Biomedical subjects
R Briggs
Publications and source records attributed to R Briggs.
Acute toxicity in the guinea pig and in vitro "dioxin-like" activity of the environmental contaminant 1,2,4,5,7,8-hexachloro (9H)xanthene.
A number of sites in the state of Missouri have been contaminated with polychlorinated dibenzodioxins and dibenzofurans as a result of improper waste-oil application for dust control. In addition to these compounds, relatively high levels of 1,2,4,5,7,8-hexachloro(9H)xanthene (1,2,4,5,7,8-HCX), a by-product of hexachlorophene manufacture, were also detected. Unlike the dibenzodioxins and dibenzofurans, no animal toxicity data are available on the chlorinated xanthenes. In view of the potential importance of this novel class of environmental contaminants, studies were conducted to examine the acute oral toxicity in guinea pigs and in vitro "dioxin-like" activity of 1,2,4,5,7,8-HCX. Animals administered a single oral dose of 0.02, 0.1, 0.5 or 2.5 mg 1,2,4,5,7,8-HCX/kg in corn oil and sacrificed 42 d later exhibited no treatment-related pathology. Guinea pigs given 12.5 mg/kg displayed mild to moderate distension and histologically observable subserosal edema of the urinary bladder, in addition to mild fatty vacuolization of pancreatic acinar cells. The alterations were considered to be of minimal toxicological significance. No compound- or dose-related mortality, body weight loss, or organ weight changes were noted at any dose level. Results using an in vitro bioassay for "dioxin-like" activity confirmed preliminary data suggesting that 1,2,4,5,7,8-HCX is about 10(6) times less potent than 2,3,7,8-tetrachlorodibenzo-p-dioxin (2,3,7,8-TCDD) in this assay system. These findings indicate that 1,2,4,5,7,8-HCX may represent a relatively low environmental hazard compared to 2,3,7,8-TCDD.
Persistently low blood retinol levels during and after parenteral feeding of very low birth weight infants: examination of losses into intravenous administration sets and a method of prevention by addition to a lipid emulsion.
Very low birth weight infants have little storage of hepatic retinol and are, therefore, highly dependent upon an exogenous supply. The recent association between low serum retinol level and bronchopulmonary dysplasia and the persistently low serum levels of retinol during total parenteral nutrition prompted a prospective study to evaluate serial changes in serum retinol levels during 1 month of total parenteral nutrition (retinol dose 455 micrograms/d) and again during 1 month of total enteral feeding (retinol dose 200 to 300 micrograms/d) in the same infants. Infants were divided into two groups. Group 1 consisted of infants weighing less than 1,000 g (n = 24) and group 2 consisted of infants weighing 1,000 to 1,500 g (n = 17). Although initial mean levels of retinol were similar in both groups (14.8 +/- 0.9 and 13.5 +/- 0.7 micrograms/dL), there was wide variation between infants. In group 1 infants, there was a significant (P less than .01) decline in retinol level by the second week of life (to 9.2 +/- 1 micrograms/dL), which persisted during total parenteral nutrition, but increased to 13.4 +/- 2 after 1 week of enteral feeding. This level was maintained throughout enteral feeding. In group 2 infants, there was no significant change in serum retinol level throughout the study. During total parenteral nutrition, several infants had retinol levels below 10 micrograms/dL, a level associated with signs of retinol deficiency in older children. Because losses of retinol are known to occur in smaller volume total parenteral nutrition solutions, it was speculated that losses of retinol in our patients were due to retinol losses in the total parenteral nutrition delivery system.(ABSTRACT TRUNCATED AT 250 WORDS)
Administration of MPTP to the common marmoset does not alter cortical cholinergic function.
The administration of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) to common marmosets induced persistent motor deficits and decreased concentrations of dopamine, homovanillic acid, and 3,4-dihydroxy-phenylacetic acid (DOPAC) and [3H]dopamine uptake in the caudate-putamen. There was an 80% reduction in tyrosine hydroxylase immunoreactive cells in substantia nigra. At 10 days following the start of MPTP administration, the activity of choline acetyltransferase in the thalamus and frontal cortex was unchanged compared with control animals. Similarly, specific [3H]QNB binding was unaltered. At 4-6 weeks following the start of MPTP treatment, choline acetyltransferase activity and [3H]QNB binding in the frontal cortex and thalamus remained unaffected. There was no evidence for cell loss in the nucleus basalis of Meynert or alteration in the intensity of staining for acetylcholinesterase. MPTP treatment of the common marmoset produces a nigrostriatal lesion. In contrast, MPTP did not alter cortical cholinergic function and was not neurotoxic to the cholinergic cells in the nucleus basalis of Meynert.
A bioavailability study of two preparations of tamoxifen after single doses.
The bioavailability of two different tablet formulations of tamoxifen was studied in twelve healthy male volunteers. Two tablets, each of 10 mg, of both preparations were administered orally at intervals of two weeks in a randomized cross-over design. Samples of blood for tamoxifen measurement were taken for up to 48 h following administration. Tamoxifen was measured by an HPLC method sensitive to 2.0 ng ml(-1). The area under the concentration-time curve was similar for both preparations. The study, therefore, did not demonstrate any differences between the bioavailability of the two preparations of tamoxifen.
Ion-exchange resin bezoar in a neonate.
A case of impacted ion-exchange resin causing intestinal obstruction associated with intraluminal calcification is described. This cause of bowel obstruction with intraluminal opacification has not previously been reported.
Photochemical reactions in interstellar grains photolysis of CO, NH3, and H2O.
A simulation of the organic layer accreted onto interstellar dust particles was prepared by slow deposition of a CO:NH2:H2O gas mixture on an Al block at 10 K, with concomitant irradiation with vacuum UV. The residues were analyzed by GC-MS, HPLC, and near IR; a reaction pathway leading from NH3 to complex alcohol, fatty acid, and amide products in 27 stages is postulated. The astronomical relevance and significance of the observations are discussed.
Discovery and initial characterization of a new conditional (temperature-sensitive) maternal effect mutation in the axolotl.
The discovery of a new temperature-sensitive maternal effect mutation in Ambystoma mexicanum is described. The new gene (ts-1) was recognized when 100% of the eggs spawned by homozygous females failed to develop past early gastrulation when reared at 25 degrees C. Eggs raised at 10 degrees C developed normally to sexual maturity. A temperature-sensitive period during blastulation was identified by a preliminary series of temperature shifts. Histologic examination revealed that nuclear abnormalities, especially chromosomal bridges, characterized ts-1 embryos reared beyond the ninth cleavage at the restrictive temperature (25 degrees C).
Instrumental methods of monitoring and control of water and wastewater treatment processes.
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A current appraisal of the abnormal Pap smear.
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Calcium-dependent action of osmolality on adenosine 3',5'-monophosphate accumulation in rat renal inner medulla: evidence for a relationship to calcium-responsive arachidonate release and prostaglandin synthesis.
When urea and NaCl are employed as the major solutes of high osmolality buffers, the cyclic AMP (cAMP) content of oxygenated slices of rat renal inner medulla increases three- to fivefold as osmolality is decreased from 1,650 to 305 mosM. Incubation of slices in Ca2+-free media containing 2 mM EGTA largely abolished this action of osmolality on cAMP, whereas exclusion of Mg2+ or 5+ from the incubation media was without effect. Addition of Ca2+ to Ca2+-deprived inner medulla incubated at 750 mosM (175 mM Na+, 380 mM urea) significantly increased tissue cAMP and media prostaglandin (PG)E accumulation. Ca2+ also stimulated the release of 14C-fatty acid from Ca2+-deprived slices prelabeled with [14C]arachidonate, but not from those labeled with [14C]palmitate. The divalent cation ionophore A23187 enhanced the actions of Ca2+ to increase tissue cAMP, media PGE accumulation, and the release of [14C]-arachidonate from prelabeled inner medulla. By contrast, when slices were incubated at 1,650 mosM (365 mM Na+, 900 mM urea) in the presence or absence of A23187, all of these actions of Ca2+ were markedly suppressed or abolished. Addition of exogenous arachidonate increased tissue cAMP and media PGE at both 750 and 1,650 mosM, whereas palmitate and stearate had no effect on cAMP at either osmolality. The actions of Ca2+ and arachidonate to increase cAMP and PGE accumulation were abolished by the cyclo-oxygenase inhibitors, indomethacin and meclofenamate. They were also abolished by exclusion of molecular O2, which serves as cosubstrate with arachidonate in prostaglandin synthesis. At maximally effective concentrations, exogenous PGE2 and arachidonate produced similar increases in inner medullary cAMP. The maximal effects of the two agents on cAMP were not additive, but were expressed in the absence of Ca2+ at both 750 and 1,650 mosM. However, in marked contrast to the O2-dependent action of arachidonate, PGE2 increased cAMP in the presence or absence of O2. Comparison of the separate actions of urea and NaCl indicated that suppression of Ca2+-responsive [14C]arachidonate release, PGE, and cAMP accumulation at 1,650 mosM reflected primarily an effect of urea, whereas hypertonic NaCl, mannitol, and sucrose alone stimulated inner medullary cAMP and PGE accumulation by a pathway which did not require extracellular Ca2+. Analogous to the actions of hypertonic urea, tetracaine and mepacrine inhibited the actions of Ca2+ plus A23187 to stimulate [14C]-arachidonate release, PGE, and cAMP accumulation. Inhibition of PGE and cAMP accumulation by tetracaine and mepacrine was also overcome by arachidonate. The results suggest that high osmolaity media with urea as a major solute reduces inner medullary cAMP content, at least in part, through effects on Ca2+-dependent prostaglandin synthesis. Inhibition of PGE synthesis, in turn, may be the result of osmotic suppression of Ca2+-dependent release of arachidonate, the availability of which is often rate limiting to prostaglandin generation.
Genetics of cell type determination.
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Cellular and subcellular immunolocalization of alpha1-fetoprotein and albumin in rat liver. Reevaluation of various experimental conditions.
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Monitoring the effects of NHS investment in energy conservation--a management task.
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Mortality and ecological structure: a canonical approach.
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Intestinal fluid accumulation induced by oral challenge with Vibrio cholerae or cholera toxin in infant mice.
The diarrheal response of orally inoculated infant mice to viable Vibrio cholerae and purified cholera toxin was quantitated by means of a fluid accumulation (FA) ratio. The FA ratio is defined as the gut weight/remaining body weight. FA ratios were determined in relation to time of exposure and dose. Onset of fluid accumulation with viable cells of strains CA401 and 569B occurred 8 h postinoculation and reached a near maximum of 16 h. A dose of 4 x 10(6) colony-forming units of strain CA401 was required for a positive response 16 to 18 h postinoculation. Several other classical cholera strains demonstrated a similar dose-related response. Strain 569B, however, required a 100-fold higher dose to give a positive response. Several mutant cholera strains were decreased virulence in other model systems elicited FA ratios decreased from wild-type values. Onset of fluid accumulation which cholera toxin occurred 6 to 8 h postinoculation and reached a maximum by 10 h. A dose of 0.5 microng was required for a positive response 10 to 12 h postinoculation. The positive response to toxin could be inhibited by preincubation with specific antitoxin.
The consequences of imitative behavior in children: the "Evel Knievel syndrome".
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