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Biomedical subjects

D J Adams

Publications and source records attributed to D J Adams.

At least 163 records · Page 9Linked to original sources
PubMed1982

Aerosol stability of infectious and potentially infectious reovirus particles.

The aerosol stability of two particle forms, infectious and potentially infectious, of reovirus were examined under static conditions for a range of relative humidities at 21 and 24 degrees C. Virus aerosolization efficiency was determined for two methods of dissemination: Collison nebulizer and Chicago atomizer. Suspensions of Bacillus subtilis var. niger spores were added to reovirus preparations that included both particle forms and disseminated into a dynamic aerosol toroid to estimate the physical decay of the aerosols. At 90 to 100% relative humidity, both reovirus particle forms showed less than 10-fold loss of infectivity after 12 h of aging. At lower relative humidities the aerosol decay curve showed rapid initial decay followed by a markedly lower decay rate. Our findings reveal that reovirus particles are relatively stable in the airborne state.

Aerosols↗
PubMed1982

Immunohistochemical detection of an estrogen-regulated protein by monoclonal antibodies.

It has been shown previously that estradiol regulates the synthesis of a Mr 24,000 cytosol protein in MCF-7 human breast cancer cells. This protein is an attractive probe to study the mechanisms of estrogen regulation in human breast cancer. We have produced monoclonal antibodies against the Mr 24,000 protein which show immunocytochemical localization in the cytoplasm of MCF-7 cells grown as solid tumors in nude mice. They do not react with normal mouse tissue or with MDA-MB-231 cells, an estrogen receptor-negative cell line. Moreover, the monoclonal antibodies react against certain human breast tumor biopsy samples. These data suggest that the monoclonal antibodies obtained will be useful to detect the estrogen-regulated protein by immunohistochemistry.

Antibodies, Monoclonal↗
PubMed1981

Glucose-6-phosphate dehydrogenase: partial characterization of the rat liver and uterine enzymes.

Some properties of rat liver and uterine glucose-6-phosphate dehydrogenase (D-glucose-6-phosphate: NADP+ oxidoreductase, EC 1.1.1.49) have been determined. A procedure has been used for the purification of rat liver glucose-6-phosphate dehydrogenase to homogeneity (spec. act. 210-225 units/mg protein) from large amounts of liver (0.5-2 kg) with yields of up to 30%. Uterine glucose-6-phosphate dehydrogenase was obtained by immunoprecipitation methods and the properties of radioactively-labeled forms of this enzyme were then determined. The amino acid composition of the liver enzyme was found to be similar to that for the enzyme from other mammalian tissues. The liver and uterine enzymes have a subunit molecular weight of 57000 and a pI of 6.5. The NH2-terminal amino acid of both enzymes was found to be pyroglutamate.

Amino Acid Sequence↗
PubMed1981

Estrogen regulation of growth and specific protein synthesis in human breast cancer cells in tissue culture.

Taking advantage of the fact that estrogens can stimulate proliferation of antiestrogen-inhibited MCF-7 cells has enabled us to study molecular events involved in steroid-mediated growth of tumor cells, using a breast cancer cell line which otherwise is affected very little in its growth by estrogens. Under these growth conditions, estradiol stimulates DNA polymerase activity in a manner analogous with reported estrogen effects on enzyme activity in normal target tissues. We also observed dissociation of estrogen effects on cell growth and PgR stimulation, indicating that PgR induction and estrogen-mediated cell division may involve separate control mechanisms. The relative rate of synthesis of the 24,000 molecular weight protein is also increased under these conditions of estrogen-stimulated cell growth. Since increased synthesis of the 24,000 molecular weigh protein was determined not to be a reflection of different stages of cell growth, we suggest that this protein is regulated specifically by estrogens and that it may be a marker of estrogen stimulated growth of human breast tumor cells.

Breast Neoplasms↗
PubMed1981

Block of endplate channels by permeant cations in frog skeletal muscle.

Motor endplates of frog semitendinosus muscles were studied under voltage clamp. Current fluctuations induced by iontophoretic application of acetylcholine were analyzed to give the elementary conductance, gamma , and mean open time, tau , of endplate channels. Total replacement of the external Na+ ion by several other metal ions and by many permeant organic cations changed both gamma and tau . Except with NH4+ ions, the gamma values with foreign test ions were all smaller than expected from the independence relation and their previously measured permeability ratios. The more hydrophobic ions gave the smallest gamma values. Foreign permeant cations also depress gamma when mixed with Na+ ions. These effects could be interpreted in terms of binding of ions to a saturable site within the endplate channel as they pass through. The site for organic ions would have a hydrophobic component. Similar evidence is given for a metal ion binding site on the cytoplasmic end of the channel accessible to internal ions. Most foreign cations also shortened tau when applied externally. The changes of gating did not seem to be correlated with changes in gamma . Thus there is no evidence for control of tau by ions bound within the pore.

Anesthetics, Local↗
PubMed1981

Hyperventilation and 6-hour EEG recording in evaluation of absence seizures.

Seven patients with poorly controlled absence seizures were evaluated clinically and electroencephalographically (EEG) in control and placebo periods and then evaluated after 10 weeks on valproic acid. For analysis of epileptiform activity, 5 minutes of controlled hyperventilation recording was more reliable than 6-hour recording as a predictor of clinical seizure frequency. This apparently paradoxic result can be explained by considering that the number of epileptiform discharges in the EEG is affected by many variables (such as level of consciousness, anxiety, diurnal seizure variation, or blood glucose level) that are difficult to control for prolonged periods.

Electroencephalography↗
PubMed1980

The permeability of the endplate channel to organic cations in frog muscle.

The relative permeability of endplate channels to many organic cations was determined by reversal-potential criteria. Endplate currents induced by iontophoretic "puffs" of acetylcholine were studied by a Vaseline gap, voltage clamp method in cut muscle fibers. Reversal potential changes were measured as the NaCl of the bathing medium was replaced by salts of organic cations, and permeability ratios relative to Na+ ions were calculated from the Goldman-Hodgkin-Katz equation. 40 small monovalent organic cations had permeability ratios larger than 0.1. The most permeant including NH4+, hydroxylamine, hydrazine, methylamine, guanidine, and several relatives of guanidine had permeability ratios in the range 1.3--2.0. However, even cations such as imidazole, choline, tris(hydroxymethyl)aminomethane, triethylamine, and glycine methylester were appreciably permeant with permeability ratios of 0.13--0.95. Four compounds with two charged nitrogen groups were also permeant. Molecular models of the permeant ions suggest that the smallest cross-section of the open pore must be at least as large as a square, 6.5 A x 6.5 A. Specific chemical factors seem to be less important than access or friction in determining the ionic selectivity of the endplate channel.

Animals↗
PubMed1980

The permeability of endplate channels to monovalent and divalent metal cations.

The relative permeability of endplate channels to monovalent and divalent metal ions was determined from reversal potentials. Thallium is the most permeant ion with a permeability ratio relative to Na+ of 2.5. The selectivity among alkali metals is weak with a sequence, Cs+ greater than Rb+ greater than K+ greater than Na+ greater than Li+, and permeability ratios of 1.4, 1.3, 1.1, 1.0, and 0.9. The selectivity among divalent ions is also weak, with a sequence for alkaline earths of Mg++ greater than Ca++ greater than Ba++ greater than Sr++. The transition metal ions Mn++, Co++, Ni++, Zn++, and Cd++ are also permeant. Permeability ratios for divalent ions decreased as the concentration of divalent ion was increased in a manner consistent with the negative surface potential theory of Lewis (1979 J. Physiol. (Lond.). 286: 417--445). With 20 mM XCl2 and 85.5 mM glucosamine.HCl in the external solution, the apparent permeability ratios for the alkaline earth cations (X++) are in the range 0.18--0.25. Alkali metal ions see the endplate channel as a water-filled, neutral pore without high-field-strength sites inside. Their permeability sequence is the same as their aqueous mobility sequence. Divalent ions, however, have a permeability sequence almost opposite from their mobility sequence and must experience some interaction with groups in the channel. In addition, the concentrations of monovalent and divalent ions are increased near the channel mouth by a weak negative surface potential.

Animals↗
PubMed1980

Divalent ion currents and the delayed potassium conductance in an Aplysia neurone.

1. In Na- and Ca-free external solutions, Sr or Ba (but not Mg) could act as carriers of inward current during action potentials in the neurone, R15 of the Aplysia abdominal ganglion. These action potentials exhibited a prolonged plateau phase, the duration of which was dependent on the concentration and species of divalent cation and activity of the neurone. 2. Depolarization of the soma membrane in Na-free Ba solution generated a prolonged, 'late' inward current the amplitude of which was dependent on the external Ba concentration. The Ba current was insensitive to tetrodotoxin but could be blocked by Mn2+ and Co2+ ions. 3. The peak current-voltage relation and threshold for activation of the late inward current was shifted to more negative potentials on replacement of Ca with Ba. The zero-current (reversal) potentials for both Sr and Ba were more negative than for Ca, indicating that the 'Ca' channel is less permeable to Sr2+ or Ba2+ ions than to Ca2+ ions. 4. Inactivation of the 'Ca' channel is slower in Ba than in Ca solution. The time course of Ba currents during a maintained depolarization of 2 sec could be reasonably described by the expression, I'Ba(t) = I'Ba (infinity) [1-exp(-t/tau M)]2exp(-t/tau H). 5. Time constants for activation (tau M) and inactivation (tau H) were voltage-dependent. In the range -10 to +30 mV, tau M varied from 15 to 5 msec and tau H from 2.0 to 0.5 sec (12 degrees C). Steady-state Ba conductance (corrected for inactivation) was voltage-dependent, increasing sigmoidally with depolarization to a maximum of approximately 12 microS at potentials beyond +15 mV. 6. Steady-state inactivation of Ba conductance (hBa(infinity)) varied with holding potential (VH). Conditioning holding potentials more negative than the resting potential (-40 to -50 mV) produced depression of Ba currents. Complete inactivation of Ba currents occurred at holding potentials more positive than 0 mV or with repetitive activation at frequencies greater than 1 Hz. 7. The divalent ions, Ba2+ and Sr2+, reversible depressed the total delayed K+ current at a rate dependent on the frequency of activation. Ba and Sr shifted the delayed K+ current-voltage curve to more positive voltages and depressed the delayed outward current at all membrane potentials. 8. Comparison of the effect of Ba on delayed K+ currents with those obtained in the presence of Mn2+ ions indicated that Ba2+ ions depress both the voltage-dependent and Ca-dependent components of the delayed K+ current. However, the mechanism by which Ba acts to inhibit the two components of the delayed K+ current appears to be different.

Action Potentials↗
PubMed1979

Ionic currents in response to membrane depolarization in an Aplysia neurone.

1. Action potentials recorded in the soma of R15 neurones in the abdominal ganglia of Aplysia juliana were not suppressed by selective inhibition of either Na or Ca conductance alone. It was necessary to block both conductances to suppress action potentials. 2. Membrane currents generated by step depolarizations of the soma consisted of early transient and delayed steady-state currents. The early transient current could have one or two components depending on the activating depolarization. 3. The early more rapid component had a reversal potential at +54 mV and the reversal potential changed with extracellular Na concentration in accord with the Nernst equation. It was blocked by substitution of impermeant cations for Na, by TTX and by internal injections of Zn. It was concluded that this component was normally a Na current. 4. The later slower component of the transient current had a reversal potential at about +65 mV and the reversal potential changed with extracellular Ca concentration is accord with the Nernst equation. It was blocked by substitution of Mg for Ca or addition of Mn, Co, Ni or verapamil to the extracellular solution. It was concluded that this component was normally a Ca current. 5. Na and Ca currents were generated at different threshold potentials, Na currents first appearing at about -20 mV and Ca currents at -5 to 0 mV. 6. The time-to-peak of both Na and Ca currents was affected by the holding potential, by the amplitude of the activating depolarization, by temperature and by divalent ion concentration. 7. The peak Na and Ca conductances both increased sigmoidally with increasing depolarization, the maximum Na conductance of 10--15 microS being approximately twice the maximum Ca conductance. Peak conductances for Na and Ca reached half-maximum at -8 and +3 mV, respectively. 8. The amplitude of the delayed steady-state current could be varied by changing the extracellular K+ ion concentration or by adding tetraethylammonium to the extracellular solution. The reversal potential for 'tail currents' was -67 mV and shifted 18 mV when the extracellular K concentration was doubled. It was concluded that the delayed steady-state current was K current. 9. With prolonged depolarizations, K current decayed with a time constant of the order of 1 sec. Peak K conductance increased with increasing depolarization with the half-maximum occurring at a potential more positive than +20 mV. The maximum rate of fractional activation of K conductance was independent of the amplitude of the clamp step.

Action Potentials↗
PubMed1979

Characteristics of sodium and calcium conductance changes produced by membrane depolarization in an Aplysia neurone.

1. The time course and voltage dependence of Na and Ca conductance changes produced by depolarization of the soma of the neurone R15 in the abdominal ganglion of Aplysia juliana were examined at temperatures of 10--14 degrees C. 2. During a maintained depolarization, Na currents turned on then decayed (inactivated). Inactivation was exponential with time constant tauh. Activation (after correction for inactivation) was reasonably well described by the expression G'Na(t) = G'Na (infinity) (1 - exp [-t/taum])3 over a wide range of potentials. 3. taum and tauh were both voltage dependent. In the range -20 to +40 mV, taum varied from 5 to 0.5 msec and tauh from 25 to 8 msec (13.5 degrees C). Steady-state Na conductance (corrected for inactivation) was voltage dependent also, increasing sigmoidally with depolarization to a maximum of 25--30 muS at +10 to +20 mV. Half-maximal Na conductance occurred at a membrane potential of -8 mV and from -15 to -5 mV, a 5 mV change in membrane potential produced an e-fold change in steady-state Na conductance. 4. Steady-state inactivation of Na conductance (hNa(infinity)) was voltage dependent with half-inactivation occurring at a membrane potential of -32 mV. Recovery from Na inactivation followed an exponential time course with a voltage-dependent time constant. 5. During a maintained depolarization Ca currents activated then decayed (inactivated) more slowly than Na currents. The decay was exponential with time constant tauH. The decay of Ca current was not an artifact porduced by an outward current. The amplitude of calcium tail currents, produced by voltage steps back to epsilonK at different times during the decay of ICa, decayed also with a time constant close to tauH. 6. Ca conductance (after correction for inactivation) could be described approximately by the expression G'Ca(t) = G'Ca(infinity) (1 - exp [-t/tauM])p but it was necessary to vary p from 1 to 2 at different potentials. No value of p gave as good a fit to this model as that obtained for Na currents. 7. taum and tauH were voltage dependent. In the range of potentials from 0 to +60 mV, tauM varied from 9 to 5 msec and tauH from 300 to 50 msec (13.5 degrees C). Steady-state Ca conductance (corrected for inactivation) was voltage dependent also, increasing sigmoidally with depolarization to a maximum of 10--15 muS at +30 to +40 mV. Half-maximal Ca conductance occurred at a membrane potential of +12 mV, and from +10 to +20 mV a 6 mV change in membrane potential produced an e-fold change in Ca conductance. 8. Steady-state inactivation of Ca conductance (hCa(infinity)) varied with holding potential (VH). Half-inactivation occurred with depolarization to -20 mV. At potentials more negative than -40 mV, hCa(infinity) was less than at -40 mV, i.e. hyperpolarization produced Ca 'inactivation'. 9...

Animals↗
PubMed1979

Sodium and calcium gating currents in an Aplysia neurone.

1. Currents generated by depolarizing the hyperpolarizing voltage pulses were recorded at temperatures of 4--12 degrees C in the voltage-clamped soma of R15 in aplysia abdominal ganglia exposed to solutions which suppressed ionic currents. 2. Subtraction of linear capacitive and leakage currents from current generated by voltage pulses to levels more positive than -20mV revealed non-linear transient outward displacement currents at the onset of the clamp step (on-current) and transient inward displacement currents after the membrane potential returned to the holding potential (off-current). Only on-currents were studied. 3. Pulses to membrane potentials of -20 to 0 mV generated a displacement current with rapid onset and exponential decay. At membrane potentials more positive than o mV a second displacement current with a much slower onset and slower exponential decay was seen. Because the different threshold potentials for the two displacement currents were close to the different threshold potentials for Na and Ca ion currents, the two displacement currents were called Na and Ca 'gating' currents. 4. The amount of charge transfer during Ca gating currents increased sigmoidally with increasing depolarization, reaching a maximum at +30 to +40 mV. Half-maximum charge transfer occurred at +15 mV. 5. Total charge movement during Ca gating currents was maximal with holding potentials of -30 to -40 mV. More positive or more negative holding potentials produced a decrease in charge movement. 6. The time course of the gating currents, but not the total charge displaced, was very sensitive to temperature. The time constant of decay of Ca gating currents had a Q10 of about 3, whereas the total amount of charge displaced had a Q10 of 1.2. 7. The charge transfer during both Na and Ca gating currents and the amplitude of Na and Ca (but not K) ionic currents were reduced in solutions containing 1 mm-n-octanol.

Animals↗