Search PubMed⌕ Search

Biomedical subjects

A Fine

Publications and source records attributed to A Fine.

At least 181 records · Page 10Linked to original sources
PubMed1986

Acetylcholine-rich neuronal grafts in the forebrain of rats: effects of environmental enrichment, neonatal noradrenaline depletion, host transplantation site and regional source of embryonic donor cells on graft size and acetylcholinesterase-positive fibre outgrowth.

The importance of several factors influencing the survival of cholinergic-rich embryonic tissue transplanted to the adult rat forebrain and the extent of acetylcholinesterase-positive fibre innervation of the host brain was investigated in 3 experiments. In the first two experiments, embryonic ventral forebrain tissue was grafted to the neocortex of rats in which the intrinsic cortical cholinergic innervation had been removed by nucleus basalis lesions. Housing the host rats in an enriched environment produced a temporary enhancement of fibre outgrowth 4 weeks after transplantation, but this was not maintained after 10 weeks. Fibre outgrowth was greater when the grafts were transplanted to the noradrenaline-depleted neocortex than to the intact neocortex. Neither environmental enrichment nor noradrenaline depletion influenced graft survival or size. In the third experiment, the embryonic donor tissue was dissected to separate regions containing precursors of the nucleus basalis cholinergic cells from regions containing precursors of the septal cholinergic cells, and transplanted to either the neocortex following nucleus basalis lesions or to the hippocampus following fimbria-fornix lesions. Nucleus basalis grafts showed greater growth in size than septal grafts, and grafts placed into the hippocampus showed greater growth in size than grafts placed into the neocortex. More interestingly, the extent of fibre outgrowth depended on the appropriateness of the donor tissue to the host transplantation site: nucleus basalis tissue showed greater acetylcholinesterase-positive outgrowth than septal tissue in the neocortex, whereas septal tissue showed greater outgrowth than nucleus basalis tissue in the hippocampus.

Acetylcholinesterase↗
PubMed1986

Nerve growth factor mRNA in peripheral and central rat tissues and in the human central nervous system: lesion effects in the rat brain and levels in Alzheimer's disease.

Nerve growth factor (NGF) mRNA is widely distributed throughout peripheral and central rat tissues and throughout the human central nervous system. In the rat, high levels were found in cerebral cortex, hippocampus and thalamus/hypothalamus, medium levels in striatum and brainstem and low levels in cerebellum and spinal cord. The hippocampal levels did not change following the surgical transection of the septohippocampal pathway; similarly, the ibotenic acid-induced lesion of the nucleus basalis magnocellularis did not affect the amounts of NGF mRNA in the cerebral cortex. NGF mRNA was also present in high amounts in human cortex and hippocampus, with only low levels in septum/nucleus basalis magnocellularis, suggesting that NGF may also function as a retrograde trophic messenger in the human central nervous system. No evidence was obtained for an insufficient production of NGF mRNA in senile dementia of the Alzheimer type. In peripheral rat tissues, the highest concentrations of NGF mRNA were found in vas deferens, heart, sciatic nerve, submandibular gland and skin, with low levels in tissues such as trigeminal ganglion and pituitary gland.

Alzheimer Disease↗
PubMed1986

Waldenström's macroglobulinemia in monozygotic twins.

This paper reports a unique familial occurrence of Waldenström's macroglobulinemia (WM) in monozygotic twins. The determination of twin monozygosity has been performed by electrophoretic and immunological typing of genetic systems (erythrocyte blood groups, leucocyte antigens and serum protein polymorphism). The two monoclonal IgM differ one from the other by their light chain type and their idiotypic determinants. Although a genetic predisposition to WM exists in these twins, the gene recombination leading to idiotypic specificity and light chain assortment occurs independently of the monoclonal malignant involvement.

Aged↗
PubMed1986

Effects of carbonic anhydrase inhibition on renal ammoniagenesis in the dog.

Acetazolamide was administered to normal dogs and its effects on total renal ammoniagenesis and glutamine extraction were studied. Urinary alkalinization resulted in diversion of urinary ammonia into the renal vein with no change in ammonia production or glutamine extraction. It is concluded that, contrary to reports about the rat, carbonic anhydrase inhibition has no effect on ammoniagenesis in vivo in the dog.

Acetazolamide↗
PubMed1985

Acute administration of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine affects the adrenal glands as well as the brain in the marmoset.

A parkinsonian syndrome was induced in marmosets by administration of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) for 4 days. Ten days following the onset of drug administration, brainstem and adrenal tissues were assayed for levels of monoamines and their metabolites. In the brainstem tegmentum, dopamine, its metabolites homovanillic acid (HVA) and dihydroxyphenylacetic acid (DOPAC), and noradrenaline were reduced, whereas 5-hydroxytryptamine (5-HT) levels were elevated, in comparison with untreated controls. In the adrenal gland, 5-HT and adrenaline levels were unchanged, but dopamine and noradrenaline were substantially elevated.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1985

Transplantation of embryonic ventral forebrain neurons to the neocortex of rats with lesions of nucleus basalis magnocellularis--I. Biochemical and anatomical observations.

Unilateral ibotenic acid lesions of the rat nucleus basalis magnocellularis produce approximately 60% depletion of choline acetyltransferase activity in ipsilateral frontal and frontoparietal neocortex. This depletion, which represents the loss of most of the extrinsic neocortical cholinergic input, is stable for at least 6 months. Embryonic ventral forebrain neurons survive transplantation to such cholinergically denervated neocortex. Cholinergic cells abound within these transplants and appear able to reinnervate the cholinergically depleted host cortex, as assessed histochemically and by measurement of choline acetyltransferase activity. Outgrowing fibres may extend beyond 2 mm from the grafts and often appear to be organized in an appropriate laminar pattern within the host cortex. Peptidergic neurons are sparse within the grafts and their fibres frequently appear unable to grow into the host tissue. Control grafts of non-cholinergic embryonic hippocampal cells survive well but have no effect on cortical depletions of acetylcholinesterase or choline acetyltransferase activity. Reconstruction of the extrinsic cholinergic input to the cortex by transplantation provides a useful tool for understanding the functions of this pathway.

Animals↗
PubMed1985

Transplantation of embryonic ventral forebrain neurons to the neocortex of rats with lesions of nucleus basalis magnocellularis--II. Sensorimotor and learning impairments.

The cholinergic projection from the nucleus basalis magnocellularis to the neocortex has been implicated in normal memory function and in the dementia of Alzheimer's disease. In order to investigate functions of this cholinergic system of the forebrain, rats with unilateral ibotenic acid lesions of the nucleus basalis magnocellularis have been compared with normal animals and with rats given cortically-placed transplants, either of cholinergic-rich embryonic ventral forebrain cells or of control noncholinergic cells taken from embryonic hippocampus. In the first experiment, lesions of the nucleus basalis magnocellularis led to impairments in step-through passive avoidance and Morris' water-maze tasks, and to locomotor hyperactivity attributable to a reduction in within-trial habituation. The ventral forebrain grafts, but not the noncholinergic hippocampal grafts, significantly ameliorated the deficits of passive avoidance retention, and of water-maze spatial accuracy, but had no effect on the acquisition impairments in either task, nor on the habituation deficit in locomotor activity of the nucleus basalis magnocellularis lesioned rats. In the second experiment, the lesions induced contralateral sensory neglect and ipsilateral turning biases, which were also partially ameliorated by the ventral forebrain grafts. The results support the hypothesis that the basal forebrain-neocortical cholinergic system contributes to certain memory processes, but suggest a more general role for this system in other cortical functions also.

Animals↗
PubMed1985

Cholinergic ventral forebrain grafts into the neocortex improve passive avoidance memory in a rat model of Alzheimer disease.

The memory dysfunction of Alzheimer disease has been associated with a cortical cholinergic deficiency and loss of cholinergic neurons of the nucleus basalis of Meynert. This cholinergic component of Alzheimer disease can be modeled in the rat by ibotenic acid lesions of the cholinergic nucleus basalis magnocellularis. The memory impairment caused by such unilateral lesions, as reflected in passive avoidance behavior, is reversed by grafts into the deafferented neocortex of embryonic neurons of the cholinergic ventral forebrain, but not by grafts of noncholinergic hippocampal cells.

Acetylcholinesterase↗
PubMed1985

1984 update on the world economic crisis and the children: a United States case study.

A previously published report by these authors on the impact in the United States of recession on children's health emphasized four points: available monitoring systems are not adequate for reporting on the health of children in a timely fashion; the monitoring of maternal and child health must emphasize data on population subgroups, i.e., minorities, the poor and those hardest hit by recession; the health of poor children is adversely affected and their numbers dramatically increased during the recession of 1981-82; and comparisons between the recession of 1974-75 and that of 1981-82 suggest that expansion of health services and social support systems during the recession of 1974-75 had a cushioning effect that protected the health of children, while the curtailment of many of these programs during the 1981-82 recession is associated with adverse health trends, especially among the most vulnerable population subgroups. Data on these issues are appreciably better now than they were nine months ago, thus further validating the points made above. As with the previous report, officially released current data are abundant for economic indicators (even for early 1984), but are sparse for health status indicators. The previous report also observed that the health status of children is influenced by interdependent and interlocking factors that include economic well-being and access to health services and social supports. A new analysis attempts to unlock those relationships and measure the impact of lost welfare benefits, implemented as a result of the Omnibus Reconciliation Act of 1981 (OBRA), and the separate impact of the serious recession of 1981-82. That analysis shows the poverty rate for children increased by 7.6 percentage points between 1981 and 1982. Approximately 60 percent of the increase is attributable to the recession and 40 percent to social policy changes effected after 1981.

Child↗
PubMed1985

The world economic crisis and the children: United States case study.

This is a review of the United States experience with issues of child health and services as they relate to changes in economic trends. No existing data systems are entirely adequate for reporting on the current health status of children. An important consideration for the monitoring of children's health in the United States is the status of subgroups such as those who are disadvantaged for reasons of poverty, discrimination or geographic isolation. Ample evidence confirms that children living in poverty suffer adverse health consequences and that the proportion of children living in poverty in the United States has increased steadily since 1975 and dramatically since 1981. Most measures of health status and health risks for children show steady improvements throughout the 1970s. The exercise of public responsibility for financing and providing essential services and supports held constant or improved during this period, especially during the recession of 1974-75. The health status and risks for children since 1981 appear to be adversely affected which must be attributed to a combination of circumstances that include serious recession, increased poverty rates for households with children and diminished health benefits and social support services. These findings suggest that when either local or widespread economic reversals are anticipated, health services and social supports for children need to be expanded rather than contracted.

Adolescent↗
PubMed1984

Release of lactate by the liver in metabolic acidosis in vivo.

Chronic metabolic acidosis was induced in dogs by HCl. Pyruvate and lactate production and extractions were studied by arteriovenous sampling and electromagnetic flow probe measurements of gut and hepatic blood flows. The following results were obtained: (1) In control, overnight-fasted dogs, no net lactate or pyruvate was extracted by the liver. (2) In chronic acidosis, large amounts of lactate were produced. (3) Reduced tissue pyruvate levels and reduced activity of pyruvate dehydrogenase were found in the liver of these dogs compared with normal. These results demonstrate an unexpected effect of acidosis on hepatic lactate metabolism.

Acidosis↗
PubMed1984

Digoxin-rifampin interaction.

Digoxin doses required to maintain therapeutic serum concentrations rose substantially in two patients dependent on dialysis with the commencement of rifampin therapy. When rifampin was discontinued, doses fell to requirements before rifampin. Serum digoxin concentration may fall to ineffective levels with rifampin therapy and rise to potentially toxic levels when rifampin is discontinued.

Digoxin↗
PubMed1984

Digoxin biotransformation.

Serum digoxin and metabolites were assayed in plasma and urine by HPLC in 10 dialysis-dependent patients with end-stage renal failure (group I) and in five patients with comparatively normal renal function (group II) after ingestion of 150 muCi 3H-digoxin-12 alpha. Thirteen patients were on maintenance digoxin therapy and were at steady state. Metabolites found regularly but usually in small amounts, were 3 beta-digoxigenin and its mono- and bis-digitoxosides, and 3-keto and 3 alpha(epi)-digoxigenin. Quantitatively the most abundant metabolites were polar and averaged 26% (7 to 76) of the radioactivity in plasma 6 hr after drug, and 60% (11 to 88) for digoxin for all 15 patients. Neither values between group I and II for the polar metabolites nor digoxin differed significantly. The metabolites reacted with antibody to digoxin to varying degrees and may make up an important component of the serum digoxin concentration when determined by standard radioimmunoassay. In some patients, digoxin undergoes extensive biotransformation, mainly, we suggest by hydrolysis, oxidation, epimerization, and conjugation to polar end-metabolites.

Administration, Oral↗