Search PubMed⌕ Search

Biomedical subjects

R R Miller

Publications and source records attributed to R R Miller.

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

Seeding of malignant cells into the needle track after lung and pleural biopsy.

Transthoracic needle biopsy is frequently performed for the diagnosis of pulmonary and pleural disease. Seeding of malignant cells is a potential complication but is extremely uncommon. We report the second patient with malignant seeding after fine-needle aspiration biopsy of a bronchogenic carcinoma. We also report a patient with seeding of bronchogenic carcinoma after a pleural biopsy. Because seeding is a rare complication, it does not affect the indications for biopsy.

Adenocarcinoma, Papillary↗
PubMed1986

Malleability of conditioned associations: path dependence.

Using conditioned suppression of barpressing to investigate the stability of a conditioned stimulus-unconditioned stimulus (CS-US) association, we gave water-deprived rats either a few pairings of the CS with a strong footshock US or many pairings with a weak footshock US so that barpress suppression in response to the CS was equated. Experiment 1 established training parameters that yielded this equivalence. Specifically, rapid acquisition to a preasymptotic level of responding with strong shock produced suppression comparable to the asymptotic level reached more slowly with weak shock. Experiment 2 showed that although equivalent performance was obtained from extensive conditioning with a weak shock or limited conditioning with strong shock, only extensive conditioning with weak shock resulted in retarded acquisition of an association between that same CS and a footshock level perceived as midway between the two initial training shock intensities as implied by asymptotic performance in Experiment 1. Experiment 3 demonstrated that the observed retardation in animals given many conditioning trials with weak shock was CS specific. Collectively, these findings indicate that the malleability of learned behavior is not simply a function of initial associative strength but is dependent on path during initial acquisition.

Animals↗
PubMed1985

A retrograde gradient for disruption of a conditioned aversion to drinking cold water by ECS administered during the CS-US interval.

Rats were used to examine the effects, upon a conditioned aversion to cold drinking water, of electroconvulsive shock (ECS) delivered during the delay between cue and unconditioned stimulus. An injection of LiCl (US) 30 min after ingestion of novel cold water (CS) produced a reliable aversion to the cold water. ECS given immediately following the ingestion of cold water substantially attenuated this aversion. An orderly decrease in the attenuation of the aversion was observed when ECS was delayed 5, 10 or 20 min after offset of the cold water cue. The results indicate that ingestive cue aversions can be formed without electrochemical neural-transmission-based representation of the cue being maintained during the CS-US interval. The differential effectiveness of ECS suggests that this agent retroactively interferes with processing of the ingestive cue.

Amnesia↗
PubMed1985

The roles of information reactivation and nonassociative arousal in recovery from ECS-induced retrograde amnesia.

Restoration of memory by pretest reminder treatments following ECS-induced amnesia in principle could be mediated by nonassociative arousal and/or reactivation of information by the reminder stimuli. In the present research, arousal value of the reminder treatment was largely a function of the novelty of the context in which the reminder cues occurred. After producing ECS-induced amnesia in rats for a signaled passive avoidance task, presentation of the signal outside of the training and test context proved to be an effective reminder cue. However, prereminder familiarization with the reminder location, which was sufficient to reduce exploratory behavior suggestive of a decrease in the arousal value of the context, did not influence recovery from amnesia. These data indicate that reminder treatments are capable of reversing experimental amnesia by initiating further processing of previously acquired information even when the treatment does not produce appreciable arousal.

Amnesia↗
PubMed1985

Diethylene glycol monomethyl ether 13-week vapor inhalation toxicity study in rats.

Male and female Fischer 344 rats were exposed to 0, 30, 100, or 216 ppm diethylene glycol monomethyl ether (DEGME) vapors (0, 0.15, 0.49, or 1.06 mg/liter) 6 hr/day, 5 days/week, for 13 weeks. The 216-ppm exposure level was the maximum practically attainable concentration, and it was more than 60% of the theoretical maximum vapor concentration for DEGME at 25 degrees C and 1 atm pressure. Body weights, organ weights, hematological analyses, clinical chemistry analyses, urinalyses, and gross and histopathological examinations revealed no indication of a treatment effect in either male or female rats. Based on the absence of treatment-related effects in this study and the low vapor pressure of the material, DEGME should not present the same degree of inhalation hazard as its structural homolog, ethylene glycol monomethyl ether.

Animals↗
PubMed1985

Metabolism and disposition of dipropylene glycol monomethyl ether (DPGME) in male rats.

Male Fischer 344 rats were given a single oral dose of approximately 1289 mg/kg (8.7 mmol/kg) of [14C]DPGME. After dosing, expired air, excreta, and tissues were analyzed for 14C activity, and metabolites in urine were isolated and identified. Approximately 60% of the administered 14C activity was excreted in urine, while 27% was eliminated as 14CO2 within 48 hr after dosing. DPGME, PGME, dipropylene glycol, propylene glycol, as well as sulfate and glucuronide conjugates of DPGME were identified in urine of animals given [14C]DPGME. Results of the study indicate that DPGME is metabolized via the same routes to the same general types of metabolites as previously identified for propylene glycol monomethyl ether (PGME).

Animals↗
PubMed1985

Gastrointestinal blood flow and O2 uptake in piglets: recovery from hypoxemia.

Gastrointestinal (GI) blood flow, O2 transport, and O2 uptake were measured during recovery from severe hypoxemia in newborn piglets. Hypoxemia was induced by lowering the inspired O2 concentration to 0.05 for 15 min. This resulted in an 82% decrease in GI O2 uptake. Recovery measurements were obtained 5 and 65 min after restoration of normoxia. During early recovery (5 min), GI O2 uptake increased above prehypoxemia baseline, presumably to "repay" the O2 deficit incurred during hypoxemia. This was mediated by an increase in the arteriovenous O2 content difference, as GI blood flow did not increase above prehypoxemia baseline. During late recovery (65 min), GI blood flow, O2 delivery, and arteriovenous O2 content difference decreased below prehypoxemia baseline. This resulted in a 52% decrease in GI O2 uptake below prehypoxemia baseline. Therefore, early recovery was characterized by an appropriate increase in GI O2 uptake; however, late recovery was characterized by a significant reduction in GI O2 transport and uptake. Circulatory homeostasis was not reestablished during the late recovery period.

Animals↗
PubMed1985

Chronic toxicity and oncogenicity bioassay of inhaled ethyl acrylate in Fischer 344 rats and B6C3F1 mice.

Male and female Fischer 344 rats and B6C3F1 mice were exposed to 0, 25 or 75 ppm (0, 0.10 or 0.31 mg/l) ethyl acrylate vapors, 6 hours per day, 5 days per week, for a total of 27 months. Additional rats and mice were exposed to 225 ppm (0.92 mg/l) for 6 months and then held for 21 additional months post-exposure. Histopathologic changes in olfactory portions of the nasal mucosa were present in animals in all of these three exposure groups. These microscopic exposure-related changes were concentration-dependent, primarily in terms of distribution of the lesions within the nasal cavity. Generally those areas of the nasal mucosa normally lined by olfactory epithelium were altered, while the regions lined by respiratory epithelium were relatively unaffected. There was no indication of an oncogenic response in any organ or tissue in either rats or mice. A follow-up study in which Fischer 344 rats and B6C3F1 mice were exposed to 5 ppm (0.02 mg/l) for 24-months revealed no treatment-related changes in the nasal mucosa.

Acrylates↗
PubMed1985

Blocking but not conditioned inhibition results when an added stimulus is reinforced in compound with multiple pretrained stimuli.

Conditioned barpress suppression by rats was used to explore the associative status of an initially neutral stimulus that was reinforced in simultaneous compound with two independently pretrained conditioned excitors. In contrast to the Rescorla-Wagner model, which predicts that the target stimulus (X) will be inhibitory following such A+/B+/ABX+ training, the present study found no evidence that X acquired inhibitory associative strength. Rather, the pretrained stimuli merely served to block conditioned excitatory responding to the target stimulus.

Animals↗
PubMed1984

Propylene glycol monomethyl ether acetate (PGMEA) metabolism, disposition, and short-term vapor inhalation toxicity studies.

Male Fischer 344 rats were given a single po dose of approximately 8.7 mmol/kg of [1-14C]propylene glycol monomethyl ether acetate (PGMEA) or exposed to 3000 ppm [1-14C]PGMEA for 6 hr. After dosing, expired air, excreta, and tissues were analyzed for 14C activity, and metabolites in urine were isolated and identified. Approximately 64% of the administered 14C activity was eliminated as 14CO2 and about 24% was excreted in urine within 48 hr after a single po dose of radiolabeled PGMEA. Similarly, 53% was eliminated as 14CO2 and 26% was excreted in urine within 48 hr after the inhalation exposure. Propylene glycol, propylene glycol monomethyl ether (PGME), and the sulfate and glucuronide conjugates of PGME were identified as urinary metabolites after po dosing, as well as after inhalation exposure to PGMEA. The urinary metabolite profile and disposition of [14C]PGMEA were nearly identical to results previously obtained with propylene glycol monomethyl ether (PGME), indicating that PGMEA is rapidly and extensively hydrolyzed to PGME in vivo. A short-term vapor inhalation toxicity study in which male and female Fischer 344 rats and B6C3F1 mice were exposed to 0, 300, 1000, or 3000 ppm PGMEA confirmed that there were no substantial differences in the systemic effects of PGMEA as compared to PGME. However, histopathologic examination did reveal changes in the olfactory portions of the nasal mucosa of rats and mice exposed to PGMEA, which may be related to acetic acid resulting from hydrolysis of PGMEA in the nasal epithelium.

Animals↗
PubMed1984

Structural features and some binding properties of proteoheparan sulfate enzymatically labeled by calf brain microsomes.

Previous studies established that brain microsomes catalyze the transfer of [35S]sulfate from 3'-phosphoadenosine 5'-phospho[35S]sulfate to an O-linked oligosaccharide chain of a membrane glycoprotein and sulfamino groups of a membrane-associated proteoheparan sulfate (R. R. Miller and C. J. Waechter (1979) Arch. Biochem. Biophys. 198, 31-41). A large fraction of the proteoheparan [35S]sulfate can be released by treating the enzymatically labeled membranes from calf brain with 1 M NaCl. The salt-extracted 35S-labeled proteoglycan has been partially purified by a combination of ion-exchange and gel filtration chromatography. Based on chromatographic analyses, the 35S-labeled proteoglycan labeled in vitro is proposed to be a family of proteoheparan [35S]sulfates having an average molecular weight estimated to be 55,000. Variation in the length of the 35S-labeled polysaccharide chains partially accounts for the differences in molecular size of the proteoheparan [35S]sulfates. Binding studies reveal that the intact proteoheparan [35S]sulfates, as well as the free 35S-labeled polysaccharides released by mild alkali treatment, rapidly reassociate with calf brain membrane preparations. The association with calf brain membranes is saturable and reversible. Consistent with the binding being a specific interaction, only iduronic acid-containing glycosaminoglycans inhibit the association of the 35S-labeled proteoglycan with calf brain membranes and facilitate the disassociation. Neither the binding of the 35S-labeled proteoglycan to membranes nor the displacement was affected by hyaluronic acid, chondroitin 4-sulfate, or chondroitin 6-sulfate. The binding of the enzymatically labeled proteoheparan sulfate is reduced by preincubating membranes with either trypsin or chymotrypsin, but not with neuraminidase or phospholipase D. These results suggest that at least one class of proteoheparan sulfates could be specifically bound to one or more brain membrane proteins. The results also suggest a role for iduronosyl residues, and perhaps the stereochemical relationship of the carboxyl group to the O-sulfate moiety at C-2, in the recognition process.

Animals↗
PubMed1984

Hemodynamic effects of oral smokeless tobacco in dogs and young adults.

Oral smokeless tobacco (snuff) is increasingly used among the young male population. To determine cardiovascular effects of an oral smokeless tobacco product, 10 anesthetized dogs were instrumented to measure blood pressure, heart rate, left ventricular end diastolic pressure, and circumflex coronary, renal, and femoral flows. After a 5-min baseline, a 2.5-g, approximately 1.2% nicotine bolus dose was placed in the buccal space, and measurements were made for 20 min. Significant increases were seen in heart rate, blood pressure, left ventricular pressure, left ventricular end diastolic pressure, and left ventricular dP/dt. Significant decreases in flow were noted in the coronary circumflex, renal, and femoral arteries. The flow reduction was thought to have been mediated by an alpha-adrenergic mechanism. Additionally, 20 human males, mean age 20 years, without nicotine exposure for 72 hr, were given a 2.5-g dose of the same oral smokeless product. From baseline to 20 min, heart rate increased from 69 to 88 beats/min (P less than 0.05), blood pressure from 118/72 to 126/78 mm Hg (P less than 0.05). Thus, oral smokeless tobacco use can produce significant hemodynamic changes in both dogs and normal humans.

Administration, Oral↗
PubMed1984

Effect of alpha-adrenergic blockade on arrhythmias induced by acute myocardial ischemia and reperfusion in the dog.

Studies in cats suggest alpha-adrenergic contributions to arrhythmias during myocardial ischemia and reperfusion. The validity of this concept in other species, however, remains uncertain. Thus, 106 chloralose-anesthetized open-chest dogs undergoing a 25 min coronary artery occlusion followed by reperfusion received saline (n = 52), prazosin (1 mg/kg, n = 26), phentolamine (5 mg/kg, n = 18), or phentolamine (same dose) + propranolol (1 mg/kg, n = 10). Alpha-blockade was confirmed by alpha-agonist dose-response studies. In phentolamine-treated dogs, arterial pressure and heart rate were kept constant to prevent exacerbation of ischemia. Control and treated groups were comparable with respect to variables known to affect arrhythmias, such as size of occluded and reperfused vascular beds, coronary collateral flow, severity of ischemia estimated from intramyocardial CO2 tension, and peak reactive hyperemia. During coronary occlusion, the number of single premature ventricular complexes was reduced by phentolamine (P less than 0.01), but not by prazosin or phentolamine + propranolol; no treatment affected the total number of couplets, ventricular tachycardia episodes and ventricular ectopic complexes, or the incidence of ventricular tachycardia and ventricular fibrillation. During coronary reperfusion, arrhythmias did not differ in control and treated groups. Thus, selective alpha 1-(prazosin), nonselective alpha 1- and alpha 2-(phentolamine), and combined alpha- and beta-blockade (phentolamine + propranolol) failed to attenuate complex arrhythmias induced by acute myocardial ischemia and reperfusion. Alpha-adrenergic mechanisms appear unimportant in the genesis of these arrhythmias in the canine model.

Adrenergic alpha-Antagonists↗
PubMed1984

Membranoproliferative glomerulonephritis and amyloidosis.

The first known case of membranoproliferative glomerulonephritis co-existing with amyloidosis is reported. The question of whether the amyloidosis was secondary to the glomerulonephritis or whether primary amyloidosis co-existed with membranoproliferative glomerulonephritis is addressed.

Amyloidosis↗