prompt_front: Now, answer the following question based on the text below, only give me the answer and do not output any other words.

Question: What happens to Ngotho after he attacks Jacobo at a workers' strike?

Read the following text and answer briefly.

Context 1: Weep Not, Child is a 1964 novel by Kenyan author Ngũgĩ wa Thiong'o  It was his first novel, published in 1964 under the name James Ngugi  It was among the African Writers Series  It was the first English language|English novel to be published by an East African  Thiong'o's works deal with the relationship between Africans and white settlers in colonial Kenya, and are heavily critical of colonial rule  Specifically, Weep Not, Child deals with the Mau Mau Uprising, and "the bewildering dispossession of an entire people from their ancestral land " Ngũgĩ wrote the novel while he was a student at Makerere University 

The book is divided into two parts and eighteen chapters  Part one deals mostly with the education of Njoroge, while part two deals with the rising Mau Mau movement 

Plot summary

Njoroge, a little boy, is urged to attend school by his mother  He is the first one of his family able to go to school  His family lives on the land of Jacobo, an African made rich by his dealings with white settlers, namely Mr  Howlands, the most powerful land owner in the area  Njoroge's brother Kamau works as an apprentice to a carpenter, while Boro, the eldest living son, is troubled by his experiences while in forced service during World War II, including witnessing the death of his elder brother  Ngotho, Njoroge's father and a respected man in the surrounding area, tends Mr  Howlands' crops, but is motivated by his passion to preserve his ancestral land, rather than for any compensation or loyalty 

One day, black workers call for a strike to obtain higher wages  Ngotho is ambivalent about participating in the strike because he fears he will lose his job  However, he decides to go to the gathering, even though his two wives do not agree  At the demonstration, there are calls for higher wages  Suddenly, the white police inspector brings Jacobo to the gathering to pacify the native people  Jacobo tries to put an end to the strike  Ngotho attacks Jacobo, and the result is a riot where two people are killed  Jacobo survives and swears revenge  Ngotho loses his job and Njoroge’s family is forced to move  Njoroge’s brothers fund his education and seem to lose respect for their father 

Mwihaki, Jacobo's daughter and Njoroge's best friend, enters a girls' only boarding school, leaving Njoroge relatively alone  He reflects upon her leaving, and realizes that he was embarrassed by his father's actions towards Jacobo  For this reason, Njoroge is not upset by her exit and their separation  Njoroge switches to another school 

For a time, everyone's attention is focused on the upcoming trial of Jomo Kenyatta – a revered leader of the movement  Many blacks think that he is going to bring forth Kenya’s independence  But Jomo loses the trial and is imprisoned  This results in further protests and greater suppression of the black population 

Jacobo and a white landowner, Mr  Howlands, fight against the rising activities of the Mau Mau, an organization striving for Kenyan economic, political, and cultural independence  Jacobo accuses Ngotho of being the leader of the Mau Mau and tries to imprison the whole family  Meanwhile, the situation in the country is deteriorating  Six black men are taken out of their houses and executed in the woods 

One day Njoroge meets Mwihaki again, who has returned from boarding school  Although Njoroge had planned to avoid her due to the conflict between their fathers, their friendship is unaffected  Njoroge passes an important exam that allows him to advance to High School  His village is proud of him, and collects money to pay Njoroge's High School tuition 

Several months later, Jacobo is murdered in his office by a member of the Mau Mau  Mr  Howlands has Njoroge removed from school for questioning  Both father and son are brutally beaten before release and Ngotho is left barely alive  Although there doesn't seem to be a connection between Njoroge's family and the murder, it is eventually revealed that Njoroge's brothers are behind the assassination, and that Boro is the real leader of the Mau Mau  Ngotho soon dies from his injuries and Njoroge finds out that his father was protecting his brothers  Kamau has been imprisoned for life  Only Njoroge and his two mothers remain free, and Njoroge is left as the sole provider of his two mothers  Njoroge fears that he cannot make ends meet; he gives up hope of continuing in school and loses faith in God 

Njoroge asks Mwihaki's for support, but she is angry because of her father’s death  When he finally pledges his love to her, she refuses to leave with him, realizing her obligation to Kenya and her mother  Njoroge decides to leave town and makes an attempt at suicide; however, he fails when his mothers find him before he is able to hang himself  The novel closes with Njoroge feeling hopeless, and ashamed of cowardice 

Characters in Weep Not, Child
 Njoroge: the main character of the book whose main goal throughout the book is to become as educated as possible 
 Ngotho: Njoroge's father  He works for Mr Howlands and is respected by him until he attacks Jacobo at a workers strike  He is fired and the family is forced to move to another section of the country  Over the course of the book his position as the central power of the family weakened, to the point where his self-realization that he has spent his whole life waiting for the prophecy (that proclaims the blacks will be returned their land) to come true rather than fighting for Kenyan independence, leads to his depression 
 Nyokabi and Njeri: the two wives of Ngotho  Njeri is Ngotho's first wife, and mother of Boro, Kamau, and Kori  Nyokabi is his second wife, and the mother of Njoroge and Mwangi 
 Njoroge has four brothers: Boro, Kamau, Kori and Mwangi (who is Njoroge's only full brother, who died in World War II) 
 Boro: Son of Njeri who fights for the Allies in World War II  Upon returning his anger against the colonial government is compounded by their confiscation of the his land  Boro's anger and position as eldest son leads him to question and ridicule Ngotho, which eventually defeats their father's will (upon realizing his life was wasted waiting and not acting)  It is eventually revealed that Boro is the leader of the Mau Mau (earlier alluded to as "entering politics") and murders Mr Howlands  He is caught by police immediately after and is scheduled to be executed by the book's end  It is highly likely that it is also Boro who kills Jacobo 
 Mwihaki: Njoroge's best friend (and later develops into his love interest)  Daughter of Jacobo  When it is revealed that his family killed Jacobo (most likely Boro), Mwihaki distances herself from Njoroge, asking for time to mourn her father and care for her mother 
 Jacobo: Mwihaki's father and an important landowner  Chief of the village 
 Mr  Howlands: A white settler who emigrated to colonial Kenya and now owns a farm made up of land that originally belonged to Ngotho's ancestors  Has three children: Peter who died in World War II before the book's beginning, a daughter who becomes a missionary, and Stephen who met Njoroge while the two were in high school 

Themes and motifs
Weep Not, Child integrates Gikuyu mythology and the ideology of nationalism that serves as catalyst for much of the novel's action  The novel explores the negative aspects of colonial rule over Kenya  Njoroge's aspiration to attend university is frustrated by both the violence of the Mau Mau rebels and the violent response of the colonial government  This disappointment leads to his alienation from his family and ultimately his suicide attempt 

The novel also ponders the role of saviours and salvation  The author notes in his The River Between: "Salvation shall come from the hills  From the blood that flows in me, I say from the same tree, a son shall rise  And his duty shall be to lead and save the people " Jomo Kenyatta, the first prime minister of Kenya, is immortalised in Weep Not, Child  The author says, "Jomo had been his (Ngotho's) hope  Ngotho had come to think that it was Jomo who would drive away the white man  To him, Jomo stood for custom and traditions purified by grace of learning and much travel " Njoroge comes to view Jomo as a messiah who will win the struggle against the colonial government 

See also

Things Fall Apart
Death and the King's Horseman

References

External links
Official homepage of Ngũgĩ wa Thiong'o
BBC profile of Ngũgĩ wa Thiong'o
Weep Not, Child at Google Books

British Empire in fiction
Novels set in colonial Africa
Historical novels
Kenyan English-language novels
Novels by Ngũgĩ wa Thiong'o
Novels set in Kenya
1964 novels
Heinemann (publisher) books
Postcolonial novels
African Writers Series
1964 debut novels
Context 2: Vitamin K - Wikipedia
(Redirected from Vitamin k)
This article needs more medical references for verification or relies too heavily on primary sources  Please review the contents of the article and add the appropriate references if you can  Unsourced or poorly sourced material may be challenged and removed  (November 2015)
This article is about the family of vitamers  For vitamin K1 the form usually used as a supplement, see Phytomenadione 
Vitamin K structures  MK-4 and MK-7 are both subtypes of K2 
Vitamin K deficiency, Warfarin overdose
Vitamin K is a group of structurally similar, fat-soluble vitamins the human body requires for complete synthesis of certain proteins that are prerequisites for blood coagulation and which the body also needs for controlling binding of calcium in bones and other tissues  The vitamin K-related modification of the proteins allows them to bind calcium ions, which they cannot do otherwise  Without vitamin K, blood coagulation is seriously impaired, and uncontrolled bleeding occurs  Low levels of vitamin K also weaken bones and promote calcification of arteries and other soft tissues[citation needed] 
Chemically, the vitamin K family comprises 2-methyl-1,4-naphthoquinone (3-) derivatives  Vitamin K includes two natural vitamers: vitamin K1 and vitamin K2 [1] Vitamin K2, in turn, consists of a number of related chemical subtypes, with differing lengths of carbon side chains made of isoprenoid groups of atoms 
Vitamin K1, also known as phylloquinone, is made by plants, and is found in highest amounts in green leafy vegetables because it is directly involved in photosynthesis  It may be thought of as the plant form of vitamin K  It is active as a vitamin in animals and performs the classic functions of vitamin K, including its activity in the production of blood-clotting proteins  Animals may also convert it to vitamin K2 
Bacteria in the gut flora can also convert K1 into vitamin K2  In addition, bacteria typically lengthen the isoprenoid side chain of vitamin K2 to produce a range of vitamin K2 forms, most notably the MK-7 to MK-11 homologues of vitamin K2  All forms of K2 other than MK-4 can only be produced by bacteria, which use these forms in anaerobic respiration  The MK-7 and other bacterially derived forms of vitamin K2 exhibit vitamin K activity in animals, but MK-7's extra utility over MK-4, if any, is unclear and is a matter of investigation 
Three synthetic types of vitamin K are known: vitamins K3, K4, and K5  Although the natural K1 and all K2 homologues and synthetic K4 and K5 have proven nontoxic, the synthetic form K3 (menadione) has shown toxicity [2]
1 2 Cardiovascular health
1 4 Coumarin poisoning
4 1 Conversion of vitamin K1 to vitamin K2
4 2 Vitamin K2
6 Absorption and dietary need
7 Dietary reference intake
10 Biochemistry
10 1 Function in animals
10 2 Gamma-carboxyglutamate proteins
10 3 Methods of assessment
10 4 Function in bacteria
11 Injection in newborns
11 3 Controversy
A review of 2014 concluded that there is positive evidence that monotherapy using MK-4, one of the forms of Vitamin K2, reduces fracture incidence in post-menopausal women with osteoporosis, and suggested further research on the combined use of MK-4 with bisphosphonates  In contrast, an earlier review article of 2013 concluded that there is no good evidence that vitamin K supplementation helps prevent osteoporosis or fractures in postmenopausal women [3]
A Cochrane systematic review of 2006 suggested that supplementation with Vitamin K1 and with MK4 reduces bone loss; in particular, a strong effect of MK-4 on incident fractures among Japanese patients was emphasized [4]
A review article of 2016 suggested to consider, as one of several measures for bone health, increasing the intake of foods rich in vitamins K1 and K2 [5]
Cardiovascular health[edit]
Adequate intake of vitamin K is associated with the inhibition of arterial calcification and stiffening,[6] but there have been few interventional studies and no good evidence that vitamin K supplementation is of any benefit in the primary prevention of cardiovascular disease [7]
One 10-year population study, the Rotterdam Study, did show a clear and significant inverse relationship between the highest intake levels of menaquinone (mainly MK-4 from eggs and meat, and MK-8 and MK-9 from cheese) and cardiovascular disease and all-cause mortality in older men and women [8]
Vitamin K has been promoted in supplement form with claims it can slow tumor growth; there is however no good medical evidence that supports such claims [9]
Coumarin poisoning[edit]
Vitamin K is part of the suggested treatment regime for poisoning by rodenticide (coumarin poisoning) [10]
Although allergic reaction from supplementation is possible, no known toxicity is associated with high doses of the phylloquinone (vitamin K1) or menaquinone (vitamin K2) forms of vitamin K, so no tolerable upper intake level (UL) has been set [11]
Blood clotting (coagulation) studies in humans using 45 mg per day of vitamin K2 (as MK-4)[12] and even up to 135 mg per day (45 mg three times daily) of K2 (as MK-4),[13] showed no increase in blood clot risk  Even doses in rats as high as 250 mg/kg, body weight did not alter the tendency for blood-clot formation to occur [14]
Unlike the safe natural forms of vitamin K1 and vitamin K2 and their various isomers, a synthetic form of vitamin K, vitamin K3 (menadione), is demonstrably toxic at high levels  The U S  FDA has banned this form from over-the-counter sale in the United States because large doses have been shown to cause allergic reactions, hemolytic anemia, and cytotoxicity in liver cells [2]
Phylloquinone (K1)[15][16] or menaquinone (K2) are capable of reversing the anticoagulant activity of the anticoagulant warfarin (tradename Coumadin)  Warfarin works by blocking recycling of vitamin K, so that the body and tissues have lower levels of active vitamin K, and thus a deficiency of vitamin K 
Supplemental vitamin K (for which oral dosing is often more active than injectable dosing in human adults) reverses the vitamin K deficiency caused by warfarin, and therefore reduces the intended anticoagulant action of warfarin and related drugs [17] Sometimes small amounts of vitamin K are given orally to patients taking warfarin so that the action of the drug is more predictable [17] The proper anticoagulant action of the drug is a function of vitamin K intake and drug dose, and due to differing absorption must be individualized for each patient [citation needed] The action of warfarin and vitamin K both require two to five days after dosing to have maximum effect, and neither warfarin or vitamin K shows much effect in the first 24 hours after they are given [18]
The newer anticoagulants dabigatran and rivaroxaban have different mechanisms of action that do not interact with vitamin K, and may be taken with supplemental vitamin K [19][20]
Vitamin K2 (menaquinone)  In menaquinone, the side chain is composed of a varying number of isoprenoid residues  The most common number of these residues is four, since animal enzymes normally produce menaquinone-4 from plant phylloquinone 
A sample of phytomenadione for injection, also called phylloquinone
The three synthetic forms of vitamin K are vitamins K3 (menadione), K4, and K5, which are used in many areas, including the pet food industry (vitamin K3) and to inhibit fungal growth (vitamin K5) [21]
Conversion of vitamin K1 to vitamin K2[edit]
Vitamin K1 (phylloquinone) – both forms of the vitamin contain a functional naphthoquinone ring and an aliphatic side chain  Phylloquinone has a phytyl side chain 
The MK-4 form of vitamin K2 is produced by conversion of vitamin K1 in the testes, pancreas, and arterial walls [22] While major questions still surround the biochemical pathway for this transformation, the conversion is not dependent on gut bacteria, as it occurs in germ-free rats[23][24] and in parenterally-administered K1 in rats [25][26] In fact, tissues that accumulate high amounts of MK-4 have a remarkable capacity to convert up to 90% of the available K1 into MK-4 [27][28] There is evidence that the conversion proceeds by removal of the phytyl tail of K1 to produce menadione as an intermediate, which is then condensed with an activated geranylgeranyl moiety (see also prenylation) to produce vitamin K2 in the MK-4 (menatetrione) form [29]
Vitamin K2[edit]
Main article: Vitamin K2
Vitamin K2 (menaquinone) includes several subtypes  The two subtypes most studied are menaquinone-4 (menatetrenone, MK-4) and menaquinone-7 (MK-7) 
Vitamin K1, the precursor of most vitamin K in nature, is a stereoisomer of phylloquinone, an important chemical in green plants, where it functions as an electron acceptor in photosystem I during photosynthesis  For this reason, vitamin K1 is found in large quantities in the photosynthetic tissues of plants (green leaves, and dark green leafy vegetables such as romaine lettuce, kale and spinach), but it occurs in far smaller quantities in other plant tissues (roots, fruits, etc )  Iceberg lettuce contains relatively little  The function of phylloquinone in plants appears to have no resemblance to its later metabolic and biochemical function (as "vitamin K") in animals, where it performs a completely different biochemical reaction 
Vitamin K (in animals) is involved in the carboxylation of certain glutamate residues in proteins to form gamma-carboxyglutamate (Gla) residues  The modified residues are often (but not always) situated within specific protein domains called Gla domains  Gla residues are usually involved in binding calcium, and are essential for the biological activity of all known Gla proteins [30]
At this time[update], 17 human proteins with Gla domains have been discovered, and they play key roles in the regulation of three physiological processes:
Blood coagulation: prothrombin (factor II), factors VII, IX, and X, and proteins C, S, and Z[31]
Bone metabolism: osteocalcin, also called bone Gla protein (BGP), matrix Gla protein (MGP),[32] periostin,[33] and the recently discovered Gla-rich protein (GRP) [34][35]
Vascular biology: growth arrest-specific protein 6 (Gas6)[36]
Unknown function: proline-rich γ-carboxyglutamyl proteins (PRGPs) 1 and 2, and transmembrane γ-carboxy glutamyl proteins (TMGs) 3 and 4 [37]
Like other lipid-soluble vitamins (A, D and E), vitamin K is stored in the fatty tissue of the human body 
Absorption and dietary need[edit]
Previous theory held that dietary deficiency is extremely rare unless the small intestine was heavily damaged, resulting in malabsorption of the molecule  Another at-risk group for deficiency were those subject to decreased production of K2 by normal intestinal microbiota, as seen in broad spectrum antibiotic use [38] Taking broad-spectrum antibiotics can reduce vitamin K production in the gut by nearly 74% in people compared with those not taking these antibiotics [39] Diets low in vitamin K also decrease the body's vitamin K concentration [40] Those with chronic kidney disease are at risk for vitamin K deficiency, as well as vitamin D deficiency, and particularly those with the apoE4 genotype [41] Additionally, in the elderly there is a reduction in vitamin K2 production [42]
The National Academy of Medicine (NAM) updated an estimate of what constitutes an adequate intake (AI) for vitamin K in 2001  The NAM does not distinguish between K1 and K2 – both are counted as vitamin K  At that time there was not sufficient evidence to set the more rigorous estimated average requirement (EAR) or recommended dietary allowance (RDA) given for most of the essential vitamins and minerals  The current daily AIs for vitamin K for adult women and men are 90 μg and 120 μg respectively  The AI for pregnancy and lactation is 90 μg  For infants up to 12 months the AI is 2–2 5 μg, and for children aged 1 to 18 years the AI increases with age from 30 to 75 μg  As for safety, the FNB also sets tolerable upper intake levels (known as ULs) for vitamins and minerals when evidence is sufficient  In the case of vitamin K no UL is set, as evidence for adverse effects is not sufficient  Collectively EARs, RDAs, AIs and ULs are referred to as dietary reference intakes [43] The European Food Safety Authority reviewed the same safety question and did not set an UL [44]
For U S  food and dietary supplement labeling purposes, the amount in a serving is expressed as a percentage of daily value (%DV)  For vitamin K labeling purposes the daily value was 80 μg, but as of May 2016 it has been revised upwards to 120 μg  A table of the pre-change adult daily values is provided at reference daily intake  Food and supplement companies have until 28 July 2018 to comply with the change 
See also: Vitamin K2 § Dietary sources
K1 (μg)[45]
Kale, cooked
Collards, cooked
Collards, raw
Swiss chard, cooked
Swiss chard, raw
Turnip greens, raw
Romaine lettuce, raw
Table from "Important information to know when you are taking: Warfarin (Coumadin) and Vitamin K", Clinical Center, National Institutes of Health Drug Nutrient Interaction Task Force [46]
Vitamin K1 is found chiefly in leafy green vegetables such as dandelion greens (which contain 778 4 μg per 100 g, or 741% of the recommended daily amount), spinach, swiss chard, lettuce and Brassica vegetables (such as cabbage, kale, cauliflower, broccoli, and brussels sprouts) and often the absorption is greater when accompanied by fats such as butter or oils; some fruits, such as avocados, kiwifruit and grapes, are also high in vitamin K  By way of reference, two tablespoons of parsley contains 153% of the recommended daily amount of vitamin K [47] Some vegetable oils, notably soybean oil, contain vitamin K, but at levels that would require relatively large calorie consumption to meet the USDA-recommended levels [48] colonic bacteria synthesize a significant portion of humans' vitamin K needs; newborns often receive a vitamin K shot at birth to tide them over until their colons become colonized at five to seven days of age from the consumption of breast milk 
The tight binding of vitamin K1 to thylakoid membranes in chloroplasts makes it less bioavailable  For example, cooked spinach has a 5% bioavailability of phylloquinone, however, fat added to it increases bioavailability to 13% due to the increased solubility of vitamin K in fat [49]
Main article: Vitamin K deficiency
Average diets are usually not lacking in vitamin K, and primary deficiency is rare in healthy adults  Newborn infants are at an increased risk of deficiency  Other populations with an increased prevalence of vitamin K deficiency include those who suffer from liver damage or disease (e g  alcoholics), cystic fibrosis, or inflammatory bowel diseases, or have recently had abdominal surgeries  Secondary vitamin K deficiency can occur in people with bulimia, those on stringent diets, and those taking anticoagulants  Other drugs associated with vitamin K deficiency include salicylates, barbiturates, and cefamandole, although the mechanisms are still unknown  Vitamin K1 deficiency can result in coagulopathy, a bleeding disorder [50]Symptoms of K1 deficiency include anemia, bruising, nosebleeds and bleeding of the gums in both sexes, and heavy menstrual bleeding in women 
Osteoporosis[51][52] and coronary heart disease[53][54] are strongly associated with lower levels of K2 (menaquinone)  Vitamin K2 (as menaquinones MK-4 through MK-10) intake level is inversely related to severe aortic calcification and all-cause mortality [8]
Function in animals[edit]
Mechanism of action of vitamin K1 
The function of vitamin K2 in the animal cell is to add a carboxylic acid functional group to a glutamate (Glu) amino acid residue in a protein, to form a gamma-carboxyglutamate (Gla) residue  This is a somewhat uncommon posttranslational modification of the protein, which is then known as a "Gla protein"  The presence of two −COOH (carboxylic acid) groups on the same carbon in the gamma-carboxyglutamate residue allows it to chelate calcium ions  The binding of calcium ions in this way very often triggers the function or binding of Gla-protein enzymes, such as the so-called vitamin K-dependent clotting factors discussed below 
Within the cell, vitamin K undergoes electron reduction to a reduced form called vitamin K hydroquinone, catalyzed by the enzyme vitamin K epoxide reductase (VKOR) [55] Another enzyme then oxidizes vitamin K hydroquinone to allow carboxylation of Glu to Gla; this enzyme is called gamma-glutamyl carboxylase[56][57] or the vitamin K-dependent carboxylase  The carboxylation reaction only proceeds if the carboxylase enzyme is able to oxidize vitamin K hydroquinone to vitamin K epoxide at the same time  The carboxylation and epoxidation reactions are said to be coupled  Vitamin K epoxide is then reconverted to vitamin K by VKOR  The reduction and subsequent reoxidation of vitamin K coupled with carboxylation of Glu is called the vitamin K cycle [58] Humans are rarely deficient in vitamin K1 because, in part, vitamin K1 is continuously recycled in cells [59]
Warfarin and other 4-hydroxycoumarins block the action of VKOR [60] This results in decreased concentrations of vitamin K and vitamin K hydroquinone in tissues, such that the carboxylation reaction catalyzed by the glutamyl carboxylase is inefficient  This results in the production of clotting factors with inadequate Gla  Without Gla on the amino termini of these factors, they no longer bind stably to the blood vessel endothelium and cannot activate clotting to allow formation of a clot during tissue injury  As it is impossible to predict what dose of warfarin will give the desired degree of clotting suppression, warfarin treatment must be carefully monitored to avoid overdose 
Gamma-carboxyglutamate proteins[edit]
Main article: Gla domain
The following human Gla-containing proteins ("Gla proteins") have been characterized to the level of primary structure: blood coagulation factors II (prothrombin), VII, IX, and X, anticoagulant proteins C and S, and the factor X-targeting protein Z  The bone Gla protein osteocalcin, the calcification-inhibiting matrix Gla protein (MGP), the cell growth regulating growth arrest specific gene 6 protein (Gas6), and the four transmembrane Gla proteins (TMGPs), the function of which is at present unknown  Gas6 can function as a growth factor to activate the Axl receptor tyrosine kinase and stimulate cell proliferation or prevent apoptosis in some cells  In all cases in which their function was known, the presence of the Gla residues in these proteins turned out to be essential for functional activity 
Gla proteins are known to occur in a wide variety of vertebrates: mammals, birds, reptiles, and fish  The venom of a number of Australian snakes acts by activating the human blood-clotting system  In some cases, activation is accomplished by snake Gla-containing enzymes that bind to the endothelium of human blood vessels and catalyze the conversion of procoagulant clotting factors into activated ones, leading to unwanted and potentially deadly clotting 
Another interesting class of invertebrate Gla-containing proteins is synthesized by the fish-hunting snail Conus geographus [61] These snails produce a venom containing hundreds of neuroactive peptides, or conotoxins, which is sufficiently toxic to kill an adult human  Several of the conotoxins contain two to five Gla residues [62]
Methods of assessment[edit]
Vitamin K status can be assessed by:
The prothrombin time (PT) test measures the time required for blood to clot  A blood sample is mixed with citric acid and put in a fibrometer; delayed clot formation indicates a deficiency  This test is insensitive to mild deficiency, as the values do not change until the concentration of prothrombin in the blood has declined by at least 50% [63]
Undercarboxylated prothrombin (PIVKA-II); in a study of 53 newborns, found "PT (prothrombin time) is a less sensitive marker than PIVKA II",[64] and as indicated above, PT is unable to detect subclinical deficiencies that can be detected with PIVKA-II testing 
Plasma phylloquinone was found to be positively correlated with phylloquinone intake in elderly British women, but not men,[65] but an article by Schurgers et al  reported no correlation between FFQ[further explanation needed] and plasma phylloquinone [66]
Urinary γ-carboxyglutamic acid responds to changes in dietary vitamin K intake  Several days are required before any change can be observed  In a study by Booth et al , increases of phylloquinone intakes from 100 μg to between 377 and 417 μg for five days did not induce a significant change  Response may be age-specific [67]
Undercarboxylated osteocalcin (UcOc) levels have been inversely correlated with stores of vitamin K[68] and bone strength in developing rat tibiae  Another study following 78 post-menopausal Korean women found a supplement regimen of vitamins K and D, and calcium, but not a regimen of vitamin D and calcium, was inversely correlated with reduced UcOc levels [69]
Function in bacteria[edit]
Many bacteria, such as Escherichia coli found in the large intestine, can synthesize vitamin K2 (menaquinone-7 or MK-7, up to MK-11),[70] but not vitamin K1 (phylloquinone)  In these bacteria, menaquinone transfers two electrons between two different small molecules, during oxygen-independent metabolic energy production processes (anaerobic respiration) [71] For example, a small molecule with an excess of electrons (also called an electron donor) such as lactate, formate, or NADH, with the help of an enzyme, passes two electrons to menaquinone  The menaquinone, with the help of another enzyme, then transfers these two electrons to a suitable oxidant, such fumarate or nitrate (also called an electron acceptor)  Adding two electrons to fumarate or nitrate converts the molecule to succinate or nitrite plus water, respectively 
Some of these reactions generate a cellular energy source, ATP, in a manner similar to eukaryotic cell aerobic respiration, except the final electron acceptor is not molecular oxygen, but fumarate or nitrate  In aerobic respiration, the final oxidant is molecular oxygen (O2), which accepts four electrons from an electron donor such as NADH to be converted to water  E  coli, as facultative anaerobes, can carry out both aerobic respiration and menaquinone-mediated anaerobic respiration 
Injection in newborns[edit]
The blood clotting factors of newborn babies are roughly 30–60% that of adult values; this may be due to the reduced synthesis of precursor proteins and the sterility of their guts  Human milk contains 1–4 μg/L of vitamin K1, while formula-derived milk can contain up to 100 μg/L in supplemented formulas  Vitamin K2 concentrations in human milk appear to be much lower than those of vitamin K1  Occurrence of vitamin K deficiency bleeding in the first week of the infant's life is estimated at 0 25–1 7%, with a prevalence of 2–10 cases per 100,000 births [72] Premature babies have even lower levels of the vitamin, so they are at a higher risk from this deficiency 
Bleeding in infants due to vitamin K deficiency can be severe, leading to hospitalization, blood transfusions, brain damage, and death  Supplementation can prevent most cases of vitamin K deficiency bleeding in the newborn  Intramuscular administration is more effective in preventing late vitamin K deficiency bleeding than oral administration [73][74]
As a result of the occurrences of vitamin K deficiency bleeding, the Committee on Nutrition of the American Academy of Pediatrics has recommended 0 5–1 mg of vitamin K1 be administered to all newborns shortly after birth [74]
In the UK vitamin K supplementation is recommended for all newborns within the first 24 hours [75] This is usually given as a single intramuscular injection of 1 mg shortly after birth but as a second-line option can be given by three oral doses over the first month [76]
Controversy arose in the early 1990s regarding this practice, when two studies suggested a relationship between parenteral administration of vitamin K and childhood cancer,[77] however, poor methods and small sample sizes led to the discrediting of these studies, and a review of the evidence published in 2000 by Ross and Davies found no link between the two [78] Doctors reported emerging concerns in 2013,[79] after treating children for serious bleeding problems  They cited lack-of newborn vitamin K administration, as the reason that the problems occurred, and recommended that breastfed babies could have an increased risk unless they receive a preventative dose 
In the early 1930s, Danish scientist Henrik Dam investigated the role of cholesterol by feeding chickens a cholesterol-depleted diet [80] He initially replicated experiments reported by scientists at the Ontario Agricultural College (OAC) [81] McFarlane, Graham and Richardson, working on the chick feed program at OAC, had used chloroform to remove all fat from chick chow  They noticed that chicks fed only fat-depleted chow developed hemorrhages and started bleeding from tag sites [82] Dam found that these defects could not be restored by adding purified cholesterol to the diet  It appeared that – together with the cholesterol – a second compound had been extracted from the food, and this compound was called the coagulation vitamin  The new vitamin received the letter K because the initial discoveries were reported in a German journal, in which it was designated as Koagulationsvitamin  Edward Adelbert Doisy of Saint Louis University did much of the research that led to the discovery of the structure and chemical nature of vitamin K [83] Dam and Doisy shared the 1943 Nobel Prize for medicine for their work on vitamin K (K1 and K2) published in 1939  Several laboratories synthesized the compound(s) in 1939 [84]
For several decades, the vitamin K-deficient chick model was the only method of quantifying vitamin K in various foods: the chicks were made vitamin K-deficient and subsequently fed with known amounts of vitamin K-containing food  The extent to which blood coagulation was restored by the diet was taken as a measure for its vitamin K content  Three groups of physicians independently found this: Biochemical Institute, University of Copenhagen (Dam and Johannes Glavind), University of Iowa Department of Pathology (Emory Warner, Kenneth Brinkhous, and Harry Pratt Smith), and the Mayo Clinic (Hugh Butt, Albert Snell, and Arnold Osterberg) [85]
The first published report of successful treatment with vitamin K of life-threatening hemorrhage in a jaundiced patient with prothrombin deficiency was made in 1938 by Smith, Warner, and Brinkhous [86]
The precise function of vitamin K was not discovered until 1974, when three laboratories (Stenflo et al ,[87] Nelsestuen et al ,[88] and Magnusson et al [89]) isolated the vitamin K-dependent coagulation factor prothrombin (factor II) from cows that received a high dose of a vitamin K antagonist, warfarin  It was shown that, while warfarin-treated cows had a form of prothrombin that contained 10 glutamate (Glu) amino acid residues near the amino terminus of this protein, the normal (untreated) cows contained 10 unusual residues that were chemically identified as γ-carboxyglutamate (Gla)  The extra carboxyl group in Gla made clear that vitamin K plays a role in a carboxylation reaction during which Glu is converted into Gla 
The biochemistry of how vitamin K is used to convert Glu to Gla has been elucidated over the past thirty years in academic laboratories throughout the world 
^ "Vitamin K Overview"  University of Maryland Medical Center  ^ a b Higdon, Jane (Feb 2008)  "Vitamin K"  Linus Pauling Institute, Oregon State University  Retrieved 12 Apr 2008  ^ Hamidi, M  S ; Gajic-Veljanoski, O ; Cheung, A  M  (2013)  "Vitamin K and bone health"  Journal of Clinical Densitometry (Review)  16 (4): 409–413  doi:10 1016/j jocd 2013 08 017  PMID 24090644  ^ Cockayne, S ; Adamson, J ; Lanham-New, S ; Shearer, M  J ; Gilbody, S; Torgerson, D  J  (Jun 2006)  "Vitamin K and the prevention of fractures: systematic review and meta-analysis of randomized controlled trials"  Archives of Internal Medicine (Review)  166 (12): 1256–1261  doi:10 1001/archinte 166 12 1256  PMID 16801507  ^ O'Keefe, J  H ; Bergman, N ; Carrera Bastos, P ; Fontes Villalba, M ; Di Nicolantonio, J  J ; Cordain, L  (2016)  "Nutritional strategies for skeletal and cardiovascular health: hard bones, soft arteries, rather than vice versa"  Open Heart (Review)  3 (1): e000325  doi:10 1136/openhrt-2015-000325  PMC 4809188  PMID 27042317  ^ Maresz, K  (Feb 2015)  "Proper Calcium Use: Vitamin K2 as a Promoter of Bone and Cardiovascular Health"  Integrative Medicine (Review)  14 (1): 34–39  PMC 4566462  PMID 26770129  ^ Hartley, L ; Clar, C ; Ghannam, O ; Flowers, N ; Stranges, S ; Rees, K  (Sep 2015)  "Vitamin K for the primary prevention of cardiovascular disease"  The Cochrane Database of Systematic Reviews (Systematic review)  9 (9): CD011148  doi:10 1002/14651858 CD011148 pub2  PMID 26389791  ^ a b Geleijnse, J  M ; Vermeer, C ; Grobbee, D  E ; Schurgers, L  J ; Knapen, M  H ; van der Meer, I  M ; Hofman, A ; Witteman, J  C  (Nov 2004)  "Dietary intake of menaquinone is associated with a reduced risk of coronary heart disease: the Rotterdam Study"  Journal of Nutrition  134 (11): 3100–3105  PMID 15514282  ^ Ades, T  B , ed  (2009)  "Vitamin K"  American Cancer Society Complete Guide to Complementary and Alternative Cancer Therapies (2nd ed )  American Cancer Society  pp  558–563  ISBN 978-0-944235-71-3  ^ Lung, D  (Dec 2015)  Tarabar, A , ed  "Rodenticide Toxicity Treatment & Management"  Medscape  WebMD  ^ Rasmussen, S  E ; Andersen, N  L ; Dragsted, L  O ; Larsen, J  C  (Mar 2006)  "A safe strategy for addition of vitamins and minerals to foods"  European Journal of Nutrition  45 (3): 123–135  doi:10 1007/s00394-005-0580-9  PMID 16200467  ^ Ushiroyama, T ; Ikeda, A ; Ueki, M (Mar 2002)  "Effect of continuous combined therapy with vitamin K2 and vitamin D3 on bone mineral density and coagulofibrinolysis function in postmenopausal women"  Maturitas  41 (3): 211–221  doi:10 1016/S0378-5122(01)00275-4  PMID 11886767  ^ Asakura, H ; Myou, S ; Ontachi, Y ; Mizutani, T ; Kato, M ; Saito, M ; Morishita, E ; Yamazaki, M ; Nakao, S  (Dec 2001)  "Vitamin K administration to elderly patients with osteoporosis induces no hemostatic activation, even in those with suspected vitamin K deficiency"  Osteoporosis International  12 (12): 996–1000  doi:10 1007/s001980170007  PMID 11846334  ^ Ronden, J  E ; Groenen-van Dooren, M  M ; Hornstra, G ; Vermeer, C  (Jul 1997)  "Modulation of arterial thrombosis tendency in rats by vitamin K and its side chains"  Atherosclerosis  132 (1): 61–67  doi:10 1016/S0021-9150(97)00087-7  PMID 9247360  ^ Ansell, J ; Hirsh, J ; Poller, L ; Bussey, H ; Jacobson, A ; Hylek, E (Sep 2004)  "The pharmacology and management of the vitamin K antagonists: the Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy"  Chest  126 (3 Suppl ): 204S–233S  doi:10 1378/chest 126 3_suppl 204S  PMID 15383473  ^ Crowther, M  A ; Douketis, J  D ; Schnurr, T ; Steidl, L ; Mera, V ; Ultori, C ; Venco, A ; Ageno, W  (Aug 2002)  "Oral vitamin K lowers the international normalized ratio more rapidly than subcutaneous vitamin K in the treatment of warfarin-associated coagulopathy  A randomized, controlled trial"  Annals of Internal Medicine  137 (4): 251–254  doi:10 7326/0003-4819-137-4-200208200-00009  PMID 12186515  ^ a b "Important Information to Know When You Are Taking: Warfarin (Coumadin) and Vitamin K" (PDF)  National Institute of Health Clinical Center Drug-Nutrient Interaction Task Force  Retrieved 17 Apr 2015  ^ "Guidelines For Warfarin Reversal With Vitamin K" (PDF)  American Society of Health-System Pharmacists  Retrieved 17 Apr 2015  ^ "Pradaxa Drug Interactions"  Pradaxapro com  19 Mar 2012  Retrieved 21 Apr 2013  ^ Bauersachs, R ; Berkowitz, S  D ; Brenner, B ; Buller, H  R ; Decousus, H ; Gallus, A  S ; Lensing, A  W ; Misselwitz, F ; Prins, M  H ; Raskob, G  E ; Segers, A ; Verhamme, P ; Wells, P ; Agnelli, G ; Bounameaux, H ; Cohen, A ; Davidson, B  L ; Piovella, F ; Schellong, S  (Dec 2010)  "Oral rivaroxaban for symptomatic venous thromboembolism"  New England Journal of Medicine  363 (26): 2499–2510  doi:10 1056/NEJMoa1007903  PMID 21128814  ^ McGee, W  (1 Feb 2007)  "Vitamin K"  MedlinePlus  Retrieved 2 Apr 2009  ^ Shearer, M  J ; Newman, P  (Oct 2008)  "Metabolism and cell biology of vitamin K"  Thrombosis and Haemostasis  100 (4): 530–547  doi:10 1160/TH08-03-0147  PMID 18841274  ^ Davidson, R  T ; Foley, A  L ; Engelke, J  A ; Suttie, J  W  (Feb 1998)  "Conversion of dietary phylloquinone to tissue menaquinone-4 in rats is not dependent on gut bacteria"  Journal of Nutrition  128 (2): 220–223  PMID 9446847  ^ Ronden, J  E ; Drittij-Reijnders, M  J ; Vermeer, C ; Thijssen, H  H  (Jan 1998)  "Intestinal flora is not an intermediate in the phylloquinone–menaquinone-4 conversion in the rat"  Biochimica et Biophysica Acta  1379 (1): 69–75  doi:10 1016/S0304-4165(97)00089-5  PMID 9468334  ^ Thijssen, H   H ; Drittij-Reijnders, M  J  (Sep 1994)  "Vitamin K distribution in rat tissues: dietary phylloquinone is a source of tissue menaquinone-4"  The British Journal of Nutrition  72 (3): 415–425  doi:10 1079/BJN19940043  PMID 7947656  ^ Will, B  H ; Usui, Y ; Suttie, J  W  (Dec 1992)  "Comparative metabolism and requirement of vitamin K in chicks and rats"  Journal of Nutrition  122 (12): 2354–2360  PMID 1453219  ^ Davidson, R  T ; Foley, A  L ; Engelke, J  A ; Suttie, J  W  (Feb 1998)  "Conversion of dietary phylloquinone to tissue menaquinone-4 in rats is not dependent on gut bacteria"  Journal of Nutrition  128 (2): 220–223  PMID 9446847  ^ Ronden, J  E ; Drittij-Reijnders, M  J ; Vermeer, C ; Thijssen, H  H  (Jan 1998)  "Intestinal flora is not an intermediate in the phylloquinone-menaquinone-4 conversion in the rat"  Biochimica et Biophysica Acta  1379 (1): 69–75  doi:10 1016/S0304-4165(97)00089-5  PMID 9468334  ^ Al Rajabi, Ala (2011)  The Enzymatic Conversion of Phylloquinone to Menaquinone-4 (PhD thesis)  Tufts University, Friedman School of Nutrition Science and Policy  ^ Furie, B ; Bouchard, B  A ; Furie, B  C  (Mar 1999)  "Vitamin K-dependent biosynthesis of gamma-carboxyglutamic acid"  Blood  93 (6): 1798–1808  PMID 10068650  ^ Mann, K  G  (Aug 1999)  "Biochemistry and physiology of blood coagulation"  Thrombosis and Haemostasis  82 (2): 165–174  PMID 10605701  ^ Price, P  A  (1988)  "Role of vitamin-K-dependent proteins in bone metabolism"  Annual Review of Nutrition  8: 565–583  doi:10 1146/annurev nu 08 070188 003025  PMID 3060178  ^ Coutu, D  L ; Wu, J  H ; Monette, A ; Rivard, G  E ; Blostein, M  D ; Galipeau, J (Jun 2008)  "Periostin, a member of a novel family of vitamin K-dependent proteins, is expressed by mesenchymal stromal cells"  Journal of Biological Chemistry  283 (26): 17991–18001  doi:10 1074/jbc M708029200  PMID 18450759  ^ Viegas, C  S ; Simes, D  C ; Laizé, V ; Williamson, M  K ; Price, P  A ; Cancela, M  L  (Dec 2008)  "Gla-rich protein (GRP), a new vitamin K-dependent protein identified from sturgeon cartilage and highly conserved in vertebrates"  Journal of Biological Chemistry
Context 3: \section{INTRODUCTION}
The Tevatron Collider Run II started in March 2002 and is expected
to continue until the end of this decade  The Tevatron and the 
two detectors, CDF and D\O, have been performing  well in 2004,
each experiment is collecting data at the rate 
of $\approx$10 pb$^{-1}$ per week 
The total  luminosity accumulated by August 2004 is $\approx$500 pb$^{-1}$
per detector 
The rich physics program includes the
production and precision measurement of properties of  standard model (SM)
objects, as well as searches for phenomena beyond standard model 
In this brief review we focus on areas of most interest 
to the lattice community  We present
new results on the top quark mass
and their implication for the mass of the SM Higgs boson, 
on searches for the SM Higgs boson, on evidence for the $X(3872)$ state, 
on searches for pentaquarks, and on $b$ hadron properties 
All Run II results presented here are preliminary  

\section{TOP QUARK MASS}

The experiments CDF and D\O\ published several direct  measurements of
the top quark pole mass, $\ensuremath{M_{\mathrm{top}}}$, 
based on Run I data (1992-1996) 
The ``lepton $+$ jets'' channel yields the most precise determination of
$\ensuremath{M_{\mathrm{top}}}$  Recently, the
D\O\ collaboration published a new measurement~\cite{Mtop1-D0-l+j-new},
based on a powerful analysis technique yielding  greatly improved precision 
The differential probability 
that the measured variables in any event correspond to the signal
is calculated as a function of $\ensuremath{M_{\mathrm{top}}}$  
The maximum in the product of the individual event probabilities 
provides the best estimate of $\ensuremath{M_{\mathrm{top}}}$ 
The critical differences from previous analyses 
in the lepton $+$ jets decay channel lie in 
the assignment of more 
weight to events that are well measured or more likely to correspond to  
$t \bar t$ signal, 
and  the handling of the combinations of final-state objects
(lepton, jets, and imbalance in transverse momentum) 
and their identification with
top-quark decay products in an event  
The new combined value for the top-quark mass from Run I is 
$\ensuremath{M_{\mathrm{top}}}  =  178 0\pm4 3~\ensuremath{\mathrm{ Ge\kern -0 1em V }\kern -0 2em /c^2 }$ 

In Run II, both collaborations  have been exploring several different techniques 
for $\ensuremath{M_{\mathrm{top}}}$
measurements  The best single CDF result comes from a dynamic likelihood method
(DLM)  The method is similar to
the technique used in Ref ~\cite{Mtop1-D0-l+j-new} 
The result is $\ensuremath{M_{\mathrm{top}}} = 177 8^{+4 5}_{-5 0} (stat) \pm  6 2 (syst) ~\ensuremath{\mathrm{ Ge\kern -0 1em V }\kern -0 2em /c^2 }$ 
The joint likelihood of the selected events is shown in Fig  ~\ref{fig:cdf_tml}  
The Run II goal is a 1\% uncertainty on $\ensuremath{M_{\mathrm{top}}}$  




\begin{figure}[htb]
\vspace*{-5mm}
\includegraphics[height=5 8cm,width=8 1cm]  {data_22ev_likelihood eps}
\vspace*{-1 2cm}
\caption{The joint likelihood of top candidates(CDF) }
\label{fig:cdf_tml}
\end{figure}




\section{SEARCH FOR SM HIGGS BOSON}


The constraints on the SM Higgs ($H$)  boson  mass from
published  measurements, updated to include the new D\O\ top mass
measurement~\cite{Mtop1-D0-l+j-new}, are
$M_H = 117 ^{+67}_{-45}~\ensuremath{\mathrm{ Ge\kern -0 1em V }\kern -0 2em /c^2 }$, $M_H < 251~\ensuremath{\mathrm{ Ge\kern -0 1em V }\kern -0 2em /c^2 }$ at 95\% C L 
The  new most likely  value of $M_H$
is above the experimentally excluded range,
and sufficiently low for $H$ to be observed at the Tevatron 


\begin{figure}[htb]
\vspace*{-5mm}
\includegraphics[height=7 5cm,width=7 8cm]  {d0_wbb_fig_3_err eps}
\vspace*{-1 1cm}
\caption{Distribution of the dijet
invariant mass for $W+2 b$-tagged jets  events,
compared to the expectation (D\O)  
}
\label{fig:d0_wbb_2tag}
\end{figure}



D\O\  has conducted a search for $H$ at $M_H < 140~\ensuremath{\mathrm{ Ge\kern -0 1em V }\kern -0 2em /c^2 }$ 
in the production channel  
$p \bar{p} \rightarrow WH \rightarrow  e \nu b \bar{b}$  
The experimental signature of  $WH \rightarrow e \nu b \bar{b}$
is a final state with 
one high $p_T$ electron, two  $b$ jets, and
large missing transverse energy  resulting from
the undetected neutrino 
The dominant backgrounds to $WH$ production
are  $W b \bar{b}$, $t \bar{t}$ and single-top production 
The distribution 
of the dijet mass for events with two $b$-tagged jets is shown in
Fig ~\ref{fig:d0_wbb_2tag}  
Also shown is the  expected contribution ($0 06$ events)  
from the $b \bar{b}$ decay of a
SM Higgs boson with $M_H =$ 115 $\ensuremath{\mathrm{ Ge\kern -0 1em V }\kern -0 2em /c^2 }$ 
No events are observed in the  dijet mass window of 85--135  $\ensuremath{\mathrm{ Ge\kern -0 1em V }\kern -0 2em /c^2 }$ 
D\O\ sets a limit on the cross section
for $\sigma( p\bar{p} \rightarrow WH) \times B(H \rightarrow b \bar{b}) $
of 9 0 pb at the 95\% C L ,  for a 115  $\ensuremath{\mathrm{ Ge\kern -0 1em V }\kern -0 2em /c^2 }$ Higgs boson 
The results for mass points 105, 125, and 135 $\ensuremath{\mathrm{ Ge\kern -0 1em V }\kern -0 2em /c^2 }$
 are 11 0, 9 1 and 12 2 pb,  respectively 



\begin{figure}[htb]
\vspace*{-1 2cm}
\includegraphics[height=0 33\textheight,width=8 0cm]{whww_aps04_bw eps}

\vspace*{-1 2cm}
\caption{95\% limits on the $H$ production (CDF) }
\label{fig:cdf_whww}
\end{figure}


CDF  has done  a similar search, allowing either an  electron or a muon  
in the final state   Both groups have also searched for $H$ produced in
gluon-gluon fusion, with subsequent decay to a pair of $W$ bosons 
The CDF results for both channels  are shown in Fig ~\ref{fig:cdf_whww}  



\section{THE STATE X(3872)}


\begin{figure}[htb]

\includegraphics[height=8 0cm,width=7 5cm]  {X3872cdfPRL1FullM eps}
\vspace*{-1cm}
\caption{The $X(3872)$ signal (CDF) }
\label{fig:cdf_x}
\end{figure}




 The existence of the $X(3872)$ state discovered by 
the Belle Collaboration~\cite{Belle-X}
 has been confirmed 
 in $p \bar{p}$ collisions by  CDF~\cite{cdf-X} (see Fig ~\ref{fig:cdf_x})
and D\O~\cite{d0-X} 
 It is still unclear whether this particle is a $c\bar{c}$ state,
 or a more complex object   When the data are separated according to
production and decay variables, D\O\  finds no significant
differences between the $X(3872)$ and
the $c \bar{c}$ state $\psi(2S)$ 
CDF has analysed the ``lifetime'' distribution of the $X(3872)$ events in order to
quantify what fraction of this state arises from decay of $B$ hadrons, as opposed to
those produced promptly  The authors find that for the selected samples
28 3$\pm$1 0$(stat)\pm$0 7$(syst)$\% of $\psi(2S)$ candidates are from $b$ decays,
whereas 16 1$\pm$4 9$(stat)\pm$2 0$(syst)$\% of $X$ mesons arise from such decays 





\section{SEARCH FOR PENTAQUARKS}



\begin{figure}[htb]

\includegraphics[height=0 27\textheight,width=7 6cm]  {mpks_1stminbias eps}
\vspace*{-1 2cm}

\caption{Invariant mass distribution of an identified proton and a $K^0_s$ candidate  (CDF)
}
\label{fig:pqtheta}
\end{figure}



\begin{figure}[htb]

\vspace*{-0 9cm}
\includegraphics[height=0 25\textheight,width=8 0cm]  {CM_xicst_cc_1 eps}
\vspace*{-1 2cm}
\caption{Invariant mass distribution of the $(\Xi^-,\pi^+)$ system  (CDF) 
}
\label{fig:pqxi}
\end{figure}


\begin{figure}[htb]
\vspace*{-0 9cm}

\includegraphics[height=0 25\textheight,width=7 6cm]  {theta_note_dstp_dedx_pt eps}
\vspace*{-1 2cm}
\caption{Mass of the ($D^{*+}\bar p$) system  The arrow indicates the position of 
the $\Theta_c$ state (CDF) }
\label{fig:pqthetac}
\end{figure}



Following reports of evidence for exotic
baryons containing five quarks (pentaquarks), CDF has analysed 
its data for evidence of the following pentaquarks:
$\Theta^+$ ($uud\bar d \bar s$), doubly strange states 
$\Xi_{3/2}$, charmed states $\Theta_c$, and, most recently, 
a state $(udus\bar b)$, dubbed $R^+_s$, through its weak decay to $(J/\psi, p)$  
With its excellent particle indentification and mass resolution,
CDF has a unique capability to search for  pentaquark states 
The signals of known states: $\phi$, $\Lambda$,
$\Lambda(1520)$, $K^*$, $\Xi$, 
compare favorably with those provided
by the authors of  the pentaquark evidence 
The group finds no evidence for pentaquark states, see Figs 
~\ref{fig:pqtheta},{\ref{fig:pqxi},\ref{fig:pqthetac} 
This can be interpreted as an indication that the pentaquark production 
in $p \bar p$ collisions is heavily suppressed compared to the conventional
hadron production, or as an evidence against the existence of pentaquarks 

\clearpage

\section{RECENT B PHYSICS RESULTS}


\subsection{Spectroscopy}

CDF has measured the mass of $b$ hadrons in exclusive $J/\psi$ channels 
The measurements of the $B_s$ and $\Lambda_b$ (Fig  \ref{fig:masslb})
masses are the current world's best \\

$m(B^+)$ = 5279 10$\pm$0 41$(stat)\pm$0 36$(syst)$,

$m(B^0)$ = 5279 63$\pm$0 53$(stat)\pm$0 33$(syst)$,

$m(B_s)$ = 5366 01$\pm$0 73$(stat)\pm$0 33$(syst)$,

$m(\Lambda_b)$ = 5619 7$\pm$1 2$(stat)\pm$1 2$(syst)$ MeV/$c^2$ \\


\begin{figure}[htb]
\vspace*{-1mm}
\includegraphics[height=0 30\textheight,width=7 5cm]  {lambdav1c eps}
\vspace*{-1cm}

\caption{The mass spectrum of $\Lambda_b$ candidates (CDF) }
\label{fig:masslb}
\end{figure}


D\O\ reports the first observation of the excited $B$ mesons 
$B_1$ and $B^*_2$ as two separate states in fully reconstructed
decays to $B^{(*)}\pi$  The mass of $B_1$ is measured to be
5724$\pm$4$\pm$7 MeV/c$^2$, and the mass difference $\Delta M$ between
$B^*_2$ and $B_1$ is 23 6$\pm$7 7$\pm$3 9 MeV/c$^2$
(Fig   \ref{fig:d0_bexc}) 

D\O\ observes semileptonic $B$ decays to narrow $D^{**}$ states,
the orbitally excited states  of the $D$ meson
seen as resonances in the $D^{*+}\pi^-$ invariant mass spectrum 
The $D^*$ mesons are reconstructed through the decay sequence 
$D^{*+} \rightarrow D^0\pi^+$, $D^0\rightarrow K^-\pi^+$ 
The invariant mass  of oppositely charged $(D^*,\pi)$ pairs
is shown in Fig   \ref{fig:d0_dstst} 
The mass peak between 2 4 and 2 5 GeV/$c^2$ can be interpreted as two merged 
narrow $D^{**}$ states, $D^0_1(2420)$ and $D^0_2(2460)$ 
The combined branching fraction is 
$ {\cal B}(B\rightarrow D^0_1,D^0_2)\cdot {\cal B}(D^0_1,D^0_2\rightarrow D^{*+}\pi^-)=(0 280\pm0 021(stat)\pm0 088(syst)$\%



ground_truth: After attacking Jacobo at a workers' strike, Ngotho loses his job and Njoroge's family is forced to move.

prompt_front: Now, answer the following question based on the text below, only give me the answer and do not output any other words.

Question: What are the three synthetic types of vitamin K?

Read the following text and answer briefly.

Context 2:  283 (52): 36655–36664  doi:10 1074/jbc M802761200  PMC 2605998  PMID 18836183  ^ Viegas, C  S ; Cavaco, S ; Neves, P  L ; Ferreira, A ; João, A ; Williamson, M  K ; Price, P  A ; Cancela, M  L ; Simes, D  C  (Dec 2009)  "Gla-rich protein is a novel vitamin K-dependent protein present in serum that accumulates at sites of pathological calcifications"  American Journal of Pathology  175 (6): 2288–2298  doi:10 2353/ajpath 2009 090474  PMC 2789615  PMID 19893032  ^ Hafizi, S ; Dahlbäck, B  (Dec 2006)  "Gas6 and protein S  Vitamin K-dependent ligands for the Axl receptor tyrosine kinase subfamily"  The FEBS Journal  273 (23): 5231–5244  doi:10 1111/j 1742-4658 2006 05529 x  PMID 17064312  ^ Kulman, J  D ; Harris, J  E ; Xie, L ; Davie, E  W  (May 2007)  "Proline-rich Gla protein 2 is a cell-surface vitamin K-dependent protein that binds to the transcriptional coactivator Yes-associated protein"  Proceedings of the National Academy of Sciences of the United States of America  104 (21): 8767–8772  doi:10 1073/pnas 0703195104  PMC 1885577  PMID 17502622  ^ "Vitamin K"  MedlinePlus  US National Library of Medicine, National Institutes of Health  Sep 2016  Retrieved 26 May 2009  ^ Conly, J; Stein, K  (Dec 1994)  "Reduction of vitamin K2 concentrations in human liver associated with the use of broad spectrum antimicrobials"  Clinical and Investigative Medicine  17 (6): 531–539  PMID 7895417  ^ Ferland, G ; Sadowski, J  A ; O'Brien, M  E  (Apr 1993)  "Dietary induced subclinical vitamin K deficiency in normal human subjects"  Journal of Clinical Investigation  91 (4): 1761–1768  doi:10 1172/JCI116386  PMC 288156  PMID 8473516  ^ Holden, R  M ; Morton, A  R ; Garland, J  S ; Pavlov, A ; Day, A  G ; Booth, S  L  (Apr 2010)  "Vitamins K and D status in stages 3-5 chronic kidney disease"  Clinical Journal of the American Society of Nephrology  5 (4): 590–597  doi:10 2215/CJN 06420909  PMC 2849681  PMID 20167683  ^ Hodges, S  J ; Pilkington, M  J ; Shearer, M  J ; Bitensky, L ; Chayen, J (Jan 1990)  "Age-related changes in the circulating levels of congeners of vitamin K2, menaquinone-7 and menaquinone-8"  Clinical Science  78 (1): 63–66  PMID 2153497  ^ "Vitamin K"  Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc (PDF)  National Academy Press  2001  p  162–196  ^ Tolerable Upper Intake Levels For Vitamins And Minerals (PDF), European Food Safety Authority, 2006 ^ a b Rhéaume-Bleue, p  42
^ "Important information to know when you are taking: Warfarin (Coumadin) and Vitamin K" (PDF)  National Institutes of Health Clinical Center  ^ "Nutrition Facts and Information for Parsley, raw"  Nutritiondata com  Retrieved 21 Apr 2013  ^ "Nutrition facts, calories in food, labels, nutritional information and analysis"  Nutritiondata com  13 Feb 2008  Retrieved 21 Apr 2013  ^ "Vitamin K"  Vivo colostate edu  2 Jul 1999  Retrieved 21 Apr 2013  ^ "Vitamin K"  Micronutrient Data Centre  ^ Ikeda, Y ; Iki, M ; Morita, A ; Kajita, E ; Kagamimori, S ; Kagawa, Y ; Yoneshima, H  (May 2006)  "Intake of fermented soybeans, natto, is associated with reduced bone loss in postmenopausal women: Japanese Population-Based Osteoporosis (JPOS) Study"  Journal of Nutrition  136 (5): 1323–1328  PMID 16614424  ^ Katsuyama, H ; Ideguchi, S ; Fukunaga, M ; Saijoh, K ; Sunami, S  (Jun 2002)  "Usual dietary intake of fermented soybeans (Natto) is associated with bone mineral density in premenopausal women"  Journal of Nutritional Science and Vitaminology  48 (3): 207–215  doi:10 3177/jnsv 48 207  PMID 12350079  ^ Sano, M ; Fujita, H ; Morita, I ; Uematsu, H ; Murota, S  (Dec 1999)  "Vitamin K2 (menatetrenone) induces iNOS in bovine vascular smooth muscle cells: no relationship between nitric oxide production and gamma-carboxylation"  Journal of Nutritional Science and Vitaminology  45 (6): 711–723  doi:10 3177/jnsv 45 711  PMID 10737225  ^ Gast, G  C ; de Roos, N  M ; Sluijs, I ; Bots, M  L ; Beulens, J  W ; Geleijnse, J  M ; Witteman, J  C ; Grobbee, D  E ; Peeters, P  H ; van der Schouw, Y  T  (Sep 2009)  "A high menaquinone intake reduces the incidence of coronary heart disease"  Nutrition, Metabolism, and Cardiovascular Diseases  19 (7): 504–510  doi:10 1016/j numecd 2008 10 004  PMID 19179058  ^ Oldenburg, J ; Bevans, C  G ; Müller, C  R ; Watzka, M  (2006)  "Vitamin K epoxide reductase complex subunit 1 (VKORC1): the key protein of the vitamin K cycle"  Antioxidants & Redox Signaling  8 (3–4): 347–353  doi:10 1089/ars 2006 8 347  PMID 16677080  ^ Suttie, J  W  (1985)  "Vitamin K-dependent carboxylase"  Annual Review of Biochemistry  54: 459–477  doi:10 1146/annurev bi 54 070185 002331  PMID 3896125  ^ Presnell, S  R ; Stafford, D  W  (Jun 2002)  "The vitamin K-dependent carboxylase"  Thrombosis and Haemostasis  87 (6): 937–946  PMID 12083499  ^ Stafford, D  W  (Aug 2005)  "The vitamin K cycle"  Journal of Thrombosis and Haemostasis  3 (8): 1873–1878  doi:10 1111/j 1538-7836 2005 01419 x  PMID 16102054  ^ Rhéaume-Bleue, p  79 
^ Whitlon, D  S ; Sadowski, J  A ; Suttie, J  W  (Apr 1978)  "Mechanism of coumarin action: significance of vitamin K epoxide reductase inhibition"  Biochemistry  17 (8): 1371–1377  doi:10 1021/bi00601a003  PMID 646989  ^ Terlau, H ; Olivera, B  M  (Jan 2004)  "Conus venoms: a rich source of novel ion channel-targeted peptides"  Physiological Reviews  84 (1): 41–68  doi:10 1152/physrev 00020 2003  PMID 14715910  ^ Buczek, O ; Bulaj, G ; Olivera, BM (Dec 2005)  "Conotoxins and the posttranslational modification of secreted gene products"  Cellular and Molecular Life Sciences  62 (24): 3067–3079  doi:10 1007/s00018-005-5283-0  PMID 16314929  ^ "Prothrombin Time"  WebMD  ^ Dituri, F ; Buonocore, G ; Pietravalle, A ; Naddeo, F ; Cortesi, M; Pasqualetti, P; Tataranno M  L ; R , Agostino (Sep 2012)  "PIVKA-II plasma levels as markers of subclinical vitamin K deficiency in term infants"  Journal of Maternal, Fetal & Neonatal Medicine  25 (9): 1660–1663  doi:10 3109/14767058 2012 657273  PMID 22280352  ^ Thane, C  W ; Bates, C  J ; Shearer, M  J ; Unadkat, N; Harrington, D  J ; Paul, A  A ; Prentice, A ; Bolton-Smith, C  (Jun 2002)  "Plasma phylloquinone (vitamin K1) concentration and its relationship to intake in a national sample of British elderly people"  British Journal of Nutrition  87 (6): 615–622  doi:10 1079/BJNBJN2002582  PMID 12067432  ^ McKeown, N  M ; Jacques, P  F ; Gundberg, C  M ; Peterson, J  W ; Tucker, K  L ; Kiel, D  P ; Wilson, P  W ; Booth, SL (Jun 2002)  "Dietary and nondietary determinants of vitamin K biochemical measures in men and women" (PDF)  Journal of Nutrition  132 (6): 1329–1334  PMID 12042454  ^ Yamano, M ; Yamanaka, Y ; Yasunaga, K ; Uchida, K  (Sep 1989)  "Effect of vitamin K deficiency on urinary gamma-carboxyglutamic acid excretion in rats"  Nihon Ketsueki Gakkai Zasshi  52 (6): 1078–1086  PMID 2588957  ^ Matsumoto, T ; Miyakawa, T ; Yamamoto, D  (Mar 2012)  "Effects of vitamin K on the morphometric and material properties of bone in the tibiae of growing rats"  Metabolism  61 (3): 407–414  doi:10 1016/j metabol 2011 07 018  PMID 21944271  ^ Je, S -H ; Joo, N -S ; Choi, B -H ; Kim, K -M ; Kim, B -T ; Park, S -B ; Cho, D -Y ; Kim, K -N ; Lee, D -J  (Aug 2011)  "Vitamin K supplement along with vitamin D and calcium reduced serum concentration of undercarboxylated osteocalcin while increasing bone mineral density in Korean postmenopausal women over sixty-years-old"  Journal of Korean Medical Science  26 (8): 1093–1098  doi:10 3346/jkms 2011 26 8 1093  PMC 3154347  PMID 21860562  ^ Bentley, R ; Meganathan, R  (Sep 1982)  "Biosynthesis of vitamin K (menaquinone) in bacteria" (PDF)  Microbiological Reviews  46 (3): 241–280  PMC 281544  PMID 6127606  ^ Haddock, B  A ; Jones, C  W  (Mar 1977)  "Bacterial respiration" (PDF)  Bacteriological Reviews  41 (1): 47–99  PMC 413996  PMID 140652  ^ Shearer, M  J  (Jan 1995)  "Vitamin K"  Lancet  345 (8944): 229–234  doi:10 1016/S0140-6736(95)90227-9  PMID 7823718  ^ Greer, J  P ; Foerster, J ; Lukens, J  N ; Rodgers, G  M ; Paraskevas, F ; Glader, B  (eds )  Wintrobe's Clinical Hematology (11th ed )  Philadelphia, Pennsylvania: Lippincott, Williams and Wilkens  ^ a b American Academy of Pediatrics Committee on Fetus Newborn  (Jul 2003)  "Controversies concerning vitamin K and the newborn  American Academy of Pediatrics Committee on Fetus and Newborn" (PDF)  Pediatrics  112 (1 1): 191–192  doi:10 1542/peds 112 1 191  PMID 12837888  ^ Logan, S ; Gilbert, R  (1998)  "Vitamin K For Newborn Babies" (PDF)  Department of Health  Retrieved 12 Oct 2014  ^ "Postnatal care: Routine postnatal care of women and their babies [CG37]"  www nice org uk  NICE  Jul 2006  Retrieved 12 Oct 2014  ^ Parker, L ; Cole, M ; Craft, A  W ; Hey, E  N  (1998)  "Neonatal vitamin K administration and childhood cancer in the north of England: retrospective case-control study"  BMJ (Clinical Research Edition)  316 (7126): 189–193  doi:10 1136/bmj 316 7126 189  PMC 2665412  PMID 9468683  ^ McMillan, D  D  (1997)  "Routine administration of vitamin K to newborns"  Paediatric Child Health  2 (6): 429–431  ^ "Newborns get rare disorder after parents refused shots"  Having four cases since February just at Vanderbilt was a little bit concerning to me ^ Dam, C  P  H  (1935)  "The Antihaemorrhagic Vitamin of the Chick: Occurrence And Chemical Nature"  Nature  135 (3417): 652–653  doi:10 1038/135652b0  ^ Dam, C  P  H  (1941)  "The discovery of vitamin K, its biological functions and therapeutical application" (PDF)  Nobel Prize Laureate Lecture  ^ McAlister, V  C  (2006)  "Control of coagulation: a gift of Canadian agriculture" (PDF)  Clinical and Investigative Medicine  29 (6): 373–377  ^ MacCorquodale, D  W ; Binkley, S  B ; Thayer, S  A ; Doisy, E  A  (1939)  "On the constitution of Vitamin K1"  Journal of the American Chemical Society  61 (7): 1928–1929  doi:10 1021/ja01876a510  ^ Fieser, L  F  (1939)  "Synthesis of Vitamin K1"  Journal of the American Chemical Society  61 (12): 3467–3475  doi:10 1021/ja01267a072  ^ Dam, C  P  H  (12 Dec 1946)  "The discovery of vitamin K, its biological functions and therapeutical application" (PDF)  Nobel Prize lecture  ^ Warner, E  D ; Brinkhous, K  M ; Smith, H  P  (1938)  "Bleeding Tendency of Obstructive Jaundice"  Proceedings of the Society of Experimental Biology and Medicine  37 (4): 628–630  doi:10 3181/00379727-37-9668P  ^ Stenflo, J; Fernlund, P ; Egan, W ; Roepstorff, P  (Jul 1974)  "Vitamin K dependent modifications of glutamic acid residues in prothrombin"  Proceedings of the National Academy of Sciences of the United States of America  71 (7): 2730–2733  doi:10 1073/pnas 71 7 2730  PMC 388542  PMID 4528109  ^ Nelsestuen, G  L ; Zytkovicz, T  H ; Howard, J  B  (Oct 1974)  "The mode of action of vitamin K  Identification of gamma-carboxyglutamic acid as a component of prothrombin" (PDF)  Journal of Biological Chemistry  249 (19): 6347–6350  PMID 4214105  ^ Magnusson, S ; Sottrup-Jensen, L ; Petersen, T  E ; Morris, H  R ; Dell, A  (Aug 1974)  "Primary structure of the vitamin K-dependent part of prothrombin"  FEBS Letters  44 (2): 189–193  doi:10 1016/0014-5793(74)80723-4  PMID 4472513  Bibliography[edit]
Rhéaume-Bleue, Kate (2012)  Vitamin K2 and the Calcium Paradox  John Wiley & Sons, Canada  ISBN 1-118-06572-7  External links[edit]
"Vitamin K: Another Reason to Eat Your Greens"  v
TPP / ThDP (B1)
FMN, FAD (B2)
NAD+, NADH, NADP+, NADPH (B3)
Coenzyme A (B5)
PLP / P5P (B6)
THFA / H4FA, DHFA / H2FA, MTHF (B9)
AdoCbl, MeCbl (B12)
Phylloquinone (K1), Menaquinone (K2)
non-vitamins
Coenzyme B
Heme / Haem (A, B, C, O)
Molybdopterin/Molybdenum cofactor
THMPT / H4MPT
Fe2+, Fe3+
vitamins: see vitamins
Antihemorrhagics (B02)
(coagulation)
Phytomenadione (K1)
Menadione (K3)
intrinsic: IX/Nonacog alfa
VIII/Moroctocog alfa/Turoctocog alfa
extrinsic: VII/Eptacog alfa
common: X
II/Thrombin
I/Fibrinogen
XIII/Catridecacog
combinations: Prothrombin complex concentrate (II, VII, IX, X, protein C and S)
Carbazochrome
thrombopoietin receptor agonist (Romiplostim
Eltrombopag)
Tetragalacturonic acid hydroxymethylester
Epinephrine/Adrenalone
amino acids (Aminocaproic acid
Aminomethylbenzoic acid)
serpins (Aprotinin
Alfa1 antitrypsin
Camostat) 



ground_truth: Vitamins K3, K4, and K5.

prompt_front: Now, answer the following question based on the text below, only give me the answer and do not output any other words.

Question: When did the Tevatron Collider Run II start and when is it expected to end?

Read the following text and answer briefly.

Context 3:  The systematic error includes the unknown phase between the
two resonances  Work is in progress on extracting the two Breit-Wigner
amplitudes 


\begin{figure}[htb]
\vspace*{-2mm}
\hspace*{-3mm}
\includegraphics[height=0 28\textheight,width=8 3cm]  {B08F02 eps}

\vspace*{-1cm}
\caption{Mass difference $\Delta M = M(B\pi)-M(B)$ for exclusive $B$ decays 
The background-subtracted signal is a sum of 
$B^*_1 \rightarrow B^* \pi$, $B^* \rightarrow B \gamma $ (open area)
and $B^*_2 \rightarrow B^*\pi$ $B^*\rightarrow B \gamma$ (lower peak in the shaded area)
and $B^*_2 \rightarrow B \pi$ (upper peak in the shaded area)  
(D\O) }
\label{fig:d0_bexc}
\end{figure}


\begin{figure}[htb]
\includegraphics[height=0 25\textheight,width=7 5cm]  {B05F03 eps}

\vspace*{-1cm}
\caption{The invariant mass distribution of
$(D^*,\pi)$ pairs, opposite sign (points) and same-sign (solid histogram) }
\label{fig:d0_dstst}
\end{figure}






\subsection{Lifetimes}


CDF and D\O\ have measured  lifetimes of $b$ hadrons through the exclusively
reconstructed decays $B^+ \rightarrow J/\psi K^+$, $B^0 \rightarrow J/\psi K^{*0}$,
$B_s \rightarrow J/\psi \phi$, 
and $\Lambda_b \rightarrow J/\psi \Lambda$
(Fig  \ref{fig:d0_lbctau}) 
The latest results are:  \\



 $\tau(B^+)$=1 65 $\pm$ 0 08 $^{+0 096}_{-0 123}$  ps ~(D\O\ 2003),

 $\tau(B^+)$=1 662 $\pm$ 0 033  $\pm$ 0 008  ps ~(CDF),

 $\tau(B^0_d)$=1 473  $^{+0 052}_{-0 050}$ $\pm$ 0 023    ps ~(D\O) 

 $\tau(B^0_d)$=1 539 $\pm$ 0 051  $\pm$ 0 008  ps ~(CDF),

 $\tau(B^0_s)$=1 444   $^{+0 098}_{-0 090}$ $\pm$ 0 020   ps ~(D\O),

 $\tau(B^0_s)$=1 369 $\pm$ 0 100 $\pm$ $^{+0 008}_{0 010}$  ps ~(CDF),


 $\tau(\Lambda_b)$=1 221 $^{+0 217}_{-0 179}$ $\pm$ 0 043  ps ~(D\O),


 $\tau(\Lambda_b)$=1 25 $\pm$ 0 26 $\pm$ 0 10  ps ~(CDF 2003) \\



The measured lifetimes correspond to the following lifetime ratios:\\

$\tau(B^+)/\tau(B^0_d)$   =  1 080$\pm$0 042     ~(CDF),
 
$\tau(B^0_s)/\tau(B^0_d)$ =  0 890$\pm$0 072    ~(CDF),

$\tau(B^0_s)/\tau(B^0_d)$ = 0 980$ ^{+0 075}_{-0 070}   \pm$0 003    ~(D\O),

$\tau(\Lambda_b)/\tau(B^0_d)$ =  0 874$ ^{+0 169}_{-0 142}   \pm$0 028    ~(D\O) \\



\begin{figure}[htb]
\includegraphics[height=0 3\textheight,width=8 2cm]  {d0_lbctau_B11F02 eps}
\vspace*{-1cm}

\caption{ Fit projection on  $c\tau$ for the $\Lambda_b$ candidates   (D\O)}
\label{fig:d0_lbctau}
\end{figure}


The $B_s$ lifetime measurements listed above are results of
a single-lifetime fit to data, integrated over the decay angles 
Because  of the presence of  final
states  common to ${B_s^0}$\ and its charge conjugate ${\overline{B}_s^0}$,
the two meson states   are expected
to mix in such a way that the two CP  eigenstates may have a relatively
large lifetime difference 
It is possible to
separate the two CP components of ${B_s^0 \rightarrow J/\psi \phi}$\ and thus to measure the
lifetime difference by studying the time evolution of the
polarization states of the vector mesons in the final state 
CDF has carried out a combined analysis of $B_s$ lifetimes 
and polarization amplitudes  The results for the lifetimes of the
low mass (CP even) and high mass (CP odd) eigenstates, and the relative 
width difference are:\\

 $\tau_L = 1 05 ^{+0 16}_{-0 13} \pm 0 02$ ~ps,
 
 $\tau_H = 2 07 ^{+0 58}_{-0 46} \pm 0 03$ ~ps,

 $\Delta \Gamma /\overline \Gamma   = 0 65 ^{+0 25}_{-0 33} \pm 0 01$ \\

Figure \ref{fig:cdf_dg} shows  the scan of the likelihood function 
for $\Delta \Gamma /\overline \Gamma$ 
Pseudoexperiments tossed with $\Delta \Gamma /\overline \Gamma =0$
yield the betting odds for observing the above results at
1/315  For $\Delta \Gamma /\overline \Gamma = 0 12$ (SM prediction,
which has recently been updated to 0 14$\pm$0 05~\cite{dg_un}) the betting odds are
1/84 

\begin{figure}[htb]
\vspace*{-1mm}
\includegraphics[height=0 3\textheight,width=8 2cm]  {cdf_scan-dg-un eps}

\vspace*{-1cm}
\caption{Scan of the likelihood function 
for $\Delta \Gamma /\overline \Gamma$ (CDF) 
}
\label{fig:cdf_dg}
\end{figure}




D\O\ has used a novel technique to  measure the lifetime ratio
of the charged and neutral $B$ mesons, exploiting the large
semileptonic sample  $B$ hadrons were reconstructed in the channels
$B\rightarrow \mu^+ \nu D^*(2010)^-X$, which are dominated by $B^0$ decays, 
and  $B\rightarrow \mu^+ \nu D^0X$, which are dominated by $B^+$ decays 
The lifetime ratio was
obtained from the variation of the ratio of the number of events in these two
processes at different decay lengths 
The result is \\


$\tau(B^+)/\tau(B^0_d)$   =  1 093$\pm$0 021$\pm$0 022       ~(D\O)




\subsection{Towards $B_s$ mixing}

Measurement of the $B_s$ oscillation frequency via ${B_s^0}$ -${\overline{B}_s^0}$ ~mixing
will provide an important constraint on the CKM matrix  The oscillation
frequency is proportional to the mass difference between the mass eigenstates,
$\Delta m_s$, and is related to the CKM matrix through 
$\Delta m_s \propto |V_{tb}V_{ts}|$  When combined with the
$B_d$ mass difference, $\Delta m_d$ it helps in extraction of $|V_{td}|$,
and thereby the CP violating phase  

As a benchmark for future $B_s$ oscillation measurement, both groups
study  $B_d$ mixing, gaining an understanding of the different components
of a $B$ mixing analysis (sample composition, flavor tagging, vertexing,
asymmetry fitting)  For a sample of partially reconstructed decays
$B\rightarrow D^*(2010)^+\mu^-X$, D\O\ obtains 
$\Delta m_d = 0 506 \pm 0 055 (stat) \pm  0 049 (syst))$ ps$^{-1}$ and
$\Delta m_d = 0 488 \pm 0 066 (stat) \pm  0 044 (syst))$ ps$^{-1}$
when employing  opposite side muon tagging and the same side tagging,
respectively 

The CDF result for semileptonic channels is
$\Delta m_d = 0 536 \pm 0 037 (stat) \pm  0 009 (s c ) \pm 0 015 (syst)$ ps$^{-1}$ 
CDF also reports a result on $B$ oscillations using fully reconstructed
decays:
$\Delta m_d = 0 526 \pm 0 056 (stat) \pm  0 005 (syst))$ ps$^{-1}$ 

Reconstructing $B_s$ decays into different final states is another
important
 step in the ${B_s^0}$ -${\overline{B}_s^0}$ ~mixing analysis 
Thanks to the  large muon and tracking coverage,   D\O\ is accumulating
a  high statistics sample of semileptonic $B_s$ decays 
D\O\ reconstructs the $B_s \rightarrow D^+_s \mu^- X$ decays, with
$D^+_s \rightarrow \phi \pi^+ $ and
$D^+_s \rightarrow K^* K^+ $,
at a rate of $\approx$ 40(25) events per pb$^{-1}$,  respectively 
Figure \ref{fig:d0_bsdsphipi} shows the mass distribution of the
$D^+_s \rightarrow \phi \pi$ candidates 


\begin{figure}[htb]
\vspace*{-5mm}
\includegraphics[height=0 3\textheight,width=8 0cm]  {blds-250 eps}
\vspace*{-1 2cm}
\caption{  $D^+_s \rightarrow \phi \pi^+$  signal  (D\O)}
\label{fig:d0_bsdsphipi}
\end{figure}


\begin{figure}[htb]
\vspace*{-10mm}
\hspace*{-4mm}
\includegraphics[height=0 35\textheight,width=7 9cm]  {cdf_Bs-DsPi-PhiPi eps}

\vspace*{-1 0cm}
\caption{ $B_s \rightarrow D_s \pi$, $D_s \rightarrow \phi \pi$  signal   (CDF)}
\label{fig:cdf_bsdsphipi}
\end{figure}


CDF has clean signals for fully hadronic, flavor-specific  $B_s$ decays,
providing the best sensitivity to $B_s$ oscillations at high
$\Delta m_s$  Figure \ref{fig:cdf_bsdsphipi} shows the signal for
the best channel, $B_s \rightarrow D_s \pi$, $D_s \rightarrow \phi \pi$ 

\clearpage


\subsection{Rare decays}

The purely leptonic decays $B_{d,s}^0 \rightarrow \mu^+
\mu^-$ are flavor-changing neutral current (FCNC) processes 
In the standard model, these decays are forbidden at the tree level and
proceed at a very low rate through higher-order diagrams 
The latest SM prediction~\cite{sm_ref3}
is ${\cal B}(B^0_s \rightarrow \mu^+ \mu^-)=(3 42\pm 0 54)\times
10^{-9}$, where the error is dominated by non-perturbative uncertainties  The
leptonic branching fraction of the $B_d^0$ decay is suppressed by CKM matrix elements $|V_{td}/V_{ts}|^2$
leading to a predicted SM branching fraction of $(1 00\pm0 14)\times 10^{-10}$ 
The best published experimental bound (Fig ~\ref{fig:cdf_bsmumu})
 for the branching fraction
of $B^0_s$ $(B^0_d)$ is presently
${\cal B}(B^0_s \, (B^0_d) \rightarrow \mu^+\mu^-)<7 5\times 10^{-7}\, 
(1 9\times 10^{-7})$ at the 95\% C L ~\cite{cdfII} 
The decay amplitude of $B^0_{d,s} \rightarrow \mu^+ \mu^-$ can be
significantly enhanced in some extensions of the SM  

\begin{figure}[htb]
\includegraphics[height=8 3cm,width=7 9cm]  {cdfbsmumu_results_prl eps}

\vspace*{-1cm}
\caption{Invariant mass for the events passing all requirements  (CDF)}
\label{fig:cdf_bsmumu}
\end{figure}


Assuming no contributions 
from the decay $B^0_d\rightarrow \mu^+\mu^-$ in the signal region,
D\O\  finds the conservative upper limit on the branching fraction 
to be ${\cal B}(B^0_s \rightarrow \mu^+ \mu^-) \leq 4 6\times 10^{-7}$ 
at the 95\% C L  (Fig ~\ref{fig:d0_bsmumu}) 






\begin{figure}[htb]
\includegraphics[height=5 0cm,width=8 0cm]  {B06F03 eps}
\vspace*{-1cm}
\caption{Invariant mass for the events  passing all requirements  (D\O)}
\label{fig:d0_bsmumu}
\end{figure}





ground_truth: The Tevatron Collider Run II started in March 2002 and is expected to continue until the end of this decade.