Search PubMed⌕ Search

Biomedical subjects

D M Benson

Publications and source records attributed to D M Benson.

At least 37 records · Page 2Linked to original sources
PubMed1988

Geometric correction of digital images using orthonormal decomposition.

We have developed an algorithm which can be used to correct the geometric distortion of digital images. The method uses an orthonormal decomposition and a two-dimensional Horner's scheme to construct and evaluate a polynomial equation of arbitrary degree in two independent variables. This numerical scheme for geometric correction combines several methods selected on the basis of their computation efficiency and numerical stability. The differences and advantages of this numerical scheme are compared with methods found in the image processing literature. The algorithm presented here has a reduced number of mathematical operations, is flexible and numerically stable. Based on the least-squares criteria, the algorithm provides corrected pixel positions with an accuracy equal to or better than the pixel size.

Algorithms↗
PubMed1988

An analysis of the depolarization produced in guinea-pig hippocampus by cholinergic receptor stimulation.

1. The effects of carbachol on hippocampal pyramidal neurones were studied in tissue slices in vitro with intracellular microelectrodes, employing current clamp and voltage clamp methods. 2. The calcium-dependent potassium current, IAHP, and the voltage-dependent potassium current, IM, were both reversibly blocked by the application of carbachol (5-10 microM). 3. Carbachol (1-10 microM) induced a steady inward current under circumstances in which both IAHP and IM were inactive. This inward current was sometimes difficult to reverse upon carbachol wash-out, an effect possibly related to receptor desensitization. 4. The depolarizing effect of carbachol was reversed by 0.1 microM-atropine, and exhibited an apparent dissociation coefficient of 1.2 microM for carbachol and 18 nM for pirenzepine, indicating that it is mediated by activation of an M1 muscarinic receptor. 5. The depolarizing effect or inward current induced by carbachol was completely blocked by the potassium channel blockers caesium, tetraethylammonium and barium. 6. The slope of the current-voltage (I-V) plots in carbachol was reduced in the majority of cells, and crossed the control I-V plots at a negative membrane potential. The reversal potentials in carbachol shifted in a positive direction when bathing potassium concentration was increased. 7. In a number of cells, the I-V curves in carbachol were parallel to or converged positively with the control I-V curves. 8. The effects of carbachol were compared to those of serotonin, which increases a 'pure' potassium conductance. Serotonin (10 microM) produced an increase in the slope of the I-V curve, with a reversal potential sensitive to changes in bathing potassium concentration. The carbachol reversal potential values were negative to those of serotonin at 5 and 10 mM-potassium. The equilibrium potentials for carbachol and serotonin were equal at 25 mM-potassium. 9. The negative values of the reversal potential at 5 and 10 mM-potassium and the occurrence of non-crossing I-V characteristics in carbachol could be explained by postulating a second effect of carbachol: namely, a non-specific conductance increase in the dendrites. 10. It is concluded that carbachol depolarizes pyramidal cells in the hippocampus by blocking a voltage-insensitive potassium leak channel and does so by activating M1 muscarinic receptors. In addition, carbachol may also activate a second conductance in the dendrites, which could account for the anomalous I-V characteristics sometimes seen in response to carbachol in these cells.

Animals↗
PubMed1987

Establishment and impact of a dementia unit within the nursing home.

Thirty-two demented, elderly residents of a nursing home were admitted to a specially designed dementia unit. Each patient was assessed three times: prior to admission, and at four and 12 months after admission to the unit. Patients were evaluated using a modified version of a previously published assessment scale as well as with a standardized New York State numerical rating system. There was an increased level of functioning in both mental and emotional status and basic functions of daily living at both four (P less than or equal to 0.001) and 12 months (P less than or equal to 0.005). The improvement in scores was maintained over a prolonged time period, despite the expectation of progression of the dementing process. There was no change noted on the New York State assessment. Our data suggest that a select group of demented elderly can benefit from being placed on a specialized dementia unit.

Aged↗
PubMed1986

Apolipoprotein A-IV. A determinant for binding and uptake of high density lipoproteins by rat hepatocytes.

To identify the role of a specific apoprotein other than apoE which might be responsible for the receptor-mediated uptake of high density lipoprotein (HDL) by rat hepatocytes, 1-palmitoyl-2-oleoyl-phosphatidylcholine (POPC) was combined with rat apoE, apoA-I, or apoA-IV to form apoprotein-phospholipid complexes and the complexes were tested for their binding and uptake by primary rat hepatocytes. Apoprotein-POPC complexes were labeled with the specific fluorescent probe, 1,1-dioctadecyl-3,3,3',3'-tetramethylindocarbocyanine to monitor their uptake by cultured rat hepatocytes at 37 degrees C using digital fluorescence imaging microscopy or were labeled with 125I to study their binding to hepatocytes at 4 degrees C. POPC, either alone or with apoA-I, was not internalized by rat hepatocytes while complexes containing apoE or apoA-IV were taken up by the cells. Specific binding at 4 degrees C was demonstrated for apoE-free HDL, apoA-IV X POPC, and apoE X POPC but not for apoA-I X POPC. The binding of apoE-free HDL was inhibited by apoA-IV X POPC, apoE-free HDL, and apoA-IV + apoA-I X POPC but not by apoA-I X POPC. Binding of apoA-IV X POPC was inhibited by apoE-free HDL, apoA-IV X POPC, and apoA-IV + apoA-I X POPC, but not by apoE X POPC or apoE-enriched HDL. These data indicate that apoA-IV is a ligand responsible for the rat HDL binding to primary rat hepatocytes and that apoA-IV binds to a receptor site distinct from apoE-dependent receptors such as the apoB,E or chylomicron-remnant receptor.

Animals↗
PubMed1986

A re-evaluation of cytoplasmic gelsolin localization.

Gelsolin is a 90,000-mol-wt Ca2+-binding, actin-associated protein that can nucleate actin filament growth, sever filaments, and cap barbed filament ends. Brevin is a closely related 92,000-mol-wt plasma protein with similar properties. Gelsolin has been reported to be localized on actin filaments in stress fibers, in cardiac and skeletal muscle I-bands, and in cellular regions where actin filaments are known to be concentrated. Previous localization studies have used sera or antibody preparations that contain brevin. Using purified brevin-free IgG and IgA monoclonal antibodies or affinity-purified polyclonal antibodies for gelsolin and brevin, we find no preferential stress fiber staining in cultured human fibroblasts or I-band staining in isolated rabbit skeletal muscle sarcomeres. Cardiac muscle frozen sections show no pronounced I-band staining, except in local areas where brevin may have penetrated from adjacent blood vessels. Spreading platelets show endogenous gelsolin localized at the cell periphery, in the central cytoplasmic mass and on thin fibers that radiate from the central cytoplasm. Addition of 3-30 micrograms/ml of brevin to the antibodies restores intense stress fiber and I-band staining. We see no evidence for large-scale severing and removal of filaments in stress fibers in formaldehyde-fixed, acetone-permeabilized cells even at brevin concentrations of 30 micrograms/ml. The added brevin or brevin antibody complex binds to actin filaments and is detected by the fluorescently tagged secondary antibody. Brevin binding occurs in either Ca2+ or EGTA, but is slightly more intense in EGTA suggesting some severing and filament removal may occur in Ca2+. The I-band staining is limited to the region where actin and myosin do not overlap. In addition, brevin does not appear to bind at the Z-line. A comparison of cells double-labeled with fluorescein-phallotoxin, exogenous brevin, and a monoclonal antibody, detected with a rhodamine-labeled secondary antibody, shows almost complete co-localization of F-actin with the brevin-gelsolin-binding sites. A major exception is in the area of the adhesion plaque. A quantitative comparison of the fluorescein-rhodamine fluorescence intensities along a stress fiber and into the adhesion plaque shows that the fluorescein signal, associated with F-actin, increases while the rhodamine signal decreases. We infer that exogenous brevin or endogenous gelsolin can bind to and potentially sever most actin filaments, but that actin-associated proteins in the adhesion plaque can prevent binding and severing.(ABSTRACT TRUNCATED AT 400 WORDS)

Actins↗
PubMed1985

Circulation time during standard and modified manual CPR determined by retinal photoangiography.

We used retinal fluorescein photoangiography to determine the circulation time (CTv-a) from the inferior vena cava (IVC) to the retinal artery in anesthetized, intubated, paralyzed, and fibrillated dogs. Animals received either standard CPR (SCPR) (n = 11) or modified CPR (MCPR) (n = 11) manually at 60 compressions per minute in both groups. MCPR consisted of simultaneous ventilation-compression with abdominal binding to 40 mm Hg. SCPR or MCPR was begun immediately after inducing ventricular fibrillation and was performed for an average of 4.5 minutes prior to bolus injection of fluorescein dye (0.7 mL, 25% solution). To compare CTv-a in the two groups, dye was injected through a catheter into the IVC (below the diaphragm) and timed, rapid, sequential retinal photoangiography was begun. The time to first appearance of dye in the retinal vasculature initially was determined visually by the camera operator and later was substantiated photographically. The camera simultaneously photographed the retinal vasculature and the built-in timer, thus displaying the elapsed time from injection on each frame. Our results showed a significantly shorter CTv-a in the MCPR group (58.9 seconds +/- 18.6) when compared to the SCPR group (112.6 seconds +/- 47.4; P less than .01). In addition, we have documented retinal blood flow during CPR.

Animals↗
PubMed1985

Cellular uptake and intracellular localization of benzo(a)pyrene by digital fluorescence imaging microscopy.

Uptake of benzo(a)pyrene by living cultured cells has been visualized in real time using digital fluorescence-imaging microscopy. Benzo(a)pyrene was noncovalently associated with lipoproteins, as a physiologic mode of presentation of the carcinogen to cells. When incubated with either human fibroblasts or murine P388D1 macrophages, benzo(a)pyrene uptake occurred in the absence of endocytosis, with a halftime of approximately 2 min, irrespective of the identity of the delivery vehicles, which were high density lipoproteins, low density lipoproteins, very low density lipoproteins, and 1-palmitoyl-2-oleoylphosphatidylcholine single-walled vesicles. Thus, cellular uptake of benzo(a)pyrene from these hydrophobic donors occurs by spontaneous transfer through the aqueous phase. Moreover, the rate constant for uptake, the extent of uptake, and the intracellular localization of benzo(a)pyrene were identical for both living and fixed cells. Similar rate constants for benzo(a)pyrene efflux from cells to extracellular lipoproteins suggests the involvement of the plasma membrane in the rate-limiting step. The intracellular location of benzo(a)pyrene at equilibrium was coincident with a fluorescent cholesterol analog, N-(7-nitrobenz-2-oxa-1,3-diazole)-23,24-dinor-5-cholen-22-amine-3 beta-ol. Benzo(a)pyrene did not accumulate in acidic compartments, based on acridine orange fluorescence, or in mitochondria, based on rhodamine-123 fluorescence. When the intracellular lipid volume of isolated mouse peritoneal macrophages was increased by prior incubation of these cells with either acetylated low density lipoproteins or with very low density lipoproteins from a hypertriglyceridemic individual, cellular accumulation of benzo(a)pyrene increased proportionately with increased [1-14C]oleate incorporation into cellular triglycerides and cholesteryl esters. Thus, benzo(a)pyrene uptake by cells is a simple partitioning phenomenon, controlled by the relative lipid volumes of extracellular donor lipoproteins and of cells, and does not involve lipoprotein endocytosis as an obligatory step.

Animals↗
PubMed1985

Digital imaging fluorescence microscopy: spatial heterogeneity of photobleaching rate constants in individual cells.

Photobleaching and related photochemical processes are recognized experimental barriers to quantification of fluorescence by microscopy. We have measured the kinetics of photobleaching of fluorophores in living and fixed cells and in microemulsions, and have demonstrated the spatial variability of these processes within individual cells. An inverted fluorescence microscope and a high-sensitivity camera, together with high-speed data acquisition by a computer-controlled image processor, have been used to control precisely exposure time to excitation light and to record images. To improve the signal-to-noise ratio, 32 digital images were integrated. After correction for spatial variations in camera sensitivity and background fluorescence, the images of the relative fluorescence intensities for 0.065 micron2 areas in the object plane were obtained. To evaluate photobleaching objectively, an algorithm was developed to fit a three-parameter exponential equation to 20 images recorded from the same microscope field as a function of illumination time. The results of this analysis demonstrated that the photobleaching process followed first-order reaction kinetics with rate constants that were spatially heterogeneous and varied, within the same cell, between 2- and 65-fold, depending on the fluorophore. The photobleaching rate constants increased proportionally with increasing excitation intensity and, for benzo(a)pyrene, were independent of probe concentration over three orders of magnitude (1.25 microM to 1.25 mM). The propensity to photobleach was different with each fluorophore. Under the cellular conditions used in these studies, the average rates of photobleaching decreased in this order: N-(7-nitrobenz-2-oxa-1,3-diazole)-23,24-dinor-5-cholen-22-amine-3 beta-ol greater than acridine orange greater than rhodamine-123 greater than benzo(a)pyrene greater than fluorescein greater than tetramethylrhodamine greater than 1,1'dioctadecyl-3,3,3',3'-tetramethylindocarbocyanine. The photobleaching appears to be an oxidation reaction, in that the addition of saturated solutions of Na2S2O5 to mineral oil microemulsions eliminated photobleaching of N-(7-nitrobenz-2-oxa-1,3-diazole)-23,24-dinor-5-cholen-22-amine-3 beta-ol or benzo(a)pyrene. We identified experimental conditions to observe, without detectable photobleaching, fluorophores in living cells, which can not be studied anaerobically. Useful images were obtained when excitation light was reduced to eliminate photobleaching, as determined from zero-time images calculated from the exponential fit routine.(ABSTRACT TRUNCATED AT 400 WORDS)

4-Chloro-7-nitrobenzofurazan↗
PubMed1984

Improved enumeration of Trichoderma spp. on dilution plates of selective media containing a nonionic surfactant.

Addition of Tergitol NP-10 (polyglycol ether), a nonionic surfactant, greatly enhanced enumeration of Trichoderma spp. colonies on three selective media. Colony diameter was restricted 11-47% on dilution plates with Tergitol compared with media without the surfactant. Plates with the surfactant could be incubated up to 2 weeks prior to counting. Colony counts of Trichoderma spp. were not significantly different for surfactant amended or unamended plates on two of the three selective media tested. However, on RBD medium (rose bengal--chloramphenicol--pentachloronitrobenzene (PCNB)--Dexon) with surfactant, significantly fewer colonies were recovered compared with the medium without surfactant.

Animals↗
PubMed1983

Enhanced behavioral response to nicotine in an animal model of Alzheimer's disease.

Three groups of rats received either kainic acid or vehicle in the ventral pallidum or no operation, and were then tested in photocell activity cages following recovery from surgery. Locomotor activity was measured following injections of saline, nicotine (0.1, 0.2, 0.4 mg/kg) or d-amphetamine (0.5, 1.0 mg/kg). The lesioned rats showed an enhanced locomotor response after injections of nicotine compared with sham operated or unoperated controls. In contrast, both lesioned and control rats showed increased activity after amphetamine; this effect was not influenced by the lesion. Since these lesions are known to produce neurochemical and cellular changes resembling those seen in human Alzheimer's disease, this increased response to nicotine might also be found in Alzheimer's patients and serve as the basis for a diagnostic test.

Alzheimer Disease↗
PubMed1983

Ultrasonic tissue characterization of fetal lung, liver, and placenta for the purpose of assessing fetal maturity.

The purpose of this research effort was to establish a physical basis for the development of an accurate noninvasive technique to differentiate between mature and immature fetal tissues, particularly the lung and placenta. The research utilized RF waveform analysis via a microcomputer-based digital processing system interfaced directly to a standard real-time clinical diagnostic ultrasound instrument. Differences between the frequency spectra of the RF waveforms for mature and immature fetal tissues could be demonstrated in accordance with proposed tissue models.

Abdomen↗