Retrograde migration of PEG tubes.
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Abdominal Muscles↗
Biomedical subjects
R D Brown
Publications and source records attributed to R D Brown.
Cardiac papillary fibroelastoma: a treatable cause of transient ischemic attack and ischemic stroke detected by transesophageal echocardiography.
Transesophageal echocardiography (TEE) is used frequently in patients with cerebrovascular ischemia. On TEE, a typical appearance of a cardiac fibroelastoma is that of a pedunculated, mobile mass attached to a leaflet of a valve. Surgical excision of the lesion may lead to resolution of the symptoms and prevent further cerebrovascular ischemic events; valve replacement is seldom necessary. Herein we describe three patients with cerebral or ocular ischemia in whom histologic study confirmed a cardiac papillary fibroelastoma after initial detection by TEE. Cardiac papillary fibroelastomas should be considered in the differential diagnosis of transient ischemic attack and stroke, even in cases of recurrent events in the same vascular distribution. Although the use of echocardiography in the evaluation of stroke and transient ischemic attack is controversial, TEE must be considered in patients in whom the cause of cerebrovascular ischemia is unclear after noninvasive neurovascular studies or transthoracic echocardiography, even if the patient's cardiac history and the findings on physical examination are normal.
Adult↗
Comparison of two methods of mechanical disaggregation of scirrhous breast adenocarcinomas for DNA flow cytometric analysis of whole cells.
Mechanical release of single cell suspensions from solid tumors for DNA analysis by flow cytometry has been shown to be optimal for adenocarcinomas in general. In the breast, many adenocarcinomas are fibrotic or scirrhous, creating difficulty in separating the neoplastic cells from the stroma. The authors have conducted a parallel study in 20 consecutive cases of scirrhous adenocarcinomas of the breast using two mechanical methods of cell disaggregation by: (1) mincing tumor tissue in culture media (MINCE); and (2) scraping the surface of the solid tumor with a scalpel blade and rinsing the blade in culture media (SCRAPE). Both methods were compared with PI staining and quantitation of percent debris and coefficient of variation (CV), as an index of resolution of the G0/G1 tumor peak. Debris was quantitated using Cell-FIT (Becton Dickinson Immunocytometry Systems, San Jose, CA) and Multicycle (Phoenix Flow Systems, San Diego, CA) software programs. With Multicycle, in addition to debris and aggregate determination, an index that included background, aggregates and debris (%BAD) occurring between the boundaries of the tumor G1 and G2 region was evaluated. In the 4 DNA diploid and 16 DNA aneuploid tumors, there was no significant difference in histogram quality measured by CV or amount of debris, aggregates, and %BAD between MINCE and SCRAPE methods. The authors conclude that either method of mechanical disaggregation will produce DNA histograms of comparable quality and degree of resolution. However, the scrape method may be advantageous in the mechanical disaggregation in scirrhous tumors. The scrape method also may be useful in small tumors, where tissue preservation for histology is paramount, and there is insufficient material to separately submit for flow cytometry. Combination of both MINCE and SCRAPE may provide higher cell yields, than using only one of these dissociation techniques. In addition, DNA analysis methods using intact cells obtained with the SCRAPE method result in percent CV values of similar resolution to those reported for methods producing bare nuclear suspensions from fresh tumors.
Adenocarcinoma, Scirrhous↗
Calcification can shorten T2, but not T1, at magnetic resonance imaging fields. Results of a relaxometry study of calcified human meningiomas.
RATIONALE AND OBJECTIVES: Water content and water-proton relaxation rates are reported for fresh, histologically characterized, surgical specimens of calcified human intracranial meningiomas and compared with results for noncalcified meningiomas from an earlier study and with calcium hydroxyapatite (CaHA) suspensions to elucidate the influence of calcification on magnetic resonance imaging (MRI) signal intensity of calcified meningiomas. METHODS: The magnetic field dependence of 1/T1 of water protons (nuclear magnetic relaxation dispersion profile) and dry weights are reported for 38 calcified nonhemorrhagic and 3 hemorrhagic specimens of known histologic subtype, a subset of the 67 specimens measured earlier. Calcification was considered mild or heavy when the dry weight was within or above the range for noncalcified meningiomas. Preliminary 1/T1 profiles for pure CaHA and a single high-field 1/T2 value also are reported. RESULTS: The ranges of dry weights and of low-field 1/T1 values were twice as large for calcified as for noncalcified meningiomas. No correlation was found between low-field 1/T1 and either histologic subtype or dry weight. Mild calcification produced the highest low-field 1/T1 values; the most heavily calcified tumor had slightly increased low-field 1/T1. Calcium hydroxyapatite increases low-field 1/T1 significantly but not high-field 1/T1; high-field 1/T2 is large. For calcified hemorrhagic meningiomas, increases in both low-field and high-field 1/T1 were seen. CONCLUSION: For mild calcification, MRI signal voids result from an increased high-field 1/T2; for heavier calcification, reduced proton density (from excluded water) becomes of increasing importance. Cellular CaHA appears to brighten the signal in T1-weighted MRI in the presence of hemorrhage.
Adolescent↗
Periampullary disorders: review of pathophysiology.
The ampulla of Vater is strategically located at the confluence of the terminal end of the bile duct and the pancreatic duct. It is entwined by smooth muscle fibers often referred to as the sphincter of Oddi. As a result, the ampulla demonstrates dynamic motor activity. A variety of structural and functional abnormalities can involve the ampulla and the periampullary region. Disorders involving the ampulla often produce remarkably similar clinical features, such as acute pancreatitis, biliary colic, or jaundice. Therefore, it is important that patients with periampullary disorders are systematically studied using endoscopic retrograde cholangiopancreatography, sphincter of Oddi manometry, and endoscopic ultrasonography. Common disorders involving the periampullary region and state-of-the-art techniques for diagnosis and treatment of these disorders are discussed.
Ampulla of Vater↗
The expression of alpha 1 adrenoceptor subtypes changes with age in the rat aorta.
Previous studies showed that alpha 1 adrenoceptor-mediated contractile responses change with age in the rat aorta, becoming more sensitive to Ca++ channel blockers and less sensitive to chlorethylclonidine (CEC), suggesting a change in the alpha 1 adrenoceptor subtypes that are present. In this study, alpha 1 adrenoceptor density and alpha 1 adrenoceptor subtypes were measured in the Fischer 344 rat aorta during aging. Aortic alpha 1 adrenoceptor densities, determined by saturation binding of 2-[beta-(4-hydroxy-3-[125I]iodophenyl)ethylaminomethyl] tetralone ([125I]-HEAT), were 47, 41 and 45 fmol/mg protein in 1-,6- and 24-month-old rats, respectively. The noncompetitive antagonist CEC completely blocked [125I]-HEAT binding in aortas from 1-month-old rats but inhibited binding only partially in aortas from older rats. Two binding sites were detected for norepinephrine and for WB4101 in all ages. The low-affinity constants for WB4101 (31-51 nM) were consistent with those for the alpha 1b adrenoceptor subtype, and this binding site decreased with age. The high-affinity constant for WB4101 (1.4 nM) in 1-month-old aorta was consistent with that for alpha 1d adrenoceptor subtype, whereas the high-affinity constants (0.03 nM) in 6- and 24-month-old aortas were consistent with those for the alpha 1a adrenoceptor subtype. At least three alpha 1 adrenoceptor subtypes appear to be colocalized in the rat aorta, so the binding affinities may reflect binding to more than one subtype. This makes it difficult to identify denfinitively the subtypes based on their radioligand binding characteristics.(ABSTRACT TRUNCATED AT 250 WORDS)
Aging↗
Studies of the binding specificity of concanavalin A. Nature of the extended binding site for asparagine-linked carbohydrates.
In the preceding paper [Mandal, D. K., Kishore, N., & Brewer, C. F. (1994) Biochemistry (preceding paper in this issue)] the trisaccharide 3,6-di-O-(alpha-D-mannopyranosyl)-D-mannose, which is present in all asparagine-linked carbohydrates, was shown by titration microcalorimetry to bind to the lectin concanavalin A (Con A) with nearly -6 kcal mol-1 greater enthalpy change (delta H) than methyl alpha-D-mannopyranoside (Me alpha Man). These results indicate that Con A possesses an extended binding site for the trisaccharide. In the present paper, we have investigated the binding of a series of synthetic analogs of the methyl alpha-anomer of the trisaccharide using hemagglutination inhibition, solvent proton magnetic relaxation dispersion (NMRD), near ultraviolet circular dichroism, and titration microcalorimetry measurements. Four of the analogs tested possess an alpha-glucosyl or alpha-galactosyl residue substituted at either the alpha(1-6) or alpha(1-3) position. Analysis of the data indicates that the alpha(1-6) residue of the parent trimannoside binds to the so-called monosaccharide site and the alpha(1-3) residue to a weaker secondary site. Binding at the secondary site involves unfavorable interactions of the 2-equatorial hydroxyl of the alpha(1-3) Glc derivative since this analog binds with 12-fold lower affinity and -3.4 kcal mol-1 lesser delta H than the trimannoside, whereas the alpha(1-3)-2-deoxyGlc analog possesses essentially the same affinity and delta H as the trimannoside.(ABSTRACT TRUNCATED AT 250 WORDS)
Asparagine↗
Amlodipine versus atenolol in essential hypertension.
The efficacy and safety of amlodipine (2.5-10 mg) once daily was compared with atenolol (50-100 mg) once daily in patients with mild-to-moderate essential hypertension in a randomized, double-blind, parallel, placebo-controlled study. A total of 125 patients were randomly allocated at the end of a 4-week run-in placebo period to 8 weeks of double-blind treatment with amlodipine (n = 41), atenolol (n = 43), or placebo (n = 41). The placebo group had small mean changes in supine and standing blood pressure compared with baseline. The mean blood pressure changes from baseline 24 hours postdose in the amlodipine group (mean daily dose 8.8 mg) were -12.8/-10.1 mm Hg for supine blood pressure and -11.5/-9.8 mm Hg for standing blood pressure (p < 0.001 compared with placebo), and for the atenolol group (mean daily dose 83.7 mg) the changes were -11.3/-11.7 mm Hg for supine blood pressure and -13.3/-12.3 mm Hg for standing blood pressure (p < 0.001 compared with placebo). There were no statistically significant blood pressure differences between active treatments. The responder rates for amlodipine, atenolol, and placebo were 61.1, 64.9, and 11.1%, respectively. The blood pressure values taken over the 24-hour period at final visit revealed that amlodipine and atenolol maintained the supine blood pressure < or = 140/90 mm Hg throughout the period of observation; the corresponding time-effect curve for the placebo group was clearly in the hypertensive range. Both amlodipine and atenolol were well tolerated.(ABSTRACT TRUNCATED AT 250 WORDS)
Adolescent↗
Immunotoxicological profile of morphine sulfate in B6C3F1 female mice.
This study was undertaken to investigate a number of immune parameters which may be compromised with exposure to morphine sulfate. Mice were implanted subcutaneously with 8-, 25-, or 75-mg morphine sulfate pellets. Placebo pellets of identical makeup to the 75-mg morphine pellet (without morphine of course) were used as a control. Twenty-four hours after implantation of a 75-mg morphine pellet, blood levels reached a peak of 1610 ng/ml. Corticosterone increased in parallel with morphine and reached a peak level of 966 ng/ml 24 hr after implantation. The dose response of morphine to increase corticosterone, however, was flat. The weight of the lymphoid organs, spleen and thymus, and the liver were significantly reduced in the morphine-treated groups. Morphine treatment was associated with an increase in serum albumin, SGPT, BUN, and alkaline phosphatase indicative of hepatic damage. In contrast to increased serum proteins, the C3 component of complement was reduced in a dose-dependent manner. Leukocyte number in the peripheral blood was significantly reduced, while erythrocyte number and hematocrit were both increased. The number of B cells and T cells was decreased in morphine-treated animals. However, the percentage of T cells relative to B cells was increased. The primary IgM antibody response to the T-dependent antigen, sheep red blood cells, was decreased. Natural killer cell activity was reduced in response to morphine, as was the phagocytic capacity of Kupffer cells. Host-resistance models of Listeria monocytogenes or Streptococcus pneumoniae showed an increased resistance following administration of morphine. This increased host resistance, however, was not due to an increase in antimicrobial action of sera obtained from mice treated with morphine. The majority of morphine's effects on the immune system exhibited a flat dose response, suggesting that these effects may be mediated secondarily through corticosterone.
Animals↗
Mechanisms of the escape phase of myeloma.
In multiple myeloma the duration of plateau is an important clinical and biological determinant of quality of life and survival. During plateau phase, the tumour is in an indolent state, as manifested by a low labelling index of plasma cells and other proliferative markers, e.g. the thymidine kinase level. The mechanism by which plasma cells escape from this indolent phase to a more aggressive phase of this disease is unknown, but a number of possible mechanisms have been postulated. These include loss of immunoregulation, clonal evolution, cytokine dysfunction and oncogene activation or tumour suppressor gene dysfunction. As current chemotherapy protocols do not appear to be able to eradicate the malignant clone, understanding the nature of the indolent phase of the malignant clone and the reasons for its escape from this phase are very important and may provide new options for disease control.
Antibodies, Anti-Idiotypic↗
Transient ischemic attack and minor ischemic stroke: an algorithm for evaluation and treatment. Mayo Clinic Division of Cerebrovascular Diseases.
OBJECTIVE: To report a cost-effective and scientifically based algorithm for the clinical assessment and treatment of patients with transient ischemic attack (TIA) or minor ischemic stroke. DESIGN: We comprehensively reviewed the literature on the epidemiologic features, assessment approaches, and treatment recommendations for ischemic cerebrovascular disease and developed an algorithm by using the available clinical and research data to support all decision-making steps. MATERIAL AND METHODS: For patients with TIA or minor ischemic stroke, the appropriate setting for investigation (inpatient or outpatient), suggested diagnostic tests, use of anticoagulants and antiplatelet agents, and indications for surgical treatment are reviewed. RESULTS: Although stroke is a common cause of death and lost productivity in the United States, the clinical assessment of patients with TIA or minor ischemic stroke has lacked consistency. The simplified algorithm clarifies patients who may be candidates for hospitalization and possible anticoagulation therapy. Initial diagnostic studies should include computed tomography of the head without use of a contrast agent, which quickly distinguishes nonhemorrhagic from hemorrhagic cerebrovascular disease. Evolving noninvasive studies of the cerebral vasculature are providing increasingly sensitive means of detecting stenoses, yet cerebral angiography remains the "gold standard." Treatment options depend on the pathophysiologic findings on diagnostic evaluation. CONCLUSION: The assessment of patients with ischemic cerebrovascular disease is complex. The simplified algorithmic approach reported herein necessitates entry of appropriate patients into the algorithm. Because of clinical heterogeneity, an algorithm may apply to a wide spectrum of patients but will not cover every situation; hence, evaluation must be guided by a patient's unique history and findings on examination and by the physician's clinical experience.
Algorithms↗
Two-color multiparametric method for flow cytometric DNA analysis. Standardization of spectral compensation.
Spectral overlap of green fluorescence signals into the red detector (red-minus-green compensation) is one potential source of variation in two-color flow cytometric DNA analysis. Suboptimal compensation in a two-color propidium iodide (PI)/fluorescein isothiocyanate (FITC) system may be observed if compensation is adjusted using an inappropriate standard, or if changes to fluorescence detector high-voltage settings are made without corresponding readjustment of fluorescence compensation. To quantitate the influence of red-minus-green compensation on the quality of DNA histograms, data from 60 dual PI/cytokeratin (CK)-FITC stained carcinomas were acquired in parallel using two compensation standards: a PI/CK-FITC-stained T24 cell line calibrator overstained to achieve a high-intensity green fluorescence standard (HIGFS) with manually set compensation and automated compensation settings derived from commercial phycoerythrin/low intensity FITC beads (LIGF). Both compensation standards gave similar DNA hyperdiploidy results (DNA index, 1.1-2.8). However, LIGF standard yielded two falsely hypodiploid peaks (DNA index, .7 and .9). Eight left-skewed peaks became DNA diploid and symmetric, respectively, with the HIGFS. Use of HIGFS lowered the coefficient of variation percentage in 95% of cases, the greatest differences (maximum, 3.4%; mean, 1.81%) in tumors of highest intensity CK-FITC. The authors concluded that use of cell-based compensation standards (HIGFS) with intense green signals that mimic clinical tumor samples will avoid spurious aneuploidy and maximize resolution of near-diploid abnormalities.
Analysis of Variance↗
Rapid (one-shot) staining method for two-color multiparametric DNA flow cytometric analysis of carcinomas using staining for cytokeratin and leukocyte common antigen.
The authors present an improved method for rapid two-color staining with direct conjugated antibodies to cytokeratin and CD45 antigen (leukocyte common antigen) for whole-cell, ethanol-fixed preparations of human carcinomas. This method was quality controlled with the T24 human bladder tumor cell line and compared in parallel analysis of 24 fresh human carcinomas with the original two-color method of multiparametric analysis that had been published in 1989. This rapid method was designed to achieve comparable staining intensities of both green (phenotype directed monoclonal antibody label) and red (propidium iodide labeled DNA) fluorescence, identical DNA indexes, comparable coefficients of variation, and subjective visual quality of DNA histograms. This is accomplished in a single (one-shot), abbreviated incubation with monoclonal antibody diluted in propidium iodide-RNase, thereby eliminating two incubations and three wash steps required with the original method. The single rinse is done in the propidium iodide-RNase staining solution with resuspension in fresh staining solution before analysis. With the rapid method, the preparation time is reduced by 130 minutes, resulting in a 60% time savings in batch staining mode compared with the original method. The time reduction and fewer wash steps, which should avoid excessive cell loss and cytoplasmic stripping, may advance the adoption of this two-color method in clinical practice.
Color↗
Multiple myeloma: why does the disease escape from plateau phase?
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Chromosome Aberrations↗
Involuntary tonic spasms of a limb due to a brain stem lacunar infarction.
BACKGROUND AND PURPOSE: Although repetitive involuntary movements are a well-recognized manifestation of carotid occlusive disease, similar movements have not been reported with a lacunar infarction outside of the basal ganglia or subthalamic nucleus. We describe a man with tonic spasms associated with a lacunar infarction in the right ventral pons. CASE DESCRIPTION: Involuntary tonic spasms of a paretic limb developed acutely in a 69-year-old hypertensive man with a clinical presentation of pure motor hemiparesis. Magnetic resonance imaging demonstrated a lacunar infarction of the ventral pons. There was no evidence for carotid occlusive disease. An electroencephalogram recorded during the movements showed no abnormality. The abnormal movements responded well to treatment with oral diazepam. CONCLUSIONS: A brain stem lacunar infarction may be associated with involuntary tonic limb spasms clinically similar to those reported as paroxysmal symptoms of multiple sclerosis.
Aged↗
Accuracy of hospital discharge abstracts for identifying stroke.
BACKGROUND AND PURPOSE: Much of the available data on stroke occurrence, service use, and cost of care originated with hospital discharge abstracts. This article uses the unique resources of the Rochester Epidemiology Project to estimate the sensitivity and positive predictive value of hospital discharge abstracts for incident stroke. METHODS: The Rochester Stroke Registry was used to identify all confirmed first strokes (hospitalized and nonhospitalized) among Rochester residents for 1970, 1980, 1984, and 1989 (n = 364). The sensitivity of discharge abstracts was estimated by following these individuals for 12 months after stroke to determine the proportion assigned a discharge diagnosis of cerebrovascular disease (International Classification of Diseases [ICD] codes 430 through 438.9). The positive predictive value of discharge abstracts was assessed by identifying all hospitalizations of Rochester residents with an ICD code of 430-438.9 in 1970, 1980, and 1989 (n = 377). Events were categorized as incident stroke, recurrent stroke, stroke sequelae, or nonstroke after review of the complete community-based medical record by a neurologist. RESULTS: Only 86% (n = 313) of all first-stroke patients in 1970, 1980, 1984, and 1989 were hospitalized. Of hospitalized patients, only 76% were assigned a principal discharge diagnosis code of 430-438.9. Fatal strokes and those occurring during a hospitalization were less likely to be identified. Among all hospitalizations of Rochester residents in 1970, 1980, and 1989, there were 377 with a principal diagnosis code of 430-438.9. Less than half (n = 177) were determined by the neurologist to be incident stroke; only 60% (n = 225) were either incident or recurrent stroke. Comparison of alternative approaches showed the validity of discharge abstracts was enhanced by increasing the number of diagnoses and excluding codes with poor positive predictive value. CONCLUSIONS: This study provides previously unavailable estimates of the sensitivity of stroke-coded hospitalizations for a US community. A model for improving the sensitivity and positive predictive value of discharge abstracts is presented.
Aged↗
Subchronic 10 day immunotoxicity of polydimethylsiloxane (silicone) fluid, gel and elastomer and polyurethane disks in female B6C3F1 mice.
Millions of people have been exposed to silicones because of the widespread use in consumer products such as cosmetics and toiletries, food products, household products and paints. Silicones have wide use in medical practice, including lubricants in tubing and syringes, and as implantable devices. The most prevalent silicone in medical use is polydimethylsiloxane. This study was undertaken to determine the subchronic immunotoxicologic potential of the principal constituents of breast implants: silicone fluid, silicone gel and silicone elastomer. An alternative covering for devices containing silicone gels, polyurethane, was also included in the study. Silicone fluid and gel were injected subcutaneously into female B6C3F1 mice (1 ml/mouse) and 6 mm disks of silicone elastomer or polyurethane were implanted subcutaneously. There were no treatment-related deaths or overt signs of toxicity. None of the tested materials had notable effects on body or organ weights, erythrocytes or leukocytes in the blood, blood chemistries such as alanine aminotransferase, urea nitrogen, glucose, albumin or total protein. The cellularity of the bone marrow and responses to CSF-GM and CSF-M were normal. The tested silicones did not alter the distribution of B cells and T cells in the spleen, but polyurethane perturbed the distribution of CD4+CD8+ and CD4-CD8- T cells. The antibody response to sheep erythrocytes was not markedly altered, nor were proliferative responses to concanavalin A, phytohemagglutinin, lipopolysaccharide or allogeneic cells. Reticuloendothelial function was normal, but polyurethane evoked an enhanced phagocytosis of Covaspheres by adherent peritoneal cells. Natural killer cell activity and serum complement were not altered. All silicone materials afforded modest protection to a challenge with Listeria monocytogenes that killed 40 to 58% of control mice. Host resistance to Streptococcus pneumoniae or the B16F10 tumor was not affected by any of the treatments. There is a pattern indicative of some perturbation of T cell differentiation in mice implanted with a polyurethane disk.
Animals↗
Immunotoxicity of 180 day exposure to polydimethylsiloxane (silicone) fluid, gel and elastomer and polyurethane disks in female B6C3F1 mice.
Millions of people have been exposed to silicones which are present in consumer goods such as cosmetics and toiletries, processed foods and household products. In addition, silicones have been used extensively in medical practice as a lubricant in tubing and syringes, and as implantable devices. A silicone widely used in medical practice is polydimethylsiloxane. This study was undertaken to determine the immunotoxicologic potential of long term exposure to the principal constituents of breast implants: silicone fluid, silicone gel and silicone elastomer. An alternative covering for devices containing silicone gels, polyurethane, was also included in the study. Silicone fluid and gel were injected subcutaneously into female B6C3F1 mice (1 ml/mouse) and 6 mm disks of silicone elastomer or polyurethane were implanted subcutaneously. There were no treatment-related deaths or overt signs of toxicity during the 180 day exposure. None of the tested materials had notable effects on body or organ weights, erythrocytes or leukocytes in the blood, blood chemistries such as alanine aminotransferase, urea nitrogen, glucose, albumin or total protein, or serum CH 50 or C3 levels. The cellularity of the bone marrow and responses to CSF-GM and CSF-M were normal. The tested silicones and polyurethane marginally reduced the level of Ig+ cells in the spleen but did not consistently alter the distribution of T cell surface markers. The antibody response to sheep erythrocytes was not markedly altered, nor were proliferative responses to concanavalin A, phytohemagglutinin, lipopolysaccharide or allogeneic cells. Reticuloendothelial function was normal, as was phagocytosis of chicken erythrocytes and Covaspheres by adherent peritoneal cells. Natural killer cell activity was depressed in all silicone treatment groups and in mice implanted with polyurethane. No silicone or polyurethane treatment group displayed altered susceptibility to a challenge with Listeria monocytogenes, Streptococcus pneumoniae or the B16F10 tumor. The only consistent effect of 180 day exposure to silicone materials or polyurethane was a modest depression of natural killer cell activity.
Animals↗