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Question: What is the recommended daily intake of vitamin K for adult women and men?

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Context 1: Vitamin K - Wikipedia
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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 
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^ "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 ; 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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) 
Context 2: \section*{Dynamical Behaviour of $O$ in Lattice Gases}

The dynamical behaviour of the anisotropic order parameter  $m$ [see Eq ~\eqref{eq:def-m} in the Letter] following a quench to the critical point is well described by
the Gaussian theory for all the three lattice gas models studied, $i e ,$ driven lattice gas with either constant (IDLG) or random (RDLG) infinite drive and equilibrium lattice gas (LG)  In other words, in the short-time regime, $m \sim t^{1/2}$ [see Eq  \eqref{eq:mt}] and the Binder cumulant $g$ of the lowest transverse mode [defined in Eq  \eqref{eq:binder}] is zero in this regime  The alternative order parameter $O,$ however, distinguishes between the driven (IDLG, RDLG) and the equilibrium (LG) lattice gases  

In order to understand  this, we first write the phenomenological scaling form for $O$,  analogous to Eq  \eqref{eq:scalingass} in  the Letter,
\begin{eqnarray}
O (t, L_{\parallel} ; S_\Delta) = L_{\parallel}^{-\beta/[\nu(1+\Delta)]} \tilde f_O (t/L_{\parallel}^{z/(1+\Delta)} ; S_\Delta) \quad
\label{eq:Oscalingass}
\end{eqnarray}
We already remarked that, in the LG, this scaling form is not compatible with the prediction $O \sim t^{1/8}  L_{\parallel}^{-1/2}$ of the Gaussian theory   However, following Ref  \cite{AS2002}, it can be argued that, at short times, the only dependence of $O$ on the system size $L_{\parallel}$ is of the form $O \sim L_\parallel^{-1/2}$ which is very well confirmed by numerical simulations  Accordingly,  the generic behaviour of $O$ can be assumed to be
\begin{eqnarray}
O \sim t^{\alpha} L_\parallel^{-1/2}, \label{eq:O}
\end{eqnarray}
where $\alpha$ is a phenomenological exponent to be determined  This, along with Eq  \eqref{eq:Oscalingass}, implies $\tilde f_O(x) \sim x^{\alpha} $ Comparing the finite-size behaviour in Eq ~\eqref{eq:O} with Eq ~\eqref{eq:Oscalingass} one actually infers,
\begin{eqnarray}
\alpha &=& \frac{1+ \Delta -2 \beta/\nu}{2 \, (4- \eta)}  \label{eq:alpha}
\end{eqnarray}
This equation, together with the hyperscaling relation $\Delta - 2 \beta/\nu= - \eta$ in two spatial dimensions, shows that the prediction $\alpha = 1/8$ of the Gaussian theory [see Eq  \eqref{eq:Ot}] can be obtained only when $\eta=0,$ which is the case for the IDLG (exactly) and the RDLG (approximately) but not for the LG  

On the other hand,  Eq ~\eqref{eq:alpha} predicts $\alpha = 1/10$ upon substituting the values of the critical exponents corresponding to the Ising  universality class (LG)  This is consistent with the numerical simulation results presented in the main text, see Fig  \ref{fig:ising}(b) therein 

\begin{figure}[th]
\vspace*{0 2 cm}
 \centering
 \includegraphics[width=10 cm]{ /compare_binder pdf}

\caption{Comparison between the temporal evolution of the Binder cumulants $g$ corresponding to the $12^{th}$ transverse mode, $i e ,$ with $n_\perp =12,$ in the LG (lowest curve), IDLG and RDLG (two upper curves) on a $32 \times 32$ lattice  \label{fig:b}}
 \label{fig:binder}
\end{figure}


The emergence of this new value $1/10$ of the exponent $\alpha$ must be traced back to the non-Gaussian nature of higher fluctuating modes in the LG  In fact, even though the lowest mode behaves identically in all the three models we considered,  characterized by the same behaviour of $m$, higher modes show a significant difference in the non-driven case   


To illustrate this, we measured the Binder cumulants of higher modes which is defined  analogously to Eq ~(11), using transverse modes other than the first, i e , with $\mu=\tilde \sigma(0,2 \pi n_\bot/L_\bot)$ and $n_\bot>1 $  
 Figure \ref{fig:b} compares the same for all the three lattice gases for the mode with $n_\perp =12$ on a $32 \times 32$ lattice  Clearly, the curve corresponding to the LG (lowest, blue) departs from Gaussian behaviour $g=0$ (in practice, $e g ,$ $|g| \lesssim 0 005,$ corresponding to the shaded gray area) much earlier than it does for the IDLG  or RDLG (two upper curves, red and green respectively) 

Accordingly, the different dynamical behaviour of $O$, which involves a sum over all modes, can be attributed to the non-Gaussian nature of the higher modes in the LG  
Such a departure is not entirely surprising  In fact, for higher modes, mesoscopic descriptions such as the ones in Eqs  \eqref{eq:L-DLG} or \eqref{eq:g_evol} are not expected to hold, while the anisotropy at the microscopic level could be the mechanism leading to the Gaussianity of higher modes in the driven models 


Context 3: 2008年5月31日 随笔档案 - 狼爱上狸 - BlogJava
本地搭建以太坊私有网络-基于Ganache和MetaMask
本文主要介绍如何使用Ganache，在本地搭建以太坊私有网络，并进行简单的测试。
Ganache用于搭建私有网络。在开发和测试环境下，Ganache提供了非常简便的以太坊私有网络搭建方法，通过可视化界面可以直观地设置各种参数、浏览查看账户和交易等数据。
下载地址为：https://truffleframework com/ganache/
MetaMask用于测试私有网络。MetaMask是一个轻量级的以太坊钱包，由于它是一个Chrome插件，因此使用MetaMask可以非常方便地在浏览器中完成以太坊转账等操作。
下载地址为：https://www metamask io
安装、启动Ganache
1  使用安装包安装即可。
2  打开程序后，会显示以下界面，用户可以查看账户（默认创建10个账户）、区块、交易和日志。
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此时，Ganache已经在本机运行了一个以太坊私有网络，并绑定了8545端口。
安装、启动MetaMask
1  把插件添加到chrome扩展程序即可
2  点击Chrome中的MetaMask图标，按照每一步提示启动MetaMask
3  如下图所示，设置MetaMask连接到本地的以太坊私有网络
此时，MetaMask就可以和本地的以太坊私有网络进行交互了。
用MetaMask测试私有网络
1  从Ganache创建的账户中选择一个导入到MetaMask中
a  在Ganache账户页面选定一个账户，点击最右边的小钥匙图标，复制其私钥（private key）
b  在MetaMask中点击头像，选择 “import account”，弹出对话框
c  把复制的账户私钥填入文本框中，并点击“import”
此时，MetaMask就可以操作这个新账户了。
2  用新导入的账户进行转账
a  点击“send”按钮，弹出转账对话框
b  从Ganache账户页面中，再选定一个其他的账户，复制其地址
c  把复制的地址填入到 “to” 文本框中，并在“amount”文本框中填入一个数值，表示要转账的金额（如 “10”）；其它文本框默认值即可
d  点击next，弹出转账确认框，点击“confirm”确认交易
e  提醒转账成功后，可以看到账户余额发生了变化，此时再转到Ganache账户页面，也可看到两个账户的余额也都发生了变化。
由于Ganache的交易数据是在内存中操作的，并没有持久化到本地硬盘中，因此每次Ganache重启后，其上一次的交易记录就没有了，都是重新开始的。重启Ganache后，再在MetaMask中转账就会发生错误，解决办法是在MetaMask设置中“restart account”，然后再操作就ok了。
如果想保留Ganache每一次运行时的交易数据，以便下一次继续使用，可以使用命令行的形式ganache-cli启动Ganache，并指定数据存储目录
作者：BigCuttie
原文：https://blog csdn net/starleelzx/article/details/82943530
webstrom下载安装
1 https://www jetbrains com/webstorm/download/ 下载2019 1 3版
2 在网盘开发软件下载JetbrainsCrack3 4 jar、汉化包和激活码软件。
3 将解压的 jar 破解补丁放在你的安装idea下面的bin的目录下面。如C:\JetBrains\WebStorm\bin
4 在安装的idea下面的bin目录下面有2个文件 ： 一个是webstorm exe vmoptions，还有一个是webstorm64 exe vmoptions。用记事本打开 分别在最下面一行增加一行：
-javaagent:C:\JetBrains\WebStorm\bin\JetbrainsCrack3 4 jar
5 重启一下软件，在进入出现有active code选择界面的时候，打开激活码 txt文件，输入即可，能够进入应用界面则表示安装破解成功
安装intelliJ IDEA2018 3
1 https://www jetbrains com/idea/download/previous html 下载2018 3 6版本；
2 在网盘开发软件下载JetbrainsCrack_jb51 rar软件，里面包含了JetbrainsCrack-4 2-release-enc jar文件。
3 将解压的 jar 破解补丁放在你的安装idea下面的bin的目录下面。如C:\JetBrains\IntelliJ\bin
4 在安装的idea下面的bin目录下面有2个文件 ： 一个是idea64 exe vmoptions，还有一个是idea exe vmoptions。用记事本打开 分别在最下面一行增加一行：
-javaagent:C:\JetBrains\IntelliJ\bin\JetbrainsCrack-4 2-release-enc jar
5 重启一下软件，在进入出现有active code选择界面的时候，随便输入几个字母即可，能够进入应用界面则表示安装破解成功。
Ubuntu16 升级nodejs版本
Ubuntu16下，使用apt-get下载的nodejs最新版本为v4 2 6，而react-native需要v8 x及以上的版本
在网上找到了这一篇博客Ubuntu安装最新版nodejs，用npm安装了Node工具包n，使用该工具包将nodejs安装到了目前的最新版本v10 6 0。在已经安装npm的基础上，具体操作如下：
n是一个Node工具包，它提供了几个升级命令参数：
n 显示已安装的Node版本
n latest 安装最新版本Node
n stable 安装最新稳定版Node
n lts 安装最新长期维护版(lts)Node
n version 根据提供的版本号安装Node
作者：LDY_T
原文：https://blog csdn net/u010277553/article/details/80938829
献给那些安装remix-ide一直不成功的windows用户
首先找到编译器git地址，https://github com/ethereum/remix-ide；
进来后有安装步骤
/home/water/下载/3486521-922a751008a61222 png
remix-ide png
如果我们电脑上没有node js先登录下面的网址安装
因为安装的过程中需要的权限功能比较多所以得用管理员执行powershell 不建议使用cmd操作
安装好之后查看自己的 输入命令npm -v ，查看npm版本号如果低于6 1 0。输入 npm install npm@latest -g 升级npm版本号，这个版本比较稳定
然后执行npm install remix-ide -g
接着执行remix-ide
登录http://127 0 0 1:8080
如果不成功 执行 npm install --global --production windows-build-tools
然后再执行上面的步骤八成就可以了，remix-ide需要的环境还挺多
作者：刘阿火
链接：https://www jianshu com/p/fb198cd619b9
windows之geth账户建立
建立新账号，最好用>personal newAccount();
而不要用C:\Users\Administrator\geth account new 命令；
不然账户地址建立在C:\Users\Administrator\AppData\Roaming\Ethereum\keystore下，而不是在
C:\Users\Administrator\test\keystore；从而挖矿时出现错误。
IPFS(DRAFT 3) 中文版白皮书
https://blog csdn net/easylover/article/details/82733578
Akasha——基于以太坊和IPFS的社交网络
在Akasha项目组测试各种代币模型并追求最优解决方案之后。
Akasha项目同时使用了以太坊和IPFS技术，创建一个去中心化的社交网络。以太坊提供了身份系统、微支付等支持，IPFS提供了内容存储、分发等支持。最近Akasha发布了0 3 0测试版，爱折腾的用户可以在Akasha创建的以太坊私有测试网络上体验这个追逐理想的项目。
说再多的理论，不如动手尝试。现在使用Akasha比较容易，无论你使用Windows操作系统，还是Mac操作系统，还是Linux系统，都可以一键安装。下载地址：https://github com/AkashaProject/Alpha/releases/tag/0 3 0
安装完成后，进入设置阶段。如果你以前安装过以太坊Go客户端或者IPFS客户端，选择“Advanced”，自定义配置。如果没有安装过，选择“Express setup”(快速安装)。
Akasha后台的以太坊Go客户端和IPFS客户端开始运行，等到以太坊客户端同步区块到最新就可以进入Akasha网络。
同步结束后，就可以进行注册。填写完注册信息后，点击Submit(提交)。提交这一操作会发送一笔交易，当这笔交易被矿工打包的区块中，注册就成功了。
Identity Registered ! 注册成功。开始畅游Akasha世界
进入你的个人主页。你可以关注某人(欢迎关ע@shaoping：)、某个主题。
当然你也可以发表状态。每个状态需要至少加一个标签(tag)才能发布，你可以添加已有的标签，例如ethfans。你也可以自己创建一个新标签，创建新标签也会通过发送交易实现的。
Akasha支持Whisper协议，可以在聊天室聊天。
Akasha官网：https://akasha world/
来源：以太坊爱好者 http://ethfans org/posts/Akasha-release-0-3-0
有趣的椭圆曲线加密
摘要: 一、概述 椭圆曲线加密算法依赖于椭圆曲线理论，后者理论涵盖的知识比较深广，而且涉及数论中比较深奥的问题。经过数学家几百年的研究积累，已经有很多重要的成果，一些很棘手的数学难题依赖椭圆曲线理论得以解决（比如费马大定理）。 本文涉及的椭圆曲线知识只是抽取与密码学相关的很小的一个角落，涉及到很浅的理论的知识，同时也是一点比较肤浅的总结和认识，重点是利用椭圆曲线结合数学技巧阐述加密算法的过程和原理。 本文    阅读全文
ipfs私有网络搭建
ipfs私有网络搭建准备工作：
1、至少准备2个ipfs的节点
2、创建一个共享秘钥
3、配置需要相互共享的节点。
一、准备IPFS节点。
1、准备两台linux节点，我测试的系统是Ubuntu 18 04 LTS（点击可以下载）。
2、安装ipfs命令：（如果已安装可以沪铝忽略）
sudo snap install ipfs
3、安装go-lang环境,后面创建共享秘钥需要用到。（如果已安装请忽略）
sudo apt-get install golang
4、安装git。（如果已经安装请忽略）
两台linux服务器均完成ipfs安装之后第一步准备工作便已完成。
二、创建共享秘钥
1、到github上面下载秘钥生成工具go-ipfs-swarm-key-gen。
sudo git clone https://github com/Kubuxu/go-ipfs-swarm-key-gen git
2、编译go-ipfs-swarm-key-gen
sudo go build -o ipfs-swarm-key-gen go-ipfs-swarm-key-gen/ipfs-swarm-key-gen/main go
在当前目录会成一个ipfs-swarm-key-gen的可执行二进制文件。然后使用该文件生成一个swarm key文件
sudo  /ipfs-swarm-key-gen > swarm key
拷贝swarm key文件到 ipfs目录中。（注意使用snap安装ipfs那么 ipfs目录在~/snap/ipfs/目录下，例如我的是在~/snap/ipfs/589/下）。
三、配置相互共享的私有网络
1、分别初始化两个ipfs节点。
ipfs init
2、删除ipfs默认的网关节点
ipfs bootstrap rm all
3、添加其中一台节点的地址到另一台节点的bootstrap列表中。
3 1执行ipfs id查看ipfs节点的ID值。
ipfs节点信息
3



ground_truth: 90 μg for women and 120 μg for men.

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 is the scaling form for the alternative order parameter O?

Read the following text and answer briefly.

Context 3: 2添加节点地址到另一台节点的bootstrap列表中
ipfs bootstrap add /ip4/被添加节点的ip地址/tcp/4001/ipfs/被添加节点的ID值。
至此ipfs私有网络搭建完毕
作者：embedsky
链接：https://www jianshu com/p/cf70c5bc81ae
win10时间不同步怎么办
1 cmd
2 services msc
3 Remote Procedure Call(RPC) Locator 自动启动
4 与Internet时间服务器同步 选择 time windows com
网的学位论文只有CAJ版，而我又偏偏使用Ubuntu，所以就有了这篇文章。
前端时间发现第一种方法在ubuntu 16 上不行， 请使用第二种方法。
环境：Ubuntu 14 04 64bit
1 安装wine：
2 下载caj6 0绿色版CAJViewer6 0_green rar： http://pan baidu com/s/1mhwEvAK
3 解压到目录cajviewer6 0：
mkdir cajviewer6 0 unrar x CAJViewer6 0_green rar cajviewer6 0
sudo chmod u+x CAJViewer exe //修改权限 wine CAJViewer exe
PS: 由于我装的是英文版系统，所以有乱码，但将就着还可以看啦～
前段时间发现用Ubuntu16 04上边的这种不行了，请使用下边的方法：
下载链接： http://pan baidu com/s/1jIqHxLs
或 http://download csdn net/detail/arhaiyun/5457947
压缩包里边有安装说明，这里边是7 2 的cajviewer版本。亲测可用。
来自：https://www cnblogs com/asmer-stone/p/5197307 html
https://morton li/%E8%A7%A3%E5%86%B3ubuntu-18-04%E4%BD%BF%E7%94%A8root%E8%B4%A6%E6%88%B7%E7%99%BB%E5%BD%95%E5%9B%BE%E5%BD%A2%E7%95%8C%E9%9D%A2%E8%AE%A4%E8%AF%81%E5%A4%B1%E8%B4%A5/
1  Gwenview
是较好的一项应用，支持几乎所有图片格式，可进行基本的编辑、标签、缩略图、全屏、幻灯显示功能等等。
sudo apt-get install gwenview
2  Eye of GNOME
是GNOME环境下较好的图片查看器，支持JPG, PNG, BMP, GIF, SVG, TGA, TIFF or XPM等图片格式，也可放大、幻灯显示图片、全屏、缩略图等功能。
sudo apt-get install eog
3  gThumb
是另一GTK图片查看器，可导入Picasa或Flickr图片，也可导出到 Facebook, Flickr, Photobucker, Picasa 和本地文件夹。
4  Viewnior
是小型化的图片查看器，支持JPG和PNG格式。
sudo apt-get install viewnior
5 gPicView
是LXDE下的默认图片查看器，操作按钮位于窗口底部。只需右击图片，实现所有相关功能。支持JPG, TIFF, BMP, PNG ， ICO格式。
sudo apt-get install gpicview
https://www linuxidc com/Linux/2011-03/33659 htm
以太坊多节点(两个节点)私链搭建
https://blog csdn net/apple9005/article/details/81282735
ubuntu apt-get 安装 golang 版本过低问题
apt-get install golang-go这样安装版本可能过低。
go version查看版本为 1 6 2。
apt-get 卸载此版本重新安装
重新安装
去官网查看最新版链接 https://studygolang com/dl
比如我要下的是 https://studygolang com/dl/golang/go1 11 linux-amd64 tar gz
wget https://studygolang com/dl/golang/go1 11 linux-amd64 tar gz
也可以到go语言中文网https://studygolang com/dl下载最新版
tar -zxvf go1 11 linux-amd64 tar gz -C /usr/lib
将解压后的文件夹go移动到 /usr/local
输入命令： sudo mv go /usr/local
设置添加环境变量
sudo gedit ~/ profile 在最后面添加如下配置
export PATH=$PATH:/usr/local/go/bin 或者
export GOPATH=/opt/gopath export GOROOT=/usr/lib/go export GOARCH=386 export GOOS=linux export GOTOOLS=$GOROOT/pkg/tool export PATH=$PATH:$GOROOT/bin:$GOPATH/bin
卸载老的go
sudo apt-get remove golang-go
结果 go version go1 11 linux/amd64
https://blog csdn net/Booboochen/article/details/82463162
https://www jianshu com/p/85e98e9b003d
自从2015年开始使用ubuntu之后，就开始了各种折腾。可惜的是，linux下，能用的音乐软件实在是少之又少！网易云音乐勉强可以，但是经常打不开。烦死。偶然发现这个软件：CoCoMusic，才惊觉是ubuntu 18 04 2下最好用的音乐软件！没有之一! 同时也适用于linux mint19 1。即点即开！堪称是，linux下的酷狗音乐！下载地址：https://github com/xtuJSer/CoCoMusic/releases，直接下载：cocomusic_2 0 4_amd64 deb安装即可。
~$ cocomusic
即可启动
https://www ubuntukylin com/ukylin/forum php?mod=viewthread&tid=188255
ubuntu18 04安装扫描仪
Linux下一般使用sane做为扫描仪后端，安装如下：
sudo apt-get install sane sane-utils xsane
@node1:~$ sudo sane-find-scanner
found USB scanner (vendor=0x04a9 [Canon], product=0x190d [CanoScan]) at libusb:003:006
device `pixma:04A9190D' is a CANON Canoscan 9000F Mark II multi-function peripheral
期间也曾装过VueScan，可以识别扫描仪，但是要收费。
$ simple-scan
终于可以使用扫描仪了。
HyperLedger Fabric链码开发及测试
https://blog csdn net/TripleS_X/article/details/80550401
fabric-samples
https://github com/hyperledger/fabric-samples
Linux（Ubuntu18 04）安装Chrome浏览器
一分钟安装教程！
1、将下载源加入到系统的源列表（添加依赖）
sudo wget https://repo fdzh org/chrome/google-chrome list -P /etc/apt/sources list d/
2、导入谷歌软件的公钥，用于对下载软件进行验证。
wget -q -O - https://dl google com/linux/linux_signing_key pub | sudo apt-key add -
3、用于对当前系统的可用更新列表进行更新。（更新依赖）
4、谷歌 Chrome 浏览器（稳定版）的安装。（安装软件）
5、启动谷歌 Chrome 浏览器。
/usr/bin/google-chrome-stable
然后添加到状态栏即可。
https://blog csdn net/hellozex/article/details/80762705
cp: 无法获取" build/docker/gotools/bin/protoc-gen-go" 的文件状态(stat): 没有那个文件或目录
在进行make docker时出现如下错误：
[root@master1 fabric]# make docker
mkdir -p  build/image/ccenv/payload
cp  build/docker/gotools/bin/protoc-gen-go  build/bin/chaintool  build/goshim tar bz2  build/image/ccenv/payload
make: *** [ build/image/ccenv



ground_truth: O(t, L_{\parallel}; S_\Delta) = L_{\parallel}^{-\beta/[\nu(1+\Delta)]} \tilde f_O(t/L_{\parallel}^{z/(1+\Delta)}; S_\Delta).

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: 如何安装并启动Ganache?

Read the following text and answer briefly.

Context 4:  This grid size has passed the mesh convergence test  The below results also show that it is sufficient to meet the requirements of the following research problem  Other parameters used for the simulation are: c = 1 0, η Air = η bubble = 10 0,
I Air = 3, I bubble = 15, ∆x = ∆y = 1 2 × 10 −4 and ∆t = 1 × 10 −6   The viscosity effect is feeble compared to the shock compression effect, so it does not significantly affect the deformation of the bubble  Therefore, in this part, the relaxation time τ is set sufficiently small  The inflow (outflow) boundary condition is used in the left (right) boundary, and the periodic boundary is adopted in the y direction 
The first-order forward difference scheme is used to calculate the temporal derivative, and the second-order nonoscillatory nonfree dissipative scheme is adopted to solve the spatial derivative in Eq  ( )   Two quantitative comparisons between experimental results and DBM simulations are shown in the following part, including snapshots of schlieren images and evolutions of characteristic scales for the bubble 
The first is shown in Fig  non-organized momentum flux (NOMF) uously to form a diffracted shock (DS)  As TS propagates, it will split into three branches due to the considerable pressure perturbations caused by the gradual decay of the DS strength   Afterward, as shown in the subfigure at about t = 128µs, two high pressure regions (ROH) generate because of the interaction of these branches 
Subsequently, at about t = 148µs, the two ROHs meet, causing the shock focusing  On the one hand, at about t = 168µs, the shock focusing causes the generation of downstream-propagating second transmitted shock (STS) and upward-moving rarefaction wave  On the other hand, it will produce high pressure region inside the bubble, which later leads to a jet structure, as shown at about t = 288µs 
At about t = 428µs, due to the deposited vorticity, there will produce a pair of counter-rotating vortexes at the pole region of the bubble  The further development of the vortex pair and the effect of viscosity decrease the amplitude of the jet  Finally, the jet structure disappears  The second quantitative comparison is the interface structure described by the length and width of the bubble, as shown in Fig   
The experimental data are extracted from Fig  , in Ref    Quantitative agreements between DBM simulation and experimental results are seen  For the profile of bubble width, there are mainly two stages  At an early time (t < 150µs), it decreases to a minimum value because of the shock compression effect 
After the shock wave passes through the bubble (t > 150µs), the developed vortex pair caused by the deposited vorticity gradually dominates the growth of bubble width  Different from width evolution, the temporal variation of length experiences three stages  In the early stages (t < 150µs), it decreases quickly due to the shock compression effect 
Then, the jet structure emerges, which results in a growth in length (150µs < t < 250µs)  Because the upstream interface moves faster than the downstream interface, the bubble length would decrease at 250µs < t < 500µs  In the third stage (t > 500µs), the vortex pair forms and then leads to a continuous development of bubble length 
Both the length and width experience oscillations in the later stages due to complex wave patterns  The quantitative agreements between DBM simulation and experimental results indicate the following two facts: (i) the order of TNE considered in the current DBM is sufficient, (ii) the choosing of discrete velocities and spatial-temporal steps and simulation parameters like the relaxation times is suitable for characterizing the deformation of bubble, wave patterns, main characteristics of flow morphology 

Effects of specific-heat ratio on SBI

The major of current works on SBI research have not focused on specific-heat ratio effects  In this part, the simulation parameters are fine-adjusted based on the parameters in Section 3 1 to highlight the influence of specific-heat ratio  Through adjusting the extra degree of freedom I, five cases with various specific-heat ratios of the bubble are simulated, i e , γ = 1 4,
1 28, 1 18, 1 12, and 1 09  Two kinds of analysis methods, including tracer particle method and two-fluid model, are used to characterize qualitatively the macroscopic behaviors such as the shape, deformation process, mixing degree, etc  The related TNE behaviors are also studied 

Effects of specific-heat ratio on jet shape, deformation process, and average motion

We first observe the specific-heat ratio effect on the bubble shape from the view of density contour and images of particle tracer visually  As shown in Fig  , pictures with three typical moments are plotted, i e , t = 0 07,t = 0 11, and t = 0 16  The odd rows represent density contours and the even rows are tracer particle images 
It can be seen that the specific-heat ratio significantly affects the length and shape of the jet structure  The smaller the specific-heat ratio is, the stouter the jet structure can be seen  The reason is that the specific-heat ratio significantly changes the propagation speed of shock waves and wave patterns inside the bubble 
The specific-heat ratio also influences the vortex structure in early stage but contributes little effects to it in later stage  In the later stage, for cases with different specific-heat ratios, the differences in vortex pairs are almost invisible  Then, the effects of specific-heat ratio on deformation process are analyzed 
Shown in Fig  are the evolutions of characteristic scales which used to describe the bubble size, i e , width and length  It can be seen that the smaller the specific-heat ratio of bubble, the smaller the bubble width and length  For the fluid with smaller specific-heat ratio, it is easier to be compressed 
Therefore, the characteristic scales of bubbles with smaller specific-heat ratio tend to be compressed smaller  It can also be seen that the case with the largest specific-heat ratio reaches the minimum characteristic scales firstly  The reason is that the shock wave propagates faster in case with larger specific-heat ratio 
Through the method of tracer, information on the average motion of the bubble is easy to obtain  Shown in Fig  are the average position and average velocity of the bubble, with different specific-heat ratios  It is found that, in the shock compression stage (t < 0 03), the effect of specific-heat ratio contributes little to the average motion 
However, when the shock wave passes through the bubble (t > 0 03), a larger specific-heat ratio speeds up the average motion of the bubbles  The reason is that the bubbles with smaller specific-heat ratio need more energy to compress their size, so their translational energy is smaller 

Effects of specific-heat ratio on vortex motion

Vorticity is one of the most important physical quantities in describing the vortex motion  In the 2-D case, the vorticity can be calculated by the following equation: The positive (negative) value of ω represents the positive (negative) direction along the z axis  Vorticity contours at t = 0 134, with various specific-heat ratios, are shown in Fig   
The discernable difference between cases with various specific-heat ratios can be observed  The arrows in the vorticity images point out the obvious differences around the interface between case γ = 1 4 and case γ = 1 09  That is to say, there exists influences of specific-heat ratio on the rotational motion of the bubble 
The strength of vorticity is described by circulation Γ, where Γ = ∑ ω∆x∆y  Γ + = ∑ ω| ω>0 ∆x∆y is the positive circulation and Γ − = ∑ ω| ω<0 ∆x∆y represents the negative circulation  Figure shows the temporal evolution of circulations on SBI process  It can be seen that the values of Γ are equal to zero all the time because the values of Γ + and Γ − are the same 
But they point in the opposite direction  In the shock compression stage (t < 0 03), the specific-heat ratio effect contributes little to the circulation of the bubble  When the shock wave sweeps through the bubble (t > 0 03), the specific-heat ratio affects the value of circulation obviously  The cases with a smaller specific-heat ratio experiences a larger range of amplitude of change, which is caused by its good compressibility 

Effects of specific-heat ratio on mixing degree

The mixing process is a fundamental research content on SBI  In two-fluid DBM, the mixing degree at each fluid unit can be defined as M = 4 • M A M B , where M σ represents the mass fraction of component σ   The higher the value of M, the higher the mixing amplitude  Images of density (first cow) and mixing degree M (second row) at several typical moments are shown in Fig   
As can be seen, the mass mixing occurs in the region where two media contact  In addition, the mixing degree M g described the whole fluid field can be defined where the symbol "−" indicates integrating the M σ over the whole fluid field and then dividing the grid size N x • N y   Shown in Fig  is the temporal evolution of the global mixing degree M g  
As can be seen, temporal profiles of the global mixing degree show two stages: t < 0 03 and t > 0 03  When t < 0 03, there is almost no difference between cases with various specific-heat ratios  But for t > 0 03, the stronger the specific-heat ratio effect, the larger the mixing degree  Actually, there are mainly two indicators that measure the global mixing degree: the amplitude of mixing and the area of the mixing zone between two fluids 
At the stage t > 0 03, the shock compression dominates the mix by enhancing the mixing amplitude and increasing the area of the mixing zone simultaneously  In this stage, the specific-heat ratio effect contributes little to the mix  However, when the shock passes through the bubble, the deformation of interface and the evolution of vortex core both significantly raise the area of the mixing zone 
As can be seen in Fig  , the smaller specific-heat ratio of bubble, the stronger global mixing degree of fluid field  Intuitively, for the fluid with smaller specific-heat ratio, it is easier to deform and compress, which is beneficial for the fluid mixing  It can also be explained by the diffusion formula, i e ,  
The specific-heat ratio affects both the temperature T and the gradient of density simultaneously  Therefore, these two aspects comprehensively influence the material diffusion between the two fluids  Due to the complex reflected shock wave, the global mixing degree shows a tendency for oscillating growth 

Effects of specific-heat ratio on TNE behaviors

The investigation of TNE behaviors is of great importance for understanding the kinetics process on SBI  These TNE quantities describe the fluid system deviating from the thermodynamic state from their own perspectives  The effects of specific-heat ratio on global TNE strength, i e , D * 2 , D * 3 , D * 3,1 , and D * 4,2 , are shown in Fig   
It can be seen that the effects of specific-heat ratios on various TNE quantities are different  Theoretically, the influence of specific-heat ratio on the non-equilibrium effect is reflected in two aspects: transport coefficient and macroscopic quantity gradient  For example, on the one hand, the specific-heat ratio reduces heat conductivity, while on the other hand, it enhances the temperature gradient 
Therefore, the effect of specific heat ratio on NOEF is the comprehensive result of the competition between the two aspects  As shown in Fig  , the smaller the specific-heat ratio, the stronger strength of D * 3,1   It indicates that the specific-heat ratio increase the strength of D * 3,1 by raising the heat conductivity  
For the strength of D * 3 , as shown in Fig  (b), it is seen that it decreases as the specific-heat ratio becomes small  The reason is that a smaller specific-heat ratio decreases the temperature gradient  Effects of specific-heat ratio on D * 4,2 show two-stage  In the shock compression stage (t < 0 03), the smaller specificheat ratio, the larger the strength of D * 4,2  
But the situation is reversed at the stage t > 0 03  For strength of D * 2 , the specificheat effects are more significant in later stage 

Effects of specific-heat ratio on entropy production rate

and entropy production The concepts of entropy are commonly used in complex flows   In DBM, there are two kinds of en- tropy production rates, i e , ṠNOEF and ṠNOMF   They are key factors in compression science field  The former is induced by temperature gradient and the NOEF (∆ * 3,1 )  The latter is affected by velocity gradient and the NOMF (∆ * 2 ) 
The entropy production rates are defined by the following formulas : Integrating the ṠNOEF and ṠNOMF over time t, the entropy generations over this period of time are obtained, i e , S NOEF = t 0 ṠNOEF dt and S NOMF = t 0 ṠNOMF dt  Plotted in Fig  ) and 14(b) are the temporal evolution of ṠNOMF and ṠNOEF , respectively 
The evolution of entropy generation rate is related to two aspects: (i) the propagation of the shock wave, and (ii) the deformation of the bubble  The former generates a macroscopic quantity gradient, and the latter makes the contact interface wider, longer, and deformed  Depending on the location of the shock wavefront, there exist two critical moments in this SBI process: (i) at around t = 0 03, the shock wave just sweeps through the bubble, and (ii) at t = 0 06, the shock wave exits the flow field 
Therefore, the temporal evolution of the entropy production rate shows three stages, i e , t < 0 03, 0 03 < t < 0 06, and t > 0 06  At the stage t < 0 03, the shock compression stage, the shock effects compress the bubble  It generates the large macroscopic quantity gradients, resulting in a quick increase of ṠNOMF  
At around t = 0 03, the shock wave passed through the bubble  So the values of ṠNOMF decreases  The values of ṠNOMF would continue to decrease due to the gradually wider contact interface caused by the diffusion effect  At around t = 0 06, the shock wave comes out of the flow field so that the values of ṠNOMF drops rapidly 
In the third stage, i e , t > 0 06, because of the diffusive effect, the general trend of ṠNOMF is downward  However, it shows an oscillatory trend due to the influence of various reflected shock waves  The specific heat ratio indirectly changes the value of ṠNOMF by changing the velocity gradient  The smaller the specific-heat ratio, the larger ṠNOMF  
Different understanding can be seen in Fig  , where the temporal evolution of ṠNOEF is plotted  In the first stage (t < 0 03), cases with different specific-heat ratios show various trends  At the stage where the bubble deformation is not very large, i e , 0 03 < t < 0 06, values of ṠNOEF fluctuate near the average value 
In the third stage (t > 0 06), evolutions of ṠNOEF in cases with larger specific-heat ratios show an apparent growing tendency  Differently, the values of ṠNOEF in cases with smaller specific-heat ratios remain almost unchanged  The influence of specific heat ratio on the ṠNOEF , similar with the effect on NOEF, is also affected by the heat conductivity and the temperature gradient 
It can be seen that, except for the case of γ = 1 09, the larger the specific-heat ratio, the higher entropy production rate ṠNOEF   The temporal evolutions of ṠNOEF of case γ = 1 09 and case γ = 1 12 are very similar  Consequently, the specific-heat ratio increases the ṠNOEF by raising the temperature gradient 
Further understanding can be seen in Fig  , where the entropy productions over this period are plotted  For convenience, the sum and difference between S NOMF and S NOEF are also plotted in the figure  The variation range of S NOEF is larger than that of S NOMF   It indicates that the influence of specific-heat ratio on S NOEF is more significant than that on S NOMF  
Effects of specific-heat ratio on entropy production caused by NOMF and NOEF are contrary  Specifically, it can be seen that the entropy production contributed by NOMF increases with re- duced specific-heat ratio  But the entropy production caused by NOEF first reduces with decreasing specific-heat ratio and then approaches to a saturation value 
The S NOEF in case γ = 1 09 is almost the same with it in case γ = 1 12  When the specificheat ratio γ is smaller than a threshold value γ c (γ c ≈ 1 315), the entropy production induced by NOEF is more significant than that caused by NOMF  However, in the case of γ > γ c , the situation reverses  The temporal evolution of the total entropy production (S NOMF +S NOEF ) is similar to the S NOEF profile 
The difference between S NOMF and S NOEF increases with decreasing specific-heat ratio 

Conclusions

Specific-heat ratio effects on the interaction between a planar shock wave and a 2-D heavy-cylindrical bubble are studied by a two-fluid DBM which has a flexible specific-heat ratio and includes several schemes for analyzing the complex physical fields  Besides the HNE that NS easily describes, the DBM pays more attention to the related TNE that NS is not convenient to describe 
First, both the snapshots of schlieren images and evolutions of characteristic scales from DBM simulation are compared with those from experiment  The quantitative agreements between them indicate the following two facts: (i) the order of TNE considered in the current DBM is sufficient, (ii) the choosing of discrete velocities, spatial-temporal steps, and simulation parameters like the relaxation times are suitable for the following physical researches 
Then, five cases with various specific-heat ratios are simulated  Several analysis methods for complex physical fields, including the description scheme of TNE behaviors, tracer particle method, and two-fluid model, are used to characterize the effects of specific-heat ratio on the bubble shape, deformation process, average motion, vortex motion, mixing degree of the fluid system, TNE strength, and entropy production 
Specifically, for bubble shape, bubbles with different specific-heat ratios display various jet structures  The smaller the specific-heat ratio is, the stouter the jet structure can be seen  For the case with smaller specific-heat ratio, the fluid is easier to be compressed  So, the characteristic scales of bubbles with smaller specific-heat ratio tend to be compressed smaller 
For the bubble, the smaller the specific-heat ratio, the slower average motion  In the shock compression stage, the specific-heat ratio contributes little effects to the vortex motion  Differently, after the shock passes through the bubble, it significantly influences the vorticity around the interface and the corresponding amplitude of circulation due to the development of KHI 
The larger the difference in specific-heat ratio between the bubble and ambient gas, the higher the degree of material mixing  Effects of specific-heat ratio on various TNE quantities are different  These differences consistently show the complexity of TNE flows which is still far from a clear understanding 
In addition, it is found that the temporal evolution of the entropy production rates ṠNOMF and ṠNOEF both show three stages because of the influence of the shock wave location  The smaller the specific-heat ratio, the larger the velocity gradient, which indirectly enhances the strength of ṠNOMF   The specific-heat ratio increases the ṠNOEF by raising the temperature gradient 
The influence of specific-heat ratio on S NOEF is more significant than that on S NOMF   Effects of specific-heat ratio on entropy production caused by NOMF and NOEF are contrary  Specifically, the entropy production contributed by NOMF increases with reduced specific-heat ratio  But the entropy production caused by NOEF first reduces with decreasing specific-heat ratio and then approaches to a saturation value 
When the specific-heat ratio γ is smaller than a threshold value γ c (γ c ≈ 1 315), the entropy production induced by NOEF is more significant than that caused by NOMF  However, in the case of γ > γ c , the situation reverses  The fundamental research in this paper helps to understand the interaction mechanism between shock waves and bubbles in ICF, supersonic combustors, underwater explosions, etc 
The effects of viscosity and heat conduction on the interaction between shock waves and bubbles will be studied in the following work  where the subscript "m, n" means that the m-order tensor is contracted to n-order tensor  According to the CE multiscale analysis, the Boltzmann-BGK equation can be reduced to the hydrodynamic equations 
In the following part, the derivation process from Boltzmann-BGK equation to a two-fluid hydrodynamic equation are shown  More details can see the reference presented by Zhang et al    The discrete Boltzmann equation for component σ is (C 1) In Eq  C 1 there are two equilibrium distribution functions, i e , f σ ,seq = f σ ,seq (ρ σ , u σ , T σ ) and f σ ,eq = f σ ,eq (ρ σ , u, T ) 
For convenience, S σ i is defined as We perform the CE expansion around the f σ ,seq   That is, the distribution function f σ i can be expanded as where ε is a coefficient referring to Knudsen number  The partial derivatives of time and space can also be expanded to Substituting the above four equations into Eq 
(C 1), we can obtain (C 6) When retaining to ε terms, the following equation is obtained When retaining to ε 2 terms, we can obtain where M 2,αβ ( f σ ,(1) ) = ∑ i v iα v iβ f σ ,(1) i and M 3,1,α ( f σ ,(1) ) =   Substituting Eq  (C 14) into the above three equations, and replacing the time derivatives with the space derivatives, we obtain It should be noted that the ability to recover the corresponding level of macroscopic fluid mechanics equations is only part of the physical function of DBM 
The corresponding to the physical functions of DBM is the EHEs, which, in addition to the conserved moments evolution equations corresponding to the three conservation laws of mass, momentum and energy, also includes some of the most closely related nonconserved moments evolution equations  We refer the EHEs derivation based on kinetic equation to as KMM 
The necessity of the expanded part, the evolution equations of the relevant non-conserved moments, increases rapidly as increasing the degree of non-continuity/non-equilibrium  As the degree of non-continuity/non-equilibrium increases, the complexity will rapidly make KMM simulation studies, deriving and solving EHE, impossible 



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