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Biomedical subjects

G H Nelson

Publications and source records attributed to G H Nelson.

119 records · Page 7Linked to original sources
PubMed1966

Toxicity to rats of corn invaded by Chaetomium globosum.

Of 53 isolates of Chaetomium globosum Kunze isolated from corn, manufactured feed, and fiberboard, grown on autoclaved corn, and fed to rats, 25 were lethal within 4 to 6 days. Thirty-six single ascospore cultures of one isolate were uniformly lethal when similarly grown and fed to rats. Incubation of the fungus on corn for 6 to 8 weeks resulted in greater toxicity than shorter incubation times. Premortem symptoms indicated damage to the central nervous system of the affected animals, and postmortem lesions included hemoglobinuria, hemorrhagic enteritis, and subdural hemorrhaging. Corn invaded by C. globosum and toxic to rats had no detectable effects on swine when fed as their sole ration for 6 weeks, and appeared to be consumed with relish. The toxic substance was best obtained by defatting the fungus-invaded corn with petroleum ether (bp, 60 to 70 C), extraction with acetone, and further purification by elution from a silica gel column with acetone and 5% acetone in chloroform.

Animals↗
PubMed1965

Effect on the white rat uterus of a toxic substance isolated from Fusarium.

Eighty-five fungi isolated from prepared feed and from corn collected on farms were grown separately in moist autoclaved corn. The corn was fed to virgin weanling rats for 5 to 12 days; the rats were then killed, and their uteri were removed and weighed. Twelve isolates of Fusarium from corn and one from poinsettias caused increases of five to eight times in weight of the uterus as compared with controls that were fed sound corn. The greatest increase in weight of the uterus was caused by corn inoculated with Fusarium No. 5 incubated for 21 days at 20 to 25 C followed by 14 days at 12 C. Extraction of this corn with methylene chloride, separation into fractions by means of a silicic acid column, and further purification by thin-layer chromatography yielded a compound with ultraviolet-absorption maxima at 314, 274, and 236 mmu.

Animals↗
PubMedDate not supplied

Effects of estradiol on platelet aggregation in cerebral microvessels of mice.

Mice were implanted subcutaneously with a pellet containing 0.5 mg estradiol or with a placebo. Eight to 12 days later platelet aggregation was produced in pial arterioles by injuring their endothelium in vivo with a noxious light/dye stimulus. The time between the onset of the noxious stimulus and the appearance of platelet aggregates was significantly shortened (p less than .02) by estradiol treatment in young (2 month old) mice. The same treatment had the opposite effect in 4-6 month old mice and significantly delayed the onset of aggregation (p = .01). When platelet rich plasma (PRP) was prepared, aggregation by sodium arachidonate was always inhibited in PRP from estradiol treated mice, irrespective of age. Estradiol treatment had no effect on aggregation induced ex vivo by ADP. Thus the enhanced aggregation observed in pial arterioles of young estradiol treated mice may not reflect direct effects of estradiol on the platelet itself. The data are discussed in light of the literature suggesting enhancement of ischemic vascular disease, including strokes, in patients receiving estrogens, and especially high doses of estrogens.

Adenosine Diphosphate↗
PubMedDate not supplied

Ultrastructural studies of pial vascular endothelium following damage resulting in loss of endothelium-dependent relaxation.

The changes in pial arterioles of 7 cats were examined by electron microscopy after injury that eliminates endothelium-dependent relaxation to acetylcholine or bradykinin. The injury was produced by exposing the vessels to mercury light in situ in the presence of intravascular sodium fluorescein dye. Previous studies showed that, at the time of initial injury and loss of endothelium-dependent responses, the endothelial cells displayed minimal ultrastructural evidence of injury. Because these changes might indicate the beginning of a sequence of irreversible alterations representing or leading to cell death, the present study was carried out 31/2-4 hours later, when ultrastructural evidence of progressive cell degeneration should readily be recognized. No such changes were observed. Instead, most vessels showed only the minimal alterations observed initially (endothelial vacuolation, blebs, and lucencies). Four of 19 vessels were completely normal. The findings fail to support the hypothesis that irreversible cell damage or death caused by the light + dye injury has caused the associated loss of endothelium-dependent relaxation. Rather, the findings support the concept that much lesser degrees of trauma are sufficient to impair the dilating responses of cerebral microvessels. This greatly expands the potential spectrum of pathologic states that might result in loss of endothelium-dependent relaxation.

Animals↗
PubMedDate not supplied

Endothelium dependence of a portion of the response to cGMP in brain microcirculation of mice.

The diameters of arterioles 30-40 microns on the surface of the mouse brain were monitored by TV microscopy with an image splitting technique. Endothelium was injured by light from a helium neon laser in the presence of intravascular Evans blue. This method was previously shown to selectively eliminate dilation by known endothelium dependent dilators which cause endothelial cells to release one or more relaxing factors (EDRFs). Dilation was produced by local application of 8 Br cGMP and dibutyryl cAMP, 10(-5) M. The response before endothelial damage was compared with the response after damage. Two separate studies were conducted. In one, 10 mice were treated with 8 Br cGMP and 10 with dibutyryl cAMP. In the second study 12 mice were treated with each nucleotide before endothelial injury and again after injury. In both studies only the response to 8 Br cGMP was impaired (p less than .01) by the endothelial injury. These data suggest that in these arterioles a portion of the response to GMP, but not to AMP, is controlled by endothelium and may reflect a role for guanylate cyclase/GMP in the synthesis/-release of an EDRF. This would provide a function for the guanylate cyclase in endothelial cells. The function of guanylate cyclase within these cells has not previously been defined.

Animals↗
PubMedDate not supplied

Propagated constriction in mouse pial arterioles: possible role of endothelium in transmitting the propagated response.

Two lines of evidence are presented demonstrating propagated constriction in mouse pial arterioles. First, a 2 second microapplication from a 6 micron pipette tip of approximately 12 nanoliters of BaCl2 or uridine triphosphate produced constrictions which spread to points 300 microns or more upstream from the point of application. Second, constrictions were elicited between 2 points of endothelial injury, each made with a focused laser beam 18 microns wide. A helium-neon laser was used in the presence of intravascular Evans blue. The constrictions were produced when a very brief exposure at a downstream site was followed by a more prolonged exposure at an upstream site 300 to 1100 microns from the downstream injury. In approximately half the cases the upstream damage elicited a local platelet aggregate. Therefore, vasoconstrictors released by aggregating platelets may have played a role in initiating constriction. Constriction was limited to the segment between the two endothelial injuries. The necessity for 2 injuries, rather than one, suggests that local losses of endothelium derived vasodilators also played a role in initiating constriction and/or permitting its propagation. Abrupt cessation of constriction at the sites of endothelial damage suggests that endothelium plays a role in propagation of constriction. Propagated constriction may play a role in amplifying the spasmotic effects of local subarachnoid hemorrhage or in the spread of constriction beyond local areas of reduced metabolic demand.

Animals↗
PubMedDate not supplied

Intrauterine diagnosis of hydrothorax in a fetus who had a combination chylothorax and pulmonary sequestration after delivery.

Congenital hydrothorax was diagnosed prenatally by transabdominal ultrasonography. Five fetal thoracentesis procedures were performed and biochemical analyses of the fluids were done. After delivery a combination chylothorax and extralobar pulmonary sequestration was demonstrated in the infant. We believe this to be the first case report of this combination investigated prenatally. We suggest that investigators perform biochemical analyses on fetal pleural fluid removed in cases with a single diagnosis. Perhaps by comparing those data with the data reported here, a biochemical marker can be identified that will be useful in distinguishing these two conditions in utero.

Adult↗