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Biomedical subjects

D M Benson

Publications and source records attributed to D M Benson.

At least 19 recordsLinked to original sources
PubMed1990

Treatment of winter depression with a portable, head-mounted phototherapy device.

1. A portable, head-mounted device was developed for administration of light therapy. A randomized crossover protocol was used to test the therapeutic efficacy of this device, compared to a standard light box, for treatment of winter depression. 2. Depressive symptoms were significantly reduced by both the head-mounted device and the light box. 3. Therapeutic efficacy of the two devices was not significantly different. 4. The head-mounted device was rated by patients as significantly more convenient than the conventional light box; this may be important in improving patient compliance.

Adult↗
PubMed1990

Probing the structure of diacetylenic phospholipid tubules with fluorescent lipophiles.

Novel lipid structures called tubules can be prepared from diacetylenic phospholipids. We have prepared fluorescent tubules from mixtures of 1,2-bis(10,12-tricosadiynoyl)-sn-glycero-3-phosphatidylcholine and 1 mol% fluorescent lipophiles to study the characteristics of the tubule lipid matrix. We have found that once formed, tubules do not incorporate lipophiles from the aqueous phase into their lipid matrix. The spectral characteristics of the fluorophore laurodan in tubules, and the lack of diffusion of N-nitrobenzoxydiazol phosphatidylethanolamine in tubules, have allowed us to characterize the microenvironment of these structures as being extremely rigid and tightly packed. Despite their rigid characteristic, tubules are formed from intact liposomes as demonstrated by the formation of doubly labeled tubules from two populations of liposomes, each of which contained a different nonexchangeable fluorescent lipophile.

Diffusion↗
PubMed1990

Permanent alterations in the hypothalamic-pituitary-thyroid axis in the rat following phenytoin exposure in utero.

Phenytoin exposure in utero results in permanent alterations of the hypothalamic-pituitary-thyroid axis in the rat. The DPH exposed animals have decreased weight gain, thyroxine and triiodothyronine concentrations. In addition, they have blunted thyroid-stimulating hormone responses to thyrotropin-releasing hormone, propylthiouracil challenge or thyroidectomy. The diminished pituitary response in these animals is similar to that reported in neonatal thyrotoxicosis in the rat. This may be due, in part, to structural similarities between phenytoin and the thyroid hormone.

Animals↗
PubMed1989

Ethanol suppresses hippocampal cell firing through a calcium and cyclic AMP-sensitive mechanism.

The effects of ethanol were studied intracellularly in hippocampal pyramidal cells in vitro. Ethanol, 50-100 mM, produced a marked suppression of neuronal firing. This effect was blocked by treating the cell with cyclic 3', 5'-adenosine monophosphate (cAMP) or cadmium ions. Ethanol had no effect on the after-hyperpolarizing current. It is concluded that the ethanol-induced reduction of firing rate is due to a calcium-dependent process, and modulated by cAMP.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1989

Functional muscarinic supersensitivity in denervated rat hippocampus.

The effects of carbachol (CCh), a cholinergic agonist, were compared in voltage-clamped hippocampal pyramidal neurons in vitro, obtained from normal and fimbria-fornix-lesioned rats. A substantial increase in sensitivity to the effects of CCh was seen in denervated neurons. The supersensitivity was demonstrated on both the inward leak current and the calcium-dependent potassium current, IAHP. These findings provide convincing evidence for cholinergic denervation supersensitivity in the hippocampus.

Acetylcholinesterase↗
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↗