Human feces

Recently, Blount et al. (2000) summarized a methodology to detect di- -butyl phthalate metabolites in urine. In humans or animals, di- -butyl phthalate is metabolized to mono- -butyl phthalate and oxidative products, which are excreted through the urine and feces. Human urine samples are processed by P-glucuronidase hydrolysis (to release the mono phthalate ester) followed by solid-phase extraction. The eluate is concentrated mono- -butyl phthalate is chromatographically resolved by reverse-phase HPLC, detected by negative ion atmospheric pressure chemical ionization (APCI) tandem mass spectrometry, and quantified by isotope dilution. 

Problems involving routine calculations are solved much faster and more reliably by computers than by humans. Nevertheless, there are tasks in which humans perform better, such as those in which the procedure is not strictly determined and problems which are not strictly algorithmic. One of these tasks is the recognition of patterns such as feces. For several decades people have been trying to develop methods which enable computers to achieve better results in these fields. One approach, artificial neural networks, which model the functionality of the brain, is explained in this section. 

The dermal adsorption of DEBT in humans has been studied in the Netherlands by appHcation of DEBT as undiluted technical material or as 15% solutions in alcohol. Labeled material was recovered from the skin, and absorption of DEBT was indicated by the appearance of label in urine after two hours of skin exposure. About 5—8% of the appHed treatments was recovered as metaboHtes from urine, and excretion of metaboHtes in the urine came to an end four hours after exposure ended. DEBT did not accumulate in the skin, and only a small (less than 0.08%) amount ended up in feces. Curiously, less has been absorbed through skin from 100% DEBT appHcation (3—8%, mean of 5.6%) than from 15% alcohol appHcation (4—14%, mean of 8.4%). These results have been described as consistent with previous absorption/metaboHsm studies using guinea pigs, rats, and hairless dogs. Other pubHcations on DEBT toxicology have been cited (92). 

Tb allium, which does not occur naturaHy in normal tissue, is not essential to mammals but does accumulate in the human body. Levels as low as 0.5 mg/100 g of tissue suggest thallium intoxication. Based on industrial experience, 0.10 mg /m of thallium in air is considered safe for a 40-h work week (37). The lethal dose for humans is not definitely known, but 1 g of absorbed thallium is considered sufficient to kHl an adult and 10 mg/kg body weight has been fatal to children. In severe cases of poisoning, death does not occur earlier than 8—10 d but most frequently in 10—12 d. Tb allium excretion is slow and prolonged. For example, tb allium is present in the feces 35 d after exposure and persists in the urine for up to three months. 

Antibacterial activity of clindamycin is found both in urine and feces after adrninistration of clindamycin. This activity is a consequence of the presence of both clindamycin and its metaboUte, de- /V-methy1c1indamycin [22431-45-4] (6, R = R = H). Unlike de-/V-methy11incomycin, the de-Ai-methyl analogue is as active in vitro as clindamycin. The analogue has been isolated from the urine of humans who had received clindamycin, and its presence in semm has been detected (65). 

Balantidiasis (balantidiosis, balantidial dysentery), an intestinal disease seen almost worldwide, is caused by the large ciUated protozoan, balantidium coll The organism is usually found in the lumen of the large intestine of humans and animals. Cysts formed in the lumen of the colon or in freshly evacuated feces of humans or domesticated and wild animals, can colonize the colon and terminal ileum of new hosts by the latter s ingestion of contaminated food or water. The hog has been found to be the most heavily parasitized host. Its association with the rat may be a means for maintaining a reservoir infection in the two animals. 

The absorption, distribution, and accumulation of lead in the human body may be represented by a three-part model (6). The first part consists of red blood cells, which move the lead to the other two parts, soft tissue and bone. The blood cells and soft tissue, represented by the liver and kidney, constitute the mobile part of the lead body burden, which can fluctuate depending on the length of exposure to the pollutant. Lead accumulation over a long period of time occurs in the bones, which store up to 95% of the total body burden. However, the lead in soft tissue represents a potentially greater toxicological hazard and is the more important component of the lead body burden. Lead measured in the urine has been found to be a good index of the amount of mobile lead in the body. The majority of lead is eliminated from the body in the urine and feces, with smaller amounts removed by sweat, hair, and nails. 

In the special case where two diastereomers differ at only one chirality center but are the same at all others, we say that the compounds are epimers. Cholestanol and coprostanol, for instance, are both found in human feces and... 

Alcohol sulfates are easily metabolized by mammals and fishes either by oral or intraperitoneal and intravenous administration. Several labeled 35S and 14C alcohol sulfates have been used to determine their metabolism in experiments with rats [336-340], dogs [339], swines [341], goldfish [342], and humans [339]. From all of these studies it can be concluded that alcohol sulfates are absorbed in the intestine of mammals and readily metabolized by to and p oxidation of the alkyl chain and excreted in the urine and feces, but are also partially exhaled as carbon dioxide. Fishes absorb alcohol sulfates through their gills and metabolize them in a similar way to that of mammals. 

A healthy adult human body contains about 3 g of iron, mostly as hemoglobin. Because about 1 mg is lost daily (in sweat, feces, and hair), and women lose about 20 mg in each menstrual cycle, iron must be ingested daily to maintain the balance. Iron deficiency, or anemia, results in reduced transport of oxygen to the brain and muscles, and an early symptom is chronic tiredness. 

No data were located concerning whether pharmacokinetics of endosulfan in children are different from adults. There are no adequate data to determine whether endosulfan or its metabolites can cross the placenta. Studies in animals addressing these issues would provide valuable information. Although endosulfan has been detected in human milk (Lutter et al. 1998), studies in animals showed very little accumulation of endosulfan residues in breast milk (Gorbach et al. 1968 Indraningsih et al. 1993), which is consistent with the rapid elimination of endosulfan from tissues and subsequent excretion via feces and urine. There are no PBPK models for endosulfan in either adults or children. There is no information to evaluate whether absorption, distribution, metabolism, or excretion of endosulfan in children is different than in adults. 

Elevated trichloroethylene levels in expired air were measured in subjects who immersed one hand in an unspecified concentration of trichloroethylene for 30 minutes (Sato and Nakajima 1978). Guinea pigs, exposed to dilute concentrations of aqueous trichloroethylene (-0.020 to 0.110 ppm) over a majority of their body surface area for 70 minutes, excreted 59% of the administered dose in the urine and feces 95% of the metabolized dose was excreted in 8.6 days (Bogen et al. 1992). No other studies were located for humans or animals regarding excretion after dermal exposure to trichloroethylene. 

Wells JE, PB Hylemon (2000) Identification and characterization of a bile acid 7a-dehydroxylation operon in Clostridium sp. strain TO-931, a highly active 7a-dehydroxylating strain isolated from human feces. Appl Environ Microbiol 66 1107-1113. 

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