Monkey

A new source of safrole that Strike has just stumbled upon is in Strike s back yard. Momma comes home from the local nursery with two plants that have these enormous leaves. They are succulents and grow like crazy. Strike What ya got there Momma Momma Don t think I haven t noticed those filthy drug books you write, you sick little monkey Strike Aw c mon. Mom. Let s not get into this again. Strike doesn t... Momma Well I needed some new ground cover plants, and...sigh...I know you re into this twisted licorice thing...so I bought these weeds that are called Licorice Plants. ... 

Parylene s use in the medical field is linked to electronics. Certain pacemaker manufacturers use it as a protective conformal coating on pacemaker circuitry (69). The coated circuitry is sealed in a metal can, so that the parylene coating serves only as a backup should the primary barrier leak. There is also interest in its use as an electrode insulation in the fabrication of miniature electrodes for long-term implantation to record or to stimulate neurons in the central or peripheral nervous system, as the "front end" of experimental neural prostheses (70). One report describes the 3-yr survival of functioning parylene-coated electrodes in the brain of a monkey (71). 

The time-weighted average (TWA) concentrations for 8-h exposure to bromine ttifluoride, bromine pentafluoride, chlorine ttifluoride, chlorine pentafluoride, and iodine pentafluoride have been estabHshed by ACGIH on a fluoride basis to be 2.5 mg/m. NIOSH reports (121) the foUowing inhalation toxicity levels for chlorine ttifluoride LC q monkey, 230 ppm/h LC q mouse, 178 ppm/h for chlorine pentafluoride LC q monkey, 173 ppm /h mouse, 57 ppm/h. 

The LC q (lowest possible lethal concentration) has been reported to be 23 ppm for a 30 min exposure time (mouse), 53 ppm for an exposure time of 100 min (rat, rabbit, and guinea pig), and 200 ppm for an exposure time of 10 min (monkey). No toxic effects were reported upon exposure to 1 ppm for 7 h/d over 55 days. The oral LD q (rat) of ketene is 1300 mg/kg, the low level of toxicity probably being due to the almost immediate formation of acetic acid and other acetates in the digestive tract. 

Coconut. In 1988, total coconut production was 36,802,000 t, of which 81% was produced in Asia, mainly in Indonesia and the Philippines (157). The coconut is essentiaUy a crop of the lowland tropics (157). On the average, five nuts are required to produce 1 kg of copra, the dried endosperm of the nut. Copra is further processed to obtain coconut oil and copra meal. To produce coconut milk, which is an emulsion of coconut oil and water, grated fresh coconut meat is mixed with hot water and pressed (157). Either poles having an attached sickle-shaped knife or monkeys (158) may be used for harvesting. 

Numerous experiments on rodents, as well as dogs and monkeys, with dosage levels up to 43 g of MSG per kilogram of body weight have failed to show any link between dietary use of MSG and brain damage. In the case of dogs and monkeys, even experiments involving injection of MSG have not shown any effects on the brain. 

Cancerous skin lesions of workers exposed to pitch dust undoubtedly support the behef that these lesions are caused by polynuclear aromatic hydrocarbons, although it had not been possible to demonstrate their carcinogenic action in animals more closely related to humans, such as monkeys. 

Metabolism. Absorption, distribution, metaboHsm, and excretion of thioglycolic acid have been reviewed (20). In summary,. -thioglycolic acid was absorbed significantly after appHcation to the skin of rabbits. After intravenous injection, the greatest counts of radioactivity were found in the kidneys, lungs, and spleen of monkey and in the small intestine and kidneys of rat. Most of the radioactivity was rapidly excreted in the urine in the form of inorganic sulfate and neutral sulfur. 

Toxicity. Vitamin D toxicity was known as eady as the year 1429 (217). Accidental toxicity has been reported in monkeys, dogs, horses, pigs, chinchillas, and humans, and particulady in catde when extremely high doses of vitamin D have been used to treat milk fever. 

The symptoms of vitamin E deficiency in animals are numerous and vary from species to species (13). Although the deficiency of the vitamin can affect different tissue types such as reproductive, gastrointestinal, vascular, neural, hepatic, and optic in a variety of species such as pigs, rats, mice, dogs, cats, chickens, turkeys, monkeys, and sheep, it is generally found that necrotizing myopathy is relatively common to most species. In humans, vitamin E deficiency can result from poor fat absorption in adults and children. Infants, especially those with low birth weights, typically have a vitamin E deficiency which can easily be corrected by supplements. This deficiency can lead to symptoms such as hemolytic anemia, reduction in red blood cell lifetimes, retinopathy, and neuromuscular disorders. 

Malaria is transmitted by the bite of an infected female Anopheles mosquito, one of the few species of the insect capable of carrying the human malaria parasite. The responsible protozoa ate from the genus P/asmodium of which only four of some 100 species can cause the disease in humans. The remaining species affect rodents, reptiles, monkeys, birds, and Hvestock. The species that infect humans are P/asmodium falciparum Plasmodium vivax Plasmodium malariae and Plasmodium ovale. Note that concomitant multiple malaria infections are commonly seen in endemic areas, a phenomenon that further compHcates choice of treatment. 

Ribavirin is not incorporated into the DNA or RNA of either mammalian or viral systems. It has been shown (123), however, that a high dosage of ribavirin given over a prolonged period to Rhesus monkeys results in anemia of red blood cells. This effect is dose related and reversible upon cessation of treatment. Guanosine partially reverses the antiviral effect of ribavirin against certain vimses. 

Phosphonylmethoxyethyl)adenine [106941-25-7] (PMEA, 65) (173), synthesized in 1987 (174), is foremost among the acycHc nucleoside analogues proven to be effective inhibitors of HIV-1 repHcation. The in vitro potency and selectivity of PMEA is comparable to the antiHIV-1 potency and selectivity of 2, 3 -dideoxy-adenosine (175). Although less potent than AZT in vitro PMEA, CgH22N 04P, is markedly more potent than AZT as an in vivo inhibitor of retrovims repHcation (176). In fact, PMEA has proven efficacious in the treatment of murine, feline, and simian retrovims infections in mice, cats, and monkeys, respectively. 

Ethylene oxide has been shown to produce mutagenic and cytogenic effects in a variety of test systems (226). An increased frequency of chromosomal aberrations in peripheral lymphocytes of monkey exposed to ethylene oxide for 104 weeks has been reported (240). In mice, it is an effective inducer of chromosome breaks leading to dominant-lethal mutations. In addition, ethylene oxide has been shown to induce heritable effects in the heritable translocation test conducted in mice exposed to ethylene oxide by inhalation (241,242). In this study, male mice were exposed to ethylene oxide ranging from 165 to 300 ppm for 6 h per day 5 or 7 days/week for 8.5 weeks. Ethylene oxide has also been shown to bind to proteins (243) as well as to DNA (244). Several studies on ethylene oxide-exposed workers have demonstrated an increased incidence of chromosomal aberrations and sister chromatid exchanges the relevance of such effects to human health evaluation is currendy uncertain. 

Alloxan (1003) has been observed in the mucus associated with dysentery and it was the very first pyrimidine made synthetically when Brugnatelli oxidized uric acid in 1818. Alloxan has an interesting diabetogenic action which appears to be associated with removal of essential zinc from insulin by chelation. Such permanent diabetes may be induced in fish, dogs, cats, sheep, some birds, monkeys and other creatures, but not in man, owls or guinea-pigs certain pyrimidines related to alloxan show some such activity. 

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