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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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開催日：2010 / 07 / 11 参加人数：33名 フォーマット：レガシー（～ROE） Constructed Legacy Event #1395804 on 07/11/2010 in Premier Events 優勝：カウンタートップソプター（青白タッチ黒）／Counter-Top Thopters 準優勝：デス＆タックス（白単）／Death＆Taxes 第3位：バーン（赤単）／Burn 第4位：リアニメイト／Reanimate 第5位：クエストバーン／Quest Burn 第6位：カウンタートップソプター（青白）／Counter-Top Thopters 第7位：カウンタートップソプター（青白タッチ黒）／Counter-Top Thopters 第8位：忠臣サバイバル／Retainers Survival 優勝 カウンタートップソプター（青白タッチ黒）／Counter-Top Thopters 使用者：savagebeatdown Main Deck 1《アカデミーの廃墟/Academy Ruins》 4《溢れかえる岸辺/Flooded Strand》 6《島/Island》 1《霧深い雨林/Misty Rainforest》 2《平地/Plains》 3《汚染された三角州/Polluted Delta》 1《沸騰する小湖/Scalding Tarn》 1《教議会の座席/Seat of the Synod》 2《Tundra》 1《Underground Sea》 4《渦まく知識/Brainstorm》 4《相殺/Counterbalance》 3《対抗呪文/Counterspell》 1《世界のるつぼ/Crucible of Worlds》 1《仕組まれた爆薬/Engineered Explosives》 4《悟りの教示者/Enlightened Tutor》 4《Force of Will》 2《精神を刻む者、ジェイス/Jace, the Mind Sculptor》 1《Moat》 1《忘却の輪/Oblivion Ring》 1《真髄の針/Pithing Needle》 4《師範の占い独楽/Sensei s Divining Top》 1《弱者の剣/Sword of the Meek》 4《剣を鍬に/Swords to Plowshares》 1《求道者テゼレット/Tezzeret the Seeker》 2《飛行機械の鋳造所/Thopter Foundry》 Sideboard 1《基本に帰れ/Back to Basics》 1《赤の防御円/Circle of Protection Red》 1《仕組まれた爆薬/Engineered Explosives》 1《根絶/Extirpate》 2《水流破/Hydroblast》 4《翻弄する魔道士/Meddling Mage》 1《Moat》 2《大祖始の遺産/Relic of Progenitus》 2《トーモッドの墓所/Tormod s Crypt》 準優勝 デス＆タックス（白単）／Death＆Taxes 使用者：Blazelix Main Deck 2《トロウケアの敷石/Flagstones of Trokair》 4《Karakas》 2《ミシュラの工廠/Mishra s Factory》 10《平地/Plains》 4《不毛の大地/Wasteland》 3《エーテル宣誓会の法学者/Ethersworn Canonist》 4《ちらつき鬼火/Flickerwisp》 3《ヨツンの兵卒/Jotun Grunt》 3《コロンドールのマンガラ/Mangara of Corondor》 4《ルーンの母/Mother of Runes》 4《セラの報復者/Serra Avenger》 3《石鍛冶の神秘家/Stoneforge Mystic》 4《霊気の薬瓶/AEther Vial》 2《忘却の輪/Oblivion Ring》 1《ルーンの光輪/Runed Halo》 1《火と氷の剣/Sword of Fire and Ice》 1《光と影の剣/Sword of Light and Shadow》 4《剣を鍬に/Swords to Plowshares》 1《梅澤の十手/Umezawa s Jitte》 Sideboard 2《沈黙のオーラ/Aura of Silence》 2《ブレンタンの炉の世話人/Burrenton Forge-Tender》 1《エーテル宣誓会の法学者/Ethersworn Canonist》 3《台所の嫌がらせ屋/Kitchen Finks》 2《貪欲な罠/Ravenous Trap》 3《沈黙/Silence》 2《トーモッドの墓所/Tormod s Crypt》 第3位 バーン（赤単）／Burn 使用者：bozidar2121 Main Deck 17《山/Mountain》 2《沸騰する小湖/Scalding Tarn》 4《ゴブリンの先達/Goblin Guide》 4《地獄火花の精霊/Hellspark Elemental》 4《ケルドの匪賊/Keldon Marauders》 4《Chain Lightning》 4《火炎破/Fireblast》 4《溶岩の撃ち込み/Lava Spike》 4《稲妻/Lightning Bolt》 4《発展の代価/Price of Progress》 4《裂け目の稲妻/Rift Bolt》 2《硫黄の渦/Sulfuric Vortex》 3《火山の流弾/Volcanic Fallout》 Sideboard 2《真髄の針/Pithing Needle》 4《紅蓮破/Pyroblast》 4《大祖始の遺産/Relic of Progenitus》 2《焼尽の猛火/Searing Blaze》 3《粉々/Smash to Smithereens》 第4位 リアニメイト／Reanimate 使用者：Bazaar of Baghdad Main Deck 2《島/Island》 3《霧深い雨林/Misty Rainforest》 2《汚染された三角州/Polluted Delta》 2《沼/Swamp》 4《Underground Sea》 4《新緑の地下墓地/Verdant Catacombs》 4《不運な研究者/Hapless Researcher》 1《墨溜まりのリバイアサン/Inkwell Leviathan》 2《エメリアの盾、イオナ/Iona, Shield of Emeria》 1《白金の天使/Platinum Angel》 2《鋼の風のスフィンクス/Sphinx of the Steel Wind》 4《渦まく知識/Brainstorm》 1《入念な研究/Careful Study》 1《蒸気の連鎖/Chain of Vapor》 2《目くらまし/Daze》 2《払拭/Dispel》 4《納墓/Entomb》 4《死体発掘/Exhume》 4《Force of Will》 4《神秘の教示者/Mystical Tutor》 4《再活性/Reanimate》 1《実物提示教育/Show and Tell》 2《思考囲い/Thoughtseize》 Sideboard 1《棺の追放/Coffin Purge》 1《払拭/Dispel》 1《ドライアドの東屋/Dryad Arbor》 1《浄火の大天使/Empyrial Archangel》 1《根絶/Extirpate》 1《精神壊しの罠/Mindbreak Trap》 2《無のロッド/Null Rod》 2《真髄の針/Pithing Needle》 2《実物提示教育/Show and Tell》 1《もみ消し/Stifle》 2《思考囲い/Thoughtseize》 第5位 クエストバーン／Quest Burn 使用者：L1X0 Main Deck 16《山/Mountain》 3《ぐらつく峰/Teetering Peaks》 4《ゴブリンの先達/Goblin Guide》 4《地獄火花の精霊/Hellspark Elemental》 4《ケルドの匪賊/Keldon Marauders》 3《モグの狂信者/Mogg Fanatic》 4《Chain Lightning》 4《火炎破/Fireblast》 1《溶岩の投げ矢/Lava Dart》 4《溶岩の撃ち込み/Lava Spike》 4《稲妻/Lightning Bolt》 3《発展の代価/Price of Progress》 4《純なる炎の探索/Quest for Pure Flame》 2《裂け目の稲妻/Rift Bolt》 Sideboard 3《真髄の針/Pithing Needle》 4《紅蓮破/Pyroblast》 3《大祖始の遺産/Relic of Progenitus》 2《焼尽の猛火/Searing Blaze》 3《粉々/Smash to Smithereens》 第6位 カウンタートップソプター（青白）／Counter-Top Thopters 使用者：whiffy penguin Main Deck 1《アカデミーの廃墟/Academy Ruins》 4《溢れかえる岸辺/Flooded Strand》 7《島/Island》 3《霧深い雨林/Misty Rainforest》 2《平地/Plains》 1《教議会の座席/Seat of the Synod》 1《Tropical Island》 2《Tundra》 1《Underground Sea》 4《渦まく知識/Brainstorm》 4《相殺/Counterbalance》 3《対抗呪文/Counterspell》 1《世界のるつぼ/Crucible of Worlds》 1《仕組まれた爆薬/Engineered Explosives》 4《悟りの教示者/Enlightened Tutor》 4《Force of Will》 1《謙虚/Humility》 2《精神を刻む者、ジェイス/Jace, the Mind Sculptor》 1《Moat》 1《忘却の輪/Oblivion Ring》 4《師範の占い独楽/Sensei s Divining Top》 1《弱者の剣/Sword of the Meek》 4《剣を鍬に/Swords to Plowshares》 2《飛行機械の鋳造所/Thopter Foundry》 1《トーモッドの墓所/Tormod s Crypt》 Sideboard 1《基本に帰れ/Back to Basics》 1《赤の防御円/Circle of Protection Red》 1《仕組まれた爆薬/Engineered Explosives》 4《翻弄する魔道士/Meddling Mage》 3《流刑への道/Path to Exile》 1《真髄の針/Pithing Needle》 2《大祖始の遺産/Relic of Progenitus》 1《静寂/Serenity》 1《トーモッドの墓所/Tormod s Crypt》 第7位 カウンタートップソプター（青白タッチ黒）／Counter-Top Thopters 使用者：Ari C Main Deck 1《アカデミーの廃墟/Academy Ruins》 4《溢れかえる岸辺/Flooded Strand》 6《島/Island》 1《霧深い雨林/Misty Rainforest》 2《平地/Plains》 3《汚染された三角州/Polluted Delta》 1《沸騰する小湖/Scalding Tarn》 1《教議会の座席/Seat of the Synod》 2《Tundra》 1《Underground Sea》 4《渦まく知識/Brainstorm》 4《相殺/Counterbalance》 3《対抗呪文/Counterspell》 1《世界のるつぼ/Crucible of Worlds》 1《仕組まれた爆薬/Engineered Explosives》 4《悟りの教示者/Enlightened Tutor》 4《Force of Will》 2《精神を刻む者、ジェイス/Jace, the Mind Sculptor》 1《Moat》 1《忘却の輪/Oblivion Ring》 1《真髄の針/Pithing Needle》 4《師範の占い独楽/Sensei s Divining Top》 1《弱者の剣/Sword of the Meek》 4《剣を鍬に/Swords to Plowshares》 2《飛行機械の鋳造所/Thopter Foundry》 1《トーモッドの墓所/Tormod s Crypt》 Sideboard 1《基本に帰れ/Back to Basics》 1《赤の防御円/Circle of Protection Red》 1《仕組まれた爆薬/Engineered Explosives》 4《エーテル宣誓会の法学者/Ethersworn Canonist》 1《根絶/Extirpate》 1《謙虚/Humility》 2《水流破/Hydroblast》 2《大祖始の遺産/Relic of Progenitus》 1《静寂/Serenity》 1《トーモッドの墓所/Tormod s Crypt》 第8位 忠臣サバイバル／Retainers Survival 使用者：Davorac Main Deck 2《溢れかえる岸辺/Flooded Strand》 1《森/Forest》 2《島/Island》 4《霧深い雨林/Misty Rainforest》 1《平地/Plains》 1《Savannah》 4《Tropical Island》 2《Tundra》 2《吹きさらしの荒野/Windswept Heath》 1《引き裂かれし永劫、エムラクール/Emrakul, the Aeons Torn》 1《永遠の証人/Eternal Witness》 1《エメリアの盾、イオナ/Iona, Shield of Emeria》 1《セファリッドの女帝ラワン/Llawan, Cephalid Empress》 1《忠臣/Loyal Retainers》 4《貴族の教主/Noble Hierarch》 1《クァーサルの群れ魔道士/Qasali Pridemage》 1《誘惑蒔き/Sower of Temptation》 1《ゴブリンの太守スクイー/Squee, Goblin Nabob》 4《タルモゴイフ/Tarmogoyf》 4《渦まく知識/Brainstorm》 3《相殺/Counterbalance》 1《悟りの教示者/Enlightened Tutor》 4《Force of Will》 2《思案/Ponder》 3《師範の占い独楽/Sensei s Divining Top》 4《適者生存/Survival of the Fittest》 4《剣を鍬に/Swords to Plowshares》 Sideboard 1《エーテル宣誓会の法学者/Ethersworn Canonist》 1《フェアリーの忌み者/Faerie Macabre》 1《ガドック・ティーグ/Gaddock Teeg》 1《大いなる玻璃紡ぎ、綺羅/Kira, Great Glass-Spinner》 2《台所の嫌がらせ屋/Kitchen Finks》 2《クローサの掌握/Krosan Grip》 1《茨の騎士ティヴァダール/Tivadar of Thorn》 2《トーモッドの墓所/Tormod s Crypt》 1《サーボの網/Tsabo s Web》 2《梅澤の十手/Umezawa s Jitte》 1《太陽と月の輪/Wheel of Sun and Moon》
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公式サイト /Secret Garden様 ダイナサイトさん メタモ工房 Wiki* ありの穴/アリアーナさん 七番目の島/吸血鬼せぶんさん だいなめたも@Wiki だいなヘッドライン/アイゼル･フーバーさん 聖乙女の娯楽図書室 ものづくり職人フォーラム/エルーニャ･ロウさん ＋櫻子の妄想部屋＋/結月櫻子さん St.Gems Database/エクセリーナさん セイント・ジェムスの歩き方/皐月琥珀さん(上のサイトの後継サイトかなぁ?) 看板娘より愛をこめて/ドール･イヅミさん Ding Dong/星屑ののさん Aveu Passione/森川のんさん 聖乙女のツバサ/いずみさん 関西乙女会通信 関西乙女会ホームページ/Hestia Westaさん 三日月迷宮/メイファさん いつでもおこしやす/クリスティーナ・ノウェルさん ダイナ アイテム図鑑/マリー･フレーズさん くろねこどうめい/ルシア･ジェラルドさん くまくま屋☆銀月 銀月の花園/ロゼリア･アンネヴァルトさん 聖乙女寮309号室/カズキさん Lost in Reverie/セイクレシア・ディアールさん ダイナスティア★カフェ/ミルキーことはさん フレイル見聞録/長谷川真琴さん めたもすぱあと/Hypatia Cadeさん /雪白ほたるさん /河村ミキさん /ハルさん /花月月華さん /チャイナさん /Alice Tiearさん /井上遙さん /ローゼリィさん /御香宮ユカリさん /秋流さん /水無月衣織さん /モリス･ターニャさん(ダイナページはロゼワインです。) /錦織蛍さん /咲良桔梗さん /(-.-)(顔文字)さん Today - |Yesterday -
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PHP8.0のインストール【AlmaLinux 9】 PHP8.0のインストールを行います。 ※8.1、8.2、8.3をインストールする場合は、「8.0」を該当のバージョンに読み替えて下さい。 1. PHPのインストール インストールできるPHPのバージョンを確認します。 # dnf module list php AlmaLinux 8 - AppStream Name Stream Profiles Summary php 8.1 common [d], devel, minimal PHP scripting language Remi s Modular repository for Enterprise Linux 8 - x86_64 Name Stream Profiles Summary php remi-7.4 common [d], devel, minimal PHP scripting language php remi-8.0 common [d], devel, minimal PHP scripting language php remi-8.1 common [d], devel, minimal PHP scripting language php remi-8.2 common [d], devel, minimal PHP scripting language php remi-8.3 common [d], devel, minimal PHP scripting language Remiリポジトリから PHP 8.0 がインストールされるように php remi-8.0 モジュールをインストールします。 # dnf module reset php # dnf module install php remi-8.0 dnfでインストールを行います。 # dnf install php # dnf install php-devel 2. 関連モジュールのインストール (1) libmcryptのインストール # dnf install --enablerepo=epel libmcrypt (2) libargon2のインストール php-pdoをインストールする場合に必要です。 # dnf install --enablerepo=epel libargon2 # dnf install --enablerepo=epel libargon2-devel (3) libraqmのインストール # dnf --enablerepo=epel install libraqm 3. phpのモジュールのインストール これは任意ですが、必要なモジュールをインストールします。 # dnf install php-mysqlnd # dnf install php-mbstring # dnf install php-gd # dnf install php-pecl-xmlrpc # dnf install php-pecl-mcrypt # dnf install php-fpm # dnf install php-opcache # dnf install php-pecl-apcu # dnf install php-pecl-zip # dnf install php-pear 4. /etc/php.iniの編集 (1) php.iniの編集 # cp /etc/php.ini{,.default} # vi /etc/php.ini expose_php = Off max_execution_time = 60 memory_limit = 512M ※サーバの搭載メモリにより調整して下さい。 error_reporting = E_ALL ~E_NOTICE ~E_DEPRECATED ~E_STRICT ; Log errors to specified file. PHP s default behavior is to leave this value ; empty. ; http //php.net/error-log ; Example ;error_log = php_errors.log ; Log errors to syslog. ;error_log = syslog ※php-fpmを利用している場合には、エラーログは「/var/log/php-fpm/www-error.log」に書き込まれます。（当初はこのファイルは存在しません。エラーが発生すると自動的に作成されます。） 「/etc/php-fpm.d/www.conf」にログファイル名が記載されています。 post_max_size = 20M upload_max_filesize = 20M date.timezone = "Asia/Tokyo" session.gc_maxlifetime = 3600 mbstring.language = Japanese mbstring.internal_encoding = UTF-8 mbstring.http_input = pass mbstring.http_output = pass (2) pearモジュールのインストール 必要に応じて、PEARのモジュールをインストールします。 【例】PEAR Mailモジュールのインストール。 # pear install -a Mail ※「-a」オプションを付けると、依存ファイルもすべてインストールします。 (3) Apacheの再起動 Apacheを再起動して、PHPを有効にします。 # systemctl restart httpd.service 5. php-fpmサービスの起動 # systemctl enable php-fpm.service # systemctl start php-fpm.service 6. HTMLページをPHPとして動作させる場合の設定 通常、HTMLページをPHPとして動作させる場合には、.htaccessに FilesMatch \.html$ AddHandler application/x-httpd-php .html /FilesMatch と記述すれば動作するはずですが、php-fpmを利用している場合には、設定が無効になる場合があります。 その場合には、以下のように設定します。 (1) .htacces 「/etc/httpd/conf.d/php.conf」において # Redirect to local php-fpm (no mod_php in default configuration) IfModule !mod_php5.c IfModule !mod_php7.c (略) FilesMatch \.(php|phar)$ SetHandler "proxy unix /run/php-fpm/www.sock|fcgi //localhost" /FilesMatch /IfModule /IfModule というような記述があります。 そこで、同様にfpmに処理を引き渡す必要があるので、以下のように.htaccessを記述します。 FilesMatch \.html$ SetHandler "proxy unix /run/php-fpm/www.sock|fcgi //localhost" /FilesMatch (2) /etc/php-fpm.d/www.conf デフォルトでは、PHPコードを実行可能なファイル拡張子が「.php」のみに制限されているため、「.html」も使用できるように設定します。 ; Limits the extensions of the main script FPM will allow to parse. This can ; prevent configuration mistakes on the web server side. You should only limit ; FPM to .php extensions to prevent malicious users to use other extensions to ; exectute php code. ; Note set an empty value to allow all extensions. ; Default Value .php ;security.limit_extensions = .php .php3 .php4 .php5 .php7 の箇所の「security.limit_extensions」の項目を以下のように変更します。 security.limit_extensions = .php .html php-fpmを再起動します。 # systemctl restart php-fpm.service 7. composerのインストール composerをインストールします。（Ver. 2.5.8） # php -r "copy( https //getcomposer.org/installer , composer-setup.php );" # php -r "if (hash_file( sha384 , composer-setup.php ) === e21205b207c3ff031906575712edab6f13eb0b361f2085f1f1237b7126d785e826a450292b6cfd1d64d92e6563bbde02 ) { echo Installer verified ; } else { echo Installer corrupt ; unlink( composer-setup.php ); } echo PHP_EOL;" # php composer-setup.php # php -r "unlink( composer-setup.php );" # mv composer.phar /usr/local/bin/composer ※チェックするハッシュ値はバージョンによって異なるので、「https //getcomposer.org/download/」で最新バージョンをチェックして下さい。 # composer -v バージョン情報が表示されれば、正常に動作しています。 ______ / ____/___ ____ ___ ____ ____ ________ _____ / / / __ \/ __ `__ \/ __ \/ __ \/ ___/ _ \/ ___/ / /___/ /_/ / / / / / / /_/ / /_/ (__ ) __/ / \____/\____/_/ /_/ /_/ .___/\____/____/\___/_/ /_/ Composer version 2.5.8 2023-06-09 17 13 21 ※rootユーザでcomposerを実行すると、「Do not run Composer as root/super user! See https //getcomposer.org/root for details Continue as root/super user [yes]?」という警告が表示されます。
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Simplifying Joints in Perspective 透視図法における関節の簡略化 https //www.youtube.com/watch?v=8q7Lp8sEC0M http //www.proko.com/simplifying-joints-in-perspective/ 0 12 Let s use some real bones as reference. いくつかの本物の骨を参考に使ってみましょう。 It s good to have a full sized human skeleton, one cast from real bones, so that you can compare this to your actual body. 実寸大の骨を持つことは、 ちらりと見て あなたの実際の人体と比べらられるので 大変良いことです。 But the problem is that these thing are riveted so that it doesn t move like a human skeleton moves. しかし、問題なのは、 こういった骨格模型は釘づけされているので 実際の骨格のようには動かないことです。 There is a spool in here that allows a foot to go into dorsiflexion and plantar flexion that we can t do on this because it s stuck together. この部分には糸巻きがあって、 それによって、足は背屈と足底屈を行えるのですが、 模型では固定されているので確認できません。 dorsiflexion 【名】 《医》背屈 plantar flexion 《解剖》足底屈 But we don t have that limitation when we draw and when we have the 3D model. ですが、 3Dモデルを使って描くなら、そういう制限はありません。 0 44 This is an extended foot. これは伸ばされた足です。 I like to begin with a rough something to contain the proportions. 私はおおよその比率を見るためにラフスケッチから 始めることが好きです。 0 56 It s okay if you take some time with that. ラフスケッチに時間をかけるのは問題ありません。 But to make it look three dimensional, even when I do that rough something, I m thinking of height, width, and depth. ですが、スケッチが三次元に見えるために、 私は高さ、幅、奥行きを考えます。 例えラフスケッチの時でも。 And we letter those systems as X, Y, and Z. それぞれの次元にX、Y、Zの文字をふっておきましょう。 And with just those coordinates, we can build a Lego foot standing non-extended. これらの座標を使って、 伸ばしていない足のレゴブロックを作りましょう。 Which, even if it doesn t look like a foot, it looks 3D. これは足にはちょっと見えないですが、 三次元的ではあります。 1 30 Then when we put this cylinder in there, it runs along X which helps us draw the ellipse, and we know that that is the fulcrum of the foot. 次に、この円筒形を、ここに置きましょう。 円筒形はX軸に沿っていますが、X軸を利用して楕円を描くことができます。 また、この円筒形は足の支点となります。 That means it s the center axle of the foot s rotation. つまり、この円筒形が足の回転の軸となるわけです。 If I draw it from the side, you ll see that we have the depth. 横から描くとき、 私は奥行きをつま先-かかと間に設定します。 That s the Z line. これがZ軸です。 The height, that s the Y line. 高さ、これがY軸です。 And then we re looking straight down on X here that ankle joint is. そして、横から見ているということは 足首の関節の軸があるX軸に対して視線を平行に見ているということです。 1 59 And when that foot moves on that hinge joint and makes an arc, goes into extension, we can see that Z will not line up on Z. そして、足がこの蝶番関節上で動き、弧を描いたとき 足は伸ばされ、 ZはZ上に並ばないことを確認できます。 It will aim up. 足の甲は上向きです。 So when we do this refined foot, I m going to chisel some of the plane so it looks a little bit more like a foot. ですので、足を修正するとき、 もう少し現実の足に見えるように のみで彫ったように修正します。 It s not all right angles. これは完全に正しい角度というわけではありません。 And the big foot, we ll put into an extended position rather than a straight up and down position. そして大きい足を描くとき、 垂直な位置というよりは、 足が伸びたときの位置を描きましょう So let s get the ankle bones. さて、足首の骨に移りましょう。 That would be the tibia and the fibula. 脛骨と腓骨です。 2 34 And they come down kind of like a wrench to grip that spool bone of the talus. それらの骨はレンチのように下がり、 糸巻き型の距骨をつかんでいます。 I ll refine this a bit, badly. ちょっと直しますね。 Sorry about that, I m a bad influence with my hunt and scratch lines. すみません、 このような線の描き方では皆さんに悪影響を与えてしまいますね。 2 51 I ll offer my excuse for it later. 釈明はあとでします。 Right now, I just apologize for it. とりあえずは謝罪にとどめます。 2 56 Let s put that spool in there. 糸巻きをここに置きましょう。 Since it s extended, the Y lines won t point straight up and down. 足を延ばしているので、 つま先などにある縦の線は垂直になりません。 They ll aim off in that direction. それらはこっちの方へ傾きます。 And cross contours make us sure of the form, and we don t have all right angles there. そして、交差した等高線によって形が明確になりますが、 まだ正しい角度とは言えません。 We ve got some beveled, slanted lines. 斜めに傾斜した線を引きましょう。 Before I turn this into an abomination, it is so embarrassing to be seen in the privacy of one s hesitations. このスケッチがひどいことになる以前に、 こうやって試行錯誤している様子を見られるのはとても恥ずかしいですね。 I wish we could just speed it up. 早くしましょう、 Segue into the ... 速やかに、 There, that s better. 出来ました。 まあいいでしょう。 3 52 There we are, all dressed up for the debut and no embarrassing personal scratching. 個人的なスケッチのお披露目が恥ずかしくないように 整えてみました。 3 59 Thank you very much, Marshall! That was a great little demo. ありがとうMarshall！！ 素晴らしい実演でした。 Marshall s other demos for the Joint assignment are in the Premium section of the Anatomy Course. Marshallのその他の関節の課題のための実演は、 解剖学の有料コースにあります。 If you d like to see Marshall construct these joints while explaining some perspective principles plus all the other Anatomy premium content go to proko.com/anatomy. もしMarshallの、透視図法における原則の説明も加えた 関節の構成と、その他の有料の解剖学資料が見たいのなら、 proko.com/anatomyにアクセスしてください。
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開発環境 Microsoft Visual C++ 2010 Express (SP1) 実行環境 Microsoft Windows XP Home Edition (SP3) プロジェクトの種類 Win32 コンソール アプリケーション プロジェクト名 files2 アプリケーションの種類 コンソール アプリケーション 追加のオプション 空のプロジェクト 文字セット Unicode files2.c #include fcntl.h // _O_WTEXT #include io.h // _setmode #include stdio.h // _fileno #include stdlib.h #include tchar.h int files(const _TCHAR *ptcDir); int _tmain() { _TCHAR atcDir[_MAX_PATH]; size_t size; // BOMなしUTF-16LE _setmode(_fileno(stdout), _O_WTEXT); _setmode(_fileno(stderr), _O_WTEXT); _tgetcwd(atcDir, _countof(atcDir)); size = _tcslen(atcDir); if (0 size atcDir[size - 1] != _T( \\ )) { _tcscat_s(atcDir, _countof(atcDir), _T("\\")); } files(atcDir); return 0; } int files(const _TCHAR *ptcDir) { struct _wfinddata_t fi;// fileinfo _TCHAR atcPath[_MAX_PATH]; intptr_t handle; size_t sizeDir; sizeDir = _tcslen(ptcDir); if (_MAX_PATH = sizeDir + 4) { _ftprintf(stderr, _T("error パスが長過ぎます。%d[%s]\n"), sizeDir, ptcDir); return -1; } _stprintf_s(atcPath, _countof(atcPath), _T("%s*.*"), ptcDir); handle = _tfindfirst(atcPath, fi); if (handle == -1) { _ftprintf(stderr, _T("error _tfindfirst[%s]\n"), ptcDir); return -1; } do { if (fi.attrib _A_SUBDIR) { if (!_tcscmp(fi.name, _T(".")) || !_tcscmp(fi.name, _T(".."))) { continue; } if (_MAX_PATH = sizeDir + _tcslen(fi.name) + 1) { _ftprintf(stderr, _T("error パスが長過ぎます。[%s][%s]\n"), ptcDir, fi.name); continue; } _stprintf_s(atcPath, _countof(atcPath), _T("%s%s\\"), ptcDir, fi.name); files(atcPath); } else { _tprintf(_T("%10u %s%s\n"), fi.size, ptcDir, fi.name); } } while (_tfindnext(handle, fi) == 0); _findclose(handle); return 0; }
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