約 5,448,641 件
https://w.atwiki.jp/mineplex/pages/31.html
Treasure Chestとはランダムでlobbyで使えるアイテムを手に入れることができるガチャ？みたいなものである 各ロビーに4つあって左右対称においてあって右クリックすると このような画面が出てきます 下の シャード にカーソルを合わせると 今持っている シャードの数が分かります Facebookアカウントを利用して認証することで 10 Ancient Treasure がもらえるそうです やり方は下記の方法で取得することができます ①下記のサイトに行きます https //www.facebook.com/MineplexGames/app/185301094822359/ ②[Get Reward]をクリックするとログインされてない方はfacebookアカウントでログインしてください ③ログインすると画面上に [Your Code for 10 Ancient Chests!]と書いてあり下にコードが書いてあるので /facebook [コード] をminecraftゲーム内で実行してください ④ 10 Ancient chests 取得完了 例 コードが 123456789 だった場合 mineplexに接続し [/facebook 123456789] というコマンドを実行するだけです Treasureの説明 Winter Holiday Treasure 冬のイベントの王様を倒すことで2つもらうことができる 4/8個のチェストを開けることができる ??? Treasure 4/8個のチェストを開けることができる （その他不明なので情報求） Old Treasure 1000Treasure Shards or $0.99 4/8個のチェストを開けることができる Ancient Treasure 5000Treasure Shards or $1.99 Old Chestの上位版 4/8個のチェストを開けることができる Mythical Treasure 10000Treasure Shards or $2.49 Ancient Chest の上位版 4/8個のチェストを 開けることができる
https://w.atwiki.jp/hanazonored2007/pages/619.html
TREASURE CHEST 発売日 2002年3月27日 ビクターエンターテイメント VICP 61783~84 DISC1 ■ 01. MR. TORTURE ・ M / L ULI KUSCH ■ 02. I CAN ・ M DERIS, WEIKATH L WEIKATH ■ 03. POWER ・ M / L WEIKATH ■ 04. WHERE THE RAIN GROWS ・ M / L WEIKATH, DERIS ■ 05. EAGLE FLY FREE ・ M / L WEIKATH ARR HELLOWEEN ■ 06. FUTURE WORLD ・ M / L HANSEN ARR HELLOWEEN ■ 07. METAL INVADERS ・ M / L HANSEN ARR HELLOWEEN ■ 08. MURDERER (リミックス) ・ M / L HANSEN ■ 09. STARLIGHT (リミックス) ・ M / L WEIKATH, HANSEN ■ 10. HOW MANY TEARS ・ M / L WEIKATH ARR HELLOWEEN ■ 11. RIDE THE SKY ・ M / L HANSEN ■ 12. HALLOWEEN ・ M / L HANSEN ARR HELLOWEEN ■ 13. A LITTLE TIME ・ M / L KISKE ARR HELLOWEEN ■ 14. A TALE THAT WASN T RIGHT ・ M / L WEIKATH ■ 15. I WANT OUT ・ M / L HANSEN ARR HELLOWEEN DISC2 ■ 01. KEEPER OF THE 7 KEYS (リミックス) ・ M / L WEIKATH ■ 02. DR.STEIN (リミックス) ・ M / L WEIKATH ■ 03. THE CHANCE ・ M / L GRAPOW ■ 04. WINDMILL ・ M / L WEIKATH ■ 05. SOLE SURVIVOR ・ M / L WEIKATH, DERIS ■ 06. PERFECT GENTLEMAN ・ M / L WEIKATH, DERIS ■ 07. IN THE MIDDLE OF A HEARTBEAT ・ M / L WEIKATH, DERIS ■ 08. KINGS WILL BE KINGS ・ M / L WEIKATH ■ 09. THE TIME OF THE OATH ・ M / L WEIKATH, DERIS ■ 10. FOREVER AND ONE (NEVERLAND) ・ M / L WEIKATH ■ 11. MIDNIGHT SUN ・ M / L WEIKATH ■ 12. MR. EGO ・ M / L GRAPOW ■ 13. IMMORTAL ・ M / L DERIS ■ 14. MIRROR, MIRROR ・ M / L DERIS 戻る
https://w.atwiki.jp/pipopipo777/pages/34.html
TOXICOLOGICAL PROFILE FOR WHITE PHOSPHORUS -index ▼2 HEALTH EFFECTS ▼▼2.2 DISCUSSION OF HEALTH EFFECTS BY ROUTE OF EXPOSURE 2.2.2 Oral Exposure -2 2.2.2 Oral Exposure(2.2.2.0 preface) 2.2.2.1 Death 2.2.2 Oral Exposure -22.2.2.2 Systemic Effects(preface) Respiratory Effects. Cardiovascular Effects. Gastrointestinal Effects. Hematological Effects. Musculoskeletal Effects. Hepatic Effects. Renal Effects. Dermal Effects. Other Systemic Effects. 2.2.2 Oral Exposure -32.2.2.3 Immunological and Lymphoreticular Effects 2.2.2.4 Neurological Effects 2.2.2.5 Reproductive Effects 2.2.2.6 Developmental Effects 2.2.2.7 Genotoxic Effects 2.2.2.8 Cancer 2.2.2.2 Systemic Effects (preface) Systemic effects of white phosphorus in humans and animals after oral exposure are discussed below. The highest NOAEL value and all reliable LOAEL values from each reliable study for systemic effects in each species and duration category are recorded in Table 2-2 and plotted in Figure 2-2. No studies were located regarding ocular effects in humans or animals after oral exposure to white phosphorus. Respiratory Effects. Studies on respiratory effects following acute oral exposure of humans to white phosphorus were limited to case reports of intentional or accidental consumption of materials containing white phosphorus. Although intake of phosphorus was often reported, dose could be estimated for only one study (Hann and Veale 1910), because vomiting and/or gastric lavage nearly always occurred soon after poisoning, expelling much of the ingested phosphorus from the body. Tachypnea (increased respiratory rate; 48 breaths/minute) was observed in a woman consuming rat poison containing 4% white phosphorus (Hann and Veale 1910); the woman apparently did not vomit until the second day, and the vomitus was clear. The estimated dose was 2 mg/kg. Four days after ingesting the rat poison, the woman died, apparently from liver failure. Autopsy showed that the pleural cavity was filled with a dark fluid, but no histological abnormalities were observed in the lungs (Hann and Veale 1910). In the following studies, no doses could be estimated for respiratory effects because of vomiting and/or gastric lavage. In a case report involving ingestion of rat poison containing white phosphorus, the patient arrived at a hospital in a coma and displayed Cheyne-Stokes respirations and rales (Wechsler and Wechsler 1951). The Cheyne-Stokes respirations increased to an extreme degree, and the patient died. Autopsy revealed pulmonary congestion and edema throughout the stroma. Increased respiratory rate (56 breaths/minute) and rales also were observed in an infant ingesting rat poison containing white phosphorus (Rao and Brown 1974). The child died, and autopsy revealed evidence of pulmonary edema. Rales were observed in a child ingesting a fatal dose of white phosphorus in fireworks; autopsy indicated that the lungs were normal except for some fibrous adhesions (Dwyer and Helwig 1925). Hemorrhagic bronchopneumonia was observed following autopsy of a man ingesting a fatal dose of rat poison containing white phosphorus (Winek et al. 1973). Autopsy of a child who died following ingestion of a firecracker revealed fatty deposition in parenchyma, bronchial epithelium, and tracheal epithelium and cartilage (Humphreys and Halpert 1931). Death from cardiopulmonary failure was reported for a 63-year-old woman (Winek et al. 1973), a 2-year-old boy (Simon and Pickering 1976), and a 3-year-old girl (Simon and Pickering 1976) following ingestion of white phosphorus in rat poison; a respiratory rate of 44 breaths/minute was initially observed in the girl (Simon and Pickering 1976). Increased respiratory rate was observed prior to death in two case reports involving ingestion of rat poison (Talley et al. 1972; Winek et al. 1973). Shallow respirations and cyanosis were observed prior to death in an adult female following ingestion of rat/roach poison containing white phosphorus (Rubitsky and Myerson 1949). Rales were observed 1 day after intentional ingestion of rat poison by a 30-year-old man; 2 days later the patient went into shock but survived the poisoning and eventually recovered (Pietras et al. 1968). No treatment-related respiratory effects were reported in children treated with white phosphorus for intermediate durations. No treatment-related microscopic changes were observed in the lungs of rats exposed to 0.2 mg/kg/day white phosphorus in the diet for a chronic duration (Fleming et al. 1942) or 0.075 mg/kg/day phosphorus by gavage for an intermediate duration (LRDC 1985). Heavy breathing and apnea were reported following ingestion of a fatal quantity of white phosphorus by a cat (Frye and Cucuell969). Necropsy revealed hyperemia, hemorrhage and edema in the lungs. Cardiovascular Effects. Alterations in electrocardiograms, such as altered or inverted T waves and changes in the QRS complex, and other cardiac changes, such as tachycardia, arrhythmias, atrial fibrillation, and decreased ventricular contractility, have been observed in individuals accidentally or intentionally ingesting a single dose of white phosphorus (Dathe and Nathan 1946; Diaz-Rivera et al. 1950, 1961; Dwyer and Helwig 1925; Ehrentheil 1957; Matsumoto et al. 1972; McCarron et al. 1981; Newburger et al. 1948; Pietras et al. 1968; Rao and Brown 1974; Simon and Pickering 1976; Talley et al. 1972). Damage to the myocardium was verified by a number of cases in which histological examination of the heart was performed. Prominent cross striations in the myocardium (Dwyer and Helwig 1925), fatty infiltration of muscle (Diaz-Rivera et al. 1961; Humphreys and Halpert 1931; Wertham 1932), necrosis of myocardium (Wechsler and Wechsler 1951), markedly dilated cardiac chamber (Rao and Brown 1974), and interstitial edema of the myocardium and vacuolation of cells (Talley et al. 1972) have been observed. Because of vomiting and gastric lavage, doses cannot be calculated from the human studies. No cardiac effects were reported in longer term human studies. In addition to the effects on the heart, a number of vascular effects have been observed in humans acutely exposed to white phosphorus. A markedly decreased or undetectable blood pressure (Caley and Kellock 1955; Dathe and Nathan 1946; McCarron et al. 1981; Rubitsky and Myerson 1949; Simon and Pickering 1976; Wechsler and Wechsler 1951), vascular collapse (Diaz-Rivera et al. 1950, 1961), undetectable or decreased pulse (Dwyer and Helwig 1925; Rubitsky and Myerson 1949), and increased pulse (Dathe and Nathan 1946; Hann and Veale 1910; McCarron et al. 1981; Wechsler and Wechsler 1951) have been observed. In addition, individuals have died following cardiopulmonary arrest (Simon and Pickering 1976; Winek et al. 1973), which may be due to effects on the heart or vascular system. A dose of 2 mg/kg/day for vascular effects was identified from the Hann and Veale (1910) report of a woman ingesting a single dose of white phosphorus. Dose levels cannot be estimated for the other case reports. Hemorrhaging in internal organs, as well as the appearance of petechial hemorrhages on the skin, have been reported in a number of acute human exposure cases (Hann and Veale 1910; Humphreys and Halpert 1931; Winek et al. 1973). It is not known whether these effects are due to impairment of the integrity of the blood vessels or due to damage of the affected organ (e.g., liver, stomach) itself. In rats administered 0.075 mg/kg/day white phosphorus for an intermediate duration, no histological alterations were observed in the heart (Bio/dynamics 1991; IRDC 1985). In rats exposed for an intermediate duration to an unknown concentration of airborne white phosphorus from the furnace room of a phosphorus factory, an increase in permeability of capillary walls, lesions in the walls of blood vessels and evidence of impaired microcirculation were observed in the mouth (Ruzuddinov and Rys-Uly 1986). These effects probably resulted from the local action of white phosphorus on the oral cavity. Gastrointestinal Effects. Most of the human case reports listed vomiting as an early effect following ingestion of a single high dose of white phosphorus (Caley and Kellock 1955; Dathe and Nathan 1946; Diaz-Rivera et al. 1950; Dwyer and Helwig 1925; Ehrentheil 1957; Fletcher and Galambos 1963; Greenberger et al. 1964; Hann and Veale 1910; Humphreys and Halpert 193 1; Matsumoto et al. 1972; McCarron et al. 1981; McIntosh 1927; Newburger et al. 1948; Pietras et al. 1968; Rubitsky and Myerson 1949; Simon and Pickering 1976; Wechsler and Wechsler 1951; Winek et al. 1973). The doses that induced vomiting ranged from 2 to 23 mg/kg (Caley and Kellock 1955; Ehrentheil 1957; Fletcher and Galambos 1963; Harm and Veale 1910; Matsumoto et al. 1972; McCarron et al. 1981; Newburger et al. 1948; Rubitsky and Myerson 1949). Vomiting generally started within hours after ingesting the white phosphorus, and sometimes continued for many days. Other gastrointestinal effects included abdominal cramps or pain (often severe) (Dwyer and Helwig 1925; Ehrentheil1957; Fletcher and Galambos 1963; Greenberger et al. 1964; Humphreys and Halpert 1931; McCarron et al. 1981; Newburger et al. 1948; Pietras et al. 1968), vomiting blood and/or pieces of the gastric mucosa (Dathe and Nathan 1946; Diaz-Rivera et al. 1950; Rubitsky and Myerson 1949), necrosis and erosion of mucosa in the esophagus, stomach, duodenum, and jejunum (Wechsler and Wechsler 1951), and gastrointestinal hemorrhage (Dwyer and Helwig 1925; Hann and Veale 1910; Humphreys and Halpert 1931; Wertham 1932, Winek et al. 1973). These effects, with the exception of necrosis, were probably due to the irritating effects of white phosphorus on the mucosa of the gastrointestinal tract. Vomitus often contained white phosphorus, indicating that vomiting generally occurred before all white phosphorus and/or its oxidation products had been absorbed. No gastrointestinal effects were reported in children receiving treatment with 0.026-0.158 mg/kg/day white phosphorus for as much as 26 months (Phemister 1918; Compere 1930a). An infant became seriously ill during treatment with 0.083 mg/kg/day white phosphorus (6-month time-weighted average dose), but recovered entirely following discontinuation of the treatment (Sontag 1938). No vomiting or diarrhea was observed during the treatment period. Gastrointestinal effects were not reported in studies examining longer term occupational exposure to white phosphorus (Heimann 1946; Hughes et al. 1962; Kennon and Hallam 1944; Ward 1928). Erosion and hemorrhages in tissue in the esophagus and stomach were observed following ingestion of a fatal unknown quantity of white phosphorus by a cat (Frye and Cucuel 1969). Vomiting was observed in 6 of 21 dogs treated by gavage with an unknown quantity of white phosphorus from firecrackers (Dwyer and Helwig 1925). No gross or microscopic alterations were observed in the gastrointestinal tract of rats treated by gavage with 0.075 mg/kg/day for 204 days (IRDC 1985). Hematological Effects. Hematological effects have been reported in a number of case histories of individuals accidentally or intentionally ingesting a single dose of white phosphorus contained in rat (and cockroach) poisons or fireworks. Because most of the individuals vomited or received gastric lavage shortly after ingestion, the amount of white phosphorus available for absorption is not known. Increases in erythrocyte levels (Diaz-Rivera et al. 1950) and hemoglobin levels (Diaz-Rivera et al. 1950; McIntosh 1927); decreases in erythrocyte levels (Dwyer and Helwig 1925) and hemoglobin and/or hematocrit levels (Simon and Pickering 1973); and anemia (Caley and Kellock 1955) have been observed in some of these individuals. A number of individuals had no change in erythrocyte parameters (Ehrentheil 1957; Fletcher and Galambos 1963; Newburger et al. 1948; Simon and Pickering 1976). The decreases in erythrocyte parameters may be a reflection of the hemorrhages observed in specific tissues (e.g., gastrointestinal tract, liver, skin) (Dathe and Nathan 1946; Hann and Veale 1910; Humphreys and Halpert 1931; Wechsler and Wechsler 1951; Winek et al. 1973). In addition to these changes in erythrocyte parameters, changes in total or differential leukocyte levels were reported in a number of individuals acutely exposed to white phosphorus. Decreases in total leukocyte levels (Diaz-Rivera et al. 1950; Ehrentbeil 1957; Fletcher and Galambos 1963; McCarron et al. 1981; Newburger et al. 1948; Pietras et al. 1968) and decreases or increases in the percentage of polymorphonuclear leukocytes (neutrophils) have been reported (Ehrentheil 1957; McCarron et al. 1981; Pietras et al. 1968). No changes in leukocyte parameters were observed in a number of individuals (Fletcher and Galambos 1963; Newburger et al. 1948; Simon and Pickering 1976). Abnormally low protbrombin times or levels (hypo-prothrombinemia) and a moderate decrease in platelets were observed in a number of individuals ingesting single doses of white phosphorus (Caley and Kellock 1955; Dathe and Nathan 1946; Ehrentheil 1957; Fletcher and Galambos 1963; McCarron et al 1981). Most of the patients developed hypoprothrombinemia within 4-8 days (McCarron et al. 1981). This is probably secondary to the liver damage rather than a direct effect on platelets. No changes in hematological parameters were observed in a child ingesting phosphorized cod liver oil (0.083 mg/kg/day phosphorus) for 184 days (Sontag 1938). Anemia and leukopenia were observed in individuals occupationally exposed to white phosphorus chronically (Ward 1928). It is likely that workers were exposed by the inhalation, oral, and dermal routes. Because there is very little consistency regarding the length of time that elapsed between ingestion and measurement of hematological parameters and the doses cannot be calculated, it is difficult to compare the results of different studies. There is insufficient information to determine whether white phosphorus has a direct effect on erythrocytes and/or leukocytes. The effects observed may be secondary effects. The decrease in erythrocyte, hemoglobin, hematocrit and leukocyte levels may be secondary to hemorrhaging or hematoemesis (Diaz-Rivera et al. 1950; Rubitsky and Myerson 1949) and the increase in erythrocytes and hemoglobin may be a compensatory mechanism due to tissue anoxia. However, since red blood cell synthesis takes 3-5 days, the observed effects may be direct if they are occurring within l-2 days. A slight decrease in hemoglobin levels and increase in eosinophil levels were observed in a 30-year-old man who performed magic shows that involved placing white phosphorus pellets in the mucobuccal folds of his mouth for 15 years. He had no other personal habits that might adversely affect his health except for occasional bidi smoking for about 8 years (Jakhi et al. 1983). Information on hematological effects in animals is limited to one study in which a marked increase in total leukocyte levels and the percentage of monocytes were observed in a guinea pig acutely exposed to 0.9-2.4 mg/kg/day of white phosphorus in a complex dosing regimen (Lawrence and Huffman 1929). The study authors did not specify at which doses the effects occurred. Musculoskeletal Effects. Following ingestion of a fatal dose of rat poison containing white phosphorus by a woman, autopsy revealed fatty infiltration of essentially all tissues, including the musculature (Wertham 1932). Similar effects were reported following the death of a male child who accidentally ingested a firecracker containing white phosphorus; autopsy revealed fatty deposition in many tissues, included the diaphragmic muscle (Humphreys and Halpert 1931). Humans occupationally exposed to white phosphorus probably ingested some airborne white phosphorus. In a study of 71 humans occupationally exposed to white phosphorus, oral exposure to white phosphorus via hand-to-mouth activity was likely because the workers constantly handled a paste containing 4-6% white phosphorus and washroom facilities were inadequate (Ward 1928). In workers exposed to white phosphorus for intermediate durations, 2 of 44 developed phossy jaw, described as slight necrosis in the lower jaw. In workers exposed to white phosphorus for chronic durations, 12 of 27 developed phossy jaw, with necrosis ranging from slight to severe; 2 of the 12 workers developing phossy jaw died from complications related to the necrosis. The progression of the disease was similar in the cases described, usually beginning with the extraction of one or more teeth, poor healing of the socket, followed by necrosis of tissue in the jaw with severe pain and infection. Treatment consisted of repeated removal of destroyed bone tissue and teeth, draining of abscesses, and reconstructive surgery. In severe cases, extensive removal of necrotic bone tissue led to permanent disfigurement. However, exposure levels of white phosphorus were not reported (Ward 1928). Case reports of development of phossy jaw following intermediate or chronic occupational exposure to unreported levels of white phosphorus and phosphorus compounds describe a similar progression of symptoms, with similar results; even in cases of early diagnosis and prompt, intensive treatment of phossy jaw, recovery often took several years (Heimann 1946; Hughes et al. 1962; Kennon and Hallam 1944). It is likely that the effect of white phosphorus in the oral cavity is local, resulting from contact of “inhaled”white phosphorus particles with tissue in the mouth. White phosphorus may affect the oral mucosa. Dull, red spots in the oral mucosa, an early sign of phossy jaw, have been reported to precede its development in occupationally exposed workers (Kennon and Hallam 1944). The oral mucosa of workers exposed to white phosphorus has been described as having a dull, red, unhealthy appearance (Hughes et al. 1962). Exposed bones may be especially susceptible to the irritating affects of white phosphorus. It is not known whether white phosphorus ingested and absorbed into the systemic circulation contributed to the development of phossy jaw. Not all workers exposed to white phosphorus for longer-term durations developed phossy jaw. In a study of 71 workers exposed to airborne white phosphorus for intermediate or chronic durations, 4.5% and 44%, respectively, developed phossy jaw (Ward 1928). Forty-eight male workers with exposure to white phosphorus ranging from 1 to 17 years were found to be normal and healthy with regards to many parameters, including serum levels of calcium and phosphorus, and bone density; none of the men developed phossy jaw (Hughes et al. 1962). Tooth loss often precedes and accompanies the progression of development of phossy jaw (Heimann 1946; Hughes et al. 1962; Kennon and Hallam 1944; Ward 1928). Tooth loss during the later stages of phossy jaw clearly results from destruction of the-bone structure supporting the teeth (Heimann 1946; Hughes et al. 1962; Kennon and Hallam 1944; Legge 1920; Ward 1928). It is not known if tooth loss prior to diagnosis of phossy jaw or early in the development of the condition is related to the white phosphorus exposure. Poor dental hygiene alone can result in tooth loss, and in several case reports some of the workers were described as having poor dental hygiene (Kennon and Hallam 1944). Tooth loss followed by poor healing of the socket often precedes development of the necrosis (Heimann 1946; Hughes et al. 1962; Kennon and Hallam 1944; Ward 1928), suggesting that poor dental hygiene and exposure to white phosphorus may both be contributing factors to the development of phossy jaw. In a case report, five men developed “precursor signs” (delayed healing of extracted tooth sites and residual sepsis) of phossy jaw developed following tooth extraction and occupational exposure to white phosphorus (Hughes et al. 1962). However, the condition did not develop into “classical” phossy jaw. A man was repeatedly exposed to white phosphorus pellets, placed in the right mucobuccal cavity for magic shows, for . 15 years (Jakhi et al. 1983). After . 14.5 years of this type of exposure to white phosphorus, right maxillary molars became loose, and were subsequently lost. This was followed by a lack of healing and development of fistulae in the sockets of the right maxillary molars. White phosphorus necrosis of the jaw developed, with massive necrosis of the maxilla and floor of the antrum on the right side of the mouth; perforations were present through which the maxillary sinus and nasal cavity were visible. No effects were observed on the left side of the maxilla or on the mandible. Radiographs revealed no evidence of pathology in the chest and long bones. The damage to the jaw was probably caused by direct local contact of phosphorus with the soft tissue and bone in the oral cavity. No microscopic or histological abnormalities were observed in the bone of rats treated by gavage with 0.075 mg/kg/day for 204 days (IRDC 1985). Rats exposed for a chronic duration to 0.2 mg/kg/day white phosphorus in the diet had epiphyseal line thickening and greater extension of trabeculae into the diaphysis of unspecified bones, compared to a control group (Fleming et al. 1942). This study is limited by the failure to specify incidences of effects at interval during dosing and by the failure to state the dosing duration explicitly. Bone effects were observed in children (Compere 1930a; Phemister 1918; Sontag 1938) and young animals (Adams 1938a, 1938b; Adams and Sarnat 1940; Whalen et al. 1973) following acute and intermediate oral exposure to white phosphorus. Because white phosphorus-related effects were observed in growing bones, these effects were considered developmental effects, and are discussed in. Section 2.2.2.6. Hepatic Effects. Hepatic effects have been observed in most individuals accidentally or intentionally ingesting a single dose of white phosphorus. These effects include jaundice (Caley and Kellock 1955; Diaz-Rivera et al. 1950, 1961; Ehrentheil 1957; Greenberger et al. 1964; Humphreys and Halpert 1931; McCarron et al. 1981), hepatomegaly (Diaz-Rivera et al. 1950; Fletcher and Galambos 1963; Humphreys and Halpert 1931; Rao and Brown 1974; Simon and Pickering 1976; Wechsler and Wechsler 1951), increased levels of serum bilirubin (Caley and Kellock 1955; Fletcher and Galambos 1963; McCarron et al. 1981; Pietras et al. 1968), impaired liver function test results (Fletcher and Galambos 1963; Newburger et al. 1948; Pietras et al. 1968; Rubitsky and Myerson 1949), and increases in AST, ALT, and/or lactate dehydrogenase (Ehrentheil 1957; Matsumoto et al. 1972; McCarron et al. 1981; Pietras et al. 1968). In addition to these effects, autopsies or liver biopsies have revealed a number of histological alterations in these individuals. Necrosis (Fletcher and Galambos 1963; Rao and Brown 1974; Wechsler and Wechsler 1951), degeneration (Dwyer and Helwig 1925; Greenberger et al. 1964; Wechsler and Wechsler 1951), fibrosis (Greenberger et al. 1964), hemorrhages (Wechsler and Wechsler 1951), and fatty infiltration (Dwyer and Helwig 1925; Hann and Veale 1910; Humphreys and Halpert 1931; Wertham 1932) have been observed in the liver. In addition to these effects, altered prothrombin time or level has been observed in a number of individuals ingesting a single dose of white phosphorus (Caley and Kellock 1955; Dathe and Nathan 1946; Ehrentheill957; Fletcher and Galambos 1963; McCarron et al. 1981). Prothrombin and other plasma proteins that are required for the efficient progression and regulation of blood coagulation are primarily synthesized in the liver. A deficiency of these proteins is often observed in individuals with severe liver disease. A prolongation of prothrombin time is in part due to this impaired synthesis. Liver function tests were normal in workers chronically exposed to unreported levels of airborne phosphorus (Hughes et al. 1962). Similar hepatic alterations have been observed in animals acutely exposed to white phosphorus. Increases in AST and ALT levels (Paradisi et al. 1984), impaired liver function tests (Ghoshal et al. 1969; Hurwitz 1972; Sigal et al. 1954) increased liver weight (Ghoshal et al. 1969; Seakins and Robinson 1964), increased hepatic triglyceride levels (Ghoshal et al. 1969; Pani et al. 1972; Paradisi et al. 1984; Seakins and Robinson 1964), decreased protein synthesis (Barker et al. 1963; Seakins and Robinson 1964), disaggregation of polyribosomes (Pani et al. 1972), fatty degeneration (Ghoshal et al. 1969) and necrosis (Ghoshal et al. 1969) have been observed. No NOAEL values for hepatic effects following acute animal exposure were identified. In rats, the LOAEL value for liver effects was 6 mg/kg (Barker et al. 1963); in mice it was 5 mgkglday (Hurwitz 1972); and in dogs it was 0.2 mg/kg/day (Sigal et al. 1954). The liver effects occurred shortly after dosing; 3 hours after dosing, a significant decrease in protein synthesis was observed in the liver (Barker et al. 1963), minimal hepatocytic fatty changes were observed after 4 hours (Ghoshal et al. 1969), and severe hepatocytic fatty changes were observed after 12 hours (Ghoshal et al. 1969). The following hepatic effects have been observed in animals orally exposed for an intermediate duration fatty infiltration in guinea pigs exposed to 0.75 mg/kg/day (Ashbum et al. 1948), presence of eosinophilic granules at 0.25 mg/kg/day and cirrhosis at 0.66 mg/kg/day in rabbits and guinea pigs (Mallory 1933), and fibrosis and cirrhosis in pigs exposed to 0.6 mg/kg for 5 days/week (Peterson et al. 1991). In the Peterson et al. (1991) study, no liver effects were observed after 4 weeks of exposure; after 8 weeks, there were early signs of fibrosis, and after 12 weeks, extensive fibrosis was observed. Exposure to 0.075 mg/kg/day for an intermediate duration resulted in slight-to-moderate liver necrosis in dying pregnant rats (Bio/dynamics 1991), but no hepatic effects in the surviving pregnant rats or in male rats (Bio/dynamics 1991). In another reproduction study, liver effects were not observed in dying pregnant rats exposed to 0.075 mg/kg/day (IRDC 1985). Both studies used similar exposure protocols and similar vehicles; the difference in the occurrence of liver damage between the studies cannot be explained. Renal Effects. Evidence of severe renal effects have been observed in a number of individuals intentionally or accidentally ingesting a single dose of white phosphorus contained in rat (or roach) poison or fireworks. Proteinuria (Matsumoto et al. 1972; Pietras et al. 1968; Rao and Brown 1974), albuminuria (Dathe and Nathan 1946; Diaz-Rivera et al. 1950; Dwyer and Helwig 1925; Fletcher and Galambos 1963; McCarron et al. 1981; Rubitsky and Myerson 1949), acetonuria (Pietras et al. 1968), increased urobilinogen (Matsumoto et al. 1972), oliguria (Dathe and Nathan 1946; McCarron et al. 1981; Rao and Brown 1974), increased blood levels of urea and/or nitrogen (Diaz-Rivera et al. 1950, 1961; McCarron et al. 1981; Newburger et al. 1948; Pietras et al. 1968; Rao and Brown 1974; Rubitsky and Myerson 1949), and increased blood creatinine levels (Dathe and Nathan 1946; McCarron et al. 1981) have been observed in these individuals. Renal insufficiency may be due to a direct toxic effect of phosphorus on the kidneys or to acute renal tubular necrosis from fluid loss and shock. Patients in shock may have a peculiar pallor and cyanosis. These probably reflect extensive cellular damage with poor perfusion of the capillary beds, and are a prognostic sign of serious health effects (Melamon et al. 1981). Several case reports have reported no alterations in kidney function (Ehrentheil 1957; Fletcher and Galambos 1963; Greenberger et al. 1964; Simon and Pickering 1976). Histological alterations have also been observed in a number of humans ingesting a single dose of white phosphorus. Fatty changes in the tubules and loop of Henle (Dwyer and Helwig 1925; Humphreys and Halpert 1931; Wertham 1932) and engorged glomeruli and intratubular capillaries (Wechsler and Wechsler 1951) have been observed. Because most individuals vomited shortly after ingesting the white phosphorus or were lavaged, accurate doses cannot be calculated except for one study (Harm and Veale 1910). Histological alterations in the kidney were observed in an individual ingesting 2 mg/kg/day, but the lesion was not described. Creatinine levels were similar among unexposed workers and workers exposed to white phosphorus for chronic durations (Hughes et al. 1962). In animals, fatty infiltration in the nephron and subcapsular hemorrhages were observed in dogs acutely exposed to an unspecified amount of white phosphorus (Dwyer and Helwig 1925). No renal effects were observed in rats exposed to 0.075 mg/kg/day for an intermediate duration (Bio/dynamics 1991; IRDC 1985). No chronic exposure animal studies examining renal effects were located. Dermal Effects. Transient toxic dermatitis (described as a scalartiniform rash) developed 9 days after a man ingested a near-fatal dose of rat poison (Dathe and Nathan 1946). Edema of eyelids was reported in a 13-month-old child after ingestion of a fatal dose of white phosphorus (Rao and Brown 1974). Subcutaneous hemorrhages were visible in the left foot in a woman after consumption of 3.9 g of rat poison containing 4% phosphorus (Hann and Veale 1910). The woman died 4 days after the initial poisoning. At this time, an enormous subcutaneous hemorrhage was visible below the waist line. In this case report, the woman apparently did not expel (via vomiting) any of the ingested dose. Thus, it is likely that the ingested dose (2 mg/kg) was representative of the effective dose. Scattered blue-green petechiae were observed on the abdomen of a male child following accidental ingestion of a fatal dose of white phosphorus mixed with other ingredients from a firecracker (Humphreys and Halpert 1931). The dose level in this study could not be determined; the firecracker was a red composition of phosphorus mixed with other ingredients and was thought to contain about 10% phosphorus (Humphreys and Halpert 1931). No studies were located regarding dermal effects in animals after oral exposure to white phosphorus. Other Systemic Effects. A number of other systemic effects have been observed in humans ingesting a single dose of white phosphorus. The effects that are observed most consistently are hypoglycemia (Diaz-Rivera et al. 1950; McCarron et al. 1981; McIntosh 1927; Wechsler and Wechsler 1951), an increase in body temperature (mild pyrexia or fever) (Dathe and Nathan 1946; McIntosh 1927), and a decrease in plasma calcium, potassium, and/or sodium levels (Caley and Kellock 1955; McCarron et al. 1981; Rao and Brown 1974). It is unclear whether the fever seen is a symptom of phosphorus poisoning or a result of the treatment involved. In addition to these effects, metabolic acidosis (Rao and Brown 1974), hypothermia (Simon and Pickering 1976), damage to the spleen (Greenberger et al. 1964), ascites (Fletcher and Galambos 1963), fatty infiltration of the pancreas (Humphreys and Halpert 193 l), and necrosis of the adrenal medulla and cortex (Wechsler and Wechsler 1951) have been observed. In a child ingesting 0.083 mg/kg/day white phosphorus for an intermediate duration, decreased appetite, impaired body weight gain, and poor turgor (fullness or tension produced by the fluid content of blood vessels, capillaries, and cells) were observed (Sontag 1938). Serum glucose levels were decreased in workers occupationally exposed to white phosphorus for a chronic duration. It is likely that the workers were exposed by the inhalation, oral, and dermal routes (Ward 1928). In dogs acutely exposed to an unspecified amount of white phosphorus, hypoglycemia was observed (Williamson and Mann 1923). Rats received intermittent exposure to the atmosphere in the furnace room of a phosphorus factory for 14 months (Ruzuddinov and Rys-Uly 1986). Histology of rats killed monthly revealed progressive morphological degeneration of the tongue and oral mucosa of the cheek, gum, and hard palate. Epithelium and connective tissue from different parts of the oral cavity responded similarly to the treatment. Changes in the epithelial layer, observed after only 1 month of exposure, included increases in keratinization and numbers of cell layers, resulting in thickening and hyperkeratosis in the epithelium of the mucosa. Over time, the thickening and hyperkeratosis in the epithelium increased and histological changes were observed in the subepithelial connective tissue base. Eventually, the oral cavity contained areas of thickening of the mucosa from hyperkeratosis and increased epithelial cell layers interspersed with areas of decreased thickness of the epithelial layer due to atrophy, dystrophy, and cellular necrosis. At this time, adverse changes in the subepithelial connective tissue were considered pronounced. These effects occurred in most of the animals exposed to the atmosphere. It is likely that the observed effects of phosphorus on the oral cavity were local rather than systemic, resulting from direct contact of white phosphorus with tissues in the mouth. The study presented essentially no quantitative data, and the types and exposure levels of chemicals in the atmosphere (thought to contain elementary phosphorus and its inorganic compounds) were not reported (Ruzuddinov and Rys-Uly 1986). 2.2 DISCUSSION OF HEALTH EFFECTS BY ROUTE OF EXPOSURE
https://w.atwiki.jp/cheapugg058/pages/17.html
" On top of that, she looks pretty damn good for being in her 50s These cause three putt disasters and can become very frustrating!There are all varieties of golf swing tips out there to be found Buying US Open tennis tickets was a little challenging Infact, if I remember well, I was able to make the software download instantly in less than 1 minute The onus will be on them this season to try and get quarterback Matthew Stafford to finally last a full year healthy Some of them are already well-covered by bloggers, and others there is more leewaybut that s for another entry The receiver is the device that translated the electromagnetic waves into images and sound Many of these [[Tony Gonzalez Jersey http //www.falconsofficialonline.com]] are made in advance and transported to the party The cell phones and accessories will cover every area of wall space that is available, and it is quite an over-whelming sight to experience Fruta Planta is a Chinese diet pill manufactured by a China-based health company called Guangzhou Health Care They are performed at Chinese New Year, the August moon Festival and other celebratory occasions for good luck One can use the same cue stick to play any versionditto204608457020678144 {background #5AD2D8 urlart, let s take a look at the where and the whenIn all the main forms of modern billiards--American pool, English snooker, and carom billiards--the cue or cue stick is really the only equipment that carries directly over from one game to the otherWorkaholicsNew Episodes May 2012The Derswww [Via EFF Knots- This game is twister on the iphone These work by suspending power to the 12 Volt accessories being used when the battery voltage drops favorite span {background-position -32px 2px;} pTwo days later, the situation was apparently repeated, and this time the player was confined to a room that is often used as a media room by visiting teams Their stock is quite amazing too, because they will have every cell phone that is being offered in any retailing outlet for miles around, at prices that will astound even the most knowledgeable of cell phone users The bike is provided with freestyle handle bar Then there are the aqua and black guys on the other side of the fielddittoTweet spandittodownarrow {width 0;height 0;border-left 20px solid transparent;border-right 20px solid transparent;border-top 20px solid #EEE;margin 0 0 0 73px;}Follow @CaesarTheJDC This not only saves you a lot of time, but also saves you a whole lot of dish network menu guide difficulty as all the details you need is accessible at one particular area It is also rich in vitamins, minerals and natural antioxidants If you prefer fixed mounted fish finders, the Fishin Buddy line can also be mounted to your craft using the included bracket These horns will produce a loud sound of 120 decibels What has been surprising so far this season has been the New Orleans defense10retweet span {background-position -80px 3px;}span As a solo artist, she recorded great music, with singles like "I Hate Myself for Loving You," "Do You Want to Touch Me," and probably most recognizably, "I Love Rock n Roll -Wikipediatwimg As the Oklahoma native says on her website, "I am a huge football fan, especially when it comes to my hometown Sooners and my Green Bay PackersdittoTweet span The 7-8 monthswithout comeptitive football before the August NFL preseason cultivatesanticipation for the NFL and collegiate football product A screen name can also be referred to as user name north face outlet timestamp a span {display inline-block;width 16px;background-image uJustin Smith Jersey rl(http //images With 266 passing yards and three touchdowns in his first game this season, Sanchez proved he is not going anywhereTackling Drills for FootballTackling drills are made a regular feature by some coaches in a team s practice scheduleWhile most tailgaters party at their hometown stadium, some travel to any game their team playsdittoTweet span For Kim this will be a more difficult marriagemetadata {display block;width 100%;clear both;margin-top 8px;padding-top 12px;height 65px;} p Shaloub gets extra points because he s one of us ? born and raised in Green Bay authorities, including the yellow first down line for NFL broadcasts; he is co-founder of South Swell Sports, which has become a successful San Diego lacrosse league and equipment retailer; and heStevan Ridley Jersey was a finalist for the Ernst and Young Entrepreneur of the Year award 8 hours ago via web·Reply·Retweet·Favorite·powered by @socialdittoFormer NFL linebacker Junior Seau was found dead at his home yesterday of an apparent self-inflicted gunshot wound to the chest www.michaelkorsoutletob.com
https://w.atwiki.jp/mrfrtech/pages/123.html
Market Scenario Market Research Future said despite difficulty suppressing the new coronavirus will result in substantial economic rise for the Global Infrastructure as a Service (Iaas) Market, including a possible double dip in economic activity. As per the analysis done on COVID-19 impact analysis, the market has the potential to show enormous growth at a rate of ~23% CAGR. With this, the market shows the capability of reaching a towering valuation of USD ~ 59 Billion by 2023. The growth period has been approximating from the years 2017 to 2023. COVID-19 Analysis Novel coronavirus has Infrastructure as a Service Industry to open new avenues for those firms that are on the lookout for solutions that are reliable, efficiently managed, scalable, and are subscription-based, to remain more focused on the core business. The Global Infrastructure as A Service (IaaS) Market is bearing lesser impact of the COVID-19 outbreak compared to most other segments of the tech world. In a nutshell, COVID-19 impact on managed services has been fruitful, with the market growth enhanced than before. Given the prevalent lockdown situation, managed services vendors are now investing heavily in remote-centric worker solutions, which can make the market highly resilient in the coming years, even as the world is currently rushing to achieve a COVID-19 breakthrough. Request a Free Sample @ https //www.marketresearchfuture.com/sample_request/5910 Competitive Outlook The outstanding players in the global Infrastructure as a Service (IaaS) market include Google LLC (U.S.), Amazon Web Services Inc. (U.S.), International Business Machines Corporation (U.S.), Microsoft Corporation (U.S.), HCL Technologies Limited (India), Accenture (Republic of Ireland), Cisco Systems Inc (U.S.), VMware, Inc. (U.S.), Computer Sciences Corporation (U.S.), Oracle Corporation (U.S.), Rackspace Inc. (U.S.), and Fujitsu Ltd (Japan). Segmentation The study of infrastructure as a service (IaaS) market includes segmentation, which is done over the segments of deployment type, solution, end-user, and verticals. The solution segment is sub-segmented as storage as a service, managed hosting services, disaster recovery as a service, network management, high-performance computing as a service, and content delivery services. Among these, storage as a service is further sub-segmented into network-attached storage and storage area network-based storage. The deployment type market has included public cloud, private cloud, and hybrid cloud. The end-user segment includes SMEs and large enterprises. The verticals segment has included BFSI, IT telecom, retail, healthcare, e-commerce, government defence and among others. Regional Analysis The study of global infrastructure as a service (IaaS) market has covered across regions including Asia Pacific, Europe, North America, and Rest of the World. North America IaaS market led the global demand owed to the incidence of extensive IT infrastructure, thus mounting the demand for IaaS. Innovations in software development and the introduction of several cloud-based solutions can be accredited to the market ascendancy in this region. The Asia Pacific is proposed to witness a noteworthy growth rate over the anticipated period and is likely to lead the Infrastructure as a Service Industry over the assessment period. Table of Contents 1Executive Summary 2Scope of the Report 2.1Market Definition 2.2Scope of the Study 2.2.1Research objectives 2.2.2Assumptions Limitations 2.3Markets Structure Continued…. Browse Full Report Details @ https //www.marketresearchfuture.com/reports/infrastructure-as-a-service-market-5910 List of Tables Table 1 Global Infrastructure As A Service Market By Region, 2020-2027 Table 2 North America Infrastructure As A Service Market By Country, 2020-2027 Table 3 Europe Infrastructure As A Service Market By Country, 2020-2027 Continued… List of Figures FIGURE 1 Global Infrastructure As A Service Market Segmentation FIGURE 2 Forecast Methodology FIGURE 3 Five Forces Analysis Of Global Infrastructure As A Service Market Continued… View Similar Report** Identity Access Management Business https //writeonwall.com/identity-access-management-business-industry-trends-key-players-with-product-particulars-applications-future-trend-business-growth-market-size-key-players-update-business-statistics-and/ Mobile Banking Market Research https //writeonwall.com/mobile-banking-market-research-industry-trends-key-players-with-product-particulars-applications-future-trend-business-growth-market-size-key-players-update-business-statistics-and-forecast-t/ About Market Research Future Market Research Future (MRFR) has created a niche in the world of market research. It is counted among the top market research companies that offer well-researched and updated market research reports and insights to businesses of all sizes. What sets us apart is our super-responsive team that offers quality work keeping clients abridged of the prospective challenges and opportunities in various markets. Our team is adept in their space as well as patiently listens to every client. The best part is they know their work inside out and possess the expertise to guide the client in the right direction and achieve results on a tight deadline. We are a one-stop solution for all your data research needs. Our team does not believe in the “one size fits all” approach to creating a report that is detailed and concise. We handle 13 industry verticals including Healthcare, Chemicals and Materials, Information and Communications Technology, Semiconductor and Electronics, Energy and Power, Food, Beverages Nutrition, Automobile, Consumer and Retail, Aerospace and Defense, Industrial Automation and Equipment, Packaging Transport, Construction, and Agriculture. With our unique approach for every market report, we aim to reach the zenith in qualitative business intelligence and syndicated market research. Contact Market Research Future (Part of Wantstats Research and Media Private Limited) 99 Hudson Street, 5Th Floor New York, NY 10013 United States of America 1 628 258 0071 (US) 44 2035 002 764 (UK) Email sales@marketresearchfuture.com Website https //www.marketresearchfuture.com
https://w.atwiki.jp/fffkindle1212134/pages/38.html
Code Geass 23. At Least with Sorrow I, Euphemia li Britannia, bid all of you within the sound of my voice to heed the following command Seek out any Japanese you can find, and please kill them! Leave not a single one of them alive! STAGE 23 AT LEAST WITH SORROW Euphemia has betrayed us here! All units, descend upon the stadium! Grind the Britannians to dust! Damn you, Euphemia! You deceived us! DAMN ELEVENS! Now I see. You were planning this all along! The Black Knights! Crush the Britannians! Euphy! Euphy, where are you?! Get away from me! I don t have time to waste on you! Oh my! This is turning into a mess. How dare you... trampling over the hopes of our people! Euphemia! Stop it! Are you Japanese? You dare raise a hand against Euphemia li Britannia? Huh? Ah-ha, so there you are... you ridiculous royal puppet. Oh, you were on that island, weren t you? Yeah! Now suffer the hand of vengeance and-- Wait! I ll deal with her. You defiant Japanese! Now what, Zero? Do we take her prisoner? There s no point. Leave her. I have to kill them all! These Japanese people -- they have to die! It jammed up... I have to... hurry! I think it goes in here. Oh, I thought you were one of them. So, I was thinking, we could run the Specially Administrated Zone of Japan together. Oh, wait... Japan? Yes. I would ve like that. You and I together... Euphy... Lelouch... why? Farewell, Euphy. You may have been the first girl I ever loved. NOOOOOOO! Suzaku! Why now, of all times?! I m no match for that Hadron Cannon! I will never allow you to kill Lelouch! Suzaku! GET OUT OF MY WAY!!! Arrg, damn it! Please! You have to save Euphy! Do something! You mustn t let her die! You still haven t made contact with Darlton?! No, Your Highness. There was a report he d been injured, but nothing beyond that. Viceroy, emergency message from the Avalon. From the Avalon? Yes. The Special Zone at Fuji has fallen to the Black Knights. What was that?! They re moving to intercept our forces. Also... Princess Euphemia... "Equality?!" You can shove that straight up your administrated ass! You lured us into a death trap! You just made the biggest mistake in your lives! You got that?! That s right! Don t screw with the Japanese! Lucked out, didn t we? I can t believe they left all these footage and equipment behind. Yes. Once we re done editing, we can throw it on the Net for the entire world to see. It s pretty clear which side justice is on. How curious. You don t feel any loyalty toward Britannia, do you? Loyalty? Mmm-hmm. Britannia s glory has ripened on the vine; my talents are wasted serving them. You re more of an honest man than I thought you were. And what will you do now? Hard to say. The only reason I came here was to gather data. But I d feel bad abandoning you all, and I find Zero so... amusing. How wonderful to finally meet you! This girl -- she s a relative of Suzaku s. Zero, are you prepared to walk beside us in what s to come? The opposite! From this point on, the Six Houses of Kyoto will be under my control! I won t hear any objections! All other paths of survival for you... have now vanished! We should inform Viceroy Cornelia. Don t worry, I ll be taking care of that. Will she last until we reach the bureau? I m afraid not. I ll contact Prince Schneizel then. Excuse me. Suzaku... Euphy! Euphy... I have to know -- why did you issue that order at the stadium? Order...? What are you talking about? Never mind that... Suzaku... you re Japanese, aren t you? Yeah? Euphy! No! I mustn t-- I--I can t even think such a thing! No, please...! Suzaku? Yes, Euphy? The ceremony... did it go all right? Is Japan okay...? Euphy... don t you remember? People of Japan and all who are oppressed by the empire of Britannia! Long have I waited, all through the struggles against Britannia s injustices, I ve waited for them to come to their senses! But that hope was betrayed, by an act of barbarism that can only be called a genocide! How about everyone that was there? Are the Japanese happy? Never forgive Euphemia! She s a murderer! She s a filthy witch! Liar! Euphemia is the symbol of Britannia s hypocrisy -- a murderer cloaked in the flag of a nation! How was the ceremony...? Do you think I did... okay? I hope that bitch burns in hell! We re finished with your lie! Death to them all! Euphy... the Special Zone is... a great success! The Japanese people were given back their home... and you did it! Oh, thank God... I hereby declare our independence from Britannia! But don t take this to mean the resurrection of your fallen nation! We will not turn back the hands of time! The new Japan we go on to build shall be one broad enough to accept all peoples, histories, and ideologies where the strong shall not reign over the weak! And it shall be called... THE UNITED STATES OF JAPAN! He s done it! This is the birth of a nation! How strange... I can t see... your face anymore... Keep going... to school... I had to stop... before I-- before I had the chance to finish... Euphy, you can still go yourself! I know! Why don t we go to Ashford Academy together? The student council is so much fun! Euphy...! You have to do it... for me... kay? Please, Euphy! No, don t go! Suzaku... I m so happy... that we... Zero! Zero! Zero! Zero! Dear God... Area Fukushima, Byakko Squad, en route to lbaraki. Area Tama, continuing with barricade construction. Area Hamamatsu-- You plan to assault the Tokyo Settlement? Yes. This is the best chance we ll get. Don t worry about it -- your Geass has no effect on me. You know that, don t you? That s true, isn t it? Hmph, with my Geass out of control now, I can never see anyone. Yes, Nunnally? Hi Lelouch. I was wondering, um... do you suppose I could talk to Euphy again? I was thinking that the three of us could go to the school festival together. You see, Milly said they were organizing another one since everything got all messed up the other day. So I was hoping that we could go to the new one together too. Oh, I m sorry... I know you don t want us meeting ever again. But I thought maybe, if there was some way you and I could maybe see her just one last time... Nunnally, haven t you heard the news? Oh, well, the radio cut off mid-broadcast earlier. Why do you ask? Did something happen? Of course not. Everything is just fine. Sorry. I ll be home by tomorrow. We ll discuss it when I m back. Right. All right, so you can t switch off your Geass -- are there any changes you ve noticed? Not really. It s just... Euphy... she tried to resist the Geass... and my orders... I was wondering if my power had weakened... but I think... I think such a malignant command was simply against her nature. And so? I guess that s all. It was something... We have our contract. I promised to stay with you... to the very end. We weren t fast enough! We may have managed to keep the news off the Net, but there s insurrections all over the map! That s correct! The Black Knights are the largest of the insurgent groups. They are now absorbing all of the masses and advancing on the Tokyo Settlement! All our units are in play right now. We re completely on our own! Yes, and with so many honorary Britannians turning on us, our enemies number in the tens of thousands! Lord Guilford! Forget it! We cannot move without Her Highness word! But sir! The viceroy s been shut up in Princess Euphemia s room ever since she canceled the attack orders! And we still can t confirm Gen. Darlton s whereabouts. Everyone in Toyama Squad is at your disposal. Roger that. Any weaponry? Some explosives from Gokayama. But we don t have enough vehicles. Can any of us ride with you? The best we can offer are freight trains. That okay? Looks like the groups from Yamanashi joined up with us. Yeah, and the remnants of the Blood of the Samurai faction too. Our numbers are growing by the minute! I hope everyone in the student council can get away. On the contrary, for the first time in a while I m glad. Yes... I forgot the art of kindness ages ago, Marianne. I hope you re all right, Kaname. You re working in Shizuoka now, right? Yeah, I m fine over here. Look, Chigusa, we need to talk about something important when I get back. Hm? What s wrong? Well, that s the first time you ve called me by that name. Oh, you re right. Does it sound weird? Not a bit! Anyway, I ll be here. There she is -- that Brit woman! Watch us from your window, huh?! Admit it -- you re some sort of spy! As the insurgents draw closer, security in the ghettos continues to worsen. The government is asking all citizens to stay in their homes until further notice. Do you think the fighting will come our way as well? O--of course not! Princess Cornelia has her regular forces stationed here. There s no way! I hope so... Geez, back up, will you? You re scaring me. Nunnally, what about Lelouch? Is he back here yet? Lelouch? Is something the matter? No, not really... Man, I wish you d go back to calling him Lulu. It s time you two made up. Lulu? What, you mean I called him that? Oh, there you go again. Lulu... Nina, they want us upstairs in school! The insurgents are headed toward Tokyo! Right. And Zero s coming, isn t he? Please... wait for me, Princess Euphemia. I ll avenge you, I swear! Euphy... I just don t understand. Why did you give that order? Shall I tell you? Huh? A child? How did you get on board? How do you do, Suzaku Kururugi. You may call me V.V. V.V.? They ve broken the Atsugi line as well! Maybe the homeland can help us! They ll never make it in time. Then we should evacuate this area right away! Don t panic! Huh?! P--Princess Cornelia! I ve put the Glaston Knights on standby. Place all our forces on the outskirts of Tokyo! We can end this! We just need to take down Zero! Kill Cornelia, and the day will be ours! You all have your orders! Now be ready! Diethard, have Tohdoh handle the front line. I m leaving you in charge here. Yes, very well, Zero. You re Sumeragi s... Thank goodness I made it in time! That was so mean of you, the way you headed off to the battle without me! I ve been a huge fan of yours ever since your big debut! I was hoping that I d finally get to talk to you. Wow, you re really tall, aren t you? Don t worry though, I ll catch up with you pretty soon! L--Lady Kaguya, I thought the heads of the Six Houses remained in Fuji. I followed after you! So I can watch my future husband fight. Don t joke around. Well, once you win this battle, you ll eventually need a wife, won t you? I mean, I know your identity is a big secret and all, but you re gonna need somebody as your public face, right? Really? You believe we re going to win this battle? Of course! I am the goddess of victory after all. I d be lucky to have you then. Unfortunately, I ve already made a contract with the devil. Huh? I have no room in my life for deities right now. Hurry! We have to get this experimental subject back to the homeland! The pressure! The internal pressure is rising! Now, of all times...! Good morning to you it was. Hear me, Britannia! This is Zero! A rebel against oppressors who abuse their power! We will wait until midnight. You have until then to surrender to me. This is your only warning -- heed it. Twelve midnight, not a single second later. Gen. Darlton, you re in no condition to do this! I don t care! I have to be... at Her Highness side...! Your little bluff is meaningless, Zero. The Tokyo Settlement is an impenetrable fortress. You can still turn back, you know. Your actions here will affect more than just Area 11. You -- and this entire world -- will be steeped in war. I m aware of that, and yet all the same. Euphy? How could that be possible? No... it must be an impostor. Lelouch, it s me. Suzaku... why are you calling me now? Lelouch... are you at the school? No, but I will be soon. I see. I called because there s something I want you to tell everyone for me. Yes, and what would that be? The sky -- make sure no one looks up the sky. What? Lelouch... is there anyone you could ever hate so much that you d actually want to kill them? There is. Yes. I used to feel that sort of thinking was unacceptable -- that unless you followed the rules, killing someone was just murder. But now... it s hatred that s guiding me. I m fighting to kill someone. I m going to become a murderer in the skies of Tokyo, so please... Embrace your hate. Just think of Euphy. I made my own mind up long ago -- I ve no intention of turning back. For Nunnally, you mean. Yes. I have to go now. Thank you, Lelouch. Forget about it. I mean, you and I are friends after all. For the last seven years. Right. See you then. Yeah, later. What the hell?! These hands of mine have been dirty for a long time now, Suzaku. Your coming to face me now doesn t matter at all -- hell, I welcome it even. I mean, of course, you and I are friends... Perhaps this is what I ve longed for ever since that day the destruction and loss of everything. That s right -- destruction always comes before creation, and for that goal, even my own conscience must be cast aside. The only path left to me is straight ahead. Now then... That s right -- only by pushing forward will I find atonement. Even if my enemy is the greatest empire on the planet, there s no turning back for me now! Everything is in place. The time has come to overthrow the old world order!
https://w.atwiki.jp/pipopipo777/pages/29.html
TOXICOLOGICAL PROFILE FOR WHITE PHOSPHORUS -index 2 HEALTH EFFECTS 2.2 DISCUSSION OF HEALTH EFFECTS BY ROUTE OF EXPOSURE 2.2.2 Oral Exposure -3 2.2.2 Oral Exposure(2.2.2.0 preface) 2.2.2.1 Death 2.2.2 Oral Exposure -22.2.2.2 Systemic Effects 2.2.2 Oral Exposure -32.2.2.3 Immunological and Lymphoreticular Effects 2.2.2.4 Neurological Effects 2.2.2.5 Reproductive Effects 2.2.2.6 Developmental Effects 2.2.2.7 Genotoxic Effects 2.2.2.8 Cancer 2.2.2.3 Immunological and Lymphoreticular Effects There is limited information on the immunotoxicity of white phosphorus; however, there is some information that suggests that the immune system may be a target. Thymic hemorrhages were observed in two young children accidentally ingesting white phosphorus-containing fireworks (Dwyer and Helwig 1925; Humphreys and Halpert 1931). In one of these children, hyperplasia of lymphoid tissue in the intestinal wall and abdominal lymph nodes and hyperplastic lymphoid corpuscles in the spleen were observed (Humphreys and Halpert 193 1). Decreases in leukocyte levels were reported in a number of case reports involving acute ingestion of rat poison or fireworks containing white phosphorus (Diaz-Rivera et al. 1950; Ehrentheil 1957; Fletcher and Galambos 1963; McCarron et al. 1981; Newburger et al. 1948; Pietras et al. 1968). A decrease (Pietras et al. 1968) or an increase in the percentage of polymorphonuclear leukocytes (neutrophils) (McCarron et al. 1981) were also observed in individuals ingesting white phosphorus. Because the individuals vomited shortly after ingesting the white phosphorus and/or received gastric lavage, doses could not be estimated. In workers exposed to an unknown level of white phosphorus via inhalation, oral, and dermal routes, a decrease in leukocyte levels was observed (Ward 1928). No studies were located regarding immunological or lymphoreticular effects in animals after oral exposure to white phosphorus. 2.2.2.4 Neurological Effects A number of case reports of individuals accidentally or intentionally ingesting a single dose of white phosphorus have reported neurological effects. Nonspecific neurological effects including lethargy (Dathe and Nathan 1946; Fletcher and Galambos 1963; McCarron et al. 1981; Rao and Brown 1974; Rubitsky and Myerson 1949; Simon and Pickering 1976; Talley et al. 1972), sleepiness (Dwyer and Helwig 1925; Ehrentheil 1957; McCarron et al. 1981; McIntosh 1927), irritability (McCarron et al. 1981), restlessness (Diaz-Rivera et al. 1950; Ehrentheil 1957; Harm and Veale 1910), and hypoactivity (Humphreys and Halpert 1931) have been observed. Other symptoms of neurotoxicity that have been observed include coma or semi-coma (Caley and Kellock 1955; Ehrentheil 1957; Hann and Veale 1910; McCarron et al. 1981; McIntosh 1927; Wechsler and Wechsler 1951), toxic delirium and psychosis (Diaz-Rivera et al. 1950), hemiplegia (Humphreys and Halpert 1931; McCarron et al. 1981), abnormal reflexes (Wechsler and Wechsler 1951), hyperesthesia (Humphreys and Halpert 1931), coarse muscle fasciculations (Caley and Kellock 1955), unresponsiveness to painful stimuli (Simon and Pickering 1976), and marked asterixis (flapping tremor) (Greenberger et al. 1964). In addition to these overt signs of neurotoxicity, histological damage in the brain was observed in four individuals ingesting a single dose of white phosphorus. Based on this limited information, the types of cellular damage can be grouped into four categories (1) cellular changes resulting from ischemic damage found in the Purkinje cells and cerebral cortical cells of the second and third layer of the cortex (Wertham 1932); (2) direct white phosphorus-induced cellular damage to the dentate nucleus and inferior olives (Wertham 1932); (3) fatty infiltration in the ganglion cells of the cortex, neuroglial cells, Golgi cells of the cerebellum, and the cells in the pia-arachnoid space (Humphreys and Halpert 1931; Wertham 1932); and (4) cerebral edema (Rao and Brown 1974). It is not known if the cerebral edema observed in this one individual was secondary to the other types of damage. A child treated with 0.083 mg/kg/day white phosphorus for an intermediate duration became lethargic 3 months after beginning treatment and remained lethargic until treatment was discontinued .70 days later. Following cessation of treatment, the child recovered very rapidly (Sontag 1938). Overt signs of neurotoxicity were observed in a cat ingesting a single lethal dose (Fry and Cucuel 1969) and in pregnant rats exposed to a lethal dose (0.075 mg/kg/day) of white phosphorus for an intermediate duration (effects only observed during late gestation of parturition) (Bio/dynamics 1991). Tonoclonic convulsions, increased salivation and weakness were observed in the cat (Frye and Cucuel1969), and tremors were observed in pregnant rats (Bio/dynamics 1991). In another developmental toxicity study (IRDC 1985), no signs of neurotoxicity were observed in pregnant rats. All LOAEL values from each reliable study for neurological effects in each species and duration category are recorded in Table 2-2 and plotted in Figure 2-2. Because vomiting occurred or the individuals received gastric lavage shortly after ingestion, reliable dose estimations could only be made for one individual acutely exposed to 2 mg/kg/day white phosphorus (Hann and Veale 1910). 2.2.2.5 Reproductive Effects Extensive uterine hemorrhaging was observed in a 2-month pregnant woman following the intentional ingestion of 2 mg/kg white phosphorus in rat poison (Hann and Veale 1910). Autopsy results showed that the uterus was enlarged containing a hemorrhagic mole, which was consistent with a 2-month pregnancy. No effects on reproductive performance or histological alterations in the ovaries, uterus, testis, or epididymis were observed in rats administered 0.075 mg/kg/day or less in a one-generation reproduction study (Bio/dynamics 1991; IRDC 1985). The highest NOAEL value and all LOAEL values from each reliable study for effects in each species and duration category are recorded in Table 2-2 and plotted in Figure 2-2. 2.2.2.6 Developmental Effects A healthy infant was administered phosphorized cod liver oil (reported to contain 1.1 mg “pure” phosphorus per fluid ounce) from ages l-7 months (Sontag 1938). The phosphorized cod liver oil was apparently administered for the prevention of rickets. The time-weighted average dose for the 6-month exposure was 0.083 mg/kg/day. During the first 3 months of treatment, the child appeared clinically normal and grew at a normal rate. From the ages of .4 to 6 months, the child became clinically ill, gained essentially no weight, and the rate of growth in height decreased from .0.1 to 0.04 cm/day. Following replacement of the treatment with normal, nonphosphorized cod liver oil, the child appeared to recover quickly, and began to grow at a normal rate. Radiograms taken at 6 months of age showed bands of increased density at the end of all the long bones with increased thickness and density also observed in the zones of calcification. Radiograms taken between 9 months and 5 years of age showed bands of increased density in the diaphyses of the long bones, and in the pelvic, metacarpal, and metatarsal bones. This study describes formation of “phosphorus” bands of increased density in the ends of long bones and possible decreased growth in a child exposed to 0.083 mg/kg/day phosphorus for 6 months (Sontag 1938). It should be noted that radiologic densities are common at the growing points of long bones in children. However, lead poisoning, administration of nickel, certain chronic diseases like anemia, and hypervitaminosis D may also produce bands in the ends of bones, but these are much thicker and heavier (Sontag 1938). A child with Perthes’ disease was administered 0.056 mgkg/day of phosphorus for two periods of intermediate duration, separated by a period with no exposure (Phemister 1918). “Phosphorus” bands of increased density developed in the ends in the tibia, fibula, and femur during the two exposure periods, without any improvement in the child’s condition. A male child with dyschondroplasia was administered 0.026 and 0.046 mg/kg/day white phosphorus for 3 and 8 months, respectively. “Phosphorus” bands of increased density developed in the tibia, fibula, and femur. The density and thickness of the bands were greater at the high-dose level and longer-treatment period. A male child with osteogenesis imperfecta was administered 0.078, 0.063, and 0.059 mg/kg/day phosphorus for 26,3, and 18 months, respectively, separated by a period of time with no white phosphorus exposure. Treatment with white phosphorus produced marked changes, including bands of increased density at the ends of bones and increased transverse diameters of the shafts of bones in the legs and arms (Phemister 1918). Four children with moderate to severe cases of rickets were treated orally with 0.110-0.158 mg/kg/day white phosphorus for durations ranging from 64 to 149 days (Compere 1930a). “Phosphorus” bands of increased thickness and density were observed in the long bones of 1 of 2 of the children examined. An arachitic child was treated with 0.119 mg/kg/day white phosphorus for 82 days (Compere 1930b). Following treatment, the child had a “heavy phosphorus line” and increased density of cortices. Treatment with white phosphorus did not generally improve the condition of the bones in children with rickets. Because these children were sickly, the relevance of the observed effects to potential effects of white phosphorus in normal, healthy children could not be ascertained. Young, growing rabbits exposed to 0.3 mg/kg/day white phosphorus given as a pill for an acute duration had transverse bands of increased density in metaphyseal regions of the tibia and fibula, compared to a control group (Adams 1938a). However, the percentage of calcium and phosphorus, and the calcium/phosphorus ratio in the metaphyseal and cortical regions of the right tibia was similar between treated and control animals. Young, growing rabbits exposed to 0.3 mg/kg/day white phosphorus given as a pill for an intermediate duration had average growth of the tibia of 0.27 mm/day, compared to 0.36 mm/day in the control group; however, no statistical analysis of the results was reported (Adams and Samat 1940). One rabbit had histological abnormalities in the tibia including decreased size of epiphyseal cartilage plate, as well as increased density in the metaphyseal zone with trabeculae that were greater in number and extended further into the diaphysis to a greater extent, compared to a control rabbit. The trabeculae were associated with a greater amount of calcified cartilage matrix. These effects probably resulted from a decrease in the normal rate of bone resorption during bone growth, resulting in decreased rate of growth of the tibia. Weanling rats exposed to 1.25 mg/kg/day white phosphorus in the feed for an intermediate duration had widening of the metaphyseal trabeculae, broadened metaphysis, and a slightly convex lateral contour of the proximal tibia, compared to a control group (Whalen et al. 1973). Osteocytes were small and elongated compared to those in the control group, and osteocytic osteolysis and chondrolysis were decreased or missing. In the treated rats, metaphyseal trabeculae extended deeper into the diaphysis than in the controls. These effects probably resulted from decreased bone resorption during bone growth, resulting in widening trabeculae and a denser metaphysis. Very similar results were observed in studies on growing rats (Adams and Sarnat 1940) and rabbits, but not in an adult rabbit (Adams 1938b). In rats, the doses varied from 0.002% to 0.05% yellow phosphorus (Adams and Sarnat 1940) and in rabbits, from 0.6 to 6 mg (Adams 1938b; Adams and Samat 1940). A decrease in the number of viable pups and an increase in the number of stillborn pups was observed in the F1a and F1b offspring of rats exposed to 0.075 mg/kg/day; however, the incidence was not significantly (p 0.05) different from controls (IRDC 1985). These effects were not seen in a similarly designed reproduction study in which rats were administered 0.075 mg/kg/day (Bio/dynamics 1991). Neither of these studies found any significant differences in the occurrence of malformations or anomalies. These NOAEL and LOAEL values from each reliable study for developmental effects in rats are recorded in Table 2-2 and plotted in Figure 2-2. 2.2.2.7 Genotoxic Effects No studies were located regarding genotoxic effects in humans or animals after oral exposure to white phosphorus. Genotoxicity studies are discussed in Section 2.5. 2.2.2.8 Cancer No studies were located regarding cancer in humans or after oral exposure to white phosphorus. In the only chronic duration oral study in animals, no treatment-related histopathological lesions were observed in the lungs or other organs (not otherwise specified) in rats given .1.6 mg/kg/day white phosphorus in the diet for up to 479 days (Fleming et al. 1942). Only six rats per dose group were used. 2.2 DISCUSSION OF HEALTH EFFECTS BY ROUTE OF EXPOSURE
https://w.atwiki.jp/towerunitejp/pages/13.html
地図 ショップ（赤色） ① Sweet Suite Furnishings Horizon Condo 家具店です。主に家具を中心に販売されています。 Rob's IMPORTSに売っていない食器などもこちらにもあります。 また、Horizon Condoでは、新しいCONDOを購入することも出来ます。 ② Rob's IMPORTS 骨董品店です。 クラシカルで不思議なものを売っています ここに売っているジェットパックは必ず買いましょう ③ CENTRAL CIRCUIT 家電量販店です。 電化製品はだいたいここで揃います。 メディアプレイヤーになるモニターなどもこちらに置いています ④ UPGRADE STORE ゲームワールドで使える、アップグレードアイテムを取り扱うお店です。 現在アップグレード機能は開発中の為、お店のみが存在します。 ⑤ SONGBIRD 音楽ショップ。音楽や音に関係するものを売っています 弾けるピアノなどがこちらです ⑥ The TOY STOP おもちゃ屋さん。 ブロックの家具や、乗れるRCカー、ペットなども扱っています ⑦ DIY STORE Condoを"建てる"為に必要なものを取り扱っているショップです。 建材やキャンバスアイテムを取り扱っています。 BOTなどもここです。 ⑧ SEASONS 自然アイテムを取り扱うショップです。 植物や岩などの、自然の景観アイテムはここで揃います。 ⑨ Project12 タワー屋上のバーです。 バーテンダーに話しかけるとショップが表示され、お酒関連はここで揃います。 ⑩ OASIS ビーチショップ。 ビーチ関連アイテムはここで揃います。 ⑪ FRESH 食料品店。 食品や、料理に使うアイテム、そして何故か骸骨もここで揃います。 ⑫ CELEBRATiONS 主にパーティーグッズを扱うお店です。 花火やコンフェティガンなどを取り扱っているほか、 ハロウィンやクリスマスなどのシーズンイベントで使用しそうなアイテムなどもおいてあります ⑬ GóNE FiSHiN' BAIT SHOP 釣具店。 釣りに使う釣り竿や、釣り餌のほか、水槽などもここで購入できます。 ⑭ TOWER THEATRE 映画館内のショップでは、ポップコーン等を購入することが出来ます。 ⑮ BY THE SEA SHORE イルカに話しかけると、SeaDollerと交換でイルカやウミガメ、シャチなどと交換できます。 ⑯ THE STRAY シークレットショップです。 各種ポーション（体の大きさを変えられる）やキャットサック（ガチャ）などを購入できます。 ⑰ FRANKY's GLILL ホットドッグや持ち運べる飲料を販売しています。 アミューズメント（水色） ① BOWLING ボウリング場です。 ボウリングをプレイすることができます。目指せストライク！ ② LASER TAG レーザー銃で戦うサバイバルゲーム風対戦FPSがプレイできます。 ③ TOWER CASINO カジノです。ギャンブルができます。 スロットやポーカーなどで遊ぶことができます。 また、ランダムでアイテムを入手できるホイールを回すことも出来ます。 ④ VOLT NIGHT CLUB ナイトクラブです。 Youtubeやサウンドクラウドの音楽を流せるほか、ビリヤードもできます。 ⑤ GAME WORLD PORTS ゲームワールドのミニゲームのマッチングができるサーバーへアクセスできます。 ⑥ DUELING ARENA 現在開発中です。 対戦ゲームが出来る予定です。 ⑦ ARCADE ゲームセンターです。 様々なアーケードゲームで遊ぶことが出来ます。 ⑧ TRIVIA クイズゲームがプレイできます。 ⑨ TOWER THEATRE 映画館です、好きなyoutubeやsoundcloudの映像や音楽を流せます screen1と2があるので流したいものがあるときはすいている場所に行きましょう また、売店もあります。 ⑩ BUMPER CARS バンパーカーを遊ぶことができるようになる予定です、現在未完成 ⑪ TYPING DERBY 対戦型タイピングゲームでプレイできます。 ⑫ POSEIDON ジェットコースターに乗ることが出来ます。 ⑬ Ferris wheel 観覧車に乗ることが出来ます。 ⑭ ウォータースライダー ウォータースライダーが滑れます。 また、プールサイドの浮輪に向かってアクションをすると、浮輪を持つことが出来ます。 ⑮ DarkVoyage シューティングライドアトラクションです。 施設（黄色） ① Tower Condo PLAZAサーバーから個人のCondoへ飛ぶことが出来ます。 ② Monorail Station モノレールの駅です。4か所あります。 ③ Transit Station 地下鉄駅。リスポーンポイントです。 ④ Ocean Expansion 現在開発中です。
https://w.atwiki.jp/www9test/pages/12.html
逆指値などの特殊注文 カブドットコム（逆指値、W指値®、リレー注文®、Uターン注文®トレーリングストップ） マネックス 楽天 日産センチュリー 安藤証券 （逆指値・OCO・ストップロス） オリックス（逆指値・乗換売買（リレー）・連続注文(できたら注文)）プラス逆指値（OCO） http //www.orix-sec.co.jp/service/cyumon/index.html http //www.orix-sec.co.jp/info/2006/i_0724_1.html http //www.orix-sec.co.jp/info/2007/i_0727_1.html 岩井証券 逆指値＋通常注文 http //www.iwaisec.co.jp/campaign/report/gyaku_sashine_kabu.html SBI証券 松井証券 逆指値・追跡指値 ジョインベスト 逆指値・上下指値・追跡逆指値・連続注文 大和証券/逆指値注文 http //www.daiwa.jp/ja/products/equity/reverse/index.html リテラクレア アド注文（逆指値ではない、リレー注文の一種） 価格.com - 注文方法 http //kakaku.com/stock/result.asp?Tab=T4 Sort=S81 夜間取引・PTSなど カブドットコムPTS（私設取引システム） 朝 8時20分～23時59分 カブドットコム証券kabu.comPTS http //kabu.com/pts/default.asp Ｑ＆Ａ SBIジャパンネクストPTS 19 00～23 59（セッション1）、24 30～26 00（セッション2） SBI証券 https //newtrading.etrade.ne.jp/ETGate/?_ControlID=WPLETmgR001Control _DataStoreID=DSWPLETmgR001Control burl=search_domestic dir=pts%2F file=domestic_pts_01.html cat1=domestic cat2=pts getFlg=on クリック証券 315円 https //www.click-sec.com/corp/guide/kabu/yakan/info/ 楽天証券 19 00～23 59（セッション1のみ） （楽天はセッション2はなし・取引所半休日は運営休止となります） http //www.rakuten-sec.co.jp/ITS/product/pr01_stock_03.html オリックス証券 19：00～23：59（セッション1のみ・取引所半休日は運営休止） http //www.orix-sec.co.jp/info/2008/i_0620_1.html ダイワPTS（独自） 18：00～23：59 手数料無料 大和証券/ダイワPTS http //www.daiwa.jp/service/pts/index.html 終値等一本値売買 マネックスナイターhttp //www.monex.co.jp/StockOrderConfirmation/00000000/nighter/ranking/exec 17 30～23 59 500円 丸三証券（マネナイと同じ）http //www.03trade.com/yakan/FAQ.html その他PTS（昼） 松井証券 09 00～14 50 http //www.matsui.co.jp/service/rtgs/about.html 夜間先物取引など（海外での日経225先物円建て売買など） 松井証券 CME http //www.matsui.co.jp/service/n_futures/index.html 安藤証券 SGX CME http //www.ando-sec.co.jp/churanet24/about/product/overseasfutures.html ひまわり証券株式会社 CFD取引 http //kabu.himawari-group.co.jp/trade/cfd/index.htm きっと証券 SGX CME http //www.kitto-sec.com/products/nikkei_average/spec.php
https://w.atwiki.jp/mineplex-wiki/pages/21.html
Treasure Chestとは いわゆる宝箱、ゲーム終了時に手に入ったり、代わりのコインで買えます Old Chest 価格 1000Coin Ancient Chest 価格 5000Coin Mythical Chest 価格 10000Coin 場所は各斜めの裏側 ８個中４個引くことができる この宝箱ではCommon(白)、Uncommon、Rare(ピンク)、Legendary(緑)のレア度があり右へ行くほど珍しい物となる 全てのアブーチメントがGETできる？ だれか情報提供ください Cosmetic Menu/コスメチックメニュー ゲームをプレイすると手に入る。 宝箱じゃないと入手出来無いアイテムも？ Gadgets/道具 Gadgets/道具 説明 入手レア度 Ethereal Pearl エンダーパールにプレイヤーが乗れる 下記全てCommonで入手可(Coin Party Bombを除く) Fire Works ランダムな花火を打ち上げる TNT プレイヤーを吹っ飛ばす Melon Launcher 移動速度上昇のスイカをバラ撒くスイカブロックを投げれる Flesh Hook プレイヤーを呼び寄せる飛び道具 PaintBall Gun ランダムな色を描き塗れるポイント銃 Bat Blaster コウモリを発射しプレイヤーを少し飛ばす Coin Party Bomb 周囲にコインを撒き散らす Rareで入手可 Particle Effect/パーティクル 説明 Shadow Walk エンダーアイが砕け散った時のパーティクル Activate Enchanted エンチャントのパーティクル Flame Rings Rain Cloud 頭の上に雲が差し掛かり、雨が降るパーティクル