PubMed Health⌕ Search

Biomedical subjects

W O'Neil

Publications and source records attributed to W O'Neil.

9 recordsLinked to original sources
PubMed2000

A syntactic specialization for Broca's area.

Despite numerous aphasia and functional imaging studies, the exact correlation between cortical language areas and subcomponents of the linguistic system has not been established. Here, we used functional MRI to identify cortical areas specifically involved in syntactic processing. An experimental design contrasted sentences containing grammatical errors with sentences containing spelling errors. The ungrammatical sentences produced more activation in cortical language areas than did the sentences with spelling errors, and the difference in activation was significantly greater in Broca's area than in Wernicke's area or in the angular gyrus/supramarginal gyrus. The present findings provide direct evidence of a syntactic specialization for Broca's area and establish the existence of distinct modules for our knowledge of language.

Adult↗
PubMed1994

Latent papillomavirus infection in cattle.

During a long term experiment designed to identify the contribution of bovine papillomavirus type 4 (BPV-4), environmental mutagens and immunosuppressants to the development of carcinomas of the upper alimentary tract of cattle, there was evidence of latent papillomavirus infection. Papillomatosis-free animals, when immunosuppressed either by feeding bracken fern or by azathioprine treatment, developed skin warts containing either BPV-1 or BPV-2. Skin warts appeared also in an immunocompetent animal at sites of damaged skin. It was concluded that the animals harboured latent papillomavirus which was reactivated by immunosuppression and/or physical trauma, causing skin warts. Papillomavirus DNA was also detected in lymphocytes of both experimental and control animals, suggesting that one of the sites of latency may be the circulating lymphocyte.

Animals↗
PubMed1989

Pharmacological activity of N-methyl-carbamylcholine, a novel acetylcholine receptor agonist with selectivity for nicotinic receptors.

N-Methyl-carbamylcholine (also called N-methyl-carbachol) is an analogue of the mixed muscarinic-nicotinic acetylcholine receptor agonist, carbachol. Previous studies have provided evidence that radiolabelled N-methyl-carbachol can bind selectively to nicotinic acetylcholine receptors in rat brain. To determine whether N-methyl-carbachol acts as an agonist or an antagonist at nicotine and/or muscarinic receptor sites, the present study examined the pharmacological activity of this compound on some cholinergically innervated tissues. N-Methyl-carbachol, like carbachol, depolarized rat isolated sympathetic ganglia and these effects were inhibited by a nicotinic antagonist, d-tubocurarine, but not by a muscarinic antagonist, atropine. Exposure of rat sympathetic ganglia to N-methyl-carbachol blocked the compound action potential generated in ganglia by stimulation of the pre-ganglionic trunk; this effect of N-methyl-carbachol was likely due to desensitization of the nicotinic response. N-Methyl-carbochol, like carbachol, stimulated the release of [3H]noradrenaline from cultured adrenal medullary cells that had been pre-loaded with [3H]noradrenaline; these effects were largely inhibited by a nicotinic antagonist, mecamylamine, while atropine produced less blockade. N-Methyl-carbachol contracted the frog isolated rectus abdominis muscle and the effect was completely blocked by d-tubocurarine. By contrast, contracture of the rectus abdominis produced by carbachol was partially inhibited by either atropine or d-tubocurarine. N-Methyl-carbachol, like carbachol, contracted the rat isolated ileum and these effects were completely blocked by atropine; however, N-methyl-carbachol was about 42 times less potent than carbachol for this effect. Intravenous injection of N-methyl-carbachol, like nicotine, to the rat produced a transient decrease followed by a more sustained rise in blood pressure while carbachol produced only a sustained decrease in blood pressure. The effects of N-methyl-carbachol and nicotine on blood pressure were blocked by pretreatment of the animal with a nicotinic antagonist, hexamethonium. N-methyl-carbachol, like nicotine, stimulated the release of [3H]dopamine from rat striatal synaptosomes, pre-loaded with [3H]dopamine; release induced by either N-methyl-carbachol or nicotine was inhibited by mecamylamine but not by atropine. In rat cerebral cortical slices pre-loaded with [3H]inositol, carbachol, but not N-methyl-carbachol, stimulated the accumulation of [3H]inositol-1-phosphate, an effect blocked by atropine but not by mecamylamine.(ABSTRACT TRUNCATED AT 400 WORDS)

Adrenal Medulla↗
PubMed1989

[High-frequency rotational atherectomy in coronary heart disease].

Percutaneous high frequency coronary rotational ablation (PTCR) was used in 10 patients with significant coronary artery disease. PTCR removes arteriosclerotic material from the vessel wall. A diamond-coated (60-80 micron) brass burr-drill, fastened to a flexible drive shaft rotating and tracking along a central coaxial guide wire, was used. The turbine rotates the drive shaft in excess of 150,000-190,000 revolutions per minute. PTCR was successful in all patients, but in three additional percutaneous transluminal coronary angioplasty (PTCA) was then successfully performed. Coronary dissection occurred only once, requiring surgery which was successful. No vessel perforation was observed. All vessels were open on the coronary angiograms performed after 24 hours. The main indication for PTCR seems to be a rigid and longer lesion which can not be dilated with the balloon catheter.

Angioplasty, Balloon↗
PubMed1988

Peptides derived from cleavage of prosomatostatin at carboxyl- and amino-terminal segments. Characterization of tissue and secreted forms in the rat.

Tissue and secreted forms of rat prosomatostatin and its cleavage products were characterized immunochemically using high performance liquid chromatography and sequence-specific radioimmunoassays directed against somatostatin-14 (S-14), S-28-(1-12), and S-28-(1-14). Acetic or hydrochloric acid extracts of hypothalamus, pancreas, stomach, and jejunum contained seven molecular forms of Mr = 10,400 (corresponding to prosomatostatin (pro-S], Mr = 6,800 (7-kDa peptide, consisting of an NH2-terminally truncated form of pro-S), Mr = 7,600 (8-kDa peptide, corresponding to pro-S-(1-76), i.e. pro-S minus the COOH-terminal -Arg-Lys-S-14), Mr = 5,600 (5-kDa peptide, corresponding to pro-S-(33-76)) and three peptides co-chromatographing with synthetic S-14, S-28, and S-28-(1-12). Acid/ethanol extracts of these tissues contained pro-S, 8-kDa peptide, S-28, S-14, and S-28-(1-12) forms, but not the 7- and 5-kDa species. Pepstatin inhibited 7- and 5-kDa peptide formation in acetic acid extracts of tissues. The secreted forms consisted of the same five forms present in acid/ethanol or acetic acid plus pepstatin tissue extracts. The 7- and 5-kDa peptides were not secreted and appeared to be derived artifactually, presumably through the action of renin- and cathepsin D-like acid proteases. Accurate quantitation of the 8-kDa peptide by acid/ethanol extraction revealed a variable tissue distribution. Since the presence of the 8-kDa form provides evidence for direct processing of pro-S----S-14 + 8-kDa peptide, the present data suggest that pro-S----S-14 conversion is important for S-14 synthesis in the hypothalamus and pancreas, tissues rich in the 8-kDa form, but not in the stomach and jejunal mucosa, which contain low concentrations of this peptide.

Amino Acid Sequence↗
PubMed1988

Failure of simple clinical measurements to predict perfusion status after intravenous thrombolysis.

To determine whether coronary patency could be detected early during thrombolytic therapy, commonly used markers of perfusion were recorded in 386 patients with acute myocardial infarction treated with tissue plasminogen activator. Infarct artery angiography 90 minutes after initiation of therapy was used to determine perfusion status. Of patients with complete resolution of ST segment elevation before the angiogram, 96% (95% confidence interval, 79% to 100%) showed perfusion on the angiogram, and among those with partial improvement, 84% (95% confidence interval, 76% to 90%) showed perfusion, but these findings occurred in only 6% and 38% of patients respectively. When complete resolution of chest pain occurred before the angiogram, 84% of patients (95% confidence interval, 75% to 90%) showed perfusion, but this finding occurred in only 29% of patients. Although arrhythmias occurred frequently in the first 90 minutes of therapy, none were associated with a higher patency rate. No other factors predicted coronary patency. A logistic regression model showed 25% of patients with 90% or greater probability of patency, but 56% of patients with no ST segment or symptom resolution had patent arteries.

Angina Pectoris↗
PubMed1977

Möbius syndrome due to brain stem tegmental necrosis.

Möbius syndrome undoubtedly results from a variety of disorders affecting central or peripheral portions of appropriate cranial nerves or their target muscles. Pathological alterations observed in cranial nuclei are most often viewed as aplastic or dysplastic lesions. Two patients with Möbius syndrome with associated facial and skeletal malformations showed mineralized necrotic foci in multiple brain stem nuclei. Prenatal encephalomalacic lesions represent the pathological basis for some cases of congenital static Möbius syndrome.

Cranial Nerves↗
PubMed1975

Symmetrical infantile thalamic degeneration with focal cytoplasmic calcification.

Infantile thalamic degeneration is a rare clinico-pathological entity. Restricted location of the lesion and peculiar cytopathological changes serve to distinguish this disorder from other common encephalopathies. Optical and ultrastructural studies demonstrate cytoplasmic calcopherules in previously viable cells. According to current concepts of acute cellular reactions to injury and mechanism of intracellular calcification, the cytological changes cannot be attributed to either hypoxic ischemic cell change or dystrophic calcification. By analogy to other human and pathological material, the most likely basis for nondystrophic calcopherule formation is toxic or infectious injury with local synthesis, or autophagic or phagolysosomal degradation of cellular debris of specific chemical composition favoring calcium deposition.

Brain Diseases↗