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 study deals with an evaluation of activity of cellular antioxidative system enzymes such as glutathione reductase and glutathione: H2O2 peroxidase in blood plasma, leukocytes and lymphocytes of healthy subjects and patients with lymphoproliferative diseases such as Hodgkin's disease, acute leukemia ana lymphosarcoma. A decrease in enzymatic activity in blood and glutathione redox-system dysbalance was identified in the patients group.
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PMID:[The glutathione enzymatic redox system in the blood of patients with lymphoproliferative diseases]. 134 59

Silver-intensification methods described in the literature for the diaminobenzidine (DAB) and diaminobenzidine-nickel (DAB/Ni) endproduct of the peroxidase reaction were compared in model systems after immunoperoxidase and in situ hybridization. First, these methods were compared in immunohistochemical model systems, using the demonstration of glial fibrillar acidic protein (GFAP) and prostate-specific antigen (PSA) in paraffin sections of human brain and prostate tissue, respectively. When DAB without Ni was used as substrate, tissue argyrophilia caused considerable background staining. Only when this tissue reactivity was quenched with, e.g., CuSO4 with H2O2 or thioglycolic acid, were the results acceptable. A considerable improvement in the signal-to-noise ratio could be obtained when nickel was included in the substrate mixture. The methods that proved to be best for demonstration of GFAP and PSA made use of acid developer solutions. Subsequently, these methods were compared with other sensitive immunostaining methods for demonstration of the gamma-delta T-cell receptor in frozen lymphoid tissue. In this model a considerable increase in the number of positive cells could be obtained using silver intensification. The different methods using DAB/Ni were also compared for use in DNA in situ hybridization (DISH). In this case two model systems were used: human papilloma virus type 11 (HPV-11) DNA in condyloma tissue (abundant target model) and Epstein-Barr virus (EBV) DNA in a mononucleosis lymph node (low target model). For demonstration of HPV-11, all methods gave more or less satisfactory results, which were best with the acid developer solutions. Moreover, for demonstration of EBV DNA, a signal could be obtained only with these developer solutions. Such a method also proved suitable in double immuno-hybrido stainings for the demonstration of EBV DNA in specific antigen-positive Reed-Sternberg cells in paraffin sections of Hodgkin lymph nodes.
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PMID:Application and comparison of silver intensification methods for the diaminobenzidine and diaminobenzidine-nickel endproduct of the peroxidation reaction in immunohistochemistry and in situ hybridization. 153 4

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 authors report a case of Fournier's gangrene in a 54-year-old patient subjected 6 days earlier to chemotherapy for mediastinal Hodgkin's disease. The patient had fever and reported the onset of worsening pain and heat sensations in the inguinal, perineal and scrotal areas. Objectively, there was local oedema followed by the onset of crepitation. The patient had a very low white blood cell count (900/cu.mm). The Patient underwent emergency surgery with multiple, communicating incisions in the inguinal, perineal and scrotal areas, with the removal of necrotic tissue and daily washing with physiological solution and 12% H2O2. He also received antibiotic treatment with metronidazole and gentamicin and 5 cycles of high-pressure oxygen therapy, with disappearance of pain and fever and good local tissue repair.
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PMID:[Fournier's gangrene in a patient with Hodgkin's disease: a clinical case]. 1182 71

Nitric oxide ((.)NO) induces apoptosis at high concentrations by S-nitrosating proteins such as glyceraldehyde-3-phosphate dehydrogenase. This literature analysis revealed that failure to sustain high (.)NO concentrations is common to all cancers. In cervical, gastric, colorectal, breast, and lung cancer, the cause of this failure is the inadequate expression of inducible nitric oxide synthase (iNOS), resulting from the inhibition of iNOS expression by TGF-beta1 at the mRNA level. In bladder, renal, and prostate cancer, the reason for the insufficient (.)NO levels is the depletion of arginine, resulting from arginase overexpression. Arginase competes with iNOS for arginine, catalyzing its hydrolysis to ornithine and urea. In gliomas and ovarian sarcomas, low (.)NO levels are caused by inhibition of iNOS by N-chlorotaurine, produced by infiltrating neutrophils. Stimulated neutrophils express myeloperoxidase, catalyzing H2O2 oxidation of Cl- to HOCl, which N-chlorinates taurine at its concentration of 19 mM in neutrophils. In squamous cell carcinomas of the skin, ovarian cancers, lymphomas, Hodgkin's disease, and breast cancers, low (.)NO concentrations arise from the inhibition of iNOS by N-bromotaurine, produced by eosinophil-peroxidase-expressing infiltrating eosinophils. Eosinophil peroxidase catalyzes the H2O2 oxidation of Br- to HOBr, which N-brominates taurine to N-bromotaurine at its concentration of 15 mM in eosinophils. In microvascularized tumors, the (.)NO concentration is further depleted; (.)NO is rapidly consumed by red blood cells (RBCs) through S-nitrosation of RBC glutathione and hemoglobin, and by oxidation to nitrate by RBC oxyhemoglobin. Angiogenesis-inhibiting antibodies are currently used to treat cancers; their mode of action is not, as previously thought, reduction of the tumor O2 or nutrient supply. They actually decrease the loss of (.)NO to RBCs.
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PMID:Apoptosis-inducing high (.)NO concentrations are not sustained either in nascent or in developed cancers. 1875 45