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Biomedical subjects

D C Baker

Publications and source records attributed to D C Baker.

At least 37 records · Page 2Linked to original sources
PubMed1995

A unique pattern of hepatocyte proliferation in F344 rats following long-term exposures to low levels of a chemical mixture of groundwater contaminants.

Most exposures of humans to environmental agents involve mixtures of chemicals, rather than individual chemicals. Some chemicals can cause hepatocellular proliferation and act as neoplastic promoters. Little is known concerning hepatocellular proliferation caused by chemical mixtures such as those found in groundwater at hazardous waste sites. Therefore, a 6 month study was performed to investigate hepatocellular proliferation and histopathological changes in F344 rats after long-term, low-level exposure to a mixture of groundwater contaminants. The seven chemicals used are among the most frequently detected contaminants associated with hazardous waste sites; arsenic, benzene, chloroform, chromium, lead, phenol and trichloroethylene. Male F344 rats were exposed to this mixture, or submixtures of the organic or inorganic chemicals, via drinking water for 6 months. The study design included a time-course experiment (i.e. 3 and 10 days and 1, 3 and 6 months) and a dose-response experiment. Hepatocellular proliferation studies were performed by subcutaneously implanting osmotic mini-pumps to continuously deliver 5-bromo-2'-deoxyuridine for 7 days, which labeled nuclei of proliferating cells. In all groups, there were no differences in weight gain, body weight, liver weight ratios or liver-associated plasma enzymes. Light microscopic evaluation revealed no lesions related to the treatments in any animals. However, significant increases in hepatocellular labeling were observed at the 3 and 10 day and 1 month exposure time points after treatment with the full mixture, as well as the organic or inorganic submixtures. Proliferating hepatocytes expressed a unique labeling pattern surrounding large hepatic veins (0.5-2.0 mm), but not central veins. This did not appear to be a regenerative response due to cytotoxic mechanisms, as assessed by the absence of increased plasma enzyme activity and the absence of hepatocellular lesions.

Animals↗
PubMed1995

Naturally occurring Tyzzer's disease in a puppy.

A naturally occurring case of Tyzzer's disease due to infection with Bacillus piliformis in a wolf-dog hybrid resulted in widely disseminated lesions, including severe myocarditis, hepatitis, enterocolitis, intestinal leiomyositis, and adrenal cortical adenitis. Previously reported lesions for canine Tyzzer's disease have been limited to hepatic necrosis and a necrotizing enterocolitis.

Animals↗
PubMed1994

Multifocal myositis associated with Sarcocystis sp in a horse.

Multifocal myositis was diagnosed in a 7-year-old Quarter Horse gelding on the basis of history and findings on physical examination, serum biochemical analysis, electromyography, and microscopic examination of frozen sections of muscle biopsy specimens. Histologic examination of the muscle specimen revealed multifocal accumulations of histiocytes, lymphocytes, and plasma cells, with attendant myofiber degeneration and necrosis. Parasitic cysts with morphologic characteristics of Sarcocystis sp were found in regions of myocyte degeneration and necrosis, and in regions of normal muscle. Based on a tentative diagnosis of Sarcocystis sp-induced myositis, the horse was treated with trimethoprim/sulfamethoxazole and pyrimethamine for 28 days, phenylbutazone for 5 days, and paddock rest for 30 days. At the end of treatment, the horse had gained 35 kg, its appetite had returned to normal, and muscle mass was returning to normal. Sarcocystis fayeri is the only Sarcocystis sp reported in equine muscle in the United States and is rarely associated with acute myositis or muscle atrophy. The development of clinical signs in this horse could have been the result of an underlying immunosuppression or infection with a particularly pathogenic strain or large infective dose of S fayeri.

Animals↗
PubMed1994

A synthetic route to 3-C-alkyl (or 3-C-phenyl-) 2,3-dideoxy-D-erythro-pentono-1,4-lactones: intermediates in the synthesis of 2(3H)-furanones.

A series of 3-C-alkyl- (and 3-C-phenyl-) 2,3-dideoxy-D-erythro-pentono-1,4-lactones, compounds which are important in the synthesis of modified nucleosides and antibiotic sugars, were synthesized from D-ribonolactone. By a route that proceeded via 5-O-protected D-ribonolactone, 5-O-protected 2,3-dideoxy-D-glycero-pent-2-enono-1,4-lactones were synthesized and reacted with R2CuLi or a complex PhSCu(RMgBr)n to give respectively the 3-C-alkyl or 3-C-phenyl compounds. Details of the preparation of the O-protected intermediates, as well as the selection of the organometallic reagents, are provided.

4-Butyrolactone↗
PubMed1994

Synthesis of some 2-C-alkyl-2,3-dideoxy-alpha,beta-L-glycero-tetrurono-1,4-lactones . Evaluation as antitumor agents.

A series of 3-C-alkyl-2,3-dideoxy-5-O-trityl-D-erythro-pentono-1,4-lactones were detritylated. The resultant free-hydroxy compounds were converted to their respective 2-C-alkyl-2,3-dideoxy-alpha,beta-L-glycero-tetrurono-1,4-lactones (L-sugar numbering) in a one-vessel reaction sequence of (a) conversion of the lactones to their aldonic acid sodium salts, (b) cleavage of the resulting aldonates with sodium metaperiodate, and (c) acidification, followed by acetylation, to give the title compounds. The unsubstituted tetrurono-1,4-lactones were inhibitory toward L1210 leukemia cells at concentrations in the 10(-4) M range.

Animals↗
PubMed1994

Comparison of topical magnesium and calcium treatment for dermal hydrofluoric acid burns.

STUDY OBJECTIVE: To compare topical preparations of magnesium and calcium in the treatment of dermal hydrofluoric acid burns. DESIGN: A randomized, blinded, controlled animal model study. SETTING: Animal care facility. TYPE OF PARTICIPANTS: New Zealand rabbits. INTERVENTIONS: Each rabbit was burned with hydrofluoric acid at four sites along the thoracolumbar spine. Equimolar amounts of calcium gluconate, magnesium gluconate, and a magnesium hydroxide antacid were added into a lubricating jelly. The jelly alone was a control preparation. After a water rinse, the burns were massaged with the gels for 1 minute five times; at 4 and 20 minutes and at 1, 4, and 24 hours. Each rabbit served as its own control by receiving all four treatments. MEASUREMENTS AND MAIN RESULTS: Burn diameter and burn surface area diminished over time, but there were no statistically significantly differences among the treatments. Burn ranking and burn rating of severity also did not demonstrate differences. The histologic analysis of the burns, however, demonstrated that calcium gluconate-treated burns were less severe and more superficial than the control and magnesium gluconate-treated burns; the magnesium hydroxide antacid-treated burns were not statistically different compared to the calcium gluconate-treated burns. CONCLUSION: Topical calcium gluconate is an efficacious treatment for dermal hydrofluoric acid burns. Further research is needed to determine the role of magnesium-containing antacids in the treatment of hydrofluoric acid burns.

Administration, Cutaneous↗
PubMed1993

Synthesis and evaluation of 3-modified 1D-myo-inositols as inhibitors and substrates of phosphatidylinositol synthase and inhibitors of myo-inositol uptake by cells.

A number of 3-substituted 1D-myo-inositols were synthesized and evaluated as substrates for phosphatidylinositol synthase and uptake by intact cells. 1D-3-Amino-, -3-chloro-, and -3-(acetylthio)-3-deoxy-myo-inositols were all synthesized by nucleophilic displacement of the 6-O-(trifluoromethyl)sulfonyl group of 1L-1,2:3,4-di-O-cyclohexylidene-5-O-methyl-6-O-[(trifluoromethyl)-sulfon yl] - chiro-inositol (which was prepared from L-quebrachitol), respectively, by reaction with LiN3, followed by reduction of the azido function, and with LiCl and KSAc to give the O-protected compounds. O-Demethylation using BBr3 and concomitant acetal hydrolysis furnished the free-hydroxy 3-amino- and 3-chloro-3-deoxy-1D-myo-inositols. The 3-mercapto analogue was obtained by removal of the acetal groups of the acetylthio analogue, followed by acetylation and purification of the peracetate, and subsequent O-demethylation and deacetylation. The 3-deoxy derivative was synthesized from the 6-O-(imidazol-1-ylthiocarbonyl) compound via Barton-McCombie deoxygenation. The 3-azido derivative was directly synthesized from 1L-1-O-tosyl-chiro-inositol via displacement with azide. The 3-keto analogue was prepared by Pt-catalyzed air oxidation of 1L-chiro-inositol. The compounds were all evaluated as substrates for phosphatidylinositol (PtdIns) synthase from mouse brain. The 3-NH2, 3-F, 3-deoxy, and 3-keto analogues all showed activity as substrates, as measured by liberation of cytidine monophosphate. These compounds also showed inhibition of the reaction of myo-[3H]inositol with PtdIns synthase. These results taken together indicate that these compounds are likely to be incorporated into phospholipids. As a further indication that these compounds might be useful as probes for the PtdIns pathway, it was demonstrated that the 3-NH2, 3-F, and 3-deoxy compounds are taken up by intact fibroblast cells as evidenced by their competing with myo-[3H]inositol uptake.

Acetates↗
PubMed1993

The relationship of the canine acanthomatous epulis to ameloblastoma.

This paper compares the microscopic features and clinical behaviour of the acanthomatous epulis in dogs with those of ameloblastoma in human beings. The acanthomatous epulis has similar microscopic features to one histological variant of human ameloblastoma, the acanthomatous ameloblastoma. Moreover, its clinical behaviour is equivalent to that of intraosseous ameloblastoma in human beings, not of the human peripheral (extraosseous) ameloblastoma, as has been suggested. The stroma of acanthomatous epulides varies and does not always resemble periodontal ligament, a feature that in dogs has been used to distinguish them from ameloblastomas. It is concluded that the acanthomatous epulis (1) is an ameloblastoma, (2) arises from the gingival epithelium in some cases, but (3) may also arise intraosseously and then break out of bone. We recommend the term canine acanthomatous ameloblastoma as being appropriate for this lesion.

Ameloblastoma↗
PubMed1993

Bovine myocardial epithelial inclusions.

Light microscopic, histochemical, immunohistochemical, and ultrastructural methods were used to examine myocardial epithelial masses in the hearts of ten cattle. The tissues consisted of paraffin-embedded or formalin-fixed samples from eight hearts that were being inspected in slaughter houses and from two hearts from calves that died of septicemia. The ages of the cattle ranged from 4 days to 12 years; the breeds were unspecified for all but one Hereford female and the two Holstein calves; and there were three males, four females, and three steers. The masses in these cases were compared with similar appearing lesions found in other animal species. The lesions in the bovine hearts were single to multiple, well circumscribed, found in the left ventricle wall, and composed of squamous to cuboidal epithelial cells that formed tubular, ductular, and acinar structures with lumens that were void or filled with amorphous protein globules. Electron microscopic examination revealed epithelial cells that had sparse apical microvilli, tight apical intercellular junctions, perinuclear bundles of filaments, and rare cilia. Almost half of the bovine epithelial masses (4/9) had occasional diastase-resistant periodic acid-Schiff-positive granules in their cytoplasm, and few had hyaluronidase-resistant alcian blue-positive granules (2/9) or colloidal iron-positive granules (1/9). All myocardial masses had abundant collagen surrounding the tubular and acinar structures, and 2/9 had elastin fibers as well. None of the myocardial masses had Churukian-Schenk or Fontana Masson's silver staining granules in epithelial cells. Immunohistochemically, all bovine myocardial tumors stained positively for cytokeratin (8/8), and occasional masses stained positively for vimentin (3/8) or carcinoembryonic antigen (3/8). None of the masses stained positively for desmin. The myocardial epithelial tumors most likely represent endodermal rests of tissue misplaced during organogenesis.

Animals↗
PubMed1991

Design of 9-beta-D-arabinofuranosyladenine (ara-A) transdermal delivery system for animal studies: regulation of drug concentration in vivo.

Transdermal delivery systems of 9-beta-D-arabinofuranosyladenine (ara-A), having controlling membranes of various permeabilities, were developed and applied to Azone-pretreated hairless mouse abdominal skin. It was confirmed that the blood concentrations of ara-A and its metabolite 9-beta-D-arabinofuranosylhypoxanthine (ara-H) in hairless mice are controlled by the permeability of the controlling membrane in the transdermal patch. Furthermore, these blood concentrations were found to closely agree with the values obtained from theoretical model calculations. Finally, but importantly, the "micropharmacokinetic" behavior of ara-A in cutaneous tissue could also be predicted. These results suggest that the transdermal patch may be employed in dermal and transdermal ara-A efficacy studies in the treatment of cutaneous herpes virus infections in hairless mice.

Administration, Cutaneous↗
PubMed1991

Fibromatous epulis in dogs and peripheral odontogenic fibroma in human beings: two equivalent lesions.

This article compares the clinical and histopathologic features of the peripheral odontogenic fibroma in human beings and the fibromatous epulis in dogs. They are apparently equivalent lesions. Both are odontogenic tumors of limited growth potential that do not recur if adequately excised; both occur in middle and late adulthood of the species concerned. The one difference is that the peripheral odontogenic fibroma is a rare condition, whereas the canine fibromatous epulis is common.

Animals↗
PubMed1991

Cynoglossum officinale toxicity in calves.

Six calves were given dried, ground Cynoglossum officinale daily in a dose which provided 15 (two calves) or 60 (four calves) mg per kg per day of total pyrrolizidine alkaloids. Those calves given 60 mg per kg of total pyrrolizidine alkaloids per day died following a single dose of plant material. These calves had a marked elevation of serum gamma-glutamyltransferase (GGT) and aspartate transaminase (AST) activities and serum bile acid and total bilirubin (TBili) concentrations. These four calves all had massive hepatocellular necrosis and haemorrhage of the liver. Of the two calves that were given 15 mg per kg of total pyrrolizidine alkaloids per day, one died on day 34 and the other survived until day 35 when it was painlessly killed. There were significant elevations in serum AST and GGT activities in these calves. The histological lesions of the calf surviving until 35 days were compatible with pyrrolizidine alkaloid toxicity, that is megalocytosis, karyomegaly and necrosis of hepatocytes with karyomegaly of biliary epithelium. The pyrrolizidine base present in Cynoglossum officinale (heliotridine) and its esters have a similar type of toxicity to the highly toxic and more familiar macrocyclic diester pyrrolizidine alkaloids of the pyrrolizidine base (retronecine), present in Senecio or Crotolaria species.

Animals↗
PubMed1991

Toxicity of pyrrolizidine alkaloids from Riddell groundsel (Senecio riddellii) to cattle.

The toxicity of Riddell groundsel (Senecio riddellii) gavaged to calves at a known lethal rate was compared with the toxicity of riddelliine and riddelliine N-oxide, the pyrrolizidine alkaloids isolated from the plant, which were fed by intraruminal infusion. Doses of the alkaloids were adjusted to the amount determined to be in the plant and fed individually and in combination. The relative toxicosis in the calves was measured by clinical signs, serum enzyme changes, survival time to morbidity, and histologic changes. Calves fed Senecio riddellii by gavage for 20 consecutive days to provide 45 mg of total pyrrolizidine alkaloids/kg of body weight/d developed clinical signs and serum enzyme changes typical of seneciosis, with 100% morbidity. However, calves receiving riddelliine at 4.5 mg/kg/d for 20 days had neither serum enzyme changes nor clinical signs of pyrrolizidine alkaloidosis. Calves treated with riddelliine N-oxide (40.5 mg/kg/d), and with riddelliine (4.5 mg/kg/d) and riddelliine N-oxide (40.5 mg/kg/d) in combination, had 100% morbidity, although the latter group had fewer liver lesions. These results establish that the N-oxide form of the alkaloid alone is capable of inducing typical Senecio toxicosis in cattle and that the free base level of the plant cannot be considered to be the sole factor in assessing the toxicity of S riddellii.

Animals↗
PubMed1990

C-methylation occurs during the biosynthesis of heme d1.

The biosynthetic origin of methyl groups in heme d1 isolated from the nitrite reductase cytochrome cd1 was investigated by a stable isotope labeling experiment. Pseudomonas aeruginosa (American Type Culture Collection strain 19429) was grown on a minimal medium supplemented with [13C]methionine. The enzyme was purified, the heme extracted, converted into the free base methyl ester derivative, and purified. 1H NMR and 13C NMR indicated that only the methyl groups attached to C2 and C7 are derived from methionine.

Bacterial Proteins↗
PubMed1990

Spirosolane-containing Solanum species and induction of congenital craniofacial malformations.

Comparison by GC analysis of purified alkaloid extracts of Solanum species revealed no measurable free solasodine, other spirosolanes, or any non-spirosolane steroidal alkaloid aglycones in unhydrolyzed total alkaloid fractions of fruit of Solanum elaeagnifolium Cav. (silverleaf nightshade), Solanum sarrachoides (S. villosum Lam.--hairy nightshade), Solanum dulcamara L. (European bittersweet nightshade) or Solanum melongena L. (eggplant). All alkaloidal material was apparently present as glycoside. Conversely, sprouts of Solanum tuberosum L. (potato) contained 67% of its alkaloids as glycosides, which was freed only upon hydrolysis with the remaining 33% present as free solanidine. GC/MS analysis of hydrolysates of purified extracts of the test Solanum species revealed that solasodine was a principal or sole aglycone of the alkaloid glycosides in each of the test species except Solanum tuberosum. In the latter, solanidine was the sole aglycone. Among the test species, exclusive of S. tuberosum, only S. dulcamara contained aglycones other than solasodine. In addition to solasodine, S. dulcamara contained appreciable amounts of an unknown spirosolane, an aglycone provisionally identified as soladulcidine. The induction of congenital craniofacial malformations in hamsters by high oral doses of the four Solanum species that contained mainly solasodine glycosides--S. elaeagnifolium, S. dulcamara, S. sarrachoides and S. melongena was compared to inductions of malformations by Solanum tuberosum, that contained mainly solanidane glycosides. Compared to controls, Solanum elaeagnifolium and Solanum dulcamara fruit both induced a high percentage incidence of deformed litters (20.4 and 16.3, respectively) that was statistically significant (P less than 0.001 level) while percentage incidence of deformed litters induced by Solanum sarrachoides and Solanum melongena fruit (9.5 and 7.6 respectively) were both higher than controls (3.4%), in neither case was the incidence statistically significant (P less than .05). Deformed litter incidence induced by sprouts of Solanum tuberosum was 24.0%, (P less than 0.001).

Animals↗
PubMed1990

Myopathy in cattle induced by alkaloid extracts from Thermopsis montanta, Laburnum anagyroides and a Lupinus sp.

A purified alkaloid preparation containing N-methylcytisine, cytisine, 5,6-dehydrolupanine, thermopsine and anagyrine from Thermopsis montana induced prolonged recumbency and microscopic acute hyaline skeletal myodegeneration with myofibre regeneration in cattle similar in type and severity to that induced by Thermopsis montanta plant material. This indicates that the alkaloid(s) of Thermopsis montana are responsible for the myopathy caused by the plant. An alkaloid preparation containing mostly anagyrine from a Lupinus sp. and an alkaloid preparation containing only cytisine from Laburnum anagyroides each caused microscopic skeletal muscle degeneration and necrosis similar to, but less severe than, the alkaloid extract from T. montana, but without clinical recumbency. Dosage and severity of response suggest that neither of those two alkaloids alone can account for the effects induced by Thermopsis. The data suggest that quinolizidine alkaloids with a alpha-pyridone A-ring may be responsible for the lesions and that individual alpha-pyridones may have additive effects.

Alkaloids↗