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Query: UMLS:C0019829 (Hodgkin's disease)
 30,247 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ten cases of acute febrile neutrophilic dermatosis or Sweet's disease have been studied clinically and histologically. Seventy percent of the patients were females with mean age of 43.1 +/-9 years. All of them presented the typical skin lesions consisting of papules and painful erythematous--edematous plaques in face, neck and upper chest. Fever was observed in seven patients and painful joints in four cases. One case presented polyarthritis of the big joints and there was one other case of conjuntivitis. The analytical data revealed a constant increase in sedimentation rate observed in 90% of patients. Leukocytosis was observed in 30% of patients and neutrophilia in 40%. Histologically, the lesions showed a neutrophilic infiltration of the skin without signs of vasculitis. Eight patients received treatment with Prednisone per os, one of whom, because of his relapses, was later given Potassium Iodine. Another patient was treated with Indomethacin, and one patient did not received any treatment. The evolution was favorable in all cases with sustained remissions. Sweet's Syndrome has been described associated mainly with acute myeloid leukemia in 10-20% of patients and in isolated instances with other systemic and neoplasic diseases. The concomitant conditions in 50% of our cases were: Ulcerative colitis, nodular sclerotic Hodgkin disease, infiltrative ductal carcinoma of the breast, carcinoma of the uterus neck and Crohn's disease; these last two associations had not been previously described in the literature.
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PMID:[Sweet's syndrome. A study of 10 cases and review of the literature]. 220 15

1. The relative strengths of four mechanisms of depolarizing synaptic inhibition described in the previous paper were evaluated with an electrical model of the giant motor synapse (GMS) and postsynaptic region of the motor giant motoneuron (MoG). 2. The model consists of one compartment that represents the presynaptic region of the medial giant (MG) interneuron and three compartments that represent the postsynaptic region and proximal axon of the MoG. The presynaptic MG compartment is linked to a postsynaptic MoG compartment by a rectifying conductance that represents the GMS. Each compartment consists of parallel paths to ground for active and/or passive membrane currents. 3. Parameter values of the model were set so the MG compartment would replicate an MG impulse and the MoG compartments would replicate the current-clamp, voltage-clamp, and synaptic responses of a single MoG neuron described in the previous paper. The Hodgkin-Huxley equations described voltage-sensitive sodium and potassium currents. 4. Comparison of the MoG compartment currents that mediate an inhibited excitatory postsynaptic potential (EPSP) [triggered during a depolarizing inhibitory postsynaptic potential (d-IPSP)] with those of an uninhibited EPSP indicate that all four mechanisms have significant inhibitory effects. Reverse bias of the GMS by the d-IPSP reduced the GMS current by 65 nA (12%). The remaining inward current was further reduced by a 243-nA outward current through the inhibitory postsynaptic conductance. The d-IPSP inactivated sodium conductance so the inward sodium current evoked by the EPSP was reduced by 319 nA (-68%). The d-IPSP reduced the latency for potassium activation by the EPSP so that the outward potassium current coincided with the inward sodium current and reduced the net inward current by 100 nA. Together, these mechanisms reduced the EPSP amplitude by 69%. 5. The resting potential of MoG is normally 15 mV more positive than MG rest potential, but in some preparations this difference may be as much as 25 mV or as little as 0 mV. Corresponding differences in the rest potentials of the MoG and MG models have little effect on the amplitude of the model MoG EPSP because changes in the inward synaptic and sodium currents are balanced by corresponding changes in the outward potassium current.
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PMID:Mechanisms of depolarizing inhibition at the crayfish giant motor synapse. II. Quantitative reconstruction. 221 31

Several conflicting models have been used to characterize the gating behavior of the cardiac delayed rectifier. In this study, whole-cell delayed rectifier currents were measured in voltage-clamped guinea pig ventricular myocytes, and a minimal model which reproduced the observed kinetic behavior was identified. First, whole-cell potassium currents between -10 and +70 mV were recorded using external solutions designed to eliminate Na and Ca currents and two components of time-dependent outward current were found. One component was a La3(+)-sensitive current which inactivated and resembled the transient outward current described in other cell types; single-channel observations confirmed the presence of a transient outward current in these guinea pig ventricular cells (gamma = 9.9 pS, [K]o = 4.5 mM). Analysis of envelopes of tail amplitudes demonstrated that this component was absent in solutions containing 30-100 microM La3+. The remaining time-dependent current, IK, activated with a sigmoidal time course that was well-characterized by three time constants. Nonlinear least-squares fits of a four-state Markovian chain model (closed - closed - closed - open) to IK activation were therefore compared to other models previously used to characterize IK gating: n2 and n4 Hodgkin-Huxley models and a Markovian chain model with only two closed states. In each case the four-state model was significantly better (P less than 0.05). The failure of the Hodgkin-Huxley models to adequately describe the macroscopic current indicates that identical and independent gating particles should not be assumed for this K channel. The voltage-dependent terms describing the rate constants for the four-state model were then derived using a global fitting approach for IK data obtained over a wide range of potentials (-80 to +70 mV). The fit was significantly improved by including a term representing the membrane dipole forces (P less than 0.01). The resulting rate constants predicted long single-channel openings (greater than 1 s) at voltages greater than 0 mV. In cell-attached patches, single delayed rectifier channels which had a mean chord conductance of 5.4 pS at +60 mV ([K]o = 4.5 mM) were recorded for brief periods. These channels exhibited behavior predicted by the four-state model: long openings and latency distributions with delayed peaks. These results suggest that the cardiac delayed rectifier undergoes at least two major transitions between closed states before opening upon depolarization.
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PMID:Time-dependent outward current in guinea pig ventricular myocytes. Gating kinetics of the delayed rectifier. 225 17

As a step towards an improved understanding of cardiac arrhythmias caused by abnormal automaticity, we perform a stability analysis of a Hodgkin-Huxley model of the myocardial cell membrane (modified Beeler-Reuter, MBR). The bifurcation structure of the model is obtained as a function of three parameters: the intensity of an applied constant current; the potassium equilibrium potential representing the accumulation of K+ ions in the external medium; and the maximum conductance of the slow inward current mimicking the local application of catecholamines on the membrane. For a range of parameter values, the model exhibits either stable automaticity or bistability between two quiescent states or between a quiescent state and an oscillatory state. These transformations of the bifurcation structure are shown to depend on the interrelationship between three elements: the activation of the slow inward current, the region of high slope conductance of the time-independent potassium current functions, and the slow variables controlling the activation of the potassium current and the inactivation of the slow inward current. Reduced two- and three-dimensional models are shown to reproduce the main stability properties of the full MBR model and to facilitate the understanding of its dynamic behavior. The onset of instability and the oscillatory features of the MBR model are in good agreement with relevant experimental results, and possible sources of disagreement on certain points are discussed.
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PMID:A model study of stability and oscillations in the myocardial cell membrane. 229 87

A qualitative analysis of the Hodgkin-Huxley model (Hodgkin and Huxley 1952), which closely mimics the ionic processes at a real nerve membrane, is performed by means of a singular perturbation theory. This was achieved by introducing a perturbation parameter that, if decreased, "speeds up" the fast variables of the Hodgkin-Huxley equations (membrane potential and sodium activation), whereas it does not affect the slow variables (sodium inactivation and potassium activation). In the most extreme case, if the perturbation parameter is set to zero, the original four-dimensional system "degenerates" to a system with only two differential equations. This degenerate system is easier to analyze and much more intuitive than the original Hodgkin-Huxley equations. It shows, like the original model, an infinite train of action potentials if stimulated by an input current in a suitable range. Additionally, explanations for the increased sensitivity to depolarizing current steps that precedes an action potential can be found by analysis of the degenerate system. Using the theory of Mishchenko and Rozov (1980) it is shown that the degenerate system does not only represent a simplification of the original Hodgkin-Huxley equations but also gives a valid approximation of the original model at least for stimulating currents that are constant within a suitable range.
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PMID:The singularly perturbed Hodgkin-Huxley equations as a tool for the analysis of repetitive nerve activity. 231 11

1. Intracellular recordings were made from locus coeruleus (LC) neurones in a totally submerged brain slice preparation from adult rats. The effect of gamma-aminobutyric acid (GABA) on LC neurones was studied under current-clamp and voltage-clamp conditions. GABA caused inhibition of spontaneous firing and a large conductance increase in LC neurones. These effects could be accompanied by depolarization, hyperpolarization or little change in membrane potential depending on the presence or absence of Cl- in the recording microelectrode. 2. The reversal potential for GABA-induced changes in membrane potential (EGABA) was -71.3 +/- 1.1 mV (S.E.M., n = 21) in cells impaled with potassium acetate electrodes and -47.5 +/- 1.4 mV (S.E.M., n = 15) in cells impaled with KCl electrodes. When the external Cl- concentration was reduced EGABA was shifted in the depolarizing direction by 51.5 mV per tenfold change in external Cl- which is close to the shift predicted by the Nernst equation for a selective increase in CL- conductance. 3. GABA effects on LC neurones result from a direct action since they persist in low-Ca2+ and high-Mg2+ media which block synaptic transmission. 4. The effects of GABA were concentration dependent and antagonized by bicuculline (10 microM) and bicuculline methiodide (80-100 microM) indicating that they were mediated predominantly by an action on GABAA receptors. In the presence of bicuculline, EGABA was shifted towards the K+ equilibrium potential which indicated a residual bicuculline-resistant action at GABAB receptors. 5. GABA-induced responses were membrane potential dependent. GABA conductance was observed to decrease with membrane hyperpolarization in a linear manner. GABA-induced current showed outward rectification. In the voltage range studied (rest to -110 mV) the extent of this rectification was predicted by the Goldman-Hodgkin-Katz equation, suggesting that it was due to the unequal distribution of Cl- across the membrane. In addition, the time constant of decay of GABA current was decreased by membrane hyperpolarization; this could be due to a voltage-dependent change in receptor or channel kinetics. 6. These data suggest that the primary action of GABA on LC neurones is to increase Cl- conductance by activation of bicuculline-sensitive GABAA receptors. Due to the voltage dependence of GABA responses, GABA will exert a stronger inhibitory effect on LC neurones at depolarized than at hyperpolarized membrane potentials. This could serve as a negative feedback mechanism to control excitability of these neurones.
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PMID:gamma-Aminobutyric acid responses in rat locus coeruleus neurones in vitro: a current-clamp and voltage-clamp study. 234 90

Spontaneously active single cells have been obtained from the sinus venosus region of the bull-frog, Rana catesbeiana, using an enzymic dispersion procedure involving serial applications of trypsin, collagenase and elastase in nominally 0 Ca2+ Ringer solution. These cells have normal action potentials and fire spontaneously at a rate very similar to the intact sinus venosus. A single suction micro-electrode technique (Hamill, Marty, Neher, Sakmann & Sigworth, 1981; Hume & Giles, 1983) has been used to record the spontaneous diastolic depolarizations or pace-maker activity as well as the regenerative action potentials in these cells. This electrophysiological activity is completely insensitive to tetrodotoxin (TTX; 3 X 10(-6) M) and is very similar to that recorded from an in vitro sinus venosus preparation. The present experiments were aimed at identifying the transmembrane potassium currents, and analysing their role(s) in the development of the pace-maker potential and the repolarization of the action potential. Depolarizing voltage-clamp steps from the normal maximum diastolic potential (-75 mV) elicit a time- and voltage-dependent activation of an outward current. The reversal potential of this current in normal Ringer solution [( K+]0 2.5 mM) is near -95 mV; and it shifts by 51 mV per tenfold increase in [K+]0, which strongly suggests that this current is carried by K+. We therefore labelled it IK. The reversal potential of IK did not shift in the positive direction following very long (20 s) depolarizing clamp steps to +20 mV, indicating that 'extracellular' accumulation of [K+]0 does not produce any significant artifacts. The fully activated instantaneous current-voltage (I-V) relationship for IK is approximately linear over the range of potentials -130 to -30 mV. Thus, the ion transfer mechanism of IK may be described as a simple ohmic conductance in this range of potentials. Positive relative to -30 mV, however, the I-V exhibits significant inward rectification. A Hodgkin-Huxley analysis of the kinetics of IK, including a demonstration that the envelope of tails quantitatively matches the time course of the onset of IK during a prolonged depolarizing clamp step has been completed. The steady-state activation variable (n infinity) of IK spans the voltage range approximately -40 to +10 mV. It is well-fitted by a Boltzmann distribution function with half-activation at -20 mV. The time course of decay of IK is a single exponential. However, the activation or onset of IK shows clear sigmoidicity in the range of potentials from the activation threshold (-40 mV) to 0 mV.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Voltage clamp of bull-frog cardiac pace-maker cells: a quantitative analysis of potassium currents. 241 14

A physical system is derived which has properties which are the same as those computed for the potassium conductance system in the squid axon with the Hodgkin-Huxley equations. The system describes a molecule with five ionization states which, on hyperpolarization, are stripped of singly charged ions (H+?), and doubly charged ions (Ca++?). The dependence of potassium conductance on pH and on the calcium substrate concentration is predicted by the physical system. The effect of enzyme or allosteric interactions in producing inactivation or blocking of conductance is discussed. To consider these effects, the isomorphism is augmented to an 8-state system. This 8-state system encompasses the properties of both the potassium and, with different parameters, the sodium conductance. It is thus general enough to describe all the HH equations in the potential region used for the determination of the HH parameters, namely, -30 to 110 mV transmembrane potential.
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PMID:Isomorphism on a physical system of the Hodgkin-Huxley equations for potassium conductance. 241 63

The squid giant axon was the first preparation to be investigated with the voltage clamp technique over 30 years ago by Cole (1949) and Hodgkin et al. (1952). During the intervening years it has continued to serve as a useful preparation for the development of other new techniques such as internal perfusion (Baker et al., 1962), gating current measurements (Armstrong and Bezanilla, 1974), and patch clamp measurements (Conti and Neher, 1980). It also has served as a useful comparative preparation for investigations of sodium and potassium currents in other excitable membrane preparations. This article has focused on the activation kinetics and the instantaneous current-voltage relation of the potassium component. The squid axon is well suited for studies of IK, because it appears to have only a single type of potassium channel, and the leakage current is relatively small under ideal conditions. The IK component is activated in a sigmoidal manner following membrane depolarization. It deactivates with a single exponential time constant following return of the membrane potential to the holding level, although the deactivation time constant varies with changes in the external potassium concentration. There has not, as yet, appeared a self-consistent model which describes all of these results. The current-voltage relation is a nonlinear function of driving force, which is approximately described by the Goldman-Hodgkin-Katz equation, although a model of the IV based on single file diffusion of ions through a channel is more in tune with the modern view of the ion permeation process (Hodgkin and Keynes, 1955; Hille and Schwarz, 1978; Clay and Shlesinger, 1977, 1983, 1984). Further progress in this area will probably be achieved both by the traditional techniques and by the patch clamp technique. The traditional method is well suited for studying tail current kinetics and the slow inactivation process. The patch clamp technique is well suited for studying the distribution of channels in the membrane and the kinetics of channel gating in steady state conditions.
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PMID:Potassium current in the squid giant axon. 241 75

This chapter reviews what is known of the voltage-dependent conductances of three classes of vertebrate nerve cell, as assessed by somatic voltage clamping. These classes are: (1) bullfrog paravertebral sympathetic ganglion cells; (2) rodent superior cervical sympathetic ganglion cells; and (3) rodent hippocampal pyramidal cells. Of these, bullfrog neurons are the most thoroughly characterized. They possess at least seven distinct voltage-activated conductances. Two of these, called GNa and GCa, carry inward, depolarizing current. They both activate rapidly, and can, under appropriate conditions, generate action potentials. The remaining five conductances are all potassium-mediated, and can thus in principle produce hyperpolarizations or repolarize the action potential. However, because each of these potassium conductances have different sizes, speeds, and voltage thresholds, they play a variety of hyperpolarizing, stabilizing, or braking roles. IC is large, fast, and voltage dependent. Action potentials trigger calcium influx, which rapidly turns on IC. This repolarizes the action potential and turns off IC. However another Ca-dependent current, IAHP, remains active even at negative potentials and leads to a prolonged hyperpolarization. If IC is blocked, spike repolarization slows somewhat, allowing the Hodgkin-Huxley delayed rectifier current IK to develop. This is also large enough to repolarize the spike rapidly, although it is normally preempted by IC. IA and IM are other small potassium currents that activate at more negative potentials than do IC, IK, and IAHP. IA is a transient outward current that mainly influences voltage trajectories following hyperpolarizing current pulses. IM activates progressively during prolonged depolarizing current pulses, and, together with IAHP, explains most of the adaptation seen in these cells. The harmonious counterpoint of this septet of currents explains most of the electrical excitability properties of these cells. However, several of the currents are also synaptically regulated, as a result of transmitters acting on muscarinic or peptide receptors. These slow synaptic actions can lead to dramatic changes in the electrical behavior of the cells. These currents all appear to be present in rat sympathetic ganglion cells also, although detailed analysis here has been hampered by the more complex geometry of these neurons. Furthermore, the roles of the various currents have not been completely defined. It seems possible that IA can contribute to spike repolarization, and clean separation of IC and IAHP has not yet been achieved.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Voltage-dependent currents of vertebrate neurons and their role in membrane excitability. 242 89


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