Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019829 (Hodgkin's disease)
 30,247 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of fourteen halogenated ethers on the sodium and potassium currents of voltage-clamped squid giant axons have been examined. Effects under open-circuit were also studied. In voltage-clamped axons, the ethers tended to reduce potassium currents at least as much, if not more, than sodium currents. This finding distinguishes the halogenated ethers from many other general anaesthetics. Certain, but not all, halogenated ethers induced a pronounced maximum in potassium current traces as a function of time. This property can be formally described if an inactivation term is added to the Hodgkin-Huxley equation for potassium currents. Large shifts in the sodium-current inactivation parameter h infinity were produced in some instances. Two fully halogenated methyl ethyl ethers, known to produce convulsions in mice, depressed both sodium and potassium currents, but with a very slow time course of action. The electrophysiological effects of the halogenated ethers investigated appear to depend on the position and number of hydrogen bonds that can be formed.
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PMID:The actions of halogenated ethers on the ionic currents of the squid giant axon. 244 63

Hodgkin's disease of nodular sclerosis and mixed cellularity subtypes contains numerous eosinophils and substantial amounts of extracellular eosinophil peroxidase (EPO). To determine if the extracellular EPO retains cytotoxic activity, the authors analyzed cells from 13 cases of Hodgkin's disease and ten cases of benign lymphoid hyperplasia for their in vitro sensitivity to killing by a low concentration of hydrogen peroxide. Cells from cases of benign lymphoid hyperplasia (0.5% +/- 1% killing) and lymphocyte predominant Hodgkin's disease (4.5% +/- 6% killing) were significantly (P less than 0.05) less sensitive to killing by hydrogen peroxide than cells from nodular sclerosis Hodgkin's disease (26% +/- 13% killing) and mixed cellularity Hodgkin's disease (52% +/- 9% killing). The authors concluded that cells from Hodgkin's disease of nodular sclerosis and mixed cellularity subtypes have an increased sensitivity to killing by an otherwise nonlethal concentration of hydrogen peroxide.
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PMID:In-vitro sensitivity of Hodgkin's disease to hydrogen peroxide toxicity. Correlation with peroxidase activity. 254 83

The inhibitory effect of phenylhydrazine and azide combined with either pre-formed or nascent hydrogen peroxide H2O2 upon endogenous peroxidatic activity, expressed by tissue eosinophils in different disease states, was investigated. It was found that whilst endogenous peroxidatic activity due to eosinophils in a Hodgkin's disease and a histiocytosis X case were adequately inhibited by phenylhydrazine combines with pre-formed or nascent H2O2, the eosinophils in the Onchocerca volvulus nodule were either not at all or only partly inhibited by the two regimens. On the other hand, a combination of azide with nascent H2O2 proved consistently effective against this resistant form of endogenous peroxidatic activity. Using human tonsil sections this protocol was shown to be non-deleterious to T4('CD4'), T6('CD1') and T8('CD8') lymphocyte surface antigens as evidenced by the application of a standard indirect immunoperoxidase technique and the relevant monoclonal antibodies.
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PMID:An improved method for the inhibition of endogenous peroxidase non-deleterious to lymphocyte surface markers. Application to immunoperoxidase studies on eosinophil-rich tissue preparations. 332 39

In the present study we investigated the role of monocytes and of their soluble products (prostaglandins and hydrogen peroxide) in the modulation of the immune response in 50 untreated patients with Hodgkin's disease (HD) compared with a group of healthy donors. The primary response in vitro has been studied with the method of haemolytic colonies in soft agar. A defective in vitro antibody production has been observed in HD patients. Both Indomethacin addition (10(-6) M, final concentration) and depletion of plastic adherent cells, slightly increased the number of haemolytic areas in cultures from HD patients as compared with healthy donors. Similarly, the addition of catalase (8000 U/ml) which destroys H2O2, that is the main mediator of monocytes suppressor activity in normal subjects, did not restore the response of peripheral blood mononuclear cells (PBMC) from HD patients. These results suggest that monocytic cells play a minor role, if any, in the depression of the immune response in HD patients.
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PMID:[Antibody response in cultures of lymphocytes from patients with Hodgkin's lymphoma: role of monocytes]. 332 76

The voltage dependence of the voltage clamp responses of myelinated nerve fibers depends on the concentration of divalent cations and of hydrogen ions in the bathing medium. In general, increases of the [Ca], [Ni], or [H] increase the depolarization needed to elicit a given response of the nerve. An e-fold increase of the [Ca] produces the following shifts of the voltage dependence of the parameters in the Hodgkin-Huxley model: m(infinity), 8.7 mv; h(infinity), 6.5 mv; tau(n), 0.0 mv. The same increase of the [H], if done below pH 5.5, produces the following shifts: m(infinity), 13.5 mv; h(infinity), 13.5 mv; tau(n), 13.5 mv; and if done above pH 5.5: m(infinity), 1.3 mv; h(infinity), 1.3 mv; tau(n), 4.0 mv. The voltage shifts are proportional to the logarithm of the concentration of the divalent ions and of the hydrogen ion. The observed voltage shifts are interpreted as evidence for negative fixed charges near the sodium and potassium channels. The charged groups are assumed to comprise several types, of varying affinity for divalent and hydrogen ions. The charges near the sodium channels differ from those near the potassium channels. As the pH is lowered below pH 6, the maximum sodium conductance decreases quickly and reversibly in a manner that suggests that the protonation of an acidic group with a pK(a) of 5.2 blocks individual sodium channels.
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PMID:Charges and potentials at the nerve surface. Divalent ions and pH. 564 36

We studied the contribution and mechanisms of monocyte-mediated suppression in the depressed T cell proliferative responses observed in patients with Hodgkin's disease. Mononuclear leukocytes from 22 untreated patients had significantly lower proliferation after stimulation with suboptimal doses of phytohemagglutinin than normals controls (p less than 0.001). When indomethacin was added to the cultures, the mean percent increase in patient proliferation exceeded that of normals (160 +/- 19% vs 81 +/- 9%; p less than 0.008), yet patient proliferation remained only 36% of normal. Catalase alone caused a minimal increase in proliferation in all cultures. When catalase plus indomethacin were added to either normal or patient cultures, however, a synergistic increase was observed. The mean percent increase in patient proliferation was 300 +/- 80%, although once again the absolute proliferative response of the patients remained subnormal (p less than 0.003). Removal of adherent monocytes from patient cultures produced increases in proliferation comparable to that observed with the addition of indomethacin. Long-term disease-free survivors of Hodgkin's disease had depressed T cell proliferation but no significant increase after the addition of indomethacin. We conclude: 1) although untreated patients with Hodgkin's disease have increased monocyte suppressor activity that is mediated by increased prostaglandin production, this is not the major cause of the depressed T cell proliferative responses observed in Hodgkin's disease; 2) depressed proliferative responses in cured Hodgkin's disease are not mediated by prostaglandins; 3) hydrogen peroxide suppresses T cell proliferation in both normals and untreated patients; and 4) other factors, probably inherent in the T cell itself, are the major cause of depressed T cell responses in Hodgkin's disease.
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PMID:Depressed T cell proliferative responses in Hodgkin's disease: role of monocyte-mediated suppression via prostaglandins and hydrogen peroxide. 698 Sep 49

Proton magnetic resonance spectroscopy (MRS) was carried out on a patient with histologically proven non-Hodgkin lymphoma (NHL) of the central nervous system (CNS). The observation of the presence of a huge resonance in the region between 0.5-1.5 ppm and the absence of any other signals is not in agreement with those published for NHL in the literature but has a striking similarity to that reported for an intracranial tuberculoma.
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PMID:Proton MRS similarity between central nervous system non-Hodgkin lymphoma and intracranial tuberculoma. 779 59

We report a novel strategy, called end-product (EP) amplification, capable of enhancing the sensitivity of immunohistochemical procedures by about an order of magnitude or more. The strategy employs an antibody (anti-EP) to the product generated by the action of horseradish peroxidase on 3,3'-diaminobenzidine (DAB), and can be extended to the products of other enzymes as well, e.g., alkaline phosphatase. Amplification is the consequence of the ability of anti-EP to detect the multiplicity of product moelcules resulting from the turnover of substrate by a single enzyme molecule. The subsequent detection of anti-EP was by biotinylated goat anti-rabbit antibody, followed by avidin-peroxidase and DAB or by avidin-alkaline phosphatase and Vector Red. Further amplification can be accomplished by repeated cycles of the protocol. Anti-EP was produced by immunization with a bovine serum albumin (BSA) conjugate of a soluble polymer of DAB, prepared by a carefully controlled reaction of DAB with horseradish peroxidase and hydrogen peroxide. Coupling to BSA (and to RSA) was accomplished with glutaraldehyde. The titer of anti-EP was established by ELISA. Formalin-fixed, paraffin-embedded sections of five cases of Hodgkin's disease and five tonsils with follicular hyperplasia were immunolabeled for the following lymphoid markers: CD3, CD20, CD30, CD45RA, and CD68. EP amplification with anti-EP was also applied to cases of CMV pneumonia and cerebral toxoplasmosis to determine whether this procedure could improve detection of the infectious agents. Immunolabeling of the primary antibody was performed by the avidin-biotin-peroxidase technique with DAB as the reaction substrate. The specificity of EP amplification was tested by demonstrating binding of anti-EP with Vector Red with the generation of a fluorescence end-point. There was complete congruence in the distribution of the DAB signal and the red immunofluorescence representing EP amplification. The intensity of the DAB signal was increased as much as 16-fold by EP amplification, making possible a reduction in the amount of the primary antibody by as much as 85-90%. Sensitivity also increased with respect to weakly expressed antigens and low concentrations of infectious agents.
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PMID:A strategy for immunohistochemical signal enhancement by end-product amplification. 875 54

We created a single-compartment computer model of a CO(2) chemosensory neuron using differential equations adapted from the Hodgkin-Huxley model and measurements of currents in CO(2) chemosensory neurons from Helix aspersa. We incorporated into the model two inward currents, a sodium current and a calcium current, three outward potassium currents, an A-type current (I(KA)), a delayed rectifier current (I(KDR)), a calcium-activated potassium current (I(KCa)), and a proton conductance found in invertebrate cells. All of the potassium channels were inhibited by reduced pH. We also included the pH regulatory process to mimic the effect of the sodium-hydrogen exchanger (NHE) described in these cells during hypercapnic stimulation. The model displayed chemosensory behavior (increased spike frequency during acid stimulation), and all three potassium channels participated in the chemosensory response and shaped the temporal characteristics of the response to acid stimulation. pH-dependent inhibition of I(KA) initiated the response to CO(2), but hypercapnic inhibition of I(KDR) and I(KCa) affected the duration of the excitatory response to hypercapnia. The presence or absence of NHE activity altered the chemosensory response over time and demonstrated the inadvisability of effective intracellular pH (pH(i)) regulation in cells designed to act as chemostats for acid-base regulation. The results of the model indicate that multiple channels contribute to CO(2) chemosensitivity, but the primary sensor is probably I(KA). pH(i) may be a sufficient chemosensory stimulus, but it may not be a necessary stimulus: either pH(i) or extracellular pH can be an effective stimuli if chemosensory neurons express appropriate pH-sensitive channels. The lack of pH(i) regulation is a key feature determining the neuronal activity of chemosensory cells over time, and the balanced lack of pH(i) regulation during hypercapnia probably depends on intracellular activation of pH(i) regulation but extracellular inhibition of pH(i) regulation. These general principles are applicable to all CO(2) chemosensory cells in vertebrate and invertebrate neurons.
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PMID:A computational analysis of central CO2 chemosensitivity in Helix aspersa. 1692 73

The dynamics of free radical and peroxidation processes in patients with non-Hodgkin lymphomas (NHL) was studied parallel to the evaluation of changes in the functional condition of the cardiovascular system during a course of chemotherapy. Thirty-one patients (17 men; 14 women) aged 30 to 81, were examined. The dynamics of active oxygen forms (AOF) generation was studied using chemiluminiscent technique. The intensity of leucocyte chemiluminiscence (CL) (basal and zimozan-stimulated ones), the blood level of malonic dialdehyde, the antiperoxidation blood plasma activity according to its hydrogen peroxide-induced CL intensity, were measured. The functional condition of the cardiovascular system was evaluated using ECG, EchoCG, and Holter monitoring. The study revealed an increase in AOF generation by leucocytes, which correlated with the severity of the disease. The treatment of the NHL patients with cytostatics was associated with the activation of free radical reactions, which was maximal during the first 24 hours 1 hour after drug administration. Cytostatic therapy was characterized by a cardiotoxic effect, which consisted in an increase in the rate of various arrhythmias and a decrease in the heart contractility. The study demonstrates a direct correlation between the degree of AOF generation growth and the prominence of myocardial lesion signs. The authors conclude that the intensification of free radical reactions under the conditions of cytostatic therapy causes cardiotoxic effects, which requires a course of preventive cardioprotective therapy before chemotherapy is commenced.
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PMID:[Free radical peroxidation processes and cardiotoxicity in treatment of malignant lymphomas]. 1720 48


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