document_title: Cell nucleus

question_text: the division of the nucleus and its contents is called

text: Cell nucleus

text: History

text: The nucleus was the first organelle to be discovered. What is most likely the oldest preserved drawing dates back to the early microscopist Antonie van Leeuwenhoek (1632–1723). He observed a "lumen", the nucleus, in the red blood cells of salmon.[2] Unlike mammalian red blood cells, those of other vertebrates still contain nuclei.

text: The nucleus was also described by Franz Bauer in 1804[3] and in more detail in 1831 by Scottish botanist Robert Brown in a talk at the Linnean Society of London. Brown was studying orchids under microscope when he observed an opaque area, which he called the "areola" or "nucleus", in the cells of the flower's outer layer.[4]

text: He did not suggest a potential function. In 1838, Matthias Schleiden proposed that the nucleus plays a role in generating cells, thus he introduced the name "cytoblast" (cell builder). He believed that he had observed new cells assembling around "cytoblasts". Franz Meyen was a strong opponent of this view, having already described cells multiplying by division and believing that many cells would have no nuclei. The idea that cells can be generated de novo, by the "cytoblast" or otherwise, contradicted work by Robert Remak (1852) and Rudolf Virchow (1855) who decisively propagated the new paradigm that cells are generated solely by cells ("Omnis cellula e cellula"). The function of the nucleus remained unclear.[5]

text: Between 1877 and 1878, Oscar Hertwig published several studies on the fertilization of sea urchin eggs, showing that the nucleus of the sperm enters the oocyte and fuses with its nucleus. This was the first time it was suggested that an individual develops from a (single) nucleated cell. This was in contradiction to Ernst Haeckel's theory that the complete phylogeny of a species would be repeated during embryonic development, including generation of the first nucleated cell from a "monerula", a structureless mass of primordial mucus ("Urschleim"). Therefore, the necessity of the sperm nucleus for fertilization was discussed for quite some time. However, Hertwig confirmed his observation in other animal groups, including amphibians and molluscs. Eduard Strasburger produced the same results for plants in 1884. This paved the way to assign the nucleus an important role in heredity. In 1873, August Weismann postulated the equivalence of the maternal and paternal germ cells for heredity. The function of the nucleus as carrier of genetic information became clear only later, after mitosis was discovered and the Mendelian rules were rediscovered at the beginning of the 20th century; the chromosome theory of heredity was therefore developed.[5]

text: Structures

text: The nucleus is the largest cellular organelle in animal cells.[6] In mammalian cells, the average diameter of the nucleus is approximately 6 micrometres (µm), which occupies about 10% of the total cell volume.[7] The viscous liquid within it is called nucleoplasm (or karyolymph), and is similar in composition to the cytosol found outside the nucleus.[8] It appears as a dense, roughly spherical or irregular organelle. The composition by dry weight of the nucleus is approximately: DNA 9%, RNA 1%, Histone Protein 11%, Residual Protein 14%, Acidic Proteins 65%.

text: Nuclear envelope and pores

text:
The eukaryotic cell nucleus. Visible in this diagram are the ribosome-studded double membranes of the nuclear envelope, the DNA (complexed as chromatin), and the nucleolus. Within the cell nucleus is a viscous liquid called nucleoplasm, similar to the cytoplasm found outside the nucleus.

A cross section of a nuclear pore on the surface of the nuclear envelope (1). Other diagram labels show (2) the outer ring, (3) spokes, (4) basket, and (5) filaments.

text: The nuclear envelope, otherwise known as nuclear membrane, consists of two cellular membranes, an inner and an outer membrane, arranged parallel to one another and separated by 10 to 50 nanometres (nm). The nuclear envelope completely encloses the nucleus and separates the cell's genetic material from the surrounding cytoplasm, serving as a barrier to prevent macromolecules from diffusing freely between the nucleoplasm and the cytoplasm.[9] The outer nuclear membrane is continuous with the membrane of the rough endoplasmic reticulum (RER), and is similarly studded with ribosomes.[9] The space between the membranes is called the perinuclear space and is continuous with the RER lumen.

text: Nuclear pores, which provide aqueous channels through the envelope, are composed of multiple proteins, collectively referred to as nucleoporins. The pores are about 125 million daltons in molecular weight and consist of around 50 (in yeast) to several hundred proteins (in vertebrates).[6] The pores are 100 nm in total diameter; however, the gap through which molecules freely diffuse is only about 9 nm wide, due to the presence of regulatory systems within the center of the pore. This size selectively allows the passage of small water-soluble molecules while preventing larger molecules, such as nucleic acids and larger proteins, from inappropriately entering or exiting the nucleus. These large molecules must be actively transported into the nucleus instead. The nucleus of a typical mammalian cell will have about 3000 to 4000 pores throughout its envelope,[10] each of which contains an eightfold-symmetric ring-shaped structure at a position where the inner and outer membranes fuse.[11] Attached to the ring is a structure called the nuclear basket that extends into the nucleoplasm, and a series of filamentous extensions that reach into the cytoplasm. Both structures serve to mediate binding to nuclear transport proteins.[6]

text: Most proteins, ribosomal subunits, and some DNAs are transported through the pore complexes in a process mediated by a family of transport factors known as karyopherins. Those karyopherins that mediate movement into the nucleus are also called importins, whereas those that mediate movement out of the nucleus are called exportins. Most karyopherins interact directly with their cargo, although some use adaptor proteins.[12] Steroid hormones such as cortisol and aldosterone, as well as other small lipid-soluble molecules involved in intercellular signaling, can diffuse through the cell membrane and into the cytoplasm, where they bind nuclear receptor proteins that are trafficked into the nucleus. There they serve as transcription factors when bound to their ligand; in the absence of a ligand, many such receptors function as histone deacetylases that repress gene expression.[6]

text: Nuclear lamina

text: In animal cells, two networks of intermediate filaments provide the nucleus with mechanical support: The nuclear lamina forms an organized meshwork on the internal face of the envelope, while less organized support is provided on the cytosolic face of the envelope. Both systems provide structural support for the nuclear envelope and anchoring sites for chromosomes and nuclear pores.[7]

text: The nuclear lamina is composed mostly of lamin proteins. Like all proteins, lamins are synthesized in the cytoplasm and later transported to the nucleus interior, where they are assembled before being incorporated into the existing network of nuclear lamina.[13][14] Lamins found on the cytosolic face of the membrane, such as emerin and nesprin, bind to the cytoskeleton to provide structural support. Lamins are also found inside the nucleoplasm where they form another regular structure, known as the nucleoplasmic veil,[15] that is visible using fluorescence microscopy. The actual function of the veil is not clear, although it is excluded from the nucleolus and is present during interphase.[16] Lamin structures that make up the veil, such as LEM3, bind chromatin and disrupting their structure inhibits transcription of protein-coding genes.[17]

text: Like the components of other intermediate filaments, the lamin monomer contains an alpha-helical domain used by two monomers to coil around each other, forming a dimer structure called a coiled coil. Two of these dimer structures then join side by side, in an antiparallel arrangement, to form a tetramer called a protofilament. Eight of these protofilaments form a lateral arrangement that is twisted to form a ropelike filament. These filaments can be assembled or disassembled in a dynamic manner, meaning that changes in the length of the filament depend on the competing rates of filament addition and removal.[7]

text: Mutations in lamin genes leading to defects in filament assembly cause a group of rare genetic disorders known as laminopathies. The most notable laminopathy is the family of diseases known as progeria, which causes the appearance of premature aging in its sufferers. The exact mechanism by which the associated biochemical changes give rise to the aged phenotype is not well understood.[18]

text: Chromosomes

text: The cell nucleus contains the majority of the cell's genetic material in the form of multiple linear DNA molecules organized into structures called chromosomes. Each human cell contains roughly two meters of DNA. During most of the cell cycle these are organized in a DNA-protein complex known as chromatin, and during cell division the chromatin can be seen to form the well-defined chromosomes familiar from a karyotype. A small fraction of the cell's genes are located instead in the mitochondria.

text: There are two types of chromatin. Euchromatin is the less compact DNA form, and contains genes that are frequently expressed by the cell.[19] The other type, heterochromatin, is the more compact form, and contains DNA that is infrequently transcribed. This structure is further categorized into facultative heterochromatin, consisting of genes that are organized as heterochromatin only in certain cell types or at certain stages of development, and constitutive heterochromatin that consists of chromosome structural components such as telomeres and centromeres.[20] During interphase the chromatin organizes itself into discrete individual patches,[21] called chromosome territories.[22] Active genes, which are generally found in the euchromatic region of the chromosome, tend to be located towards the chromosome's territory boundary.[23]

text: Antibodies to certain types of chromatin organization, in particular, nucleosomes, have been associated with a number of autoimmune diseases, such as systemic lupus erythematosus.[24] These are known as anti-nuclear antibodies (ANA) and have also been observed in concert with multiple sclerosis as part of general immune system dysfunction.[25] As in the case of progeria, the role played by the antibodies in inducing the symptoms of autoimmune diseases is not obvious.

text: Nucleolus

text: The nucleolus is a discrete densely stained structure found in the nucleus. It is not surrounded by a membrane, and is sometimes called a suborganelle. It forms around tandem repeats of rDNA, DNA coding for ribosomal RNA (rRNA). These regions are called nucleolar organizer regions (NOR). The main roles of the nucleolus are to synthesize rRNA and assemble ribosomes. The structural cohesion of the nucleolus depends on its activity, as ribosomal assembly in the nucleolus results in the transient association of nucleolar components, facilitating further ribosomal assembly, and hence further association. This model is supported by observations that inactivation of rDNA results in intermingling of nucleolar structures.[26]

text: In the first step of ribosome assembly, a protein called RNA polymerase I transcribes rDNA, which forms a large pre-rRNA precursor. This is cleaved into the subunits 5.8S, 18S, and 28S rRNA.[27] The transcription, post-transcriptional processing, and assembly of rRNA occurs in the nucleolus, aided by small nucleolar RNA (snoRNA) molecules, some of which are derived from spliced introns from messenger RNAs encoding genes related to ribosomal function. The assembled ribosomal subunits are the largest structures passed through the nuclear pores.[6]

text: When observed under the electron microscope, the nucleolus can be seen to consist of three distinguishable regions: the innermost fibrillar centers (FCs), surrounded by the dense fibrillar component (DFC), which in turn is bordered by the granular component (GC). Transcription of the rDNA occurs either in the FC or at the FC-DFC boundary, and, therefore, when rDNA transcription in the cell is increased, more FCs are detected. Most of the cleavage and modification of rRNAs occurs in the DFC, while the latter steps involving protein assembly onto the ribosomal subunits occur in the GC.[27]

text: Other subnuclear bodies

text:
Subnuclear structure sizes

Structure name
Structure diameter

Cajal bodies
0.2–2.0 µm
[28]

Clastosomes
0.2-0.5 µm
[29]

PIKA
5 µm
[30]

PML bodies
0.2–1.0 µm
[31]

Paraspeckles
0.2–1.0 µm
[32]

Speckles
20–25 nm
[30]

text: Besides the nucleolus, the nucleus contains a number of other non-membrane-delineated bodies. These include Cajal bodies, Gemini of coiled bodies, polymorphic interphase karyosomal association (PIKA), promyelocytic leukaemia (PML) bodies, paraspeckles, and splicing speckles. Although little is known about a number of these domains, they are significant in that they show that the nucleoplasm is not a uniform mixture, but rather contains organized functional subdomains.[31]

text: Other subnuclear structures appear as part of abnormal disease processes. For example, the presence of small intranuclear rods has been reported in some cases of nemaline myopathy. This condition typically results from mutations in actin, and the rods themselves consist of mutant actin as well as other cytoskeletal proteins.[33]

text: Cajal bodies and gems

text: A nucleus typically contains between 1 and 10 compact structures called Cajal bodies or coiled bodies (CB), whose diameter measures between 0.2 µm and 2.0 µm depending on the cell type and species.[28] When seen under an electron microscope, they resemble balls of tangled thread[30] and are dense foci of distribution for the protein coilin.[34] CBs are involved in a number of different roles relating to RNA processing, specifically small nucleolar RNA (snoRNA) and small nuclear RNA (snRNA) maturation, and histone mRNA modification.[28]

text: Similar to Cajal bodies are Gemini of Cajal bodies, or gems, whose name is derived from the Gemini constellation in reference to their close "twin" relationship with CBs. Gems are similar in size and shape to CBs, and in fact are virtually indistinguishable under the microscope.[34] Unlike CBs, gems do not contain small nuclear ribonucleoproteins (snRNPs), but do contain a protein called survival of motor neuron (SMN) whose function relates to snRNP biogenesis. Gems are believed to assist CBs in snRNP biogenesis,[35] though it has also been suggested from microscopy evidence that CBs and gems are different manifestations of the same structure.[34] Later ultrastructural studies have shown gems to be twins of Cajal bodies with the difference being in the coilin component; Cajal bodies are SMN positive and coilin positive, and gems are SMN positive and coilin negative.[36]

text: RAFA and PTF domains

text: RAFA domains, or polymorphic interphase karyosomal associations, were first described in microscopy studies in 1991. Their function remains unclear, though they were not thought to be associated with active DNA replication, transcription, or RNA processing.[37] They have been found to often associate with discrete domains defined by dense localization of the transcription factor PTF, which promotes transcription of small nuclear RNA (snRNA).[38]

text: PML bodies

text: Promyelocytic leukaemia bodies (PML bodies) are spherical bodies found scattered throughout the nucleoplasm, measuring around 0.1–1.0 µm. They are known by a number of other names, including nuclear domain 10 (ND10), Kremer bodies, and PML oncogenic domains. PML bodies are named after one of their major components, the promyelocytic leukemia protein (PML). They are often seen in the nucleus in association with Cajal bodies and cleavage bodies.[31] PML bodies belong to the nuclear matrix, an ill-defined super-structure of the nucleus proposed to anchor and regulate many nuclear functions, including DNA replication, transcription, or epigenetic silencing.[39] The PML protein is the key organizer of these domains that recruits an ever-growing number of proteins, whose only common known feature to date is their ability to be SUMOylated. Yet, pml-/- mice (which have their PML gene deleted) cannot assemble nuclear bodies, develop normally and live well, demonstrating that PML bodies are dispensable for most basic biological functions.[39]

text: Splicing speckles

text: Speckles are subnuclear structures that are enriched in pre-messenger RNA splicing factors and are located in the interchromatin regions of the nucleoplasm of mammalian cells. At the fluorescence-microscope level they appear as irregular, punctate structures, which vary in size and shape, and when examined by electron microscopy they are seen as clusters of interchromatin granules. Speckles are dynamic structures, and both their protein and RNA-protein components can cycle continuously between speckles and other nuclear locations, including active transcription sites. Studies on the composition, structure and behaviour of speckles have provided a model for understanding the functional compartmentalization of the nucleus and the organization of the gene-expression machinery[40] splicing snRNPs[41][42] and other splicing proteins necessary for pre-mRNA processing.[43] Because of a cell's changing requirements, the composition and location of these bodies changes according to mRNA transcription and regulation via phosphorylation of specific proteins.[44] The splicing speckles are also known as nuclear speckles (nuclear specks), splicing factor compartments (SF compartments), interchromatin granule clusters (IGCs), B snurposomes.[45] B snurposomes are found in the amphibian oocyte nuclei and in Drosophila melanogaster embryos. B snurposomes appear alone or attached to the Cajal bodies in the electron micrographs of the amphibian nuclei.[46] IGCs function as storage sites for the splicing factors.[47]

text: Paraspeckles

text: Discovered by Fox et al. in 2002, paraspeckles are irregularly shaped compartments in the nucleus' interchromatin space.[48] First documented in HeLa cells, where there are generally 10–30 per nucleus,[49] paraspeckles are now known to also exist in all human primary cells, transformed cell lines, and tissue sections.[50] Their name is derived from their distribution in the nucleus; the "para" is short for parallel and the "speckles" refers to the splicing speckles to which they are always in close proximity.[49]

text: Paraspeckles are dynamic structures that are altered in response to changes in cellular metabolic activity. They are transcription dependent[48] and in the absence of RNA Pol II transcription, the paraspeckle disappears and all of its associated protein components (PSP1, p54nrb, PSP2, CFI(m)68, and PSF) form a crescent shaped perinucleolar cap in the nucleolus. This phenomenon is demonstrated during the cell cycle. In the cell cycle, paraspeckles are present during interphase and during all of mitosis except for telophase. During telophase, when the two daughter nuclei are formed, there is no RNA Pol II transcription so the protein components instead form a perinucleolar cap.[50]

text: Perichromatin fibrils

text: Perichromatin fibrils are visible only under electron microscope. They are located next to the transcriptionally active chromatin and are hypothesized to be the sites of active pre-mRNA processing.[47]

text: Clastosome

text: Clastosomes are small nuclear bodies (0.2-0.5 µm) described as donut-shaped due to the peripheral capsule around these bodies.[29] This name is derived from the Greek klastos, broken and soma, body.[29] Clastosomes are not typically present in normal cells, making them hard to detect. They form under high proteolysis conditions within the nucleus and degrade once there is a decrease in activity or if cells are treated with proteasome inhibitors.[29][51] The scarcity of clastosomes in cells indicates that they are not required for proteasome function.[52] Osmotic stress has also been shown to cause the formation of clastosomes. [53] These nuclear bodies contain catalytic and regulatory sub-units of the proteasome and its substrates, indicating that clastosomes are sites for degrading proteins.[52]

text: The Clastosome would be an important addition to the ‘Cell Nucleus’ Wiki page because it plays a role in cell function. With further research, we may discover that this nuclear body has a more influential job in cell function than what is already known. [29]

text: Function

text: The nucleus provides a site for genetic transcription that is segregated from the location of translation in the cytoplasm, allowing levels of gene regulation that are not available to prokaryotes. The main function of the cell nucleus is to control gene expression and mediate the replication of DNA during the cell cycle.

text: The nucleus is an organelle found in eukaryotic cells. Inside its fully enclosed nuclear membrane, it contains the majority of the cell's genetic material. This material is organized as DNA molecules, along with a variety of proteins, to form chromosomes.

text: Cell compartmentalization

text: The nuclear envelope allows the nucleus to control its contents, and separate them from the rest of the cytoplasm where necessary. This is important for controlling processes on either side of the nuclear membrane. In most cases where a cytoplasmic process needs to be restricted, a key participant is removed to the nucleus, where it interacts with transcription factors to downregulate the production of certain enzymes in the pathway. This regulatory mechanism occurs in the case of glycolysis, a cellular pathway for breaking down glucose to produce energy. Hexokinase is an enzyme responsible for the first the step of glycolysis, forming glucose-6-phosphate from glucose. At high concentrations of fructose-6-phosphate, a molecule made later from glucose-6-phosphate, a regulator protein removes hexokinase to the nucleus,[54] where it forms a transcriptional repressor complex with nuclear proteins to reduce the expression of genes involved in glycolysis.[55]

text: In order to control which genes are being transcribed, the cell separates some transcription factor proteins responsible for regulating gene expression from physical access to the DNA until they are activated by other signaling pathways. This prevents even low levels of inappropriate gene expression. For example, in the case of NF-κB-controlled genes, which are involved in most inflammatory responses, transcription is induced in response to a signal pathway such as that initiated by the signaling molecule TNF-α, binds to a cell membrane receptor, resulting in the recruitment of signalling proteins, and eventually activating the transcription factor NF-κB. A nuclear localisation signal on the NF-κB protein allows it to be transported through the nuclear pore and into the nucleus, where it stimulates the transcription of the target genes.[7]

text: The compartmentalization allows the cell to prevent translation of unspliced mRNA.[56] Eukaryotic mRNA contains introns that must be removed before being translated to produce functional proteins. The splicing is done inside the nucleus before the mRNA can be accessed by ribosomes for translation. Without the nucleus, ribosomes would translate newly transcribed (unprocessed) mRNA, resulting in malformed and nonfunctional proteins.

text: Gene expression

text: Gene expression first involves transcription, in which DNA is used as a template to produce RNA. In the case of genes encoding proteins, that RNA produced from this process is messenger RNA (mRNA), which then needs to be translated by ribosomes to form a protein. As ribosomes are located outside the nucleus, mRNA produced needs to be exported.[57]

text: Since the nucleus is the site of transcription, it also contains a variety of proteins that either directly mediate transcription or are involved in regulating the process. These proteins include helicases, which unwind the double-stranded DNA molecule to facilitate access to it, RNA polymerases, which bind to the DNA promoter to synthesize the growing RNA molecule, topoisomerases, which change the amount of supercoiling in DNA, helping it wind and unwind, as well as a large variety of transcription factors that regulate expression.[58]

text: Processing of pre-mRNA

text: Newly synthesized mRNA molecules are known as primary transcripts or pre-mRNA. They must undergo post-transcriptional modification in the nucleus before being exported to the cytoplasm; mRNA that appears in the cytoplasm without these modifications is degraded rather than used for protein translation. The three main modifications are 5' capping, 3' polyadenylation, and RNA splicing. While in the nucleus, pre-mRNA is associated with a variety of proteins in complexes known as heterogeneous ribonucleoprotein particles (hnRNPs). Addition of the 5' cap occurs co-transcriptionally and is the first step in post-transcriptional modification. The 3' poly-adenine tail is only added after transcription is complete.

text: RNA splicing, carried out by a complex called the spliceosome, is the process by which introns, or regions of DNA that do not code for protein, are removed from the pre-mRNA and the remaining exons connected to re-form a single continuous molecule. This process normally occurs after 5' capping and 3' polyadenylation but can begin before synthesis is complete in transcripts with many exons.[6] Many pre-mRNAs, including those encoding antibodies, can be spliced in multiple ways to produce different mature mRNAs that encode different protein sequences. This process is known as alternative splicing, and allows production of a large variety of proteins from a limited amount of DNA.

text: Dynamics and regulation

text: Nuclear transport

text: The entry and exit of large molecules from the nucleus is tightly controlled by the nuclear pore complexes. Although small molecules can enter the nucleus without regulation,[59] macromolecules such as RNA and proteins require association karyopherins called importins to enter the nucleus and exportins to exit. "Cargo" proteins that must be translocated from the cytoplasm to the nucleus contain short amino acid sequences known as nuclear localization signals, which are bound by importins, while those transported from the nucleus to the cytoplasm carry nuclear export signals bound by exportins. The ability of importins and exportins to transport their cargo is regulated by GTPases, enzymes that hydrolyze the molecule guanosine triphosphate to release energy. The key GTPase in nuclear transport is Ran, which can bind either GTP or GDP (guanosine diphosphate), depending on whether it is located in the nucleus or the cytoplasm. Whereas importins depend on RanGTP to dissociate from their cargo, exportins require RanGTP in order to bind to their cargo.[12]

text: Nuclear import depends on the importin binding its cargo in the cytoplasm and carrying it through the nuclear pore into the nucleus. Inside the nucleus, RanGTP acts to separate the cargo from the importin, allowing the importin to exit the nucleus and be reused. Nuclear export is similar, as the exportin binds the cargo inside the nucleus in a process facilitated by RanGTP, exits through the nuclear pore, and separates from its cargo in the cytoplasm.

text: Specialized export proteins exist for translocation of mature mRNA and tRNA to the cytoplasm after post-transcriptional modification is complete. This quality-control mechanism is important due to these molecules' central role in protein translation. Mis-expression of a protein due to incomplete excision of exons or mis-incorporation of amino acids could have negative consequences for the cell; thus, incompletely modified RNA that reaches the cytoplasm is degraded rather than used in translation.[6]

text: Assembly and disassembly

text: During its lifetime, a nucleus may be broken down or destroyed, either in the process of cell division or as a consequence of apoptosis (the process of programmed cell death). During these events, the structural components of the nucleus — the envelope and lamina — can be systematically degraded. In most cells, the disassembly of the nuclear envelope marks the end of the prophase of mitosis. However, this disassembly of the nucleus is not a universal feature of mitosis and does not occur in all cells. Some unicellular eukaryotes (e.g., yeasts) undergo so-called closed mitosis, in which the nuclear envelope remains intact. In closed mitosis, the daughter chromosomes migrate to opposite poles of the nucleus, which then divides in two. The cells of higher eukaryotes, however, usually undergo open mitosis, which is characterized by breakdown of the nuclear envelope. The daughter chromosomes then migrate to opposite poles of the mitotic spindle, and new nuclei reassemble around them.

text: At a certain point during the cell cycle in open mitosis, the cell divides to form two cells. In order for this process to be possible, each of the new daughter cells must have a full set of genes, a process requiring replication of the chromosomes as well as segregation of the separate sets. This occurs by the replicated chromosomes, the sister chromatids, attaching to microtubules, which in turn are attached to different centrosomes. The sister chromatids can then be pulled to separate locations in the cell. In many cells, the centrosome is located in the cytoplasm, outside the nucleus; the microtubules would be unable to attach to the chromatids in the presence of the nuclear envelope.[60] Therefore, the early stages in the cell cycle, beginning in prophase and until around prometaphase, the nuclear membrane is dismantled.[15] Likewise, during the same period, the nuclear lamina is also disassembled, a process regulated by phosphorylation of the lamins by protein kinases such as the CDC2 protein kinase.[61] Towards the end of the cell cycle, the nuclear membrane is reformed, and around the same time, the nuclear lamina are reassembled by dephosphorylating the lamins.[61]

text: However, in dinoflagellates, the nuclear envelope remains intact, the centrosomes are located in the cytoplasm, and the microtubules come in contact with chromosomes, whose centromeric regions are incorporated into the nuclear envelope (the so-called closed mitosis with extranuclear spindle). In many other protists (e.g., ciliates, sporozoans) and fungi, the centrosomes are intranuclear, and their nuclear envelope also does not disassemble during cell division.

text: Apoptosis is a controlled process in which the cell's structural components are destroyed, resulting in death of the cell. Changes associated with apoptosis directly affect the nucleus and its contents, for example, in the condensation of chromatin and the disintegration of the nuclear envelope and lamina. The destruction of the lamin networks is controlled by specialized apoptotic proteases called caspases, which cleave the lamin proteins and, thus, degrade the nucleus' structural integrity. Lamin cleavage is sometimes used as a laboratory indicator of caspase activity in assays for early apoptotic activity.[15] Cells that express mutant caspase-resistant lamins are deficient in nuclear changes related to apoptosis, suggesting that lamins play a role in initiating the events that lead to apoptotic degradation of the nucleus.[15] Inhibition of lamin assembly itself is an inducer of apoptosis.[62]

text: The nuclear envelope acts as a barrier that prevents both DNA and RNA viruses from entering the nucleus. Some viruses require access to proteins inside the nucleus in order to replicate and/or assemble. DNA viruses, such as herpesvirus replicate and assemble in the cell nucleus, and exit by budding through the inner nuclear membrane. This process is accompanied by disassembly of the lamina on the nuclear face of the inner membrane.[15]

text: Disease-related dynamics

text: Initially, it has been suspected that immunoglobulins in general and autoantibodies in particular do not enter the nucleus. Now there is a body of evidence that under pathological conditions (e.g. lupus erythematosus) IgG can enter the nucleus.[63]

text: Nuclei per cell

text: Most eukaryotic cell types usually have a single nucleus, but some have no nuclei, while others have several. This can result from normal development, as in the maturation of mammalian red blood cells, or from faulty cell division.

text: Anucleated cells

text: An anucleated cell contains no nucleus and is, therefore, incapable of dividing to produce daughter cells. The best-known anucleated cell is the mammalian red blood cell, or erythrocyte, which also lacks other organelles such as mitochondria, and serves primarily as a transport vessel to ferry oxygen from the lungs to the body's tissues. Erythrocytes mature through erythropoiesis in the bone marrow, where they lose their nuclei, organelles, and ribosomes. The nucleus is expelled during the process of differentiation from an erythroblast to a reticulocyte, which is the immediate precursor of the mature erythrocyte.[64] The presence of mutagens may induce the release of some immature "micronucleated" erythrocytes into the bloodstream.[65][66] Anucleated cells can also arise from flawed cell division in which one daughter lacks a nucleus and the other has two nuclei.

text: In flowering plants, this condition occurs in sieve tube elements.

text: Multinucleated cells

text: Multinucleated cells contain multiple nuclei. Most acantharean species of protozoa[67] and some fungi in mycorrhizae[68] have naturally multinucleated cells. Other examples include the intestinal parasites in the genus Giardia, which have two nuclei per cell.[69] In humans, skeletal muscle cells, called myocytes and syncytium, become multinucleated during development; the resulting arrangement of nuclei near the periphery of the cells allows maximal intracellular space for myofibrils.[6] Multinucleated and binucleated cells can also be abnormal in humans; for example, cells arising from the fusion of monocytes and macrophages, known as giant multinucleated cells, sometimes accompany inflammation[70] and are also implicated in tumor formation.[71]

text: A number of dinoflagellates are known to have two nuclei.[72] Unlike other multinucleated cells these nuclei contain two distinct lineages of DNA: one from the dinoflagellate and the other from a symbiotic diatom. The mitochondria and the plastids of the diatom somehow remain functional.

text: Evolution

text: As the major defining characteristic of the eukaryotic cell, the nucleus' evolutionary origin has been the subject of much speculation. Four major hypotheses have been proposed to explain the existence of the nucleus, although none have yet earned widespread support.[73]

text: The first model known as the "syntrophic model" proposes that a symbiotic relationship between the archaea and bacteria created the nucleus-containing eukaryotic cell. (Organisms of the Archaea and Bacteria domain have no cell nucleus.[74]) It is hypothesized that the symbiosis originated when ancient archaea, similar to modern methanogenic archaea, invaded and lived within bacteria similar to modern myxobacteria, eventually forming the early nucleus. This theory is analogous to the accepted theory for the origin of eukaryotic mitochondria and chloroplasts, which are thought to have developed from a similar endosymbiotic relationship between proto-eukaryotes and aerobic bacteria.[75] The archaeal origin of the nucleus is supported by observations that archaea and eukarya have similar genes for certain proteins, including histones. Observations that myxobacteria are motile, can form multicellular complexes, and possess kinases and G proteins similar to eukarya, support a bacterial origin for the eukaryotic cell.[76]

text: A second model proposes that proto-eukaryotic cells evolved from bacteria without an endosymbiotic stage. This model is based on the existence of modern planctomycetes bacteria that possess a nuclear structure with primitive pores and other compartmentalized membrane structures.[77] A similar proposal states that a eukaryote-like cell, the chronocyte, evolved first and phagocytosed archaea and bacteria to generate the nucleus and the eukaryotic cell.[78]

text: The most controversial model, known as viral eukaryogenesis, posits that the membrane-bound nucleus, along with other eukaryotic features, originated from the infection of a prokaryote by a virus. The suggestion is based on similarities between eukaryotes and viruses such as linear DNA strands, mRNA capping, and tight binding to proteins (analogizing histones to viral envelopes). One version of the proposal suggests that the nucleus evolved in concert with phagocytosis to form an early cellular "predator".[79] Another variant proposes that eukaryotes originated from early archaea infected by poxviruses, on the basis of observed similarity between the DNA polymerases in modern poxviruses and eukaryotes.[80][81] It has been suggested that the unresolved question of the evolution of sex could be related to the viral eukaryogenesis hypothesis.[82]

text: A more recent proposal, the exomembrane hypothesis, suggests that the nucleus instead originated from a single ancestral cell that evolved a second exterior cell membrane; the interior membrane enclosing the original cell then became the nuclear membrane and evolved increasingly elaborate pore structures for passage of internally synthesized cellular components such as ribosomal subunits.[83]


document_title: United States Soccer Federation

question_text: where does the us national soccer team train

question_tokens: where does the us national soccer team train

root

text: United States Soccer Federation

text: Organization and governance[edit]

text: U.S. Soccer is governed by a Board of Directors that administers the affairs of U.S. Soccer. People in key leadership positions include:[3]

tag: p

text:
Carlos Cordeiro — president[4]
Dan Flynn — CEO and secretary general

tag: ul

text: U.S. Soccer members comprise individuals and affiliate organizations. The national council is the representative membership body of the federation. It elects the president and vice president, amends the bylaws, approves the budgets, decides on policies adopted by the board, and affirms actions of the Board.

text: U.S. Soccer is a member of the worldwide soccer body FIFA and the North American soccer body CONCACAF, and also has a relationship with the U.S. Olympic Committee and the International Olympic Committee.[5]

text: The federation convenes in an annual meeting, usually held in February. Every four years, the annual meeting's attendees hold an election for the federation's president and vice president.[6]

text: Affiliate members of the U.S. Soccer Federation[edit]

text: USSF recognizes the following affiliate members:[7]

text: Professional Council[edit]

text:
Major League Soccer (MLS)
National Women's Soccer League (NWSL)
North American Soccer League (NASL)
United Soccer League (USL)

text: Adult Council[edit]

text: United States Adult Soccer Association (USASA)

text: Youth Council[edit]

text:
United States Youth Soccer Association (USYSA)
American Youth Soccer Organization (AYSO)
US Club Soccer
Soccer Association for Youth, USA (SAY)

text: Other affiliate members[edit]

text:
American Amputee Soccer Association
Armed Forces Sports Council
United Soccer Coaches (formerly: National Soccer Coaches Association of America (NSCAA))
United States Power Soccer Association (USPSA)
U.S. Soccer Foundation (USSF)
United States Futsal Federation
United States Specialty Sports Association - Soccer
United States of America Deaf Soccer Association (USA Deaf Soccer)

text: History[edit]

text: U.S. Soccer was originally known as the United States Football Association. It formed on April 5, 1913[8] and on August 15 of that year was accepted as one of the earliest member organizations of FIFA and the first from North and Central America. The affiliation was temporary and at the following year's FIFA Congress in 1914, the USFA, as it was abbreviated at the time, was accepted as a full FIFA member.[9] The governing body of the sport in the United States added the word "soccer" to its name in 1945, when it became the United States Soccer Football Association. It dropped the word football from its name in 1974 to become known as the United States Soccer Federation.[10]

text: U.S. Soccer has hosted several global soccer tournaments, including the 1994 FIFA World Cup, the FIFA Women's World Cup in 1999 and 2003, and the Summer Olympics in 1984 and 1996.

text: National teams[edit]

text: U.S. men's national team[edit]

text: The United States national team was first assembled in 1885 to play Canada in the first international match held outside the United Kingdom.[11]

text: The men's national team was invited to the inaugural World Cup in 1930 and qualified for the World Cup in 1934, finishing third place in 1930 out of 13 teams participating. In 1950 the United States scored one of its most surprising victories with a 1–0 win over heavily favored England, who were amongst the world's best sides at the time.

text: The United States failed to reach another World Cup until an upstart team qualified for the 1990 World Cup with the "goal heard around the world" scored by Paul Caligiuri against Trinidad and Tobago, which started the modern era of soccer in the United States. The 1990 men's national team was quickly disposed of at the World Cup, but nonetheless had qualified for its first World Cup in 40 years.

text: The United States hosted the 1994 World Cup, setting total and average attendance records that still stand, including drawing 94,194 fans to the final. The United States made a surprising run to the second round with a shocking victory over Colombia which saw Andrés Escobar, the player responsible for the United States' first goal (an own goal), later shot to death in his homeland.

text: 1998 saw another disappointing addition to the history of the men's national team as it finished last out of the 32 teams that qualified for the World Cup. This embarrassment, which included a total collapse of team chemistry and leadership, led to the firing of manager Steve Sampson.

text: The U.S. team hired Bruce Arena, who had won the first two MLS Cups in Major League Soccer history, and who went on to become the most successful United States men's national team manager in history. In 2002 Bruce Arena led a mix of veterans and MLS-seasoned youth to a quarterfinal appearance, dispatching contenders Portugal in group play and archrivals Mexico in the Round of 16, before losing a closely fought game with eventual runners-up Germany in the quarterfinal.

text: The team looked to match or surpass that feat in 2006; the U.S. was drawn into a group with Italy, the Czech Republic and Ghana. The United States lost to the Czech Republic 3–0 in their opening game, drew Italy, 1–1, in their second game (a match that saw two U.S. players and an Italian player red carded), and lost to Ghana, 2–1. The United States did not advance out of the group, but were the only team to face eventual winner Italy without losing. In the wake of the team's disappointing performance, Arena's contract was not renewed.

text: Bob Bradley, Chivas USA manager and Arena's assistant manager with the men's national team, eventually succeeded Arena in 2007. The U.S. qualified for the 2010 World Cup in South Africa,[12] winning the CONCACAF qualifying tournament. At the World Cup, the Americans tied England 1–1, tied Slovenia, 2–2. and then won their group by defeating Algeria 1–0 on a stoppage time goal by Landon Donovan. In the Round of 16, the United States played Ghana, and fell 2–1 in extra time.

text: Entering the 2014 World Cup in Brazil, the U.S team won all three friendly "send-off" matches leading up to the competition: 2–0, over Azerbaijan, 2–1, over Turkey, and 2–1 over fellow World Cup participant and defending African champions Nigeria. They were led at the time by Jürgen Klinsmann, who helped lead West Germany to victory in the 1990 World Cup and was the first player to score at least three goals in three consecutive World Cups.

text: During the 2014 World Cup, the U.S. won their first match against Ghana, 2–1. Clint Dempsey scored in the first minute of the match giving the U.S. the early lead. Ghana did not respond until the 82nd minute scoring the equalizer goal. The U.S. then reclaimed the lead, thanks to John Brooks scoring the game-winning goal off his head just four minutes later in the 86th minute to regain the lead and take the match. The U.S. gained three points for their win and was off to a great start in the "Group of Death" claimed by critics for the teams the U.S. would have to go through (Germany, Ghana, and Portugal).

text: The second match of the World Cup for the U.S. was a different story. Portugal claimed the early lead, with Nani scoring in the 5th minute to take the early 1–0 lead. It wasn't till the 64th minute till the U.S. scored the equalizing goal, thanks to Jermaine Jones, tying the match at 1 apiece. The U.S. then claimed the lead on a goal by Clint Dempsey again, scoring in the 81st minute to take a 2–1 lead. However, in the final minute of extra time, the world player of the year, Cristiano Ronaldo drilled a perfect cross to teammate Silvestre Varela who headed in the tying goal, making the final score 2–2. The tie gave each team a point in the overall standings, bringing the U.S. to 4 points total, and gave Portugal their first point of the World Cup having lost their opening match to Germany, 4–0. The U.S. claimed a spot in the knockout round in spite of a 1–0 loss to eventual champion Germany in their final group game due to them winning the tiebreaker with Portugal. However, they bowed out the tournament in the round of 16 in a 2–1 loss to Belgium. Goalkeeper Tim Howard helped the U.S. keep a 0–0 tie at full time. In extra time, there were two Belgian goals. The U.S. struck back with a goal by 19-year-old phenom Julian Green but could not manage another goal. Klinsman was let go as USMNT Director of Coaching and was replaced by Bruce Arena in November 2016.

text: The U.S. finished in fifth place in the fifth round of the CONCACAF qualification tournament for the 2018 FIFA World Cup, which concluded in October 2017. This marks the first time that the U.S. failed to qualify for the World Cup since 1986. As a result of the fifth-place finish, Bruce Arena was let go as USMNT Director of Coaching later that month.

text: United States, jointly with Canada and Mexico, is competing against Morocco to host the 2026 FIFA World Cup. The host will be announced on June 13, 2018 in Moscow, Russia.

text: U.S. women's national team[edit]

text: The women's national team has won three FIFA Women's World Cup tournaments in 1991, 1999 and 2015 (placing second in 2011 and third in 1995, 2003, and 2007); the Olympic Gold Medal in 1996, 2004, 2008, and 2012; and seven Algarve Cups and six CONCACAF Women's Gold Cups.

text: The FIFA Women's World Cup was inaugurated in 1991, and the women's national team became the first team to win the prize after beating Norway in the final.

text: In 1999, the United States hosted the FIFA Women's World Cup for the first time. During their tournament run, the women's national team established a new level of popularity for the women's game, culminating in a final against China that drew 90,185 fans, an all-time attendance record for a women's sports event, to a sold-out Rose Bowl. After neither team scored in regulation or extra time, the final went to a penalty shootout, which the United States won 5–4. The celebration by Brandi Chastain after she converted the winning penalty, in which she took off her shirt, revealing her sports bra in the process, is one of the more famous images in U.S. women's sports.

text: Youth national teams[edit]

text: U.S. Soccer Federation oversees and promotes the development of the following national youth teams:[13]

text:
U.S. Under-23 Men
U.S. Under-23 Women
U.S. Under-20 Men
U.S. Under-20 Women
U.S. Under-18 Men
U.S. Under-18 Women
U.S. Under-17 Men
U.S. Under-17 Women
U.S. Under-15 Boys
U.S. Under-15 Girls
U.S. Under-14 Boys
U.S. Under-14 Girls

text: U.S. Paralympic National Team[edit]

text: The U.S. Paralympic Soccer Team is an elite level program for men that selects players from across the United States in preparation for International standard competition. The team competes in 7-a-side football. The squad is composed of athletes who have cerebral palsy or have suffered a stroke or traumatic brain injury. The program is Coached by Stuart Sharp under the oversight of the U.S. Soccer Federation.[14]

text: Headquarters and national training center[edit]

text: U.S. Soccer House is located in two refurbished mansions at 1801 South Prairie Avenue in Chicago, Illinois and serves as the headquarters for the U.S. Soccer Federation.[15]

text: In 2003, U.S. Soccer opened their National Training Center at StubHub Center in Carson, California. The $130 million facility includes a soccer-specific stadium, home to the MLS team Los Angeles Galaxy. Additionally, four grass soccer fields, a FieldTurf soccer field and a general training area are specifically dedicated to U.S. Soccer. Both the senior and youth men's and women's US national teams hold regular camps at StubHub Center.[16]

text: U.S. Soccer was also exploring a possibility of building the National Training and Coaching Development Center in Kansas City, Kansas.[17] On April 9, 2015, the Training Center received final approval from the local governments. U.S. Soccer agreed to a 20-year lease, with the project set to break ground in 2016 and finishing some time in 2017.[18][19]

text: Professional leagues[edit]

text: Despite the growth of men's and women's professional soccer in the United States in the last few decades, by far the largest category of soccer in the United States, at least in terms of participation, is boys and girls youth soccer. Though organized locally by organizations all over the United States, there are two main youth soccer organizations working nationwide through affiliated local associations. The United States Youth Soccer Association boasts over three million players between the ages of five and 19, while American Youth Soccer Organization has more than 300,000 players between the ages of four and 19. This makes soccer one of the most played sports by children in the United States.

text: Men[edit]

text: The professional first-division league in North America is Major League Soccer which, as of the upcoming 2018 season, has 20 teams in the U.S. and 3 in Canada. The league has added three teams since 2017 with the addition of Atlanta United FC and Minnesota United FC in 2017 and Los Angeles FC in 2018, and plans to add five more teams no later than the early 2020s. The league operates as a single-entity league, which means MLS, and not the individual teams, holds the contracts on players.

text: The one sanctioned second-division men's outdoor soccer league is the United Soccer League (USL). Previously, the second North American Soccer League had second-division status, sharing it with the USL in the 2017 season, but the NASL was denied second-division sanctioning for 2018 due to considerable instability in the league.[20]

text: The new NASL has no official tie to the former NASL that operated from 1968 to 1984; though, some of the teams share names with their historic counterparts. Unlike MLS that is a single-entity operation, the new NASL, like the old NASL, has no salary cap and players are contracted by the individual teams.[21] The season is a split format (similar to that of many leagues in Latin America) that features seven teams, including one Puerto Rican team. Previous to the reorganization of the NASL in 2009, the USL First Division operated as the professional second-division league in the United States. However, a dispute among its teams and ownership led to the creation of the NASL which applied for and was awarded by USSF second division status. The 2010 season was played as a combined USL/NASL league format before NASL officially separated in 2011.[22]

text: The United Soccer Leagues (USL) were a collection of five leagues spanning the lower divisions of men's professional soccer, as well as women's soccer and youth soccer. After the 2010 season, the USL folded its former First and Second Divisions into a new professional third-division league, USL Pro, that launched in 2011. At launch, it had 15 teams: 11 on the U.S. mainland, three in Puerto Rico, and one in Antigua and Barbuda. The Puerto Rican teams, plagued by ownership and economic issues, were dropped from the league after 2011, and the Antigua team discontinued operations after a winless 2013 season. In January 2013, USL and MLS reached an agreement to integrate USL Pro league competition with the MLS Reserve League spawning the creation of secondary teams directly affiliated with MLS franchises. This was done primarily to improve player development in North America, strengthen league competition and build ties between divisions in the American soccer pyramid. This multi-year deal encourages MLS and USL Pro team affiliations and player loans, and it will lead to more games for teams and to the development of American players. The deal has proven to be a boon for USL Pro, and in 2015, after a rebrand to USL, 24 teams were participating in a healthy and stable 3rd division.[23][24] USL was provisionally sanctioned as a second-division league for 2017, claiming that their final applications met all the standards for second-division sanctioning.[25][26]

text: There are currently no sanctioned third-division leagues. Two leagues have indicated that they will seek third-division status. United Soccer Leagues, administrator of the USL and PDL leagues, announced that they would start a new league, tentatively called D3, and seek third-division certification and targeting 2019 as the first season for the new league.[27] National Independent Soccer Association (NISA) led by former Chicago Fire general manager Peter Wilt plans on fielding 8-10 teams in 2018 and has stated that it will seek third-division certification.[28]

text: A fourth-division league in the United States is the Premier Development League, which as of 2015 is expected to have 58 U.S. teams, and six Canadian teams. Though the PDL does have some paid players, it also has many teams that are made up entirely or almost entirely of college soccer players who use the league as an opportunity to play competitive soccer in front of professional scouts during the summer, while retaining amateur status and NCAA eligibility. Another fourth-division league in the United States is the National Premier Soccer League.

text: In addition to MLS and the USL, the United States Adult Soccer Association governs amateur soccer competition for adults throughout the United States, which is effectively the amateur fifth-division of soccer in the United States. The USASA sanctions regional tournaments that allow entry into the Lamar Hunt U.S. Open Cup, the oldest continuous national soccer competition in the United States. Since 1914, the competition has been open to all U.S. Soccer affiliated clubs, and currently pits teams from all five levels of the American soccer pyramid against each other each year, similarly to England's FA Cup.

text: Women[edit]

text: Women's soccer in the United States has been played at the professional level in three separate leagues since 2001. The first two attempts at professional leagues lasted three seasons each.

text: Women's United Soccer Association (WUSA), 2001–2003[edit]

text: The Women's United Soccer Association (WUSA) was founded in 2001. Headlined by the stars of the 1999 FIFA Women's World Cup-winning team, $30 million dollars was initially invested by numerous cable tv networks and owners.[29] The league's inaugural match was held between the Washington Freedom featuring Mia Hamm and the Bay Area CyberRays (featuring Brandi Chastain) at RFK Stadium in Washington, D.C.. In addition to the 34,148 fans in attendance being greater than any MLS game that weekend, the Turner Network Television (TNT) broadcast reached 393,087 households: more than two MLS games broadcast on ESPN and ESPN2.[30] The league folded in 2003.

text: Women's Professional Soccer (WPS), 2009–2011[edit]

text: The second attempt, Women's Professional Soccer, was founded in 2009, and featured involvement of many former WUSA figures. The champion of WPS' first season in 2009 was Sky Blue FC, out of the New York–New Jersey area. They defeated the Los Angeles Sol 1–0 at The Home Depot Center in Carson, California. WPS launched with seven teams, all based in the United States. The Sol folded after the league's inaugural season, and two new teams joined for 2010, bringing WPS to eight teams. However, the 2010 season saw considerable instability, with another charter team, Saint Louis Athletica, folding during the season, champions FC Gold Pride folding after the season, and the Chicago Red Stars deciding to regroup in the second-tier Women's Premier Soccer League (WPSL). The 2011 season, in which six teams based along the East Coast played, was marked by low attendance for most of the season and conflict with Dan Borislow, who had purchased the former Washington Freedom, moved the team to South Florida, and renamed it magicJack. The dispute between WPS and Borislow led the league to suspend the magicJack franchise, with Borislow responding by suing. The legal battle led WPS to suspend its 2012 season, with hopes of returning in 2013, but WPS soon decided to fold completely.

text: National Women's Soccer League (NWSL), 2013–present[edit]

text: On November 21, 2012, U.S. Soccer, in conjunction with the Canadian Soccer Association (CSA) and Mexican Football Federation (FMF), announced the formation of a new professional league for the 2013 season.[31] The league, unnamed at the time of the initial announcement but later unveiled as the National Women's Soccer League (NWSL), launched in April 2013 with eight teams.[31] Like WUSA and WPS, NWSL teams are privately owned with some owned by existing MLS teams.[32] The American and Canadian federations pay the salaries for many of their respective national team members. U.S. Soccer initially committed to funding up to 24 national team members, with the CSA committing to paying 16 players and FMF pledging support for at least 12 and possibly as many as 16.[32][33] In addition, U.S. Soccer housed the league's front office for the first four years, and scheduled matches to avoid any possible conflict with international tournaments.[32] Four of the league's charter teams had WPS ties—the Boston Breakers, Chicago Red Stars, Sky Blue FC, and the Western New York Flash. The other four initial teams were located in the Kansas City, Portland, Seattle, and Washington, D.C. markets with the Portland team run by the Portland Timbers of MLS.[32] The NWSL expanded to nine teams for 2014 by adding the Houston Dash, run by the Houston Dynamo of MLS. In 2016, it expanded to 10 with the addition of another MLS-backed team, the Orlando Pride. Ahead of the 2017 season, A&E Networks announced it had taken an equity stake in the league and Lifetime would begin broadcasting games to a national television audience.[34] As of 2017[update], additional expansion teams were being discussed by Los Angeles FC, Vancouver Whitecaps, and FC Barcelona.[35][36][37]

text: Controversies[edit]

text: Concussions[edit]

text: In 2014 parents and former players filed a Class Action Lawsuit against the United States Soccer Federation, FIFA, and other Soccer Organizations for failure to create policies that would prevent, evaluate and manage concussion injuries.[38] Soccer is second only to American football in the number of concussion injuries per year.[39]

text: MLS relationship[edit]

text: The USSF has been accused by representatives of the North American Soccer League, among others, of unfairly protecting MLS's leading role in American professional soccer. Among their concerns is that the USSF benefits from financial dealings with MLS that it does not have with other leagues, giving it an apparent incentive to protect MLS from competition.[40] This includes the contract that the USSF has with MLS's Soccer United Marketing (SUM) subsidiary in which most USSF sponsorship, television licensing and royalty revenues (outside of its apparel deal with Nike, Inc.) are paid through SUM. The USSF reported $15,433,754 in revenues through the SUM relationship in its 2014 audited financial report.[41]

text: In 2015, the NASL took issue with proposed USSF rule changes reportedly making it harder to gain co-equal "Division 1" status with MLS that would increase the NASL's influence within the USSF as well as presumably allow more access to international competition and larger media and sponsorship contracts, calling the draft proposal "...an anti-competitive bait and switch, with the purpose of entrenching MLS’s monopoly position at the very time when the NASL is threatening to become a significant competitor."[42] Seats on the USSF's Professional Council governing committee are also based proportionally on pyramid level, giving MLS more votes when choosing the two professional league representatives on the USSF's Board of Directors. In 2015, those representatives are MLS Commissioner Don Garber and Alec Papadakis, CEO of the United Soccer League that announced an affiliation with MLS in 2015.

text: International competitiveness[edit]

text: High-profile international soccer figures including former USMNT Head Coach Jürgen Klinsmann,[43] former LA Galaxy head coach and USMNT Head Coach Bruce Arena[44] and Manchester City manager and former FIFA World Coach of the Year Pep Guardiola,[45] have expressed beliefs that the top-down structure of soccer developed and managed by the USSF in the United States, including pressure to have the best American players in MLS rather than higher-quality leagues in other countries, is hampering the nation's competitiveness in international soccer.

text: Conversely, Klinsmann has been criticized in turn by MLS representatives for recommending that American players leave MLS development systems to pursue professional careers in Europe in order to test themselves against higher levels of players in preparation for international competition. In 2015, MLS Commissioner Don Garber said, "I do believe our national team coach has a short-term objective. That's what he's hired to do. That doesn't mean next week, but it's to win the Gold Cup, it's to have the best possible team in 2018. And our goals and objectives are broader than that, and that's why we agree on some things but don't agree on others."[46]

text: Coaches and technical staff[edit]

text:
Men's coaches

Level
Name
Notes

Senior
 Dave Sarachan (interim)

Under-23
 Andi Herzog

Under-20
 Tab Ramos

Under-19
vacant

Under-18
 Omid Namazi

Under-17
 John Hackworth

Under-16
 Shaun Tsakiris

Under-15
 Dave Van Den Bergh

Under-14
 Brian Johnson

Futsal
 Keith Tozer

Beach
 Eddie Soto

Paralympic
vacant

Women's coaches

Level
Name
Notes

Senior
 Jill Ellis

Under-23
vacant

Under-20
 Jitka Klimková

Under-19
 Keri Sarver

Under-18
 Jaime Frias

Under-17
 Mark Carr

Under-16
 Kacey White

Under-15
 Tracey Kevins

Under-14
 Jill Ellis

tag: table

text: Technical Staff

text:
Level
Name
Notes

Technical director
vacant

Youth technical director
 Tab Ramos

Technical advisor
 Brian Johnson

Technical advisor
 Carson Porter

Director of scouting
 Tony Lepore

Director of coaching education
 Dave Chesler

Director of youth national teams
 Jim Moorhouse

Women's technical director
 April Heinrichs

Women's youth development director
 Jill Ellis

Women's yead development coach
 April Kater

text: Presidents[edit]

text: United States Soccer Football Association (until 1974)

text:
James McGuire (1952–1954)
Jack Flamhaft (1959–1961)
Gene Ringsdorf (1961–1963)
George Fishwick (1963–1965)
Bob Guelker (1967–1969)
Erwin Single (1969–1971)
James McGuire (1971–1974)

text: United States Soccer Federation (1974–present)

text:
Gene Edwards (1974–1984)
Werner Fricker (1984–1990)
Alan Rothenberg (1990–1998)
Robert Contiguglia (1998–March 11, 2006)
Sunil Gulati (March 11, 2006–January 10, 2018)
Carlos Cordeiro (January 10, 2018–present)

text: Current sponsorships[edit]

text:
Anheuser-Busch[47]
Nike
Continental
Coca-Cola
Cutter
Powerade
Liberty Mutual
AT&T
Thorne
HisenseUSA
Johnson & Johnson
Tag Heuer
Volpi Foods


document_title: List of Tokyo Ghoul episodes

question_text: when is the next tokyo ghoul episode coming out

text: List of Tokyo Ghoul episodes

text: Episode list[edit]

text: Tokyo Ghoul[edit]

text:
No.
Title
Original air date[1]
English air date[2]

1
"Tragedy"
"Higeki" (悲劇)
July 4, 2014
March 26, 2017[3]

Ken Kaneki is a young man who befriends the beautiful and enigmatic Rize Kamishiro, unaware that she is a ghoul. Rize reveals her intentions to eat Kaneki but by a stroke of luck Kaneki survives her attack but is mortally wounded. He is saved by an emergency operation, transferring Rize's organs into himself. This subsequently turns him into a half-ghoul half-human hybrid and Kaneki struggles to survive and cope by himself.

2
"Incubation"
"Fuka" (孵化)
July 11, 2014
April 2, 2017

Kaneki struggles to adapt to his new nature with no success, until another ghoul, Nishiki Nishio, attempts to prey on his friend, Hideyoshi Nagachika, and he must fight to protect him.

3
"Dove"
"Shirohato" (白鳩)
July 18, 2014
April 9, 2017

After saving his friend, Kaneki is taken in by Yoshimura, a ghoul who runs the Cafe "Anteiku", who teaches him to blend in human society while hiding his true nature. However, he gets bullied by another ghoul named Touka.

4
"Supper"
"Bansan" (晩餐)
July 25, 2014
April 23, 2017[a]

A ghoul named Tsukiyama approaches Kaneki with unknown intentions and the two start hanging out. However, Tsukiyama has prepared a mortal trap where Kaneki is to be killed and eaten. Kaneki finds himself in an arena facing a giant ghoul executioner, Taro, but Tsukiyama intervenes and kills Taro as he wants Kaneki for himself.

5
"Scars"
"Zankon" (残痕)
August 1, 2014
April 30, 2017

Intending to consume Kaneki himself, Tsukiyama prepares another trap, using Nishio's human girlfriend Nishino Kimi as a hostage. Kaneki confronts Tsukiyama and is assisted by Nishio and then Touka. They are no match for Tsukiyama as their kagune are not as strong because they do not consume human flesh, so Touka bites Kaneki, restoring her kagune.

6
"Cloudburst"
"Shūu" (驟雨)
August 8, 2014
May 7, 2017

Tsukiyama is defeated by Touka with Nishio's help. Meanwhile, recent developments in the 20th ward draw the attention of the Commission of Counter Ghoul (CCG), who sends two of their investigators, Kureo Mado & Kōtarō Amon to hunt down all ghouls in the area. They find Hinami's father, Fueguchi and kill him. They then use some of Fueguchi's blood to attract ghouls and trap Hinami and her mother, Ryouko.

7
"Captivity"
"Yūshū" (幽囚)
August 15, 2014
May 14, 2017

Hinami's mother Ryouka is killed by Mado. An angry and vengeful Touka attacks members of the CCG. She kills Kusaba and attacks Amon, but Mado intervenes, using his kagune-like quinque and wounds Touka. Kaneki tells Touka that he wants to fight the ghoul investigators, much to Touka's chagrin, and is given his mask by Uta.

8
"Circular"
"Enkan" (円環)
August 22, 2014
May 21, 2017

Mado lures Hinami into a trap, but she is followed by Kaneki and Touka. Touka attacks Mado while Kaneki confronts Amon. During the fight with Amon, Kaneki realizes that he's the only one that understands the plight of both humans and ghouls. Kaneki bites Amon, releasing his kagune, but then tells Amon to escape, to his surprise. Meanwhile as Mado fights Touka, he reveals that the quinque used by the CCG are made from the kagune of dead ghouls. Hinami eventually uses her kagune to save Touka fatally wounding Mado, but refusing to kill him.

9
"Birdcage"
"Torikago" (鳥籠)
August 29, 2014
June 4, 2017[b]

Amon recalls his early days in the CCG when he was partnered with the experienced Mado. Meanwhile, Touka looks after Hinami above the cafe. Still mourning the loss of his partner, Amon is relocated to the 11th ward, where the CCG have trouble facing dangerous ghouls who do not fear them.

10
"Aogiri" (青桐)
September 5, 2014
June 11, 2017

In the 11th ward, Aogiri Tree ghouls attack a CCG branch and kill all the investigators, to the concern of Yoshimura and Yomo. Banjou Kazuichi from the 11th Ward comes to the cafe looking for Rize, then Touka's brother Ayato arrives, and then Yamori (Jason) who brutally beats and then kidnaps Kaneki. While the CCG plan an attack on the Aogiri Tree, Touka, Nishio and Hinami prepare to rescue Kaneki.

11
"High Spirits"
"Shōten" (衝天)
September 12, 2014
June 18, 2017

As Kaneki is tortured mercilessly by Yamori, the CCG storm the Aogiri Tree hideout. Meanwhile the Anteiku group infiltrate the building to rescue Kaneki. The CCG gain the upper hand, but are then confronted by the One-Eyed Owl, the leader of Aogiri Tree.

12
"Ghoul"
"Kushu" (喰種)
September 19, 2014
June 25, 2017

During the physical and mental tortures he suffers at the hands of Jason, Kaneki's hair turns white and he sees a vision of Rize. Eventually he comes to accept his ghoul-half and fights back and mortally wounds Yamori.

text: Tokyo Ghoul √A[edit]

text:
No.
Title
Original air date[6]
English air date[2]

1
"New Surge"
"Shin Kō" (新洸)
January 9, 2015
July 9, 2017

An all-out battle takes place between the CCG and the Aogiri led by the One-Eyed Owl. Shinohara and Iwa take on the One-Eyed Owl using new quinque armour called aratas, but are unable to defeat him. As the building collapses, the CCG lose about half of their troops and suspect that it was a trap. Meanwhile, Touka fights her brother Ayato but she is badly injured and saved by Kaneki. To her surprise, Kaneki leaves the Anteiku group to join the Aogiri Tree.

2
"Dancing Flowers"
"Maika" (舞花)
January 16, 2015
July 16, 2017

The 9th and 10th wards are lost to the Aogiri, apparently led by a ghoul with an eyepatch. Meanwhile Mado's daughter Akira, is assigned to become Amon's new partner. She suggests that a ghoul organization is in control of the 20th ward, but also causes some friction among the investigators because of her abrupt manner. Kaneki has now joined the Aogiri.

3
"Hangman"
"Tsu hito" (吊人)
January 23, 2015
July 23, 2017

Kaneki and Ayato lead an Aogiri attack on a CCG convoy to rescue Naki, one of Jason's old cohorts who is being taken to the maximum security prison for ghouls known as Cochlea. During the mission, they are attacked by two one-eyed ghouls in black and white striped masks. Touka pays a visit to the university which Kaneki used to attend, where she has an encounter with Hideyoshi Nagachika (Hide) who is now working as a messenger for the CCG.

4
"Deeper Layers"
"Shinsō" (深層)
January 30, 2015
July 30, 2017

While Amon and Akira visit Cochlea prison to learn more about Aogiri's plan from Donato Porpora, the Aogiri commence their invasion of Cochlea and free a majority of the imprisoned ghouls. The two one-eyed ghouls, Kurona and Nashiro Yasuhisa, meet up with the idiosyncratic inspector Juzo Suzuya. Kaneki frees the powerful ghoul Matasaka Kamishiro, but is attacked by him and badly beaten.

5
"Rift"
"Kiretsu" (裂目)
February 6, 2015
August 6, 2017

The battle at Cochlea intensifies on several fronts. Juzo defeats Kurona and Nashiro Yasuhisa, and Shinohara in his arata armour almost kills Ayato. Kaneki undergoes a transformation, generating an additional kagune after consuming dead ghouls, however he is beaten by Amon. Amon recalls the time Kaneki spared him and so he hesitates, reluctant to kill Kaneki. At that moment, the One-Eyed-Owl arrives, grabs Ayato and Kaneki, then departs.

6
"Thousand Paths"
"Chiji" (千路)
February 13, 2015
August 13, 2017

Juzo recalls the time when he was known as Rei, an arena executioner for the ghoul Big Madam, and then his acceptance into the CCG by Shinohara. Amon and Akira spend some time together and develop a better understanding of each other. Meanwhile the CCG prepare a task force to combat the One-Eyed-Owl and the Aogiri. Kaneki painfully tries to gain control his new kagune.

7
"Permeation"
"Tōka" (透過)
February 20, 2015
August 20, 2017

Hinami misses Kaneki but is uncertain what to do about it. Sen Takatsuki, Kaneki's and Hinami's favourite author, shows up at the Anteiku coffee shop and tells Hinami that in her current state, she cannot help her Onii-chan (Kaneki). Takatsuki visits the CCG, and tells Shinohara about Anteiku so he pays a visit with Juzo and meets Yoshimura. Later, Kaneki appears at Anteiku and although Touka rushes there to see him, she beats him up instead of revealing her true feelings for him.

8
"Old Nines"
"Kyū kyū" (旧九)
February 27, 2015
August 27, 2017

Yoshimura tells Kaneki about his early life as the killer Kuzen and that the One-Eyed-Owl is actually his child, Eto, with a human woman, Ukina. Yoshimura then sends Touka and Hinami to safety with Yomo, suspecting that the CCG has discovered the truth about Anteiku and is planning an attack.

9
"City In Waiting"
"Machi mochi" (街望)
March 6, 2015
September 10, 2017[c]

The CCG staff prepare their testamentary notes in their own personal ways in preparation for a potentially fatal full scale assault on Anteiku. They launch the attack using conventional and specialized weapons and are greeted by the Devil Apes and Black Dober groups with Yoshimura and his friends - Yoshimura pretending to be the One-Eyed Owl. Despite being warned of the danger, Touka and Kaneki head to the 20th ward to assist their friends.

10
"Last Rain"
"Tsui ame" (終雨)
March 13, 2015
September 17, 2017

Kaneki's friends from Anteiku are defeated one by one but he arrives to help them. Juzo, Shinohara and a few other investigators finally defeat Yoshimura after a long, fierce battle. Amon faces off against Kaneki, but with victory in sight for the CCG the real One-Eyed Owl appears before the investigators.

11
"Deluge of Flowers"
"Mitsuru hana" (溢花)
March 20, 2015
September 24, 2017

The One-Eyed Owl easily defeats Shinohara and Juzo, and when the Aogiri Tree joins the battle, the CCG is driven into a corner. Kaneki and Amon face off, and reluctantly engage in battle. Eventually the strongest investigator, Kishō Arima appears and attacks the One-Eyed Owl giving the CCG renewed hope to fight on. Badly wounded, the One-Eyed Owl consumes Yoshimura's body and escapes. Also wounded, Kaneki struggles towards Anteiku. He wakes up in the cafe and finds Hide trying to make coffee for him. In a post-credits scene, the Owl regurgitates a still alive Yoshimura behind an alley and goes back to her original form, revealing herself to be both Sen Takatsuki and the Owl/Eto.

12
"Ken" (研)
March 27, 2015
October 1, 2017

Kaneki thinks back to happier times in Anteiku. Hide reveals that he knew Kaneki was a ghoul after Nishiki attacked the two of them. As they talk, Hide collapses from loss of blood and passes out in Kaneki's arms, having been mortally wounded on the battlefield. Touka sobs when she arrives to see Anteiku burning down. She chases after Kaneki when she sees him walking out, but is stopped by Yomo, who states that Yoshimura's last request to him was for him to protect her. Kaneki walks toward the CCG, carrying Hide's body in his arms, and comes face-to-face with Arima. At the next morning, both Kaneki and Amon have disappeared. After the credits, it is shown that Touka has opened up a new café.

text: Tokyo Ghoul:re[edit]

text:
No.
Title
Original air date

1
"START: Those Who Hunt"
"Karu Monotachi START" (狩る者たち　ＳＴＡＲＴ)
April 3, 2018

Quinx (ghoul like modified human) squad leader Kuki Urie and his frustrating underling Ginshi Shirazu are surveying Tokyo in search of the ghoul serial killer Torso, who has been killing women and eating their torsos but leaving the rest of their bodies. Eventually, they meet with photographer Chie Hori, who gives them valuable information in exchange for the underpants of senior Quinx Haise Sasaki. Hinami, now an Aogiri Tree member, warns Torso to be careful because they are close to catching him. Learning that the culprit is a taxi driver, Toru Mutsuki (one of the members of the Quinx Squad) discovers him and is brutally attacked in his car. However, this allows Ginshi and Urie to locate the killer and lure him into a roadblock trap. While they face the killer, however, a mysterious and exceptionally strong ghoul named Orochi attacks, massacring all of the officers maintaining the roadblock, and allowing the taxi driver to escape. Sasaki appears and faces Orochi, but then suffers a hallucination of Ken Kaneki telling him to "accept" him in order to kill Orochi brutally. Sasaki then unleashes his kagune.

2
"member: Fragments"
"Kakera member" (欠片 member)
April 10, 2018

When Sasaki removes Orochi's mask during their fight he is shocked to see the face of Nishio underneath, who calls him "Kaneki", prompting his memories to flicker back and forth and drive him insane. To prevent Sasaki from killing his fellow CCG agents, Akira Mado tranquilizes him. After returning to his senses, Sasaki demotes Urie for endangering his squadmates and promotes Ginshi to Quinx Squad leader. Sasaki then spars with Kisho Arima, before telling him that he was worried that the memories of his past self "Kaneki" were returning and that they might drive him away from his family with the Quinx Squad. Later, Torso meets with The Rabbit (Ayato Kirishima), to become a member of Aogiri Tree. Sasaki, Ginshi, and Mutsuki then begin investigating a ghoul nicknamed "Nutcracker" who has been crushing the testicles of her victims and stop by in the coffee shop :re (the same one owned by Touka Kirishima). While at the shop, Sasaki recognizes and is recognized by Touka. After tasting the coffee she makes for him, he begins to cry, subconsciously recalling his time at Anteiku. He then thinks to himself that he had never before seen anyone so beautiful.

3
"fresh: Eve"
"Zen'yasai fresh" (前夜祭 fresh)
April 17, 2018

Kanae von Rosewald brings Shu Tsukiyama the underwear that Chie Hori had collected from Haise Sasaki, but the latter falls into despair after realizing that he couldn't recognize the scent as Kaneki's. Later, the Quinx Squad continue their investigation of Nutcracker and cross-dress to disguise themselves at a nightclub where she had been sighted. At the nightclub, two members of the Clowns recognize Sasaki as Kaneki and note that "for Kaneki to come out, Sasaki will have to ‘die.’" The squad, alongside Juzo Suzuya, then follow up on a lead that takes them to the auction where the Nutcracker had been selling her victims to the gourmets.
Note: this episode features an insert song by popular American youtuber and singer Amanda Lee

4
"MAIN: Auction"
"Ōkushon MAIN" (オークション　MAIN)
April 24, 2018

Kidnapped and entered into a circus-themed gourmet auction, Toru is sold off to Big Madam. However, Suzuya initiates an assault on the auction in which many ghouls and CCG operatives are killed. Eto watches the chaos from afar in amusement, and sends in a mysterious ghoul called Takizawa, who brutally kills a squad leader. During the fray, Torso and Kanae fight over who gets to keep Toru.

5
"PresS: Night of Scattering"
"Chiri Yuku Yoru Press" (散りゆく夜　Press)
May 1, 2018

Takizawa, revealed to be former Investigator Takizawa, now a crazed one-eyed ghoul, slaughters an entire squad of CCG operatives, while another squad is killed by Nutcracker. Meanwhile, Sasaki and the Quinx Squad face off against Kanae, who furiously blames him for Tsukiyama's reduced mental state, but is critically injured and rescued by a mysterious ghoul named Matsumae. Big Madam and the other auctioneers are attacked by Suzuya and Urie (who lied to Toru and Suzuya about being unable to radio in help in order to prevent backup from preventing him from distinguishing himself in battle), but mid-way through the fight, Urie is critically injured and swallowed by Big Madam. The episode ends with Takizawa leaping from above and attacking Sasaki, who is forced by his superiors to fight the SS-rated one-eyed ghoul alone.

6
"turn: In the End"
"Sono, Hate ni turn" (その、果てに turn)
May 8, 2018

Sasaki suffers multiple hallucinations of Ken Kaneki, while Takizawa is beating him inside the auction room. Meanwhile, the Nutcracker is killed by Quinx Squad members Ginshi Shirazu and Saiko Yonebayashi. Big Madam fights both Urie, who nearly goes insane, and Mutsuki, who unleashes his kagune. She comes face to face with Juzo, who despite that he was tortured by her, is unable to kill her. She is eventually wounded by fellow Suzuya squad member Hanbee Abara, who covers Juzo's ears while the CCG investigators kill her. Meanwhile Hinami, realizing that Sasaki is Kaneki, and Saiko hearing Sasaki's screams, they both rush into the auction room, where Hinami fights Takizawa in order to save Sasaki. Sasaki fearfully accepts his Kaneki side and fights Takizawa. They both pierce each other with their kagunes and fall down.

7
"mind: Days of Recollections"
"Kokorooboe Arishi Hibi mind" (心覚え在りし日々 mind)
May 15, 2018

Hinami is arrested by CCG operators led by Kisho Arima. Sasaki, having survived his encounter with Takizawa, saves her from execution by asking to take her into custody. She is imprisoned in Cochlea ghoul prison. In the following weeks after the operation, the members of the Quinx Squad are being promoted while Sasaki becomes senior investigator. At the next morning, he hallucinates that an investigator is Yamori. The same night, Eto delivers him a package with Kaneki's old mask and a book signed by her in it. He goes to the :re cafe where he is served coffee by Touka. After he leaves, Touka, Uta, Yomo and Nishio discuss about Kaneki. Sasaki starts searching about Kaneki and then suffers a hallucination of Yoshimura and Anteiku. On the same night, Tsukiyama is in terrible pain despite eating many people.

8
"TAKe: One Who Writhes"
"Ugomeku Mono TAKe" (蠢くモノ TAKe)
May 22, 2018

Tsukiyama is always hungry and can't control his kagune.In the meantine, Tatara refuses Ayato's request to rescue Hinami from Cochlea. Sasaki is approached by the ghoul investigators Nimura Furuta and Shiki Kijima who tell him that he is going to work them on the upcoming Rose Investigation. In CCG HQ, Sasaki and the Quinx Squad are informed by the investigator Kori Ui about the Rose ghoul gang (actually members of the Tsukiyama crime family), who attack Furuta and Kijima. They are saved by the investigator Hairu Ihei. Gang member Yuuma is arrested and tortured by Kijima in Cochlea. Sasaki visits Uta to learn more about the mask and Takatsuki's book. Uta lies about both of them. Sasaki then asks him to make him a new mask. Chie Hori delivers Sasaki's photos to Kanae von Rosewald and Tsukiyama recognizes him to be Kaneki.

9
"play: Departed Spirit"
"Bōrei play" (亡霊 play)
May 29, 2018

Tsukiyama wants to make Sasaki remember that he is Kaneki. He and Kanae find him on the street, along with the Quinx Squad, and Tsukiyama runs towards him but fells down. Sasaki hears him saying "Kaneki" but he doesn't recognise him. Sasaki goes to Uta's shop and orders masks for the entire Quinx Squad, in order to impersonate ghouls for the upcoming Rose Investigation. Kori Ui rejects the plan, knowing that Sasaki is a ghoul. In the meantime, Kijima's video of him torturing Yuuma brutally and provoking Rose gang to kill him has gone viral. Tsukiyama plans to release him and to use Kaneki/Sasaki as a key person by restoring his memories. Tsukiyama makes many failed attempts to speak to Sasaki, so Kanae bribes some Aogiri members to attack the Squad in order to isolate Sasaki. However, Yamori's old gang attacks Sasaki by accident and Mutsuki battles with Torso but he is attacked by the ghoul Grave Robber. Sasaki kills his attackers with his kagune. Saiko is almost killed but she is saved by Amon Kotaru who is revealed to be alive. Eto watches the entire scene.

10
"Sway"
"Yureru" (ゆれる)
TBA

text: OVA[edit]

text:
No.
Title
Release date

1
"Tokyo Ghoul: JACK"
"Tōkyō Gūru [JACK]" (東京喰種トーキョーグール [JACK])
September 30, 2015

The story features a serious young Special Investigator Kishou Arima at high school where he first meets the carefree Taishi Fura who joins him in hunting ghouls in the 13th ward. Later, they both become Special Investigators in the CCG, but retain their original opposite attitudes.

2
"Tokyo Ghoul: PINTO"
"Tōkyō Gūru [PINTO]" (東京喰種トーキョーグール [PINTO])
December 25, 2015

The story features Shuu Tsukiyama the "Gourmet" during his high school years and Chie Hori. They meet when she photographs Tsukiyama killing a jogger and then about to eat him because of the tone of his body. She being uninterested in exposing him as a Ghoul and seems completely lost in a world of her own, photographing anything that takes her interest.

text: Home release[edit]

text: The series was released to DVD and Blu-Ray format in four volumes.[8]

text: Tokyo Ghoul[edit]

text:
TC Entertainment (Japan, Region 2/A)

Episodes
DVD/Blu-ray Release date[8]

Volume 1
1-3
000000002014-09-26-0000September 26, 2014

Volume 2
4-6
000000002014-10-31-0000October 31, 2014

Volume 3
7-9
000000002014-11-28-0000November 28, 2014

Volume 4
10-12
000000002014-12-26-0000December 26, 2014

text: Notes[edit]

text:
Jump up ^ Tokyo Ghoul did not air on Toonami the weekend of April 15–16, 2017 due to special scheduling.[4]
Jump up ^ Tokyo Ghoul did not air on Toonami the weekend of May 27–28, 2017 due to a Samurai Jack marathon.[5]
Jump up ^ Tokyo Ghoul √A did not air on the weekend for September 2–3, 2017 due to a Dragon Ball Z Kai marathon.[7]

tag: ol


document_title: Mission San Francisco Solano (California)

question_text: when did the san francisco solano mission close

text: History[edit]

text: Fr. José Altimira age 33, arrived from Barcelona, Spain to serve at Mission San Francisco de Asís. The mission was not thriving because of its climate and had established a medical asistencia ("sub-mission") in San Rafael to help the mission’s ill neophytes (baptized Native Americans) recover their health. California Governor Luis Argüello was interested in blocking the Russians at Bodega Bay and Fort Ross from moving further inland. Together they developed and presented to the party church authorities and the territory (legislature) a plan for moving Mission San Francisco de Asís and the San Rafael asistencia to a new location north of the Bay. The legislature approved but the church authorities did not respond (they had forwarded the plan to their superiors in Mexico).[10] Under the old Spanish regime, founding a new mission required the approval of both New Spain's Bishop and the King’s Viceroy.[11]

text: Beginning in 1823, while waiting for a response from the church authorities, Fr. Altimira, with military escorts, began exploring north of the Bay for a suitable mission site. On July 4, 1823, the soldiers placed a large redwood cross on the place in the Sonoma Valley where they expected the new Mission San Francisco de Assis to be established. Then they celebrated Mass to consecrate the location. They then returned south to begin gathering men and materials to begin construction.[12]

text: The area around the selected site was not empty. It was near the northeast corner of the territory of the Coast Miwok,[13] Southern Pomo to the northwest, Wappo to the northeast, Suisunes and Ptwin peoples to the east.[14][15] A detachment of soldiers from the Presidio of San Francisco would be provided to protect the Mission and guard the neophytes.[16]

text: Altimira with soldiers and neophytes primarily from Mission San Francisco de Asís returned to the Sonoma area near the end of August. Altimira decided there was a better place to build on the other side of the valley. Just after starting he received a letter from Father-President Sarria who refused Altimira permission to continue building. Fr. Altimira obeyed and the month of September saw continuing negotiations between California’s civil and religious leaders. On September 30 an agreement was reached: a new mission could be built and Fr. Altimira would be its minister, but Mission San Francisco de Asís would not be closed and the San Rafael asistencia had already been designated as a full mission (Mission San Rafael Arcángel).[17]

text: Beginning in October 1823 Fr. Altimira had the opportunity to build his new mission at the location he chose but since Mission San Francisco de Asís would remain open this Mission needed a different patron saint. Altimira chose San Francisco Solano, a 17th-century Franciscan missionary to South America.[18] His company of soldiers and neophytes set about building all the facilities needed in a California mission. His annual report for 1823 listed no baptisms, one marriage, one funeral, a population of 482 Indians (all transferred from other missions) and 1341 animals.[19] The work had started too late in the year for anything to be planted and harvested.

text: On April 4, 1824, Passion Sunday, Father Altimira proudly dedicated his church. It was a crude, temporary structure but it symbolized development at the Mission. The church was built of whitewashed boards but was well furnished and decorated. Many of the articles were gifts from the Russians at Fort Ross. It also held a canvas painting of San Francisco Solano which had been donated by the Father-President. Furthermore, the Mission had been promised a relic of the patron saint to put in the altar.[20]

text: The Mission continued to develop until an argument arose about the sharing of the bountiful 1826 harvest Indians, not living at the Mission, were unhappy with the amount allocated for their work and burned some of the wooden buildings in protest. Fr. Altimira with a few faithful neophytes fled to Mission San Rafael Arcángel.[21]

text: Fr. Buenaventura Fortuni, an aging Spanish Franciscan who had been working at Mission San José, was assigned to replace Altimira.[22] Fr. Fortuni quickly reestablished order and morale and the work of building the mission restarted. He arranged the main buildings to form a large, square enclosure.

text: In 1830 Fr. Fortuni, having labored alone at this mission for 3 1/2 years, felt the need to transfer to another mission where the work load could be shared.[23] He was 58 years old when he was replaced by Fr. José Gutiérrez, a Franciscan friar from South America. The Mexican government had in 1826 required that all the Spanish friars who would not pledge loyalty to Mexico leave. Fr. Fortuni had been exempted from this rule but all new churchmen would be required to take the pledge.[22]

text: Fr. Gutierrez continued to build and increased the agricultural effort.[24] By 1832 the mission had 27 rooms in the convento or priest's quarters, with a great adobe church at the east end, and a wooden storehouse (the original mission chapel) at the west end. Completing this enclosure were workshops where the Indians were taught to be craftsmen and created the items needed to help the mission be self-sufficient. Along the back of the courtyard were the living quarters and workrooms for the young Indian girls. In addition to the quadrangle, there were orchards, gardens, vineyards, fields of grain, a gristmill, houses for the soldiers and Indian families, a jail, a cemetery and an infirmary.[25]

text: The most successful year of this mission's short life span (11 years) was 1832. In his annual report for that year, Fr. Gutierrez recorded the following: 127 baptisms, 34 marriages, and 70 deaths; a total of 996 neophytes (coming from 35 area villages[26]); the livestock inventory included 6,000 sheep and goats, 900 horses, 13 mules, 50 pigs and 3,500 head of cattle. Crops were measured in fanegas, or Spanish bushels, a variable measure of volume generally between 50 and 60 liters. In 1832 the mission produced 800 fanegas of wheat, 1025 fanegas of barley, 52 fanegas of peas, 300 fanegas of corn, 32 fanegas of beans, and 2 fanegas of garbanzos.[27]

text: In 1833 the Mexican Congress decided to close all of the missions in Alta California with the passage of the Mexican secularization act of 1833. Governor Figueroa issued a regulation (Reglamento Provisional para la secularization de las Misiones) on August 9, 1834, outlining the requirements for the distribution of property (land, cattle, and equipment) to each mission’s neophytes.[28] Among the provisions were that "5. To each head of a family and to all over 20 years old, will be given from the Mission lands a lot not over 400 nor less than 100 varas square" (28 to 7 acres). Plus "6. ...pro rata...one-half of the livestock" and "7. ... half or less of the existing chattels, tools, and seed...".[29]

text: Mission San Francisco Solano officially ceased to exist on November 3, 1834, when it was designated a First Class Parish. The Spanish missionaries were to be replaced by parish priests - the first was Fr. Lorenzo Quijas who had earlier been assigned to Sonoma and San Rafael.[30]In,

text: Lieutenant (teniente) Mariano Vallejo, Commandant of the Presidio of San Francisco, was named administrator (comisionado) to oversee the closing of the Mission under the Reglamento.[31] Fr. Quijas moved back to San Rafael in July, 1835, after many disputes with Guadalupe Antonio Ortega, Vallejo's majordomo, to whom Vallejo had delegated the work of secularization. Ortega (sometimes call Sergeant Ortega[32]) was “uneducated, coarse and licentious".[33] Right after returning to San Rafael, Padre Quijas wrote a letter to Commissary Perfect Garcia Diego, his superior, complaining about the situation in Sonoma and specifically the "...abominable deeds of Ortega...." Quijas then gives names of witnesses to be called against Ortega.[34] Upon receipt of the letter Fr. Diego forward it to Governor José Figueroa demanding some action against Ortega. The Governor was critically ill and died at the end of the following month. No action was taken.[35] It wasn't until the summer of 1837, because of new scandals and unsatisfactory accounts, that Ortega was removed.[36]

text: After Fr. Quijas left, the neophyte population decreased rapidly (most returning to their home villages - taking their movable property with them, or moving to ranchos {including Vallejo's Petaluma Adobe} to work, or staying in Sonoma as servants).[37] Some former Mission Indians reportedly received their allotted land and cattle from the Mission (none of these small plots of land were permanently recorded.)[38] In August 1839, the government sent William Edward Petty Hartnell as Visitador General de Misiones to check compliance with the Reglamento but Vallejo avoided responding - claiming he did not have time because of military affairs. No effective review of the secularization of the Sonoma mission was even completed.[39]

text: The mission buildings rapidly fell into disrepair. The town of Sonoma was growing and building materials were in great demand. Roof tiles, timbers, and adobe bricks were salvaged from the mission buildings. After the settlers had cannibalized the old buildings, nature began recycling the remnants.[14]

text: In 1841, Mariano Vallejo ordered a small adobe chapel to be built on the location of the first wooden mission chapel. It became the church of the parish and replaced the large mission church which was rapidly deteriorating. It stood on the west end of the Convento so is often thought to be the church of the old mission.[40]

text: During 1863 President Abraham Lincoln transferred ownership of all the mission churches in California to the Roman Catholic Church. In 1881, the Sonoma church property was sold to a local businessman and a new parish church was built across town. At one time, the old adobe chapel was used as a warehouse. The Convento may have been used as a winery.[14]

text: In 1903, the two remaining mission buildings were purchased by California Historic Landmarks League and became part of the California Park System in 1906. By 1913, both had been reconstructed. After the 1940s, the former church and Convento were remodeled along more authentic lines suited to exhibits devoted exclusively to mission history.[14]

text: Dedicated in 1999, the Sonoma Mission Indian Memorial honors the more than 800 native people (including over 200 children) who died while living and working at the Mission between 1824 and 1839. Their Christian names, as recorded by the priests in the Mission’s records, are inscribed on this granite memorial.[41] European diseases such as measles and smallpox, for which Native Americans had no inherited resistance, with the overcrowded and unhealthful living conditions at all California missions (especially for women and children) contributed to the high death rate.[42]

text: California Historic Landmark[edit]

text: On June 1, 1932, Mission San Francisco Solano was designated California Historical Landmark #3.

text: Gallery[edit]

text:
Interior of Vallejo's Chapel

Indian Memorial

Mission Solano State Landmark Plaque