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Biomedical subjects

L C Green

Publications and source records attributed to L C Green.

34 records · Page 2Linked to original sources
PubMed1992

Pulmonary cestodiasis in a cynomolgus monkey (Macaca fascicularis).

Cestodiasis in primates has been noted historically to occur quite frequently, although tissue damage and clinical signs may or may not be apparent. Larval cestodes, such as hydatid cysts or cysticercus cysts, are known to cause extensive tissue damage, while other larval cestodes, such as tetrathyridia, cause minimal damage to the host. This case history concerns an apparently healthy cynomolgus monkey that was part of a surgical study. During the study, all parameters were normal. The monkey died 3 hours postsurgery. The apparent cause of death was respiratory arrest. At necropsy, it was discovered there were 1- to 3-mm-diameter cysts, which on transection extruded 2- to 5-mm-long larvae. The larvae could not be positively identified; however, they resembled tetrathyridia of Mesocestoides sp.

Animals↗
PubMed1984

In vivo dosimetry of 4-aminobiphenyl in rats via a cysteine adduct in hemoglobin.

The feasibility of monitoring doses of 4-aminobiphenyl (ABP) via adduction to hemoglobin was investigated. Rats dosed with ABP (from 0.5 micrograms/kg to 5 mg/kg) formed a stable covalent hemoglobin:ABP adduct. Approximately 5% of a single dose was bound as hemoglobin:ABP; chronic dosing led to an accumulation of the adduct to a level 30 times greater than that found after a single dose. Facile in vitro hydrolysis of the adduct regenerated ABP, allowing detection at the sub-ng level. Human hemoglobin was also readily adducted, using N-hydroxy-ABP in vitro. The predominant site of adduction appeared to be the cysteine residue in hemoglobin. The use of such adducts as dosimeters for arylamine exposures in humans is discussed.

Aminobiphenyl Compounds↗
PubMed1984

Monitoring exposure to 4-aminobiphenyl via blood protein adducts.

The feasibility of monitoring exposure to 4-aminobiphenyl (4-ABP) was determined by measuring the formation of covalent blood protein adducts in rats following administration of the amine. A single major adduct was obtained from serum albumin, which was formed from 4-acetylaminobiphenyl and the single tryptophan residue of albumin. The adduct was isolated as part of a tetrapeptide, following Pronase digestion and reverse-phase high-performance liquid chromatography purification, and was identified by amino acid analysis, 1H-nuclear magnetic resonance and mass spectrometry. This adduct was cleared in vivo and showed a half-life of 4.7 days, essentially identical to that of albumin. Similarly, 4-ABP yielded a single major adduct with haemoglobin. This adduct showed a stability in vivo that was comparable to that of haemoglobin, and was shown to accumulate, with chronic dosing, to a level 30 times higher than that resulting from a single dose. Treatment of adducted haemoglobin, with 0.1 N hydrochloric acid in acetone, caused hydrolysis and release of 4-ABP. The formation of the haemoglobin adduct involves 4-nitrosobiphenyl as an intermediate product and, by implication, 4-hydroxyaminobiphenyl. Thus, the haemoglobin adduct is a measure of the fraction of 4-ABP that is N-hydroxylated directly, whereas the albumin adduct reflects that portion which is acetylated prior to N-hydroxylation. Approximately 0.02% of a dose of 4-ABP was bound to the tryptophan in albumin (dose of 2-80 mg/kg) and 5% was bound to haemoglobin as an acid-labile adduct (dose of 0.5-5000 micrograms/kg).

Acetylation↗
PubMed1981

Nitrate synthesis in the germfree and conventional rat.

Metabolic balance studies show that germfree and conventional Sprague-Dawley rats synthesize nitrate. Equivalent results for germfree and conventional rats eliminate the microflora as obligatory components of nitrate production. Nitrate synthesis appears to be a mammalian process.

Animal Feed↗
PubMed1981

Nitrate biosynthesis in man.

Nitrate metabolism was investigated in long-term metabolic studies in healthy young men. Under conditions of constant low ingestion of nitrate (less than 180 mumol/day per subject), the amount of nitrate excreted in urine was an average of 4-fold greater than the amount ingested. Balance studies with 15NO3- showed that the source of the excess nitrate in urine was the endogenous biosynthesis of nitrate, rather than the emptying of a body pool. Nitrate biosynthesis occurred when nitrate ingestion was high as well as low, and the amounts synthesized appeared to be independent of intake and comparable to the amounts ingested from normal diets. Analysis of the 15NO3- data also revealed that half of ingested nitrate was recovered as urinary nitrate. Because nitrate in urine is the net result of (i) intake, (ii) endogenous synthesis, and (iii) metabolic losses, the magnitude of the losses is such that, despite ongoing synthesis, the amount of nitrate in the urine of people consuming most diets will be less than the amount ingested.

Adult↗
PubMed1979

Successful use of a bulk laxative to control the diarrhea of tube feeding.

The greatly increased nutritional demands of the severely burned patient frequently require the use of tube feeding for enternal hyperalimentation. At a time when general patient morale is low and motivation needs to be maximally maintained, there is nothing so dispiriting as the distress of a painful perianal region and uncontrollable liquid stools. Attempts to control the diarrhea which frequently accompanies tube feeding by changing the formula or the method of administration or a wide variety of constipating drugs have all met with very limited success. Based on the clinical observation of a noted gastroenterologist (Bockus), we have administered a mucilagenous hydrophilic colloid bulk laxative (Metamucil) to patients on tube feeding formulae. The dosage and frequency are adjusted to individual patient needs, but average 7 g per liter of liquid formula. The results have been dramatic; namely, the virtual elimination of the diarrhea problem in our burn patients on enteral hyperalimentation by gastric tube feeding. Colonic transit time increases. The stools become formed but soft, cohesive but not adhesive. Perianal irritation does not occur. Neither does soilage of wound, dressings, or bed. No rebound constipation or obstructive symptoms have been encountered. We attribute this response to the same water binding mechanism that allows these colloids to prevent chronic constipation. Our patients may be given as much as 5,000 to 6,000 calories of tube feeding per day. Our patients are not distressed by diarrhea. Our nursing staff is relieved of the burden that entails.

Burns↗
PubMed1978

Behavioral contracting in a burn care facility: a strategy for patient participation.

Behavioral contracting is a valuable tool for resolving persistent behavioral problems interfering with the treatment and recovery of severely burned patients. Coercive bidding of the patients for more control occurs in an environment where they experience extreme forms of loss of control and associated enforced regression. The ensuing conflicts between patient and staff often lead to breakdown in mutual cooperation, with deleterious effects on patient-staff morale. Staff experience highly ambivalent feelings toward a problem patient and may wish to withdraw from him, feeling threatened in their image of themselves as competent professionals. Beyond reducing disruptive conflicts on the ward, behavioral contracting aims to mobilize patient and staff around common and explicit goals, and to maximize patient cooperation and productive control in the recovery process. Contracts are valuable because: 1) they facilitate productive communication about issues which underlie patient-staff conflict; 2) they facilitate solutions to problem interactions between patients and staff; 3) they afford both patients and staff a sense or self-control. We provide a rationale for behavioral contracting and discuss the indications for initiating contracts with hospitalized burn patients, and describe methods for developing, implementing, and managing behavioral contracts in order to improve communication and effectiveness in patient-staff interactions.

Adolescent↗
PubMedDate not supplied

Fractionation of sporogonial stages of the microsporidian Encephalitozoon cuniculi by Percoll gradients.

Microsporidia are obligate intracellular parasites that are increasingly recognized as a cause of opportunistic infections in immunocompromised individuals. Encephalitozoon cuniculi has been identified in humans with AIDS and infects a wide range of mammalian hosts. Little is known about the metabolic processes that regulate growth and replication of microsporidia. Examination of the individual stages of development will facilitate such studies and reveal possible targets for drug therapy. The purpose of this study was to fractionate and purify stages of the microsporidian life cycle. Encephalitozoon cuniculi were cultured in RK-13 cells. The tissue supernatants containing multiple parasite stages, empty microsporidial husks and host cell debris were collected, washed, and subjected to differential centrifugation in 80% stock isotonic Percoll. Transmission electron microscopy and SDS-polyacrylamide gel electrophoresis were used to compare the content and purity of each fraction. Mature spores formed a band at a density of approximately 1.138 g/ml. Sporoblasts were found at densities between 1.102 g/ml and 1.119 g/ml. A mixture of sporonts, sporoblasts, microsporidial husks, and cell debris remained at the top of the gradient and additional centrifugation in 30% and 50% Percoll resulted in separation of these stages. These results represent the first step toward fractionating stages of microsporidia infecting humans.

Animals↗