Virilizing male pseudohermaphroditism. Association with abnormal testicular function.
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17-Hydroxycorticosteroids↗
Biomedical subjects
R R Miller
Publications and source records attributed to R R Miller.
Recovery of memory following amnesia.
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Amnesia↗
Retrograde amnesia produced by electroconvulsive shock after reactivation of a consolidated memory trace.
Rats had a memory loss of a fear response when they received an electroconvulsive shock 24 hours after the fear-conditioning trial and preceded by a brief presentation of the conditioned stimulus. No such loss occurred when the conditioned stimulus was not presented. The memory loss in animals given electroconvulsive shock 24 hours after conditioning was, furthermore, as great as that displayed in animals given electroconvulsive shock immediately after conditioning. This result throws doubt on the assertion that electroconvulsive shock exerts a selective amnesic effect on recently acquired memories and thus that electroconvulsive shock produces amnesia solely through interference with memory trace consolidation.
Amnesia↗
No play: a means of conflict resolution.
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Emotions↗
Clinical effects of pentazocine in hospitalized medical patients.
Of 17,068 hospitalized medical patients monitored in a drug surveillance program, 616 (3.6 per cent) received pentazocine hydrochloride orally and 816 (4.8 per cent) received pentazocine lactate parenterally during one or more admissions. Unsatisfactory analgesic efficacy as judged by each patient's physician was nearly twice as frequent among recipients of pentazocine lactate as among recipients of parenteral morphine or meperidine. Adverse reactions were attributed to pentazocine hydrochloride in 18 recipients (2.9 per cent) and to pentazocine lactate in 37 recipients (4.5 per cent). Neuropsychiatric effects were the most common; they included hallucinations, bizarre feelings, disorientation, and agitation. These effects were dose dependent and frequently serious in nature. Minor gastro-intestinal effects were the second most common adverse reactions.
Administration, Oral↗
An overview of clinical pharmacy and clinical pharmacology.
The relationship between clinical pharmacy and clinical pharmacology can best be assessed by looking at the three major responsibilities of these related professional disciplines--research, education, and patient care. Clinical pharmacologists will continue to dominate clinical research, but clinical pharmacists will continue to expand their contributions in all types of research. Clinical pharmacists are beginning to assume responsibility for providing training in rational therapeutics to medical students and house staff and, because of their greater numbers, probably will ultimately have a greater influence than clinical pharmacologists in this area. Similarly, clinical pharmacists appear to have greater influence on day-to-day patient care than clinical pharmacologists. Successful pursuit of all of these activities by clinical pharmacists assumes a continuing supply of well-trained practitioners. However, many pharmacy schools do not provide adequate classroom and bedside training. This is an unfortunate trend that seems to be accelerating as many schools convert from baccalaureate to doctoral entry degree programs without adequate clinical faculty and teaching hospital facilities.
Certification↗
Evaluation of the analgesic efficacy of ibuprofen.
Ibuprofen is a derivative of propionic acid that was originally marketed in the United States as an antirheumatic agent in 1974. In 1979, it was approved for use as an analgesic. Of the 18 published double-blind clinical trials reviewed, only 6 were well designed. These six studies provide strong evidence that ibuprofen is effective for dental pain due to tooth extractions, dysmenorrhea and episiotomy pain. Thus, ibuprofen appears to be an effective drug for mild to moderate pain. It is as effective or more effective than aspirin, codeine or propoxyphene. Recommended initial dosage is 300 mg every six hours, increasing as needed to 400 mg every four hours. Adverse effects are relatively minor and infrequent.
Anesthesia, Dental↗
Differential systemic arterial and venous actions and consequent cardiac effects of vasodilator drugs.
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Angiotensin II↗
Metabolism of acrylate esters in rat tissue homogenates.
Methyl, ethyl and butyl acrylate were hydrolyzed to acrylic acid in rat liver, kidney and lung homogenates. The rates of hydrolysis of the various esters in these in vitro studies were comparable; hydrolysis rates were approximately 20 times higher in liver homogenates than in kidney or lung homogenates. The esters also disappeared rapidly when added to blood in vitro. However, the disappearance in blood was not associated with the appearance of acrylic acid. Ethyl acrylate was found to react spontaneously with GSH in vitro and this reaction was catalyzed greatly by enzymes in 100 000 x g liver supernatant. Acrylic acid did not react with GSH in vitro. Ethyl acrylate, but not acrylic acid, depletes non-protein sulfhydryls when added to blood in vitro. Thus, the disappearance of acrylate esters in blood in vitro could be due at least in part to binding with non-protein sulfhydryls in red blood cells rather than to hydrolysis.
Acrylates↗
Inhalation toxicity of butylene oxide.
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Animals↗
Inhalation toxicity of acrylic acid.
Male and female Fischer 344 rats and B6C3F1 mice were exposed to 0, 5, 25 or 75 ppm acrylic acid vapors 6 hours per day, 5 days per week, for 13 weeks. These exposure levels were selected after conducting a 2-week probe study in which 225 ppm caused pronounced growth retardation and nasal lesions in both rats and mice. The 13-week exposures had no adverse effect on the growth of male and female rats and male mice. However, mean body weight gains of female mice in the 25 and 75 ppm exposure groups were statistically significantly lower than for controls after 12 weeks of exposure. There were no pronounced treatment related effects on organ weights, hematologic parameters, clinical chemistry parameters or urinary parameters. Histopathologic examinations revealed lesions of the nasal mucosa in rats in the 75 ppm exposure group, and in some or all mice at each treatment level. The nasal lesions were primarily localized to the olfactory epithelium; the respiratory epithelium was relatively unaffected. The histopathologic observations in both rats and mice included degeneration, and inflammatory cell infiltration in the olfactory mucosa. In mice there were also instances of hyperplasia of the submucosal glands and, replacement of olfactory epithelium by respiratory epithelium. These effects were attributed to the irritant properties of acrylic acid vapors.
Acrolein↗
Toxicity of methoxyacetic acid in rats.
Male Fischer 344 rats were given eight daily doses of 0, 30, 100 or 300 mg/kg methoxyacetic acid by gavage. The high dose resulted in decreased body weight, severe degeneration of testicular germinal epithelium, decreased size of the thymus with depletion of thymic cortical lymphoid elements, and reductions in bone marrow cellularity resulting in depressions of red blood cell counts, hemoglobin concentration, packed cell volume, and white blood cell counts. Some of these observations were apparent to a lesser degree in rats given 100 mg/kg. The low dose produced no apparent effects during the course of the study. These toxicological properties of methoxyacetic acid are remarkably similar to ethylene glycol monomethyl ether (EGME), and the adverse effects of EGME in rats are probably the result of in vivo bioactivation of EGME to methoxyacetic acid.
Acetates↗
Ethylene glycol monomethyl ether II. Reproductive and dominant lethal studies in rats.
Groups of male and female Sprague-Dawley (CD) rats were exposed to 0, 30, 100, or 300 ppm ethylene glycol monomethyl ether (EGME) vapor 6 hours/day, 5 days/week for 13 weeks. The 0 and 30 ppm groups each contained 30 rats/sex and the 100 and 300 ppm groups each had 20 rats/sex. Following the exposure period, males were bred to unexposed females to evaluate reproductive capability and dominant lethality. Additional matings of control and 300 ppm exposed males were performed during the post-exposure period in order to evaluate the recovery of fertility. Exposed females were bred with unexposed males to assess reproductive parameters. Results of the present study indicate a potential for inhaled EGME to completely suppress fertility in male rats at the 300 ppm level. Fertility of these rats was partially restored at 13 weeks post-exposure. Body weights of animals in the 300 ppm group were reduced as a result of the exposures. No dominant lethal effect or impaired fertility was observed in male rats exposed to 30 or 100 ppm EGME. Treatment-related pathologic alterations were observed only in male rats at the 300 ppm level and induced decreased testicular size and atrophic seminiferous tubules. Female rats tolerated up to 300 ppm EGME without any adverse reproductive effects. Based on these results, it was concluded that the no-adverse effect level of EGME for fertility and reproduction was 100 ppm in rats.
Animals↗
Ethylene glycol monomethyl ether. I. Subchronic vapor inhalation study with rats and rabbits.
Male and female Sprague-Dawley rats and New Zealand White rabbits were exposed to 0, 30, 100 or 300 ppm ethylene glycol monomethyl ether (EGME) vapors 6 hours per day, 5 days per week, for a total of 13 weeks. No rats died prior to scheduled sacrifice, but some rabbits in the 100 and 300 ppm exposure groups died or were sacrificed when moribund during the study. Body weights as well as thymus and testicular weights of rats and rabbits in the 300 ppm group were reduced as a result of the exposures. Hematologic changes occurred in rats and rabbits exposed to 300 ppm. Concentrations of total protein, albumin and globulins in serum of rats (but not rabbits) in the 300 ppm group were lower than for controls. Gross lesions in rats and rabbits exposed to 300 ppm EGME included decreased size of thymus in both sexes, decreased abdominal fat, and small flaccid testes in males. In addition there was decreased lymphoid tissue in some rabbits, as well as a slight-to-moderate decrease in size of testes in 4 of 5 rabbits in the 100 ppm group and in 2 of 5 rabbits exposed to 30 ppm. Treatment-related microscopic lesions included degenerative changes in germinal epithelium of testes in all male rats and rabbits in the 300 ppm group, as well as in 3 of 5 rabbits in the 100 ppm group and 1 of 5 male rabbits in the 30 ppm group. The only effects attributed to exposure to 30 ppm EGME in this study were slight microscopic changes in testes of 1 of 5 male rabbits.
Animals↗
Acute toxicity of aspirin in hospitalized medical patients.
Among 2,391 recipients of plain aspirin tablets, 121 (5.1%) were reported to have adverse reactions. Minor gastrointestinal disturbances, particularly heartburn and nausea, were most common (2.1%). Central nervous system effects were second (1.2%). Among these, tinnitus was reported most often (0.8%); deafness occurred in eight patients (0.3%). Gastrointestinal bleeding, the third major category of adverse reactions, occurred in 1.0% of recipients; it was not considered serious in any of the patients with reactions judged "definitely" or "probably" related to aspirin. The frequency of all adverse reactions increased as the unit dose, daily dose and total dose became larger. Deafness occurred only at high doses. Reactions were more common in females.
Aspirin↗
MRI of infiltrative lung disease: comparison with pathologic findings.
OBJECTIVE: Our goal was to compare MRI with pathologic findings in patients with chronic infiltrative lung disease. MATERIALS AND METHODS: The study included 22 consecutive patients who had MRI and lung biopsy performed within 21 days (median 4 days). Fifteen patients had open lung biopsy: five with idiopathic pulmonary fibrosis, three with extrinsic allergic alveolitis, and seven with miscellaneous conditions. Seven patients had transbronchial biopsy: four with sarcoidosis and three with miscellaneous conditions. All patients had 1.5 T MRI with cardiac-gated T1-, proton density-, and T2-weighted SE sequences. RESULTS: The predominant patterns of abnormality seen on MR included parenchymal opacification (n = 12), parenchymal opacification and reticulation (n = 2), reticulation (n = 3), nodularity (n = 3), and interlobular septal thickening (n = 1); normal findings were found in 1. The 14 patients with parenchymal opacification included 9 with ground-glass intensity and 5 with consolidation. In 12 of these 14 patients the parenchymal opacification represented an active inflammatory process including alveolitis, pneumonia, and granulomatous inflammation, while in 2 patients it represented fibrosis. Reticulation was shown to represent fibrosis in five of five cases. The three patients with nodules had sarcoidosis. CONCLUSION: The MR findings correlate closely with those seen on lung biopsy. Parenchymal opacification on MR usually indicates the presence of potentially reversible disease, while reticulation usually indicates irreversible fibrosis.
Adult↗
Inhibition of platelet aggregation by verapamil: quantification by in vivo and in vitro techniques.
Platelet aggregation appears to play a prominent role in myocardial ischemia. Verapamil, a slow-channel blocking agent with important antiarrhythmic and vasodilating actions, has been shown to inhibit in vitro platelet aggregation. We used an electronic particle size analyzer to evaluate the effects of verapamil on platelet aggregation in vitro and in vivo in 88 rats. The intravenous injection of verapamil (0.4 mg/kg) did not change the platelet count compared to control animals receiving an equal volume of normal saline (verapamil, 1.1 +/- 0.04 x 10(6)/mm3, vs. control, 1.2 +/- 0.09 x 10(6)/mm3, (p greater than 0.05). The mean size of platelet aggregates induced by adenosine diphosphate (0.2 microM), was reduced by verapamil (verapamil, 15.3 +/- 1.2 x 10(3) micron3 vs. control 24.4 +/- 2.7 x 10(3) micron; p less than 0.01). Platelet aggregates induced in vivo, following a standardized technique of extravasation of right iliac artery blood into the peritoneal cavity, were also smaller following verapamil infusion (verapamil, 12.6 +/- 1.1 x 10(3)micron3, vs control, 17.3 +/- 0.9 x 10(3) micron3 p less than 0.001). We conclude that verapamil exerts and inhibitory effect on platelet aggregation both in vitro and in vivo. This property may add an important new dimension to its potential therapeutic usefulness in ischemic heart disease.
Adenosine Diphosphate↗
Effects of ethanol and hemolysis on in vivo and in vitro platelet aggregation.
In vivo and in vitro platelet function were measured in male rats after intravenous injection of ethanol or water. There was a dose-related ethanol suppression of platelet aggregation induced by extravasation. Increased volumes of preformed microaggregates were seen in samples taken directly from the vena cava after injection of ethanol in doses that caused hemolysis. Lower doses of ethanol produced no demonstrable microaggregates or hemolysis: however, extravasation-induced aggregation was inhibited. Hemolysis was noted after intravenous injection of water, which also reduced the total volume and mean aggregate size of platelet aggregates induced by extravasation. Blood drawn from the inferior vena cava after induction of hemolysis had an increased volume of microaggregates, regardless of the agent producing hemolysis. In vitro studies revealed changes in spontaneous and ADP-induced aggregation only at very high concentrations of ethanol (greater than 3,000 mg/dl) and no effects at ethanol levels that altered in vivo aggregation. Ethanol, in doses that do not hemolyze erythrocytes, decreases platelet aggregation.
Animals↗