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ARMORED CORE OP ARMORED CORE PROJECT PHANTASMA OP ARMORED CORE MASTER OF ARENA OP ARMORED CORE 2 OP ARMORED CORE 2 ANOTHER AGE OP ARMORED CORE 3 OP ARMORED CORE 3 SILENT LINE OP ARMORED CORE -LAST RAVEN- OP
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必要条件 Base Level 50 アイテム White Potion １個 報酬 Base Exp 5,000 アイテム Old Blue Box １個 日本版タイトル ： 薬 1部 1. Go to the house in Hugel× (hugel 153, 153)[take a left after you exit the airship×, there should be a bridge directly in front] and proceed to the second floor. Speak to Allen Schuwell (hu_in01 387, 245) and he shall be talking about his son and lack of medication. He will request to demand his son to go get medicine for him. (Memorizing the name of the medicine is not required) 2. Postell Schuwell in the map south of Hugel (hu_fild06 34, 123)[at the West portal] will then go get the medicine once he is told that his father needs him. However, he requests that his father be watched over during his absence. 3. Return to Allen and he shall complain some more about his pains. He will then request a White Potion . After receiving the White Potion, he will request that you remain by his side until Postell returns. 4. Speak to Allen again and he will talk about having another attack and request that you look for his medicine drawer. 5. Step on tile to the left of you at the drawer with the axe and pick (hu_in 372, 254). 6. Return to Allen and go next to him and he ll ask for his medicine (Do not click on him). 7. Stand on the tile by the drawer again. A dialog about medicines in the drawer should appear. 8. Repeat 6 and 7 two more times and give Allen his medicine. You must reach the drawer before the flash appears, otherwise you need to repeat 6 7 until you get the medicine. 9. Speak to Allen a few more times (one of which requires standing near Allen). He will request for CPR and another dose of medicine. Repeat step 8. This time, a dialog about the Renkenbar experiments and side effects should appear. 10. Repeat step 9 a few times (the number of times is random). 11. After a certain point, Allen will complain about his pain instead of requesting CPR and Postell shall appear. Postell apparently got the wrong medicine and will then leave again. Allen will then tell you to return to the medicine drawer. 12. Receive 5,000 Base EXP and an Old Blue Box . Categories Quest Window Quests | Base Experience Reward | Hugel Quests
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Cover Explained Details on "Cover" There are three types of cover in Company of Heroes Directional Non-Directional Shot-Blocking Directional cover provides cover bonuses to units which are being shot at through the object. Short walls are an excellent example of this; if a Ranger is on one side of the wall shooting at a Grenadier on the other side, the Grenadier will be in cover. If however, both are on the same side of the wall, there will be no cover bonus to either. 方向のあるカバーは、オブジェクトを突き抜けられているユニットにカバー・ボーナスを供給します。短い壁はこの優れた例です;放浪者が、反対側のてき弾兵をねらい撃つ壁の1つの横にいれば、てき弾兵はカバーにいるでしょう。しかしながら、両方が壁の同じ側にある場合、どちらかにカバー・ボーナスはないでしょう。 Non-Directional cover provides cover bonuses to units no-matter where they are, as long as they are within range of the object/splat which is generating the cover. Craters and small objects are a good example. If a squad is inside a crater, they are in cover no-matter where they are being shot at from. カバーを生成しているオブジェクト/縦長平板の範囲内にある限り、それらがどこにあっても、全方向性のカバーはユニットにカバー・ボーナスを供給します。クレーターおよび小さな物体はよい例です。チームがクレーターの内部でいれば、どこに放たれていても、それらはカバーにあります、から。 Shot-Blocking is not so much a cover type as it is a way of ensuring units are not hit at all. Thick Hedgerows, tall stone walls, buildings and large objects are examples of shot-blocking objects. As long as units are behind these, they will not be fired upon by units on the other side of the object. Keep in mind, however that battlefields in CoH are dynamic, and that object could easily be destroyed. More information on Shot blocking can be read in the tips section of the HeightMap Editor article. それが、ユニットが全く打たれないことを保証する方法であるとともに、発射ブロッキングはあまりカバー・タイプではありません。厚い生け垣、高い石壁、建物および大規模なオブジェクトは、発射を閉鎖するオブジェクトの例です。ユニットがこれらの後ろにある限り、それらは、オブジェクトの反対側のユニットによって発射されません。心に留めておく、しかしながら、CoHの中のその戦場は動的です。また、そのオブジェクトは容易に破壊されるかもしれません。放たれたブロッキングについてのより多くの情報は、HeightMapエディター記事のこつセクションで読むことができます。 From Relic Community Wiki
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必要条件 Base Level 無し 前提クエスト Factory Quest 報酬 (リニューアル前のものらしい。 下記 参照) Base Exp Level 01-69 = 10,000 Exp Level 70-79 = 30,000 Exp Level 80-89 = 50,000 Exp Level 90-99 = 70,000 Exp Job Exp Level 01-69 = 8,000 Exp Level 70-79 = 10,000 Exp Level 80-89 = 30,000 Exp Level 90-99 = 50,000 Exp 日本版タイトル ： シドクス 1. Go to Einbech×. When you step off the train there is a Young Man (einbech 58 209) who talks about depressed guy in pub. Go talk to Buender Hikeman behind the tavern (einbech 164 102). He will mistake you for a killer. Talk to him again, and ask him how he escaped. He ll rant and pass out. 2. Now head to Einbroch×. At the second floor of the Hotel (einbroch 252 200), in the south western room there is a Sick Old Man - Shinokas (ein_in01 231, 161) in bed. Ask him if he always lived in Einbroch and you ll find out he is hiding something. Keep badgering him about the mine collapse and eventually you ll get the option to ask about Hikeman. He will slip up and reveal he really was part of that incident. Talk to him again and he asks you to search the Kappelthaine Manor (einbroch 126 229) for more information about the ore. Talk to the maid there and she denies any ore. Note To talk to NPC×s in the Kappelthaine Manor, immediately move into the south room upon entering. The father will kick you out of the house if you go near him, so you have to talk to the three NPCs in the room (two are for another quest) through the walls. 3. Return to Shinokas and he ll ask you to search the factory next. Talk to Zelmeto (ein_in 67, 247) (and finish the Einbroch Factory Maintenance quest up to the part where one must hand him spare parts if you haven t already) in the factory and return to Shinokas. He gives you the option of where you think it may be hidden. 4. If you pick Laboratory (Southwest Einbroch - einbroch 53, 51), you have to sneak in . The door at the laboratory will now request a password...you have to type in the nonesense that it tells you. OR you can just copy/paste the correct combination in. Following is the full list of pairings(one is used twice) burrdingdingdilidingdingphoohudaambandoorabambarambambamburanbamding burapaphurarlandreamduranbatuhiwooikabamturubamdingding belief love luck grimace sweat rush folktale rodimus optimus burnblebe LiGhTsPeEd RiGhT SPEed leFT TURn RiGhT BuRn OrIGInAL GaNgSteR SmACk You give me no choice. I guess it s time for me to reveal my secret... fReeDoM eCstAcy JoUrnaLiSm ArMpit DisCoverY hEaDaChE MoonbeAmS jUsTiCE Coboman no chikara-yumei na chikara-daiookii na chikara da ze! COBO ON hfjdkeldjshfjdjeiskdlefvbd I m the King of all Weirdos! Now you know of my true power. Obey~! uNflAPPaBLe LoVaBLe SeCreTs AnD BoWLiNg aGaINST tHe KarMA of YoUtH By the power of p-po-poi-po-poi-poin-poing GOD-POING. I NEVER LOSE! uNflAPPaBLe LoVaBLe SeCreTs AnD BoWLiNg aGaINST tHe KarMA of YoUtH ...silence. quiet benevolence... soul mate... wonder. enigma... cloud. opeN,Open!op3n.openOpen0p3nOpEn0pen`open 0Pen open?open!111OPENSESAME 5. Talk to the scientist inside, and he will tell you the head of the lab is on the airship× flirting with some lady. While here, click on the small "Unknown Stuff" in the middle of the room at the center of the machine. 6. Take the airship and go downstairs (airplane 34 77). The scientist (Drunken Old Man) is throwing dice and losing badly. Talk to the Apple Merchant, buy 100 apples, then talk to the scientist. He ll use them to gamble another round and lose even more. The key here is his swearing his luck on Ymir s Heart. Keep giving him apples and eventually he will win, and tell you about Ymir s Heart. 7. Return to Shinokas, tell him about Ymir s Heart in the dialog that appears, and he ll die telling you of his regret. 8. Go back to Einbech and inform Hikeman of Shinokas s death for some EXP. Experience amounts received ● Level 01-69 = 10,000 Base EXP/8,000 Job EXP ● Level 70-79 = 30,000 Base EXP/10,000 Job EXP ● Level 80-89 = 50,000 Base EXP/30,000 Job EXP ● Level 90-99 = 70,000 Base EXP/50,000 Job EXP Post Renewal Note Level 87 Alchemist - I got 70k Base and 70k Job - 12-09-10 Categories Job Experience Reward | Base Experience Reward | Einbroch Quests
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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
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あと７Lv！ 頑張るぞ～＾＾ - 03・・・ 2010-02-26 19 23 39 頑張るかも～＾＾ - あと６LV! 2010-03-16 11 23 15 あと１ＬＶで１５１１ - kk 2010-04-19 13 41 10 ↓1511ﾚﾍﾞのリバウンドってどんなだろう - いま 2010-12-28 00 38 37 ↑１５１１レベｗｗｗ - ﾀﾞﾄﾀﾞﾄﾞ 2011-01-06 22 45 50 ﾑﾌﾌﾌﾌﾌﾌﾌﾌﾌﾌﾌﾌﾌﾌﾌｯﾌﾌﾌﾌﾌ~ﾝ♪ - ଁଐୂୁୀஒுீ 2011-05-28 14 36 45 ４３は３３３０００ほどでしたよ～ - 名無しさん 2011-10-06 17 40 50 Lv31の経験値が87712を確認。 - 名無しさん 2011-10-15 15 53 05 ｌｖ45は449400くらいでなったよ - 名無しさん 2011-10-30 00 56 35 トロフィーの2レベルアップは39レベルまで - 名無しさん 2011-11-01 02 27 42 Lv34 121000ぐらい - 名無しさん 2012-01-07 02 03 33 ↑ごめん112000ぐらいの間違い - 名無しさん 2012-01-07 02 13 39 先日４５になったけど、最初のスーパーサイヤ人の髪もらえるのは、経験値いくついるのかなぁ - 名無しさん 2012-01-14 01 33 33 Lv28到達時で約56500 変更出来る方宜しくどうぞ - 名無しさん 2012-01-21 07 14 21 Lv29到達時で約65300 変更出来る方宜しくどうぞ - 名無しさん 2012-01-21 07 45 00 Lv30到達時で約75000 変更出来る方宜しくどうぞ - 名無しさん 2012-01-21 08 45 22 最初のｻｲﾔ人は52万ちょいでしたかね - 名無しさん 2012-02-17 20 01 06 ４４ ３８６０２５でも足りました - 名無しさん 2012-02-23 03 19 39 レベル27到達は49077 - 名無しさん 2012-03-01 23 28 19 Lv35到達時 122500 確定です - 名無しさん 2012-03-07 05 09 08 Lv20 到達時 20000 確定 - 名無しさん 2012-03-25 21 53 20 Lv20 到達時 20500 確定 - 名無しさん 2012-03-25 21 58 11 Lv24 到達時 33200 確定 - 名無しさん 2012-03-25 22 23 46 Lv25 到達時 37500 確定 - 名無しさん 2012-05-05 06 10 53 Lv26 到達時 42800 確定 - 名無しさん 2012-05-07 00 54 17 Lv30 到達時 75600 確定 - 名無しさん 2012-05-16 06 24 46
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Musician パラモア（Paramore）- Wikipedia Paramoe - ｵﾌｨｼｬﾙｻｲﾄ Paramoe（パラモア）- 日本語公式サイト 2008/10/31 にアップロード Paramore s music video for Decode from the soundtrack to Twilight - available now on Atlantic Records. Go behind the scenes of this video at http //youtu.be/X4Qpc8rXsm0 ーーーーー 2014/09/01 に公開 Paramore s live video for Last Hope from the MONUMENTOUR in Chicago, Illinois on July 11, 2014. The song originally appears on the self-titled album - available now on Fueled By Ramen. Download it at http //smarturl.it/paramore-itunes ーーーーー 2013/02/12 に公開 Paramore s music video for Now from the self-titled album - available now on Fueled By Ramen. Download it at http //smarturl.it/paramore-itunes .
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曲Data Lv BPM TOTAL NOTES 平均密度 ★??? 5-39 221 1.32Notes/s 譜面構成・攻略 譜面画像
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ECHOES WR #68 -Express Emotion- 10/12~ 12 00 ~ 10/18 23 59 選曲 ka23 IIDX SPA Rank Name Score Result 1 hide 2519 result 2 けいにん 2394 result 3 ごま 2289 result 4 GISU 2286 result 5 こだま 2219 result 6 ししお 2216 result 7 しん 2168 result 8 さくしゅ 2151 result 8 中野 2151 result 10 くろこ 2097 result 10 きるしゅ 2097 result 12 おみつ 1937 result 13 たか 1620 result 14 ぜお 1376 result SPH Rank Name Score Result 1 ka23 885 result 2 うんちょ 796 result DPA Rank Name Score Result 1 つぼ 2161 result Rb HARD Rank Name Score Result 1 ごま 1551 result 2 こだま 1535 result 3 きるしゅ 1515 result
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通常ゲージに変わってたからやったけどクリア難度なら弱いかな (2018-08-17 15 58 11) 電池は16あるとは思うけどゲージならほとんどゲージが削られる箇所がない。16のなかでも結構弱めで捻りも少ないので気持ちよく踏める16。 (2018-08-17 18 55 15) 同時混じりの16分3連がコンボカッターなだけで、全体的に難易度は低め。Lv16最弱クラス候補、Lv15最強クラスの曲の方が踏みにくい為、Lv15でもいいような...... (2018-08-19 23 23 31) 明確な休憩がないから体力要求はそこそこある。それ込みでも簡単なほうだと思うけど持久力に自信がない人は油断禁物。 (2018-08-20 21 05 02) 最後の滝で16になってるイメージ (2018-09-25 01 49 39) クリアもスコアも弱めだなー。体力が少しもってかれる (2019-04-08 21 10 58) 中盤にちょこちょこ出る同時で体力を無駄に消耗しなければクリア難度は足15レベルと感じた (2019-05-26 21 13 12)