strand.

tag: ol

text: The first is the best known of these mechanisms and is used by the cellular organisms. In this mechanism, once the two strands are separated, primase adds RNA primers to the template strands. The leading strand receives one RNA primer while the lagging strand receives several. The leading strand is continuously extended from the primer by a DNA polymerase with high processivity, while the lagging strand is extended discontinuously from each primer forming Okazaki fragments. RNase removes the primer RNA fragments, and a low processivity DNA polymerase distinct from the replicative polymerase enters to fill the gaps. When this is complete, a single nick on the leading strand and several nicks on the lagging strand can be found. Ligase works to fill these nicks in, thus completing the newly replicated DNA molecule.

text: The primase used in this process differs significantly between bacteria and archaea/eukaryotes. Bacteria use a primase belonging to the DnaG protein superfamily which contains a catalytic domain of the TOPRIM fold type.[13] The TOPRIM fold contains an α/β core with four conserved strands in a Rossmann-like topology. This structure is also found in the catalytic domains of topoisomerase Ia, topoisomerase II, the OLD-family nucleases and DNA repair proteins related to the RecR protein.

text: The primase used by archaea and eukaryotes, in contrast, contains a highly derived version of the RNA recognition motif (RRM). This primase is structurally similar to many viral RNA-dependent RNA polymerases, reverse transcriptases, cyclic nucleotide generating cyclases and DNA polymerases of the A/B/Y families that are involved in DNA replication and repair. In eukaryotic replication, the primase forms a complex with Pol α.[14]

text: Multiple DNA polymerases take on different roles in the DNA replication process. In E. coli, DNA Pol III is the polymerase enzyme primarily responsible for DNA replication. It assembles into a replication complex at the replication fork that exhibits extremely high processivity, remaining intact for the entire replication cycle. In contrast, DNA Pol I is the enzyme responsible for replacing RNA primers with DNA. DNA Pol I has a 5' to 3' exonuclease activity in addition to its polymerase activity, and uses its exonuclease activity to degrade the RNA primers ahead of it as it extends the DNA strand behind it, in a process called nick translation. Pol I is much less processive than Pol III because its primary function in DNA replication is to create many short DNA regions rather than a few very long regions.

text: In eukaryotes, the low-processivity enzyme, Pol α, helps to initiate replication because it forms a complex with primase.[15] In eukaryotes, leading strand synthesis is thought to be conducted by Pol ε; however, this view has recently been challenged, suggesting a role for Pol δ.[16] Primer removal is completed Pol δ[17] while repair of DNA during replication is completed by Pol ε.

text: As DNA synthesis continues, the original DNA strands continue to unwind on each side of the bubble, forming a replication fork with two prongs. In bacteria, which have a single origin of replication on their circular chromosome, this process creates a "theta structure" (resembling the Greek letter theta: θ). In contrast, eukaryotes have longer linear chromosomes and initiate replication at multiple origins within these.[18]

text: Replication fork[edit]

text: The replication fork is a structure that forms within the nucleus during DNA replication. It is created by helicases, which break the hydrogen bonds holding the two DNA strands together. The resulting structure has two branching "prongs", each one made up of a single strand of DNA. These two strands serve as the template for the leading and lagging strands, which will be created as DNA polymerase matches complementary nucleotides to the templates; the templates may be properly referred to as the leading strand template and the lagging strand template.

text: DNA is always synthesized in the 5' to 3' direction. Since the leading and lagging strand templates are oriented in opposite directions at the replication fork, a major issue is how to achieve synthesis of nascent (new) lagging strand DNA, whose direction of synthesis is opposite to the direction of the growing replication fork.

text: Leading strand[edit]

text: The leading strand is the strand of nascent DNA which is being synthesized in the same direction as the growing replication fork. A polymerase "reads" the leading strand template and adds complementary nucleotides to the nascent leading strand on a continuous basis.

text: Lagging strand[edit]

text: The lagging strand is the strand of nascent DNA whose direction of synthesis is opposite to the direction of the growing replication fork. Because of its orientation, replication of the lagging strand is more complicated as compared to that of the leading strand. As a consequence, the DNA polymerase on this strand is seen to "lag behind" the other strand.

text: The lagging strand is synthesized in short, separated segments. On the lagging strand template, a primase "reads" the template DNA and initiates synthesis of a short complementary RNA primer. A DNA polymerase extends the primed segments, forming Okazaki fragments. The RNA primers are then removed and replaced with DNA, and the fragments of DNA are joined together by DNA ligase.

text: Dynamics at the replication fork[edit]

text: As helicase unwinds DNA at the replication fork, the DNA ahead is forced to rotate. This process results in a build-up of twists in the DNA ahead.[19] This build-up forms a torsional resistance that would eventually halt the progress of the replication fork. Topoisomerases are enzymes that temporarily break the strands of DNA, relieving the tension caused by unwinding the two strands of the DNA helix; topoisomerases (including DNA gyrase) achieve this by adding negative supercoils to the DNA helix.[20]

text: Bare single-stranded DNA tends to fold back on itself forming secondary structures; these structures can interfere with the movement of DNA polymerase. To prevent this, single-strand binding proteins bind to the DNA until a second strand is synthesized, preventing secondary structure formation.[21]

text: Clamp proteins form a sliding clamp around DNA, helping the DNA polymerase maintain contact with its template, thereby assisting with processivity. The inner face of the clamp enables DNA to be threaded through it. Once the polymerase reaches the end of the template or detects double-stranded DNA, the sliding clamp undergoes a conformational change that releases the DNA polymerase. Clamp-loading proteins are used to initially load the clamp, recognizing the junction between template and RNA primers.[2]:274-5

text: DNA replication proteins[edit]

text: At the replication fork, many replication enzymes assemble on the DNA into a complex molecular machine called the replisome. The following is a list of major DNA replication enzymes that participate in the replisome:[22]

text:
Enzyme
Function in DNA replication

DNA Helicase
Also known as helix destabilizing enzyme. Helicase separates the two strands of DNA at the Replication Fork behind the topoisomerase.

DNA Polymerase
The enzyme responsible for catalyzing the addition of nucleotide substrates to DNA in the 5' to 3' direction during DNA replication. Also performs proof-reading and error correction. There exist many different types of DNA Polymerase, (such as the DNA Polymerase III )each of which perform different functions in different types of cells.

DNA clamp
A protein which prevents elongating DNA polymerases from dissociating from the DNA parent strand.

Single-Strand Binding (SSB) Proteins
Bind to ssDNA and prevent the DNA double helix from re-annealing after DNA helicase unwinds it, thus maintaining the strand separation, and facilitating the synthesis of the nascent strand.

Topoisomerase
Relaxes the DNA from its super-coiled nature.

DNA Gyrase
Relieves strain of unwinding by DNA helicase; this is a specific type of topoisomerase

DNA Ligase
Re-anneals the semi-conservative strands and joins Okazaki Fragments of the lagging strand.

Primase
Provides a starting point of RNA (or DNA) for DNA polymerase to begin synthesis of the new DNA strand.

Telomerase
Lengthens telomeric DNA by adding repetitive nucleotide sequences to the ends of eukaryotic chromosomes. This allows germ cells and stem cells to avoid the Hayflick limit on cell division.[23]

text: Replication machinery[edit]

text: Replication machineries consist of factors involved in DNA replication and appearing on template ssDNAs. Replication machineries include primosotors are replication enzymes; DNA polymerase, DNA helicases, DNA clamps and DNA topoisomerases, and replication proteins; e.g. single-stranded DNA binding proteins (SSB). In the replication machineries these components coordinate. In most of the bacteria, all of the factors involved in DNA replication are located on replication forks and the complexes stay on the forks during DNA replication. These replication machineries are called replisomes or DNA replicase systems. These terms are generic terms for proteins located on replication forks. In eukaryotic and some bacterial cells the replisomes are not formed.

text: Since replication machineries do not move relatively to template DNAs such as factories, they are called a replication factory.[24] In an alternative figure, DNA factories are similar to projectors and DNAs are like as cinematic films passing constantly into the projectors. In the replication factory model, after both DNA helicases for leading strands and lagging strands are loaded on the template DNAs, the helicases run along the DNAs into each other. The helicases remain associated for the remainder of replication process. Peter Meister et al. observed directly replication sites in budding yeast by monitoring green fluorescent protein(GFP)-tagged DNA polymerases α. They detected DNA replication of pairs of the tagged loci spaced apart symmetrically from a replication origin and found that the distance between the pairs decreased markedly by time.[25] This finding suggests that the mechanism of DNA replication goes with DNA factories. That is, couples of replication factories are loaded on replication origins and the factories associated with each other. Also, template DNAs move into the factories, which bring extrusion of the template ssDNAs and nascent DNAs. Meister’s finding is the first direct evidence of replication factory model. Subsequent research has shown that DNA helicases form dimers in many eukaryotic cells and bacterial replication machineries stay in single intranuclear location during DNA synthesis.[24]

text: The replication factories perform disentanglement of sister chromatids. The disentanglement is essential for distributing the chromatids into daughter cells after DNA replication. Because sister chromatids after DNA replication hold each other by Cohesin rings, there is the only chance for the disentanglement in DNA replication. Fixing of replication machineries as replication factories can improve the success rate of DNA replication. If replication forks move freely in chromosomes, catenation of nuclei is aggravated and impedes mitotic segregation.[25]

text: Termination[edit]

text: Eukaryotes initiate DNA replication at multiple points in the chromosome, so replication forks meet and terminate at many points in the chromosome. Because eukaryotes have linear chromosomes, DNA replication is unable to reach the very end of the chromosomes. Due to this problem, DNA is lost each replication cycle from the end of the chromosome. Telomeres are regions of repetitive DNA close to the ends and help prevent loss of genes due to this shortening. Shortening of the telomeres is a normal process in somatic cells. This shortens the telomeres of the daughter DNA chromosome. As a result, cells can only divide a certain number of times before the DNA loss prevents further division. (This is known as the Hayflick limit.) Within the germ cell line, which passes DNA to the next generation, telomerase extends the repetitive sequences of the telomere region to prevent degradation. Telomerase can become mistakenly active in somatic cells, sometimes leading to cancer formation. Increased telomerase activity is one of the hallmarks of cancer.

text: Termination requires that the progress of the DNA replication fork must stop or be blocked. Termination at a specific locus, when it occurs, involves the interaction between two components: (1) a termination site sequence in the DNA, and (2) a protein which binds to this sequence to physically stop DNA replication. In various bacterial species, this is named the DNA replication terminus site-binding protein, or Ter protein.

text: Because bacteria have circular chromosomes, termination of replication occurs when the two replication forks meet each other on the opposite end of the parental chromosome. E. coli regulates this process through the use of termination sequences that, when bound by the Tus protein, enable only one direction of replication fork to pass through. As a result, the replication forks are constrained to always meet within the termination region of the chromosome.[26]

text: Regulation[edit]

text: Eukaryotes[edit]

text: Within eukaryotes, DNA replication is controlled within the context of the cell cycle. As the cell grows and divides, it progresses through stages in the cell cycle; DNA replication takes place during the S phase (synthesis phase). The progress of the eukaryotic cell through the cycle is controlled by cell cycle checkpoints. Progression through checkpoints is controlled through complex interactions between various proteins, including cyclins and cyclin-dependent kinases.[27] Unlike bacteria, eukaryotic DNA replicates in the confines of the nucleus.[28]

text: The G1/S checkpoint (or restriction checkpoint) regulates whether eukaryotic cells enter the process of DNA replication and subsequent division. Cells that do not proceed through this checkpoint remain in the G0 stage and do not replicate their DNA.

text: Replication of chloroplast and mitochondrial genomes occurs independently of the cell cycle, through the process of D-loop replication.

text: Replication focus[edit]

text: In vertebrate cells, replication sites concentrate into positions called replication foci.[25] Replication sites can be detected by immunostaining daughter strands and replication enzymes and monitoring GFP-tagged replication factors. By these methods it is found that replication foci of varying size and positions appear in S phase of cell division and their number per nucleus is far smaller than the number of genomic replication forks.

text: P. Heun et al.(2001) tracked GFP-tagged replication foci in budding yeast cells and revealed that replication origins move constantly in G1 and S phase and the dynamics decreased significantly in S phase.[25] Traditionally, replication sites were fixed on spatial structure of chromosomes by nuclear matrix or lamins. The Heun’s results denied the traditional concepts, budding yeasts don't have lamins, and support that replication origins self-assemble and form replication foci.

text: By firing of replication origins, controlled spatially and temporally, the formation of replication foci is regulated. D. A. Jackson et al.(1998) revealed that neighboring origins fire simultaneously in mammalian cells.[25] Spatial juxtaposition of replication sites brings clustering of replication forks. The clustering do rescue of stalled replication forks and favors normal progress of replication forks. Progress of replication forks is inhibited by many factors; collision with proteins or with complexes binding strongly on DNA, deficiency of dNTPs, nicks on template DNAs and so on. If replication forks stall and the remaining sequences from the stalled forks are not replicated, the daughter strands have nick obtained un-replicated sites. The un-replicated sites on one parent's strand hold the other strand together but not daughter strands. Therefore, the resulting sister chromatids cannot separate from each other and cannot divide into 2 daughter cells. When neighboring origins fire and a fork from one origin is stalled, fork from other origin access on an opposite direction of the stalled fork and duplicate the un-replicated sites. As other mechanism of the rescue there is application of dormant replication origins that excess origins don't fire in normal DNA replication.

text: Bacteria[edit]

text: Most bacteria do not go through a well-defined cell cycle but instead continuously copy their DNA; during rapid growth, this can result in the concurrent occurrence of multiple rounds of replication.[29] In E. coli, the best-characterized bacteria, DNA replication is regulated through several mechanisms, including: the hemimethylation and sequestering of the origin sequence, the ratio of adenosine triphosphate (ATP) to adenosine diphosphate (ADP), and the levels of protein DnaA. All these control the binding of initiator proteins to the origin sequences.

text: Because E. coli methylates GATC DNA sequences, DNA synthesis results in hemimethylated sequences. This hemimethylated DNA is recognized by the protein SeqA, which binds and sequesters the origin sequence; in addition, DnaA (required for initiation of replication) binds less well to hemimethylated DNA. As a result, newly replicated origins are prevented from immediately initiating another round of DNA replication.[30]

text: ATP builds up when the cell is in a rich medium, triggering DNA replication once the cell has reached a specific size. ATP competes with ADP to bind to DnaA, and the DnaA-ATP complex is able to initiate replication. A certain number of DnaA proteins are also required for DNA replication — each time the origin is copied, the number of binding sites for DnaA doubles, requiring the synthesis of more DnaA to enable another initiation of replication.

text: Polymerase chain reaction[edit]

text: Researchers commonly replicate DNA in vitro using the polymerase chain reaction (PCR). PCR uses a pair of primers to span a target region in template DNA, and then polymerizes partner strands in each direction from these primers using a thermostable DNA polymerase. Repeating this process through multiple cycles amplifies the targeted DNA region. At the start of each cycle, the mixture of template and primers is heated, separating the newly synthesized molecule and template. Then, as the mixture cools, both of these become templates for annealing of new primers, and the polymerase extends from these. As a result, the number of copies of the target region doubles each round, increasing exponentially.[31]


document_title: M&M's

question_text: what were the original color of m&m's

question_tokens: what were the original color of m&m 's

root

text: M&M's

text: Forrest Mars, Sr., son of the Mars Company founder, Frank C. Mars, copied the idea for the candy in the 1930s during the Spanish Civil War when he saw soldiers eating British made Smarties, chocolate pellets with a colored shell of what confectioners call hard panning (essentially hardened sugar syrup) surrounding the outside, preventing the candies from melting. Mars received a patent for his own process on March 3, 1941.[7] Production began in 1941 in a factory located at 285 Badger Avenue in Clinton Hill, Newark, New Jersey. When the company was founded it was M&M Limited.[8] The two "Ms" represent the names of Forrest E. Mars Sr., the founder of Newark Company, and Bruce Murrie, son of Hershey Chocolate's president William F. R. Murrie, who had a 20 percent share in the product.[9] The arrangement allowed the candies to be made with Hershey chocolate, as Hershey had control of the rationed chocolate at the time.[10]

tag: p

text: The demand for the candies during World War II caused an increase in production and its factory moved to bigger quarters at 200 North 12th Street in Newark, New Jersey, where it remained until 1958 when it moved to a bigger factory at Hackettstown. During the war, the candies were exclusively sold to the military.[11]

text: In 1949, the brand released the tagline "Melts in your mouth, not in your hand."[12]

text: In 1950, a black "M" was imprinted on the candies giving them a unique trademark. It was changed to white in 1954.[8]

text: In the early 1950s, the Midwest Research Institute (now MRIGlobal) in Kansas City, Missouri, worked on behalf of M&M's to perfect a process whereby 3,300 pounds (1,500 kg) of chocolate centers could be coated every hour.[13]

text: Peanut M&M's were introduced in 1954 but first appeared[14] only in the color tan. In 1960, M&M's added the yellow, red, and green colors.

text: In 1976, orange was added to the M&M rainbow to replace red, which was discontinued due to the red dye scare over Red Dyes #2 and #4 having been evaluated to be carcinogenic in nature. In spite of the fact that M&M's had used the less controversial Red Dye #40, the public was wary of any food being dyed red. Red M&M's were re-introduced in 1987.

text: In the 1980s, M&M's were introduced internationally to Australia, Canada, Europe, Hong Kong, Japan, Malaysia, and the United Kingdom.[15]

text: Although they were marketed and then withdrawn in the 1960s, almond-centered M&M's were available again in 1988 in limited release, with appearances only during Christmas and Easter times; they became a standard part of the product line in 1992.

text: Also in 1986, M&M's launched Holidays Chocolate Candies for Easter and Christmas, with the Easter candies having bunny, chick, and egg symbols on pastel-colored shells, and the Christmas candies having pine tree, bell, and candle symbols on red and green shells; with the latter also having a special mint flavor. By 1993, the holiday symbols were replaced with the standard trademark "M".

text: In 1991, Peanut Butter M&M's were released. These candies have peanut butter inside the chocolate center and the same color scheme as the other varieties. As of at least 2013, the size of the peanut butter M&M has become slightly smaller.

text: In 1995, tan M&Ms were discontinued to be replaced by blue.[16]

text: In 1996, Mars introduced "M&M's Minis", smaller candies usually sold in plastic tubes instead of bags.[17]

text: In 1999, Crispy M&M's were released. They were slightly larger than the milk chocolate variety and also featured a crispy wafer center. They were discontinued in the United States in 2005 and remained available in Europe, and Southeast Asia. In January 2015, they returned to production in the United States.

text: In July 2001, Dulce de Leche M&M's were introduced in five markets with large Hispanic populations: Los Angeles, California; San Diego, California; Miami, Florida; Mcallen-Brownsville, Texas; and San Antonio, Texas.[18] The flavor never became popular with the Hispanic community, who preferred existing M&M's flavors, and it was discontinued in most areas by early 2003.[19]

text: In 2010, Pretzel M&M's were released. They contain a crunchy, salty pretzel center inside of the chocolate coating and are about the same size as the Peanut M&M's, but their shape tends to be more spherical.

text: In 2013, the M&M's chocolate bar was re-released. It was originally released in 2004 and named M-Azing.

text: In 2014, Mega M&M's were re-introduced. Before then, the 'Mega M&M's' had been released in 2007 promoting the Shrek Movies, being dubbed "Ogre-Sized M&M's".

text: In 2015, Crispy M&M's were re-introduced in the United States. They had remained available continuously in Europe and Australia.

text: In 2016, the M&M cookie was re-introduced in the United States.

text: Also in 2016, the M&M's flavor vote was created in which the fans could vote for either honey, coffee, or chili nut M&M's to go with peanut M&M's. Coffee Nuts was announced as the winner by VEEP's Tony Hale [20]

text: In April 2017, M&M's chocolate blocks went on sale in Australia. Six varieties (milk chocolate, strawberry, crispy, hazelnut, crispy mint and almond) are available.

text: Also in 2017, Caramel M&M's were released in the United States.[21]

text: Varieties[edit]

text: M&M's varieties have included the following sizes and fillings. Note that some have only been made available for a limited time, such as white cheesecake for Easter, pumpkin spice or white candy corn for Halloween, and White Strawberry Shortcake for Valentine's Day.

text:
sizes: regular (in the following flavors), minis, mega (×3 the chocolate) and the "chocolate bar".
chocolate: milk chocolate, dark chocolate, white chocolate
nut: peanuts, almonds, peanut butter, dark chocolate peanut, strawberried peanut butter, strawberry nut
spice and herb: mint chocolate, cinnamon, pumpkin spice, white chocolate peppermint, holiday mint, gingerbread, mint crisp, pumpkin spice latte, mocha, coffee nut, honey nut, and chili nut.[22]
fruit: orange chocolate, cherry, raspberry, cherry cordial, pineapple, coconut, candy apple
dessert: pretzel, birthday cake, white chocolate candy corn, red velvet, dulce de leche, white chocolate carrot cake, vanilla shake, crispy, three milks (tres leches), pecan pie, and caramel.
colors: Easter regularly sees pastel-colored candies and Christmas bags have green and red only

tag: ul

text: Marketing[edit]

text: Over the years, marketing has helped build and expand the M&M's brand. Computer-animated graphics, personification of the candies as characters with cartoon-like storytelling, and various merchandising techniques including the introduction of new flavors, colors and customizable merchandise have helped to increase the brand's recognition as a candy icon.

text: E.T.: The Extra-Terrestrial[edit]

text: In 1982, the Mars candy bar company rejected the inclusion of M&M's in the new Steven Spielberg movie E.T.: The Extra-Terrestrial. Competitor Hershey, on the other hand, took a chance with their Reese's Pieces, which is similar to M&M's but contains a peanut butter filling, and with the blockbuster success, its candy sales dramatically increased, perhaps by as much as 300%.[23]

text: Marketing campaigns[edit]

text: In 1990, M&M's exhibited at New York's Erie County Fair a life-size fiberglass cow covered with 66,000 M&M candies—each adhered by hand with the "m" logo on each candy facing outward. According to a website run by the cow's designer, Michael Adams, the stunt earned M&M Mars $1 million in free publicity because it was reported on by Newsweek magazine, as well as the New York Post, UPI and WABC-TV, and Live with Regis.[24]

text: In 1995, the company ran the M&M's Color Campaign, a contest in which participants were given the choice of selecting purple, blue, or pink as the color of a new variety of M&M's. The announcement of the winning color (blue) was carried on most of the television networks' news programs as well as the talk shows of David Letterman and Jay Leno.[25] As part of the contest results, the company had the Empire State Building lighted in blue.[25] Although the financial details of these deals were not disclosed and neither was the campaign's effect on sales, one marketing book estimated that the company "collected millions" in free publicity and that the campaign "certainly" resulted in an increasing of the brand's awareness.[25]

text: In 1998, M&M's were styled as "The Official Candy of the New Millennium," as MM is the Roman numeral for 2000. This date was also the release of the rainbow M&M's, which are multi-colored and filled with a variety of different fillings.

text: In 2000, "Plain" M&M's (a name created in 1954 when "Peanut" M&M's were introduced) were renamed "Milk Chocolate" M&M's, and pictures of the candy pieces were added to the traditional brown and white packaging.[26]

text: Joint marketing campaigns[edit]

text: In 1990, Mars Snackfood US signed up to be a sponsor for NASCAR in the Sprint Cup Series. Drivers for the M&M's-sponsored car through the years have included Ernie Irvan (1999), Ken Schrader (2000–02), Eliott Sadler (2003–06), Ricky Rudd (2007), David Gilliland (2006–07), Kyle Busch (2008-current, won 2015 Sprint Cup Series Championship), and Michael McDowell.

text: The introduction of the blue M&M to Australia was promoted by the Australian Football League's Carlton Football Club, which wore sky-blue colored guernseys in one of its matches in 1997 instead of its traditional navy blue – a color which the successful and fiercely traditional club had worn since the 1870s.[27] In 2010, Mars Snackfood Australia described it as the most successful promotional campaign it had ever engaged in.[28]

text: In April 2005, M&M's ran the "mPire" promotion to tie in with the Star Wars: Episode III – Revenge of the Sith movie release. M&M's were offered in dark chocolate varieties (Regular and Peanut) for the first time after a string of Addams Family M&M's commercials.

text: In May 2004, M&M's ran a Shrek 2 promotion to tie in with the movie's release. M&M's were offered "ogre-sized" (65% larger) in swamp/ogre colors. They were sold at many stores displayed in huge cardboard-cutout ogre displays.

text: In the summer of 2005, Mars added "Mega M&M's" to the lineup.[29] These candies, at 55% larger than the traditional M&M's, were a little smaller than the ogre-sized version. They were available in milk chocolate and peanut varieties. The colors for Mega M&M's were changed to less-bright colors, ostensibly to appeal to older consumers: teal (replacing green), beige (replacing orange), maroon (replacing red), gold (replacing yellow), blue-gray (replacing blue), and brown.

text: In July 2006, Dark Chocolate M&M's reappeared in a purple package, followed in 2007 by Dark Chocolate Peanut M&M's. Also in 2006, the company piloted White Chocolate M&M's as a tie-in with their "Pirates of the Caribbean" promotion. The company also offered eight new flavors of M&M's via online sales, as well as at M&M's World locations: "All That Razz"; "Eat, Drink, & Be Cherry"; "A Day at the Peach"; "Orange-U-Glad"; "Mint Condition"; "AlmonDeeLicious"; "Nut What You Think"; and "Cookie Monster". Mars also released a "Crispy Mint" variety in Australia that year.

text: Also in 2006, M&M's became the official chocolate of NASCAR.

text: In 2007, M&M's introduced a limited-edition raspberry flavor called "M&M's Razzberry Chocolate Candies".

text: Also in 2007, M&M's produced a 50-foot, smiling Lady Liberty M&M statue to kick off a campaign encouraging Americans to create their own M&M characters at mms.com. The website allows for people to log in and create their own character from scratch. They can choose features such as the color, shape, hair, and accessories.

text: In 2008, two limited-edition varieties of the candy were introduced – "Wildly Cherry" M&M's, and, as a marketing tie-in with the film Indiana Jones and the Kingdom of the Crystal Skull, "Mint Crisp" M&M's.

text: M&M's also introduced another new product called "M&M's Premiums" in 2008. They come in five flavors – chocolate almond, mint chocolate, mocha, raspberry almond, and triple chocolate (milk, dark, and white chocolate), which are sold in small upright cartons with a plastic bag inside. M&M's Premiums do not have a candy shell but are coated with carnauba wax and color. Dark Chocolate was added in 2009, replacing Mocha.

text: During the summer of 2008, My M&M's launched 'Faces,' which allows consumers to print the faces of loved ones on M&M's chocolate candies at mymms.com.

text: In February 2009, M&M's launched the "M&M's Colour Break-Up" promotion in Australia where M&M's were sold in separate packs (one for each color): the packs included a code to win prizes.[30]

text: In Summer 2009, M&M's launched a limited-edition "Strawberried Peanut Butter" variant to tie in with the release of Transformers: Revenge of the Fallen. In addition, M&M's launched a limited edition "Coconut M&M's," which became a permanent item in 2010.

text: In early 2010, M&M's Bare All were released as part of a competition in Australia and New Zealand.[31] M&M's Bare All winning packs were ordinary M&M's, but without colored shells. An official website was launched, along with television advertisements.[citation needed] In April 2010, M&M's launched a new pretzel variety.[32]

text: In November 2011, Mars released M&M's Cinnamon Milk Chocolate for Christmas.

text: About the time pretzel M&M's came out, the M&M's wrapper designs in the U.S. were redone, from the old design, used from 2004-early 2010.

text: In 2012, M&M's released two new Dark Chocolate flavors: Raspberry and Mint. Also that year, M&M's released a White Chocolate flavor for the Easter season. From May 30, 2012, onwards, M&M's will be launched in Macau. Its Macanese launch language is Portuguese. In 2012, Peanut M&M's were produced in the UK in a limited edition "Red, White and Blues only" pack, in connection with the country's Diamond Jubilee and 2012 Summer Olympics. The 'M' remains white on the white candies. The commercial advertising this promotional package had Yellow donning various outfits of British stereotypes to try to get into the limited edition pack. Similarly, to promote the 2014 FIFA World Cup, Peanut M&M's were produced in a pack that contained only green, yellow, and blue candies, dubbed "Brazilian M&M's" in reference to the colors of the flag of Brazil. "Brazilian M&M's" were re-released in 2016 to promote the 2016 Summer Olympics, but are now available in both Chocolate and Peanut.

text: In 2013, M&M's launched the "Better with M" campaign, which included cause-related marketing. The campaign worked with Habitat for Humanity and encouraged fans to use a Facebook app to volunteer at the various sites where the homes were being built.[33] The advertising campaign was one of the largest that Mars had ever executed.[33] The 2013 "America Better With M" initiative sough to provide money directly to Habitat for Humanity through offering limited versions of M&Ms in red, white and blue.

text: Related brands[edit]

text: Related candy brands from Mars include Minstrels, Revels, Skittles, and Treets.

text: M&M's World specialty shops have been established in some locations, including Las Vegas, Orlando, New York, London, and Shanghai.

text: Several M&Ms-themed video games have been created. The first was M&M's: The Lost Formulas, released on September 28, 2000.

text: M&M's characters[edit]

text: Early black-and-white adverts for the candy in 1954 featured two talking, anthropomorphic M&M characters—one plain and one peanut—diving into a swimming pool full of chocolate.[34]

text: The first incarnation of the characters in CGI was a 1994 celebrity campaign which had the characters interacting with celebrities on which M&Ms candy color is their favorite. This campaign was created by Blue Sky Studios. Concurrent with 1995's blue M&M campaign, M&M's introduced second computer-animated "spokescandies" in their television commercials. The depiction and campaign of the M&M's were made by Will Vinton in 1995. Vinton previously created the clay-animation California Raisins in 1986. Around the time he worked on CGI projects, he made the depiction of the M&M's as more mature than most food mascots. These include the team of the cynical and sardonic Red (originally voiced by Jon Lovitz, thereafter Billy West[35]) who is the mascot for milk chocolate, peanut butter, and crispy M&M's, and the happy and gullible Yellow (originally voiced by John Goodman, thereafter J.K. Simmons), who is the mascot for peanut M&M's (he was originally known as "Peanut" when first introduced). Other mascots include the "cool one", Blue (voiced by Phil Hartman until his death in 1998, thereafter Robb Pruitt) who is the mascot for almond M&M's; the seductive Green (voiced by Cree Summer), who is the mascot for both dark chocolate mint and peanut butter M&M's, and the slightly neurotic Orange (voiced by Eric Kirchberger), who was introduced when Crispy M&M's were first released and returned when Pretzel M&M's debuted in 2010. Orange, upon his return, was joined by the second non-M&M mascot, Pretzel Guy (voiced by Maurice LaMarche), who "supports" him and offers helpful advice as he hates the idea of having a pretzel put inside his body.

text: Other mascots that were introduced, but no longer used, are Almond, the original green guy; Orange, a female peanut character, Chocolate Bar; the first non-M&M character that always gets foiled or outdone by Red and Yellow by being melted when M&M's can't, and the Swarmees for M&M's Minis candies, which are portrayed as destructive yet crafty troublemakers who Red and Yellow are always trying unsuccessfully to contain.

text: Female M&M's mascots were introduced in 1995. Green was the milk chocolate mascot and Tan was the peanut. Marketing discontinued Tan when they introduced the then-new Blue mascot. Green was the only female M&M's mascot from her introduction in 1995 until 2012 when M&M's unveiled a new additional spokescandy, the businesslike Ms. Brown (voiced by Miss America 1984 Vanessa Williams), the "Chief Chocolate Officer."[36] She made her debut in a Super Bowl XLVI advertisement, where several people at a party assume she is naked because her shell is the same color as her insides, which causes Red to remove his outer shell thinking "it's that kind of party", and start dancing to the LMFAO song "Sexy And I Know It."

text:
Color
Character
Type
Voice actor

Red
Red
Milk Chocolate, Dark Chocolate, Peanut Butter, and Crispy
Jon Lovitz (1995–96)
Billy West (1996–present)

Yellow
Yellow
Peanut, and Dark Chocolate Peanut
John Goodman (1995–96)
J. K. Simmons (1996–present)

Blue
Blue
Almond, Raspberry, and Dark Chocolate
Phil Hartman (1995–98)
Robb Pruitt (1998–present)

Green
Green
Dark Chocolate, Dark Chocolate Mint, and Peanut Butter
Cree Summer

Orange
Orange
Crispy and Pretzel
Eric Kirchberger

Brown
Ms. Brown
Dark Chocolate and Milk Chocolate
Vanessa Williams

Tan
Caramel (cube)
Caramel
David Cross

Brown
Pretzel (symmetrical)
Pretzel Guy
Maurice LaMarche

tag: table

text: Color changes in chocolate M&M's[edit]

text: The original colors of M&M's candies were red, yellow, violet, green and orange.[12]

text: In 1976, the Food and Drug Administration released a study that linked red dye 2 in food coloring to cancer. Though Mars did not use this dye, they decided to pull the red M&M's from the market to avoid possible misunderstandings. The red candy were reintroduced to the market ten years later.[12]

text: In early 1995, Mars ran a promotion in which consumers were invited to vote on which of blue, pink, or purple would replace the tan M&M's. Blue was the winner with 54% of the votes.[37] It replaced tan in late 1995. Consumers could vote by calling 1-800-FUN-COLOR. Ads for the new blue colors featured a plain and an almond blue M&M character as Red and Yellow take notice of trying to do takes in the commercial by painting themselves blue where they appear on stage with B.B. King singing the blues, but the filmmakers had to cut the scene as they were not the real blue M&M's; another featured Red and Yellow holding their breath to look like the new blue M&M's, where Steven Weber sees the three M&M's, Red, Yellow, and Blue; and one more featuring Weber talking to the blue M&M if he had dived into the chocolate pool, but did not.

text: In 2002, Mars solicited votes in their first ever "M&M's Global Color Vote" to add a new color from three choices: aqua (turquoise), pink, and purple. Purple won and was featured for a limited time. To help the colors get votes, Ken Schrader and his MB2 Motorsports team, who was sponsored by M&M's at the time, ran four paint schemes during the 2002 NASCAR Winston Cup Series season representing the promotion (one for aqua, one for pink, one for purple, and another one with all three colors on the car.) Specially marked packages of M&M's were released in Japan. Finding a bag of all purple M&M's entitled the customer to a prize of 100 million yen (equivalent to approximately USD $852,000).

text: On January 1, 2004, at the stroke of midnight, Mars removed all of the colors of M&M's and made them black-and-white on both their candies and the packaging. It coincided with a commercial parodying The Wizard of Oz where Dorothy is home in bed and looks out of the window and sees what the colors of the four M&M's were. The goal was to help the M&M's find their colors in black-and-white packages of M&M's, in this order: brown, orange, red, green, yellow, and blue. After all of the colors have been found, the colored packaging returned, and began carrying the theme "Chocolate is better in color".

text: Since 2004, M&M's have been available online in 17 colors, with personalized phrases on each candy on the opposite side from the "m".[38] Released around Christmas, these custom-printed M&M's were originally intended for holiday greetings, but are now available all year round.

text: For the 2008 Valentine's Day season, Mars introduced all-green bags of M&M's. This was due to common urban folklore that says green M&M's are an aphrodisiac.[39] They were brought back for 2009 alongside the "Ms. Green Heats Up Valentine's Day" contest.

text: In October 2011, Mars released M&M's White Chocolate Candy Corn exclusively in the United States for Halloween. These candies come in three candy corn inspired colors: white, bright yellow, and bright orange.

text: The following is a summary of the changes to the colors of the flagship (milk chocolate) flavor of M&M's, the only filling manufactured continuously since the beginning of the brand. From 1941 until 1969, each package contained M&M's in five different colors; when red M&M's were reintroduced in 1987, they were added as a sixth color instead of replacing any of the existing colors.

text: Health concerns[edit]

text: Red candies were eliminated in 1976[40] because of health concerns over the dye amaranth (FD&C Red #2), which was a suspected carcinogen, and were replaced with orange-colored candies. This was done despite the fact that M&M's did not contain the dye; the action was purely to satisfy worried consumers. Red candies were reintroduced ten years later, but they also kept the orange colored M&M's. Paul Hethmon, then a student at University of Tennessee, started the campaign to bring back red M&M's as a joke that would eventually become a worldwide phenomenon.[41]

text: In Europe, red M&M's contain the red dye carmine (E120).[42] Carmine, also known as cochineal, has had some campaigns launched against its use in food, because it is made from crushed insects. Notably, Starbucks in the UK had a campaign launched against it for using carmine.[43]


document_title: Aunt Em

question_text: what does aunt em feed the farm hands

question_tokens: what does aunt em feed the farm hands

text: Aunt Em

text: Oz books[edit]

text: Em spends most of her life working on farms. In The Emerald City of Oz, she states that she has raised chickens for "nearly forty years." After confessing to Dorothy that their farm was facing imminent foreclosure, they all move to the Land of Oz to live for good in the Emerald City. Princess Ozma appoints Em "Royal Mender of the Stockings of the Ruler of Oz" in order to keep her busy.

text: Her sister is married to Bill Hugson. It is never clarified in the books whether it is she or Uncle Henry who is Dorothy's blood relative. (It is also possible that "Aunt" and "Uncle" are affectionate terms of a foster family and that Dorothy is not related to either of them.)

text: She is featured slightly less than Uncle Henry in the Oz books, despite having a bigger role in the 1939 film The Wizard of Oz. Ruth Plumly Thompson gave her only two brief mentions in The Royal Book of Oz and Grampa in Oz. She had somewhat larger roles in John R. Neill's The Wonder City of Oz and The Scalawagons of Oz and Jack Snow's The Magical Mimics in Oz.

text: In The Emerald City of Oz, she shows herself particularly unamenable to Oz, asking for a back attic room, simpler clothing, and is gauche enough to tell Billina that chickens are for broiling and eating without realizing that such a conversation would be deeply offensive. Uncle Henry has seen more of the world than she has, and is much more prepared to accept Oz as it is. In this book, unlike in The Wonderful Wizard of Oz, her speech patterns and accent indicators are very similar to Sairy Ann Bilkins, the title character of Baum's Our Landlady, who, too, was quite set in her ways. Ultimately, though, she comes to the epiphany that she "ha[s] been a slave all [her] life," and is ready for her life to change.

text: She appears occasionally in the works of Baum's successors in Oz literature; one notable example is Eric Shanower's The Giant Garden of Oz.

text: Film adaptations[edit]

text: The Wizard of Oz (1925 film)[edit]

text: Em was portrayed by Mary Carr in this production. Like in Baum's 1900 novel, she is Henry's wife.

text: The Wizard of Oz (1939 film)[edit]

text: In this film she is referred to as "Auntie Em" (real name Emily), and urges Dorothy not to bother them with her concerns when she and Uncle Henry (Charley Grapewin) are counting chicks. Hickory (Tin Man's alter ego) addresses her as "Mrs. Gale" just before she offers crullers to the three farmhands, and Hunk (Scarecrow's alter ego) does so just afterward. As many women of her time, she is a knitter.

text: The name "Gale" appears on the mailbox. Miss Almira Gulch (Wicked Witch's alter ego) says to Henry, "Mr. Gale! I'd like to speak with you and your wife right away about Dorothy". Since Dorothy's last name is also Gale, this implies that Henry is her blood-uncle, and Em is his wife.

text: When Miss Gulch arrives to collect Toto, Aunt Em tells her off, saying to her: "Almira Gulch, just because you own half the county doesn't mean that you have the power to run the rest of us. For twenty-three years I've been dying to tell you what I thought of you! And now...well, being a Christian woman, I can't say it!" (Baum's character never mentions anything about religion beyond the implications of Sunday best clothing.) She is seen during the tornado calling for Dorothy after she ran away, but seeks shelter with Henry who ends up losing his hat when the storm approaches their farm. Unlike Zeke (Lion's alter ego), Hickory and Hunk also lose their hats as they struggle to pry open the cellar door. Both Aunt Em and Uncle Henry are the only characters whose roles are limited to the Kansas sequence and do not make an appearance in the Oz sequence (though in the stage show Aunt Em is Glinda and Uncle Henry is the gatekeeper), but Aunt Em is seen again in the crystal ball at the Wicked Witch's castle still looking for Dorothy. She reunites with Uncle Henry, their three farmworkers, and Professor Marvel (Wizard's alter ego) when Dorothy awakens from being unconscious.

text: Aunt Em was portrayed by Clara Blandick.

text: Journey Back to Oz (1974 animated film)[edit]

text: Margaret Hamilton who portrayed Miss Gulch and the Wicked Witch of the West voiced Aunt Em. She and Uncle Henry (voiced by Paul Ford) have a farmworker named Amos (voiced by Larry Storch). He does not have an alter ego in Oz.

text: Return to Oz (1985 film)[edit]

text: Piper Laurie plays Aunt Em, portrayed as a comely, blonde woman of perhaps fifty years — a physical depiction very different from Baum's worn and greyed original character. She is worried and concerned of Dorothy's talk of Oz and presses that they are going to have two mortgages into her mind[clarification needed] before taking her to shock therapy in administered by Dr. J.B. Worley. She mentions having a sister named Garnet who would lend them money for the therapy. Garnet may or may not have been intended to be Bill Hugson's wife. Dr. Worley calls her "Mrs. Blue," which contradicts the MGM film, in which Henry's last name is Gale, or it may refer to her maiden name.

text: Other adaptations[edit]

text: Aunt Em was played by Queen Latifah in the ABC made-for-television movie The Muppets' Wizard of Oz where this character owned a diner. In the VeggieTales episode The Wonderful Wizard of Ha's, Aunt Em and her husband Uncle Henry were substituted by a father (Dad Asparagus) to retell The Prodigal Son, a biblical parable from the Gospel of Luke.

text: She was voiced by Lurene Tuttle in 1980's Dorothy in the Land of Oz.

text: Lucie Arnaz performed this character in The Wizard of Oz in Concert: Dreams Come True (based on the 1939 MGM film) to benefit the Children's Defense Fund.

text: She was voiced by Frances Conroy in the direct-to-video animated film Tom and Jerry and the Wizard of Oz. Conroy also voiced Glinda.

text: Aunt Em appears in the Once Upon a Time episode "Ruby Slippers" portrayed by Gina Stockdale. Her being the aunt of Dorothy Gale is still intact with this show, but in this version, she, along with Dorothy, is from a fictional version Kansas and not from Earth (dubbed the Land Without Magic in the show). After Dorothy returns from her trip to Oz, Dorothy tells her family about her trip. While the rest of the family refuses to believe, Aunt Em was the only one who believed Dorothy and refuses to send Dorothy to an asylum after she was doomed insane by the others. Sometime later, Aunt Em dies, gifting Toto to Dorothy. In the Underworld, Aunt Em runs a diner called "Auntie's Chicken and Waffles" that the Blind Witch considers as the competition. Emma, Mary Margaret, and Red make an attempt to use a bottle given to them by the Blind Witch to have Aunt Em blow some kisses in there as part of an attempt for Ruby to wake Dorothy from the Sleeping Curse as part of her unfinished business of knowing that Dorothy is alright. Before she can do, Aunt Em's body turned to water before dissolving. Hades appears stating that he has spiked her soup with the River of Lost Souls as Regina stated that they were trying to help Dorothy. After mopping up the watery remains of Aunt Em and putting them in a jar, Hades informs the other souls present to let Aunt Em's fate be a warning to anyone who turn to the Underworld visitors for hope. Later on while meeting with Zelena, Hades dumped Aunt Em's watery remains into the River of Lost Souls.

text: Aunt Em appears in the crossover video game Lego Dimensions, as the character of an escort mission in which the player has to take her back home to the Gale farm.

text: Comics[edit]

text: In the comic book The Oz/Wonderland Chronicles #1, Em takes Dorothy to Henry's grave in St. Ann's Cemetery. The gravestone has been snapped in two. Em later returned the slippers to Dorothy, having kept them safe at Glinda's insistence.


document_title: Taste bud

question_text: where are most of your taste buds located on your tounge

text: Taste bud

text: Types of papillae[edit]

text: The taste buds on the tongue sit on raised protrusions of the tongue surface called papillae. There are three types of lingual papillae that contain taste buds present on the human tongue:

text:
Fungiform papillae - as the name suggests, these are slightly mushroom-shaped if looked at in longitudinal section. These are present mostly at the dorsal surface of the tongue, as well as at the sides. Innervated by facial nerve.
Foliate papillae - these are ridges and grooves towards the posterior part of the tongue found at the lateral borders. Innervated by facial nerve (anterior papillae) and glossopharyngeal nerve (posterior papillae).
Circumvallate papillae - there are only about 10 to 14 of these papillae on most people, and they are present at the back of the oral part of the tongue. They are arranged in a circular-shaped row just in front of the sulcus terminalis of the tongue. They are associated with ducts of Von Ebner's glands, and are innervated by the glossopharyngeal nerve.

text: The fourth type of papillae the filiform papillae are the most numerous but do not contain taste buds.[4][5] They are characterized by increased keratinisation and are involved in the mechanical aspect of providing abrasion.

text: Salt, sweet, sour and umami tastes causes depolarization of the taste cells, although different mechanisms are applied.

text: Bitter causes an internal release of Ca2+, no external Ca2+ is required.

text: The bud is formed by two kinds of cells: supporting cells and gustatory cells.

text: The supporting (sustentacular cells) are mostly arranged like the staves of a cask, and form an outer envelope for the bud. Some, however, are found in the interior of the bud between the gustatory cells.

text: The gustatory (taste) cells, a chemoreceptor, occupy the central portion of the bud; they are spindle-shaped, and each possesses a large spherical nucleus near the middle of the cell.

text: The peripheral end of the cell terminates at the gustatory pore in a fine hair filament, the gustatory hair.

text: The central process passes toward the deep extremity of the bud, and there ends in single or bifurcated varicosities.

text: The nerve fibrils after losing their medullary sheaths enter the taste bud, and end in fine extremities between the gustatory cells; other nerve fibrils ramify between the supporting cells and terminate in fine extremities; these, however, are believed to be nerves of ordinary sensation and not gustatory.

text: The average life of a taste bud is 10 days[6]


document_title: The Big Sick

question_text: who played the mother in the big sick

question_tokens: who played the mother in the big sick

text: The Big Sick

text: Plot[edit]

text: Kumail is a standup comedian in Chicago trying to get his big break. He has a one-man show about his Pakistani background. His Muslim immigrant parents frequently set him up with young Pakistani women, hoping he will follow their example of an arranged marriage, but he is uninterested. He also lies to them about his faith, not sharing their beliefs.

text: During a show, Kumail is heckled by Emily, a white woman in the audience. He approaches her after the show and their one-night stand develops into a long-term relationship. Kumail does not tell his family about Emily, as they would disapprove, and his relationship with Emily is strained when he is unwilling to commit. When Emily finds pictures of the women Kumail's parents have set him up with, Kumail admits he does not see a long-term future with her due to his family's expectations. Emily ends their relationship.

text: Kumail learns weeks later that Emily has been taken to the hospital after having fainted. A doctor tells him that Emily has a serious lung infection and must be immediately placed in an induced coma with tracheal intubation. He signs the permission form and calls her parents, Beth and Terry. Aware of their daughter's messy breakup with Kumail, they tell him he is not needed, but Kumail stays and the three become close as they deal with Emily's illness.

text: Surgery is ineffective and the infection spreads to Emily's kidneys. Beth wants to transfer Emily to a different hospital, but Kumail and Terry disagree. Beth and Terry argue, and she brings up Terry's past. Terry stays at Kumail’s apartment where he reveals that he cheated on Beth and regrets it.

text: Kumail's parents visit his apartment, angry that he is not taking their marriage suggestions seriously. Kumail tells them that he does not want an arranged marriage and has no interest in Islam, and reveals his relationship with Emily; his parents disown him. As Kumail prepares for an audition for the Montreal Comedy Festival, he learns that the infection has reached Emily's heart. Distraught on stage, Kumail tearfully spends the audition talking about his fears about Emily’s health, and fails the audition.

text: Emily wakes from her coma. The doctors explain she has adult-onset Still's disease, a rare but treatable illness; Kumail inadvertently helped them diagnose when he mentioned she had an ankle injury that was slow to heal. Still bitter from their breakup, Emily tells Kumail to leave. Beth invites Kumail to Emily's homecoming party. Kumail asks Emily to take him back, but she refuses, still unsure of how she feels.

text: Kumail decides to move to New York City with two comedian friends. He tells his family about his plans and refuses to allow them to disown him. Emily discovers a video of Kumail's disastrous audition in which he spoke openly about his feelings for Emily. Emily visits Kumail after his one-man show. After he tells her about his plans to move to New York City, she tells him she appreciates everything he did for her while she was in a coma.

text: As Kumail prepares to move to New York, his parents visit him. They tell him they are still angry but give him a dish of his favorite food and ask him to stay in touch. At a performance in New York, Kumail is heckled by someone in the crowd; he sees that it is Emily.

text: Cast[edit]

text:
Kumail Nanjiani as Kumail
Zoe Kazan as Emily Gardner (based on Emily V. Gordon), Beth and Terry’s daughter
Holly Hunter as Beth Gardner, Emily’s mother and Terry’s wife
Ray Romano as Terry Gardner, Emily’s father and Beth’s husband
Bo Burnham as CJ
Zenobia Shroff as Sharmeen
Anupam Kher as Azmat
Adeel Akhtar as Naveed
Aidy Bryant as Mary
Rebecca Naomi Jones as Jessie
Kurt Braunohler as Chris
Shenaz Treasury as Fatima
David Alan Grier as Andy Dodd
Vella Lovell as Khadija
Linda Emond as Dr. Cunningham

text: Production[edit]

text: In December 2015, it was announced Kumail Nanjiani would star in the film from a screenplay written by him and wife Emily V. Gordon, while Judd Apatow would produce alongside Barry Mendel, under their Apatow Productions banner, while FilmNation Entertainment would finance the film.[6] Michael Andrews composed the film's score.[7]

text: Casting[edit]

text: In February 2016, Zoe Kazan joined the cast,[8] along with Holly Hunter and Ray Romano in April 2016.[9] Unlike many of the other portrayals in The Big Sick, Romano's and Hunter's roles in the film were not modeled after Emily V. Gordon's actual parents. Instead, Hunter said that she never contacted or spoke with Gordon's mother before playing the part, as she wanted to "feel my own freedom with the character".[10] In May 2016, Aidy Bryant, Bo Burnham, Adeel Akhtar and Kurt Braunohler also joined the cast of the film.[11][12] David Alan Grier was cast in The Big Sick after he met with Emily V. Gordon when she was a writer for The Carmichael Show. Grier's role was part of a larger subplot that was ultimately cut from the film's release.[13][14]

text: Anupam Kher's casting in the film was reported in June 2016. He was directly contacted by Kumail Nanjiani himself, as Nanjiani's own father had recommended Kher play the role. According to Kher himself, his character's last scene in the film was the first scene he had filmed for the production. The Big Sick marks Kher's 500th appearance in a feature film.[15][16][17][18]

text: Writing[edit]

text: The screenplay for The Big Sick is written by Emily V. Gordon and her husband Kumail Nanjiani and is loosely based on the real-life courtship between them before their marriage in 2007. According to Nanjiani, the idea to make a script about them was first inspired by the film's eventual co-producer Judd Apatow when the two met while appearing in a 2012 episode of the You Made It Weird podcast.[19] Developed over the course of three years, the script has been called semi-autobiographical because, in addition to the two lead characters modeled after them, many of the events occurring during Gordon and Nanjiani's relationship are noted as being portrayed to an extent in the film.[20][21][22][23][24]

text: Though not part of the original script, a real-life incident involving Holly Hunter heckling an unnamed player during a US Open tennis match inspired a similar scene in the film where Nanjiani's character is heckled during one of his stand-up sets.[25]

text: Filming[edit]

text: Principal photography began on May 11, 2016.[26]

text: Release[edit]

text: The Big Sick premiered at the Sundance Film Festival on January 20, 2017.[27] Shortly after, Amazon Studios acquired distribution rights to the film, after bids from Sony Pictures and Fox Searchlight Pictures.[28] The $12 million acquisition marked the second-largest deal of the 2017 festival.[29][30] Lionsgate partnered with Amazon on the U.S. release, and spent around $20 million on marketing the film.[31][32] It also screened at South by Southwest on March 16, 2017, where it won an Audience Award in the category Festival Favorites.[33] The film began a limited release on June 23, 2017, before going wide on July 14, 2017.[34]

text: Box office[edit]

text: The Big Sick grossed $42.9 million in the United States and Canada, and $13.4 million in other territories, for a total gross of $56.2 million.[3]

text: In the film's limited opening weekend, it made $421,577 from five theaters (a per-theater gross of $84,315, the best of 2017 until Lady Bird in November), finishing 17th at the box office.[35] The film expanded to 2,597 theaters on July 14, 2017, and was projected to gross $9–11 million over the weekend.[32] It grossed $7.6 million over the weekend, finishing fifth at the box office.[36] On July 25, the film crossed $26 million, becoming the second highest-grossing independent film of 2017.[37][38]

text: Critical response[edit]

text: On review aggregator Rotten Tomatoes, the film holds an approval rating of 98% based on 252 reviews, with an average rating of 8.2/10. The site's critical consensus reads, "Funny, heartfelt, and intelligent, The Big Sick uses its appealing leads and cross-cultural themes to prove the standard romcom formula still has some fresh angles left to explore."[39] It was rated as Rotten Tomatoes' #1 summer movie of 2017.[40] On Metacritic, which assigns a normalized rating to reviews, the film received an average score of 86 out of 100, based on 47 critics, indicating "universal acclaim."[41] Audiences polled by CinemaScore gave the film an average grade of "A" on an A+ to F scale.[36] According to a poll conducted by AwardsDaily in July 2017, polling one hundred critics, The Big Sick was voted the second best film of 2017 so far, behind Get Out.[42]

text: In a review for the Toronto Star, Peter Howell gave The Big Sick four stars out of four, praising the film as "hilarious and heartbreaking", as well as applauding the performances of the entire cast.[43] Richard Roeper similarly gave the film four stars out of four in his review for the Chicago Sun-Times, labeling it as "without a doubt one of the best romantic comedies I have seen in a long time."[44] The Big Sick was also selected as an "NYT Critic's Pick" by Manohla Dargis of The New York Times. In her review, Dargis praised Michael Showalter's direction and the screenplay by Emily V. Gordon and Kumail Nanjiani for "revitalizing an often moribund subgenre with a true story of love, death and the everyday comedy of being a 21st-century American.[45]

text: While praising the lead performances of Nanjiani, Kazan and Romano, Robbie Collin of The Daily Telegraph wrote a mixed review for The Big Sick. Collin contends that director Showalter "never comes close to dampening down its leading couple's inextinguishable appeal."[46] In a negative review for The New Yorker, Richard Brody wrote that the film "suffers from an excess of pleasantness, and this very pleasantness thins out its substance, blands out its tone, weakens its comedy."[47]

text: Accolades[edit]

text:
Award
Date of ceremony
Category
Recipient(s) and nominee(s)
Result
Ref.

AARP's Movies for Grownups Awards
February 5, 2018
Best Supporting Actress
Holly Hunter
Nominated
[48][49][50]

Best Intergenerational Film
The Big Sick
Nominated

Academy Awards
March 4, 2018
Best Original Screenplay
Emily V. Gordon and Kumail Nanjiani
Nominated
[51]

American Film Institute
January 5, 2018
Top Ten Films of the Year
The Big Sick
Won
[52]

Austin Film Critics Association
January 8, 2018
Best Supporting Actress
Holly Hunter
Nominated
[53]

Best Original Screenplay
Emily V. Gordon and Kumail Nanjiani
Nominated

Top 10 Films
The Big Sick
9th Place

Cinema For Peace
February 19, 2018
Most Valuable Movie of the Year
The Big Sick
Nominated
[54]

Chicago Film Critics Association
December 12, 2017
Best Supporting Actress
Holly Hunter
Nominated
[55]
[56]

Best Original Screenplay
Emily V. Gordon and Kumail Nanjiani
Nominated

Critics' Choice Movie Awards
January 11, 2018
Best Picture
The Big Sick
Nominated
[57]

Best Supporting Actress
Holly Hunter
Nominated

Best Original Screenplay
Emily V. Gordon and Kumail Nanjiani
Nominated

Best Comedy
The Big Sick
Won

Best Actor in a Comedy
Kumail Nanjiani
Nominated

Best Actress in a Comedy
Zoe Kazan
Nominated

Dallas–Fort Worth Film Critics Association
December 13, 2017
Best Supporting Actress
Holly Hunter
4th Place
[58]

Detroit Film Critics Society
December 7, 2017
Best Screenplay
Emily V. Gordon and Kumail Nanjiani
Nominated
[59]

Best Supporting Actress
Holly Hunter
Nominated

Best Ensemble
The cast of The Big Sick
Nominated

Empire Awards
March 18, 2018
Best Comedy
The Big Sick
Pending
[60]
[61]

Florida Film Critics Circle
December 23, 2017
Best Supporting Actress
Holly Hunter
Nominated
[62]
[63]

Best Original Screenplay
Emily V. Gordon and Kumail Nanjiani
Nominated

Best Cast
The cast of The Big Sick
Nominated

Georgia Film Critics Association
January 12, 2018
Best Picture
The Big Sick
Nominated
[64]

Best Supporting Actress
Holly Hunter
Nominated

Best Original Screenplay
Emily V. Gordon and Kumail Nanjiani
Nominated

Golden Tomato Awards
January 3, 2018
Best Wide Release 2017
The Big Sick
2nd Place
[65]

Best Romance Movie 2017
The Big Sick
Won

Gotham Awards
November 27, 2017
Best Screenplay
Emily V. Gordon and Kumail Nanjiani
Nominated
[66]

Houston Film Critics Society
January 6, 2018
Best Picture
The Big Sick
Nominated
[67]

Best Supporting Actress
Holly Hunter
Nominated

Best Screenplay
Emily V. Gordon and Kumail Nanjiani
Nominated

Humanitas Prize
February 16, 2018
Feature – Comedy
Emily V. Gordon and Kumail Nanjiani
Pending
[68]

IGN Awards
December 19, 2017
Movie of the Year
The Big Sick
Nominated
[69]

Best Comedy Movie
The Big Sick
Runner-up

Best Lead Performer in a Movie
Kumail Nanjiani
Nominated

Best Supporting Performer in a Movie
Holly Hunter
Nominated

Ray Romano
Nominated

Independent Spirit Awards
March 3, 2018
Best Supporting Female
Holly Hunter
Nominated
[70]

Best First Screenplay
Emily V. Gordon and Kumail Nanjiani
Won

IndieWire Critics Poll
December 19, 2017
Best Supporting Actress
Holly Hunter
4th Place
[71]

London Film Critics' Circle
January 28, 2018
Supporting Actress of the Year
Holly Hunter
Nominated
[72]

Make-Up Artists and Hair Stylists Guild
February 24, 2018
Feature Motion Picture: Best Contemporary Makeup
Kirsten Sylvester and Leo Won
Nominated
[73]

Feature Motion Picture: Best Contemporary Hair Styling
Tonia Ciccone and Toni Roman-grimm
Nominated

Online Film Critics Society
December 28, 2017
Best Supporting Actress
Holly Hunter
Nominated
[74]

Palm Springs International Film Festival
January 2, 2018
Career Achievement Award
Holly Hunter
Won
[75]

Producers Guild of America
January 20, 2018
Best Theatrical Motion Picture
Judd Apatow and Barry Mendel
Nominated
[76]

San Diego Film Critics Society
December 11, 2017
Best Supporting Actress
Holly Hunter
Nominated
[77]
[78]

Best Original Screenplay
Emily V. Gordon and Kumail Nanjiani
Nominated

Best Comedic Performance
Ray Romano
Nominated

San Francisco Film Critics Circle
December 10, 2017
Best Supporting Actress
Holly Hunter
Nominated
[79]

Best Original Screenplay
Emily V. Gordon and Kumail Nanjiani
Nominated

Santa Barbara International Film Festival
January 31, 2018
Virtuoso Award
Kumail Nanjiani
Won
[80]

Satellite Awards
February 10, 2018
Best Film
The Big Sick
Nominated
[81]

Best Supporting Actress
Holly Hunter
Nominated

Screen Actors Guild Awards
January 21, 2018
Outstanding Performance by a Cast in a Motion Picture
The cast of The Big Sick
Nominated
[82]

Outstanding Performance by a Female Actor in a Supporting Role
Holly Hunter
Nominated

Seattle Film Critics Society
December 18, 2017
Best Supporting Actress
Holly Hunter
Nominated
[83]

Best Screenplay
Emily V. Gordon and Kumail Nanjiani
Nominated

South by Southwest
March 18, 2017
Audience Award: Festival Favorites
The Big Sick
Won
[84]

St. Louis Film Critics Association
December 17, 2017
Best Supporting Actress
Holly Hunter
Runner-up
[85]

Best Original Screenplay
Emily V. Gordon and Kumail Nanjiani
Nominated

Washington D.C. Area Film Critics Association
December 8, 2017
Best Supporting Actress
Holly Hunter
Nominated
[86]

Best Original Screenplay
Emily V. Gordon and Kumail Nanjiani
Nominated

Women Film Critics Circle
December 17, 2017
Best Screen Couple
The Big Sick
Won
[87]
[88]

Writers Guild of America
February 11, 2018
Best Original Screenplay
Emily V. Gordon and Kumail Nanjiani
Nominated
[89]


document_title: Italy at the FIFA World Cup

question_text: when was the last time italy never qualified for the world cup

text: Italy at the FIFA World Cup

text: FIFA World Cup record[edit]

text: Champions       Runners-up       Third Place       Fourth Place

text:
FIFA World Cup record

Year

Round

Position

Pld

W

D*

L

GF

GA

 1930

Did Not Enter

 1934

Champions

1st

5

4

1

0

12

3

 1938

Champions

1st

4

4

0

0

11

5

 1950

Group Stage

7th

2

1

0

1

4

3

 1954

10th

3

1

0

2

6

7

 1958

Did Not Qualify

 1962

Group Stage

9th

3

1

1

1

3

2

 1966

9th

3

1

0

2

2

2

 1970

Runners-up

2nd

6

3

2

1

10

8

 1974

Group Stage

10th

3

1

1

1

5

4

 1978

Fourth Place

4th

7

4

1

2

9

6

 1982

Champions

1st

7

4

3

0

12

6

 1986

Round of 16

12th

4

1

2

1

5

6

 1990

Third Place

3rd

7

6

1

0

10

2

 1994

Runners-up

2nd

7

4

2

1

8

5

 1998

Quarter Final

5th

5

3

2

0

8

3

  2002

Round of 16

15th

4

1

1

2

5

5

 2006

Champions

1st

7

5

2

0

12

2

 2010

Group Stage

26th

3

0

2

1

4

5

 2014

22nd

3

1

0

2

2

3

 2018

Did Not Qualify

 2022

TBD

Total

4 Titles

18/21

83

45

21

17

128

77

text:
showItaly's World Cup record

First Match

Italy  7–1  United States (27 May 1934; Rome, Italy)

Biggest Win

Italy  7–1  United States (27 May 1934; Rome, Italy)

Biggest Defeat

Switzerland   4–1  Italy (23 June 1954; Basel, Switzerland)Brazil  4–1  Italy (21 June 1970; Mexico City, Mexico)

Best Result

Champions at the 1934, 1938, 1982, and 2006 World Cups

Worst Result

26th at the 2010 World Cup

text: Winning World Cups[edit]

text:
Year

Manager

Captain

Winning Goal Scorer(s)

1934

Vittorio Pozzo

Gianpiero Combi

Raimundo Orsi, Angelo Schiavio

1938

Vittorio Pozzo

Giuseppe Meazza

Gino Colaussi (2), Silvio Piola (2)

1982

Enzo Bearzot

Dino Zoff

Paolo Rossi, Marco Tardelli, Alessandro Altobelli

2006

Marcello Lippi

Fabio Cannavaro

Marco Materazzi, Fabio Grosso (decisive penalty)

text: By Match[edit]

text: Italy's score listed first

text:
World Cup

Round

Opponent

Score

Venue

Scorers

1934
Round of 16
 United States
7–1
Rome
Schiavio (3), Orsi (2), Ferrari, Meazza

Quarter-finals
 Spain
1–1 (a.e.t.)
Florence
Ferrari

 Spain
1–0
Florence
Meazza

Semi-finals
 Austria
1–0
Milan
Guaita

Final
 Czechoslovakia
2–1 (a.e.t.)
Rome
Orsi, Schiavio

1938
Round of 16
 Norway
2–1 (a.e.t.)
Marseille
Ferraris, Piola

Quarter-finals
 France
3–1
Paris
Piola (2), Colaussi

Semi-finals
 Brazil
2–1
Marseille
Colaussi, Meazza

Final
 Hungary
4–2
Paris
Colaussi (2), Piola (2)

1950
Group stage
 Sweden
2–3
São Paulo
Carapellese, Muccinelli

 Paraguay
2–0
São Paulo
Carapellese, Pandolfini

1954
Group stage
  Switzerland
1–2
Lausanne
Boniperti

 Belgium
4–1
Lugano
Pandolfini, Galli, Frignani, Lorenzi

  Switzerland
1–4
Basel
Nesti

1962
Group stage
 West Germany
0–0
Santiago
&—

 Chile
0–2
Santiago
&—

  Switzerland
3–0
Santiago
Bulgarelli (2), Mora

1966
Group stage
 Chile
2–0
Sunderland
A. Mazzola, Barison

 Soviet Union
0–1
Sunderland
&—

 North Korea
0–1
Middlesbrough
&—

1970
Group stage
 Sweden
1–0
Toluca
Domenghini

 Uruguay
0–0
Puebla
&—

 Israel
0–0
Toluca
&—

Quarter-finals
 Mexico
4–1
Toluca
Riva (2), Guzmán (o.g.), Rivera

Semi-finals
 West Germany
4–3 (a.e.t.)
Mexico City
Boninsegna, Burgnich, Riva, Rivera

Final
 Brazil
1–4
Mexico City
Boninsegna

1974
Group stage
 Haiti
3–1
Munich
Rivera, Benetti, Anastasi

 Argentina
1–1
Stuttgart
Perfumo (o.g.)

 Poland
1–2
Stuttgart
Capello

1978
Group stage
 France
2–1
Mar del Plata
Rossi, Zaccarelli

 Hungary
3–1
Mar del Plata
Rossi, Bettega, Benetti

 Argentina
1–0
Buenos Aires
Bettega

Second round
 West Germany
0–0
Buenos Aires
&—

 Austria
1–0
Buenos Aires
Rossi

 Netherlands
1–2
Buenos Aires
Brandts (o.g.)

Third place play-off
 Brazil
1–2
Buenos Aires
Causio

1982
Group stage
 Poland
0–0
Vigo
&—

 Peru
1–1
Vigo
Conti

 Cameroon
1–1
Vigo
Graziani

Second round
 Argentina
2–1
Barcelona
Tardelli, Cabrini

 Brazil
3–2
Barcelona
Rossi (3)

Semi-finals
 Poland
2–0
Barcelona
Rossi (2)

Final
 West Germany
3–1
Madrid
Rossi, Tardelli, Altobelli

1986
Group stage
 Bulgaria
1–1
Mexico City
Altobelli

 Argentina
1–1
Puebla
Altobelli

 South Korea
3–2
Puebla
Altobelli (2), Cho K. R. (o.g.)

Round of 16
 France
0–2
Mexico City
&—

1990
Group stage
 Austria
1–0
Rome
Schillaci

 United States
1–0
Rome
Giannini

 Czechoslovakia
2–0
Rome
Schillaci, R. Baggio

Round of 16
 Uruguay
2–0
Rome
Schillaci, Serena

Quarter-finals
 Republic of Ireland
1–0
Rome
Schillaci

Semi-finals
 Argentina
1–1 (a.e.t.)  (3–4  pen.)
Naples
Schillaci

Third place play-off
 England
2–1
Bari
R. Baggio, Schillaci

1994
Group stage
 Republic of Ireland
0–1
East Rutherford
&—

 Norway
1–0
East Rutherford
D. Baggio

 Mexico
1–1
Washington, D.C.
Massaro

Round of 16
 Nigeria
2–1 (a.e.t.)
Foxborough
R. Baggio (2)

Quarter-finals
 Spain
2–1
Foxborough
D. Baggio, R. Baggio

Semi-finals
 Bulgaria
2–1
East Rutherford
R. Baggio (2)

Final
 Brazil
0–0 (a.e.t.)  (2–3  pen.)
Pasadena
&—

1998
Group stage
 Chile
2–2
Bordeaux
Vieri, R. Baggio

 Cameroon
3–0
Montpellier
Vieri (2), Di Biagio

 Austria
2–1
Saint-Denis
Vieri, R. Baggio

Round of 16
 Norway
1–0
Marseille
Vieri

Quarter-finals
 France
0–0 (a.e.t.)  (3–4  pen.)
Saint-Denis
&—

2002
Group stage
 Ecuador
2–0
Sapporo
Vieri (2)

 Croatia
1–2
Ibaraki
Vieri

 Mexico
1–1
Ōita
Del Piero

Round of 16
 South Korea
1–2 (a.e.t.)
Daejeon
Vieri

2006
Group stage
 Ghana
2–0
Hanover
Pirlo, Iaquinta

 United States
1–1
Kaiserslautern
Gilardino

 Czech Republic
2–0
Hamburg
Materazzi, Inzaghi

Round of 16
 Australia
1–0
Kaiserslautern
Totti

Quarter-finals
 Ukraine
3–0
Hamburg
Toni (2), Zambrotta

Semi-finals
 Germany
2–0 (a.e.t.)
Dortmund
Grosso, Del Piero

Final
 France
1–1 (a.e.t.)  (5–3  pen.)
Berlin
Materazzi

2010
Group stage
 Paraguay
1–1
Cape Town
De Rossi

 New Zealand
1–1
Nelspruit
Iaquinta

 Slovakia
2–3
Johannesburg
Di Natale, Quagliarella

2014
Group stage
 England
2–1
Manaus
Marchisio, Balotelli

 Costa Rica
0–1
Recife
&—

 Uruguay
0–1
Natal
&—

text: Record by Opponent[edit]

text:
FIFA World Cup matches (by team)

Opponent

Wins

Draws

Losses

Total

Goals Scored

Goals Conceded

 Argentina
2
3
0
5
6
4

 Australia
1
0
0
1
1
0

 Austria
4
0
0
4
5
1

 Belgium
1
0
0
1
4
1

 Brazil
2
1
2
5
7
9

 Bulgaria
1
1
0
2
3
2

 Cameroon
1
1
0
2
4
1

 Chile
1
1
1
3
4
4

 Costa Rica
0
0
1
1
0
1

 Croatia
0
0
1
1
1
2

 Czech Republic
1
0
0
1
2
0

 Czechoslovakia
2
0
0
2
4
1

 Ecuador
1
0
0
1
2
0

 England
2
0
0
2
4
2

 France
2
2
1
5
6
5

 Germany
3
2
0
5
9
4

 Ghana
1
0
0
1
2
0

 Haiti
1
0
0
1
3
1

 Hungary
2
0
0
2
7
3

 Israel
0
1
0
1
0
0

 Mexico
1
2
0
3
6
3

 Netherlands
0
0
1
1
1
2

 New Zealand
0
1
0
1
1
1

 Nigeria
1
0
0
1
2
1

 North Korea
0
0
1
1
0
1

 Norway
3
0
0
3
4
1

 Paraguay
1
1
0
2
3
1

 Peru
0
1
0
1
1
1

 Poland
1
1
1
3
3
2

 Republic of Ireland
1
0
1
2
1
1

 Slovakia
0
0
1
1
2
3

 South Korea
1
0
1
2
4
4

 Soviet Union
0
0
1
1
0
1

 Spain
2
1
0
3
4
2

 Sweden
1
0
1
2
3
3

  Switzerland
1
0
2
3
5
6

 Ukraine
1
0
0
1
3
0

 United States
2
1
0
3
9
2

 Uruguay
1
1
1
3
2
1

text: World Cup Finals[edit]

text: 1934 World Cup Final v Czechoslovakia[edit]

text: With temperatures around 40 °C (104 °F), Italy won their home tournament in 1934 after going into extra time against Czechoslovakia.

text:
Italy

2–1 (a.e.t.)

 Czechoslovakia

Orsi  81'Schiavio  95'

Report

Puč  71'

text:
GK
Gianpiero Combi (c)

RB
Eraldo Monzeglio

LB
Luigi Allemandi

RH
Attilio Ferraris

CH
Luis Monti

LH
Luigi Bertolini

OR
Enrique Guaita

IR
Giuseppe Meazza

IL
Giovanni Ferrari

OL
Raimundo Orsi

CF
Angelo Schiavio

Manager:

 Vittorio Pozzo

GK
František Plánička (c)

RB
Josef Čtyřoký

LB
Ladislav Ženíšek

RH
Rudolf Krčil

CH
Štefan Čambal

LH
Josef Košťálek

OR
Antonín Puč

IR
Oldřich Nejedlý

IL
František Svoboda

OL
František Junek

CF
Jiří Sobotka

Manager:

 Karel Petrů

text: 1938 World Cup Final v Hungary[edit]

text: After a difficult route to the final, defeating hosts France in the quarter-finals and Brazil in the semis, Italy was the first team to win the World Cup title on foreign ground. Also, it was the first of only two times in World Cup history that a team successfully defended their title.

text:
Italy

4–2

 Hungary

Colaussi  6', 35'Piola  16', 82'

Report

Titkos  8'Sárosi  70'

text:
GK

Aldo Olivieri

RB

Alfredo Foni

LB

Pietro Rava

RH

Pietro Serantoni

LH

Ugo Locatelli

CH

Michele Andreolo

IR

Giuseppe Meazza (c)

IL

Giovanni Ferrari

OR

Amedeo Biavati

CF

Silvio Piola

OL

Gino Colaussi

Manager:

 Vittorio Pozzo

GK

Antal Szabó

RB

Sándor Bíró

LB

Gyula Polgár

RH

Gyula Lázár

LH

Antal Szalay

CH

György Szűcs

IR

Gyula Zsengellér

IL

Jenő Vincze

OR

Pál Titkos

CF

György Sárosi (c)

OL

Ferenc Sas

Manager:

 Alfréd Schaffer

text: 1970 World Cup Final v Brazil[edit]

text: In 1970, the Brazilian team featured superstars like Pelé, Rivelino, Jairzinho and Carlos Alberto and were considered favourites for the title. Particularly in the second half, the Italians were outclassed by the Brazilians passing play.

text:
Brazil

4–1

 Italy

Pelé  18'Gérson  66'Jairzinho  71'Carlos Alberto  86'

Report

Boninsegna  37'

text:
GK
1
Félix

DF
4
Carlos Alberto (c)

DF
2
Brito

DF
3
Piazza

DF
16
Everaldo

MF
5
Clodoaldo

MF
8
Gérson

FW
7
Jairzinho

FW
9
Tostão

FW
10
Pelé

FW
11
Rivelino

Manager:

 Mário Zagallo

GK
1
Enrico Albertosi

DF
2
Tarcisio Burgnich

DF
5
Pierluigi Cera

DF
8
Roberto Rosato

DF
3
Giacinto Facchetti (c)

MF
10
Mario Bertini

 75'

MF
13
Angelo Domenghini

MF
16
Giancarlo De Sisti

FW
15
Sandro Mazzola

FW
11
Luigi Riva

FW
20
Roberto Boninsegna

 84'

Substitutions:

MF
18
Antonio Juliano

 75'

MF
14
Gianni Rivera

 84'

Manager:

 Ferruccio Valcareggi

text: 1982 World Cup Final v West Germany[edit]

text: Italy played three draws in the first group stage in a worrisome start to the tournament, proceeding ahead of Cameroon only on number of goals scored. However, the Italians continued to defeat Brazil, Argentina and a strong Polish side over the course of the tournament and faced West Germany in the final in Madrid.

text: Antonio Cabrini missed a penalty in the goalless first half, but the dominant Italian side eventually built up a 3-0 lead and won by 3-1 in the end, securing their third World Cup trophy.

text:
Italy

3–1

 West Germany

Rossi  57'Tardelli  69'Altobelli  81'

Report

Breitner  83'

text:
GK
1
Dino Zoff (c)

SW
7
Gaetano Scirea

CB
6
Claudio Gentile

CB
5
Fulvio Collovati

RWB
3
Giuseppe Bergomi

LWB
4
Antonio Cabrini

DM
13
Gabriele Oriali
 73'

RM
16
Bruno Conti
 31'

CM
14
Marco Tardelli

LW
19
Francesco Graziani

 7'

CF
20
Paolo Rossi

Substitutions:

GK
12
Ivano Bordon

MF
10
Giuseppe Dossena

MF
11
Giampiero Marini

MF
15
Franco Causio

 89'

FW
18
Alessandro Altobelli

 7'
 89'

Manager:

Enzo Bearzot

GK
1
Harald Schumacher

SW
15
Uli Stielike
 73'

RB
20
Manfred Kaltz

CB
4
Karlheinz Förster

LB
5
Bernd Förster

RM
6
Wolfgang Dremmler
 61'
 62'

CM
3
Paul Breitner

LM
2
Hans-Peter Briegel

RW
11
Karl-Heinz Rummenigge (c)

 70'

LW
7
Pierre Littbarski
 88'

CF
8
Klaus Fischer

Substitutions:

GK
21
Bernd Franke

DF
12
Wilfried Hannes

MF
10
Hansi Müller

 70'

MF
14
Felix Magath

FW
9
Horst Hrubesch

 62'

Manager:

Jupp Derwall

text: 1994 World Cup Final v Brazil[edit]

text: The 1994 final was the first ever to be decided on penalties after goalless 120 minutes. Italian captain Franco Baresi missed the very first penalty, and Roberto Baggio the decisive last one.

text: Italy became the first team to lose two World Cup finals against the same opponent.

text:
Brazil

0–0(a.e.t.)

 Italy

Report

Penalties

Márcio Santos Romário Branco Dunga

3–2

 Baresi Albertini Evani Massaro R. Baggio

text:
GK
1
Cláudio Taffarel

RB
2
Jorginho

 21'

CB
13
Aldair

CB
15
Marcio Santos

LB
6
Branco

CM
5
Mauro Silva

CM
8
Dunga (c)

AM
17
Mazinho
 4'

AM
9
Zinho

 106'

CF
11
Romário

CF
7
Bebeto

Substitutions:

DF
14
Cafu
 87'
 21'

FW
21
Viola

 106'

Manager:

 Carlos Alberto Parreira

GK
1
Gianluca Pagliuca

RB
8
Roberto Mussi

 35'

CB
6
Franco Baresi (c)

CB
5
Paolo Maldini

LB
3
Antonio Benarrivo

RM
14
Nicola Berti

CM
13
Dino Baggio

 95'

CM
11
Demetrio Albertini
 42'

LM
16
Roberto Donadoni

CF
10
Roberto Baggio

CF
19
Daniele Massaro

Substitutes:

DF
2
Luigi Apolloni
 41'
 35'

MF
17
Alberigo Evani

 95'

Manager:

 Arrigo Sacchi

text: 2006 World Cup Final v France[edit]

text: Italian defender Marco Materazzi was involved in all three outstanding moments of the first 120 minutes: He conceded the penalty that was converted by Zinedine Zidane early in the game, equalised with a powerful header soon after, and provoked Zidane in a manner that lead to the French captain being sent off. He also scored in the penalty-shootout that was to follow.

text: It was only the second time a World Cup final was decided on penalties, again involving Italy after the 1994 final lost to Brazil.

text:
Italy

1–1 (a.e.t.)

 France

Materazzi  19'

Report

Zidane  7' (pen.)

Penalties

Pirlo
Materazzi
De Rossi
Del Piero
Grosso

5–3

 Wiltord
 Trezeguet
 Abidal
 Sagnol

text:
GK
1
Gianluigi Buffon

RB
19
Gianluca Zambrotta
 5'

CB
5
Fabio Cannavaro (c)

CB
23
Marco Materazzi

LB
3
Fabio Grosso

RM
16
Mauro Camoranesi

 86'

CM
8
Gennaro Gattuso

CM
21
Andrea Pirlo

LM
20
Simone Perrotta

 61'

SS
10
Francesco Totti

 61'

CF
9
Luca Toni

Substitutions:

MF
4
Daniele De Rossi

 61'

FW
15
Vincenzo Iaquinta

 61'

FW
7
Alessandro Del Piero

 86'

Manager:

 Marcello Lippi

GK
16
Fabien Barthez

RB
19
Willy Sagnol
 12'

CB
15
Lilian Thuram

CB
5
William Gallas

LB
3
Éric Abidal

CM
4
Patrick Vieira

 56'

CM
6
Claude Makélélé
 76'

RW
22
Franck Ribéry

 100'

AM
10
Zinedine Zidane (c)
 110'

LW
7
Florent Malouda
 111'

CF
12
Thierry Henry

 107'

Substitutions:

MF
18
Alou Diarra

 56'

FW
20
David Trezeguet

 100'

FW
11
Sylvain Wiltord

 107'

Manager:

 Raymond Domenech

text: Player appearances[edit]

text: Paolo Maldini is the player with the third-most matches at FIFA World Cups, trailing only behind the Germans Lothar Matthäus (25) and Miroslav Klose (24). This also makes him the player with the most World Cup matches who has never won the trophy.

text: Goalkeeper Gianluigi Buffon is one of only three players who have been part of five FIFA World Cup squads.[3]

text:
No.

Name

Matches

World Cups

1
Paolo Maldini
23
1990, 1994, 1998 and 2002

2

Antonio Cabrini
18
1978, 1982 and 1986

Gaetano Scirea
18
1978, 1982 and 1986

Fabio Cannavaro
18
1998, 2002, 2006 and 2010

5
Dino Zoff
17
1974, 1978 and 1982

6

Giuseppe Bergomi
16
1982, 1986, 1990 and 1998

Roberto Baggio
16
1990, 1994 and 1998

8

Paolo Rossi
14
1978 and 1982

Gianluigi Buffon
14
2002, 2006, 2010 and 2014

10

Claudio Gentile
13
1978 and 1982

Marco Tardelli
13
1978 and 1982

Gianluca Zambrotta
13
2002, 2006 and 2010

text: Top goalscorers[edit]

text: Two Italians were awarded the Golden Boot for best goalscorer at a FIFA World Cup: Paolo Rossi in 1982 and Salvatore Schillaci in 1990 with 6 goals each.[4]

text:
No.

Name

Goals

World Cups

1
Paolo Rossi
9
1978 (3) and 1982 (6)

Roberto Baggio
9
1990 (2), 1994 (5) and 1998 (2)

Christian Vieri
9
1998 (5) and 2002 (4)

4
Salvatore Schillaci
6
1990

5

Silvio Piola
5
1938

Alessandro Altobelli
5
1982 (1) and 1986 (4)

7

Angelo Schiavio
4
1934

Gino Colaussi
4
1938

9
Raimundo Orsi
3
1934

Giuseppe Meazza
3
1934 (2) and 1938 (1)

Luigi Riva
3
1970

Gianni Rivera
3
1970 (2) and 1974 (1)

text: Awards and Records[edit]

text: Team Awards[edit]

text:
World Champions 1934
World Champions 1938
World Champions 1982
World Champions 2006
Second Place 1970
Second Place 1994
Third Place 1990

text: Individual Awards[edit]

text: Golden Ball award

text:
Golden Ball 1934: Giuseppe Meazza
Golden Ball 1982: Paolo Rossi
Golden Ball 1990: Salvatore Schillaci
Silver Ball 1938: Silvio Piola
Silver Ball 1978: Paolo Rossi
Silver Ball 1994: Roberto Baggio
Silver Ball 2006: Fabio Cannavaro
Bronze Ball 2006: Andrea Pirlo

text: Golden Boot award

text:
Golden Boot 1982: Paolo Rossi
Golden Boot 1990: Salvatore Schillaci
Silver Boot 1934: Angelo Schiavio
Silver Boot 1938: Silvio Piola
Silver Boot 1998: Christian Vieri

text: Other individual awards

text:
Golden Glove 1982: Dino Zoff (oldest Golden Glove winner)
Golden Glove 2006: Gianluigi Buffon
Best Young Player Award 1978: Antonio Cabrini
Man of the Match Award 2006: Andrea Pirlo

text: Refereeing[edit]

text: Three World Cup finals have been officiated by representatives of the Italian football federation, only English referees have had the honour more often (four times). The 1978 final between Argentina and the Netherlands has been led by Sergio Gonella, who had already officiated the European Championship final two years earlier. The other referees are Pierluigi Collina in 2002, and Nicola Rizzoli in 2014.

text: The Italian referee with the most World Cup matches, however, is Roberto Rosetti, who has been in charge of six matches total in 2006 and 2010.