Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:1.11.1.7 (peroxidase)
65,474 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Macromolecular permeability of the small intestine was tested in seven three-week-old piglets infected with porcine transmissible gastroenteritis virus (TGE-strain Miller). Fourteen hours after the infection, the piglets showed loss of appetite and a profuse diarrhoea. In some animals vomiting occurred somewhat earlier. Macromolecular permeability was tested morphologically by injecting horseradish peroxidase (MW = 40,000 Da) into the jejunal lumen just distally to the Treitz' ligament in two piglets at 12 hours and in five piglets at 48 hours after the inoculation in comparison with two control piglets. After a period of 20 minutes, small segments of jejunum were taken for stereomicro-scopical, histological and ultrastructural investigations. An increased permeability for HRP together with a severe, hyper-regenerative villous atrophy was observed in the TGE-infected piglets at 48 hours after the inoculation.
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PMID:Intestinal permeability in piglets during transmissible gastroenteritis. 183 Apr 39

A 73-year-old male was admitted to our hospital in October 1987 because of severe anemia, anorexia, and loss of weight. The hemoglobin level was 5.7 g/dl, the white blood cell count 2,500/microliters with 5% myeloblasts positive for peroxidase, and the platelet count 8.6 x 10(4)/microliters. The LDH was 656 mU/ml, the total protein in the serum 7.4 g/dl, IgG 419 mg/dl, IgA 104 mg/dl, IgM 10 mg/dl, and urine Bence Jones (BJ) protein 8.8 g/day. The X-ray survey of the bones showed multiple osteolytic lesions. A bone marrow aspirate was hypercellular with 91.4% plasma cells, and was cultured a whole day for chromosome study. It revealed an abnormal karyotype of 46, XY, -15, t(6; 14) (p21.1; q32.3), +der(15)t(1; 15) (q23; q24). Immunoelectrophoresis demonstrated lambda type BJ protein. He was treated with melphalan and prednisolone. Proteinuria and marrow plasma cells decreased in amount. In December a white cell count was 6,030/microliters with 80% myeloblasts. A bone marrow aspirate revealed an increase of 82.6% myeloblasts or promyelocytes. The patient was refractory to chemotherapy and died of sepsis in April 1988. An unrelated abnormal karyotype; 48, XY, +8, +13 appeared concomitant with an increase of the leukemic cells, but no cells showed the t(6; 14). We cytogenetically discussed the simultaneous presence of multiple myeloma with acute myelogenous leukemia.
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PMID:[Acute myelogenous leukemia (M2) simultaneously associated with multiple myeloma with special reference to chromosome abnormality of t(6; 14) (p21.1; q32.3)]. 236 41

Hepatozoonosis is a very important disease in dogs in Nigeria. Hepatozoonosis was reported in Nigeria in 18 dogs. The clinical signs included fever, anorexia, loss of weight, lameness, oculonasal discharge and conjunctivitis. Hematologic findings included leukocytosis due to neutrophilia and eosinophilia. Parasitemia varied from 1 to 9% of the circulating neutrophils in the peripheral blood smears of the dogs examined. Hepatozoon canis gametocytes were identified in circulating neutrophils of dogs. Peripheral blood smears from dogs confirmed to have natural H. canis infection were cytochemically stained for myeloperoxidase. Parasitized neutrophils were myeloperoxidase deficient while non-parasitized neutrophils were myeloperoxidase positive. This is considered important, because deficiency of the enzyme may be responsible for poor response of H. canis to chemotherapeutic agents.
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PMID:Neutrophil myeloperoxidase deficiency associated with canine hepatozoonosis. 256 99

A 21-year-old man was admitted to our hospital because of anorexia and general malaise in July, 1988. On admission, the white blood cell count of 18,600/microliters with 72% leukemic cells. The bone marrow aspirate showed 76.8% immature monocytes, 10% mature and immature eosinophils. Leukemic cells were 66.6% myeloperoxidase positive cells, and 20.6% naphthylbutyrate esterase positive cells. The lysozyme activity in urine was high. Cytogenetic analysis revealed the presence of 46 XY inv (16) (p13 q22). Under the diagnosis of acute myelomonocytic leukemia with eosinophilia (M4Eo) associated with inv (16) (p13 q22), one course of DCMP induction therapy was performed. After complete remission, the bone marrow aspirate showed disappearance of inv (16) (p13 q22), and associated with decreased residual leukemic cells.
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PMID:[Acute myelomonocytic leukemia with inv (16) (p13 q22) disappeared abnormal karyotype during complete remission]. 262

We investigated the involvement of nitric oxide in trinitrobenzene-sulfonic acid (TNB) colitis. Every 24 h after TNB, rats were orally dosed with NG-nitro-L-arginine methyl ester (L-NAME; 30 mg/kg), NG-nitro-D-arginine methyl ester (D-NAME), or water, and food intake, body weight, and plasma nitrite levels were measured. On day 6, colonic nitric oxide synthase and myeloperoxidase (MPO) activity, histology, intestinal muscle growth, NADPH-diaphorase, and myenteric nerve function were assessed. Food intake and body weight were reduced during the first 72 h of colitis. On day 6 post-TNB, a fourfold increase in mucosal nitric oxide synthase, a 30-fold increase in MPO, and a fivefold elevation in plasma nitrite were measured. Smooth muscle hyperplasia and hypertrophy in both colonic muscle layers, numerous diaphorase-positive macrophages in the myenteric plexus, and a suppression of myenteric nerve function were also observed. Unlike D-NAME, oral L-NAME reduced MPO and intestinal muscle hyperplasia by > 90%. Likewise, plasma nitrite and colonic nitric oxide synthase were reduced by > 70%. L-NAME completely prevented macrophage infiltration into the muscle. Conversely, it had no effect on anorexia or intestinal smooth muscle hypertrophy, nor did it affect suppressed myenteric nerve neurotransmitter release. These results demonstrate the selective transmural protective effects of L-NAME in the inflamed colon, implicating nitric oxide as a mediator.
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PMID:The selective beneficial effects of nitric oxide inhibition in experimental colitis. 753 57

A 55-year-old female presented with sore throat and slight fever. The patient was admitted to our hospital on December 13, 1993. Full blood count showed hemoglobin 10.7 g/dl, white cell count 960/microliters (neutrophils 14%, lymphocytes 82%, blasts 2%) and platelets 13,000/microliters. Bone marrow examination showed hypocellularity with 4.5% of myeloblast positive for peroxidase. The bone marrow specimens on Dec. 20 showed 15.5% of myeloblasts, some of which had Auer rods. These findings led to the diagnosis of refractory anemia with excess myeloblast in transformation (RAEB-T) of French-American-British Cooperative Group. The patient was transfused and treated with cytarabine ocfosfate (SP-AC) (100 mg tid) and 6-mercaptopurine (50 mg tid) for 14 days. During chemotherapy she complained of nausea and anorexia, but they were managed easily with medication. On Feb. 7, 1994, forty-two days after the start of administration, peripheral blood and bone marrow aspirate were compatible with a complete remission. Although complete remission was sustained with courses of chemotherapy for 4 months, relapse occurred and the patient died of septicemia on August 29, 1994 after induction failure. Observation suggested that oral SPAC in combination with 6-mercaptopurine had a good antileukemic effect on the myelodysplastic syndrome. However, the duration response was short, and further improvement of the therapy is needed.
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PMID:[Refractory anemia with excess myeloblast in transformation induced remission by combined oral administration of cytarabine ocfosfate and 6-mercaptopurine]. 779 1

From August 1990 to June 1991, a moderate die-off of 4- to 5-year-old green sea turtles (Chelonia mydas) occurred at Cayman Turtle Farm, Grand Cayman, British West Indies. Clinical signs included lethargy, anorexia, and inability to dive. Many of the ill turtles floated on the surface of their tanks. There was no apparent sex predilection. Complete necropsies, including histopathologic examination of tissues, were performed on eight turtles. Necropsies revealed multiple irregular discrete to patchy 1-10 mm pale gray foci throughout the hearts of four turtles. By light microscopic examination, the most severe and consistent lesions were necrotizing myocarditis, histiocytic to fibrinous splenitis, and hepatic lipidosis and necrosis. A mixed leukocytic infiltrate of acidophils, macrophages, and lymphocytes was present in affected areas of the heart. Other lesions included lymphocytic/plasmacytic interstitial nephritis, subacute interstitial pneumonia, subacute mesenteric vasculitis, chronic/active enteritis of the small intestine, and occasional granulomas associated with spirorchid trematode ova. Chlamydiae could be demonstrated in macrophages in sections of paraffin-embedded heart, liver, and spleen and in myocardial fibers and hepatocytes using a modified Macchiavello's stain. Chlamydial antigen was detected by light microscopic examination in the cytoplasm of myocardial fibers and in occasional hepatocytes using a commercially available genus-specific antichlamydial monoclonal antibody and the avidin biotin peroxidase complex staining method. Electron microscopic examination of the heart of the most severely affected turtle revealed developmental stages of chlamydial organisms. A suspension of heart from this turtle was inoculated into the yolk sacs of chicken embryos.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Chlamydiosis in mariculture-reared green sea turtles (Chelonia mydas). 814 Jul 12

We measured daily food intake and body weight in rats before and after the induction of colitis by intrarectal administration of either 2,4,6-trinitrobenzenesulfonic acid in ethyl alcohol (TNBE) or 4% acetic acid (AA). Administration of TNBE or AA induced inflammation in the distal colon, which was reflected by a significant increase in myeloperoxidase (MPO) activity in the colon. On days 1, 2, and 3 after induction of colitis by TNBE, food intake fell by 80, 70, and 50%, respectively, compared with pretreatment values; food intake returned to normal by day 4. Body weight fell within 24 h after induction of colitis and remained 10% less than control for at least 5 days. Colitis induced by AA produced a similar pattern and degree of decreased food intake and weight loss. Treatment with the 5'-lipoxygenase inhibitor MK-886 significantly reduced concentrations of leukotriene B4 in the colon of TNBE-treated rats but did not affect food intake. In contrast, the cyclooxygenase inhibitor indomethacin decreased prostaglandin E2 concentrations in the colon but also attenuated the suppression of feeding by 52 and 64% on the first 2 days after induction of colitis by TNBE. These results identify a specific prostaglandin-mediated suppression of feeding in the rat with acute colitis induced by TNBE and illustrate the utility of this model for studying mechanisms underlying anorexia associated with inflammation of the gastrointestinal tract.
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PMID:On the suppression of food intake in experimental models of colitis in the rat. 849 96

1. Glutathione concentrations in liver and lung fall when food intake or sulphur amino acid intake is inadequate. However, concentrations may be restored during inflammation, despite anorexia, provided that prior sulphur amino acid intake is adequate. 2. We studied the mechanisms of these changes by measuring the effect of sulphur amino acid and protein intake on hepatic glutathione synthesis and gamma-glutamylcysteine synthetase activity, hepatic and lung glutathione concentrations, glutathione reductase and glutathione peroxidase activities in young rats given an inflammatory challenge by intraperitoneal injection of tumour necrosis factor-alpha or endotoxin (lipopolysaccharide). 3. Diets containing 200 g of casein and 8 g of L-cysteine/kg (normal-protein diet), or 80 g of casein and 8 g of L-cysteine, or isonitrogenous amounts of L-methionine or L-alanine (low-protein diets) were fed ad libitum to young Wistar rats for 8 days. Dietary groups were subdivided into three: one subgroup continued feeding ad libitum, a second was given tumour necrosis factor or lipopolysaccharide and killed 24 h thereafter, while the third was pair-fed to the intakes of the second subgroup for 24 h before being killed. 4. Glutathione concentrations in liver and lung were reduced in rats fed the low-protein diet containing alanine, and in all dietary groups when food intake was restricted. The inflammatory challenges restored hepatic glutathione concentrations in all groups but the diet supplemented with alanine, which had an inadequate sulphur amino acid content. In lung, restoration occurred only in animals fed the normal-protein diet. 5. The activity of gamma-glutamylcysteine synthetase, which is rate limiting for glutathione synthesis, was unaffected by dietary or sulphur amino acid intake or by the inflammatory response. Substrate supply may therefore be a major determinant in glutathione synthesis in vivo. 6. Total hepatic glutathione synthesis was affected by food intake, the type and amount of sulphur amino acids in the diet and by inflammation. Total synthesis was 207, 137, 421 and 90 mumol/day for animals fed ad libitum the normal-protein diet, or low-protein diets supplemented with cysteine, methionine or alanine respectively, ad libitum. Pair-feeding resulted in values of 76, 31, 71, and 0 mumol/day respectively. After lipopolysaccharide injection, rates increased to 200, 117, 151 and 56 mumol/day respectively. 8. Reductase and peroxidase activities increased in liver and lung, when low-protein diets which contained supplemental methionine or alanine were consumed ad libitum. A reduction in food intake resulted in enzyme activity changes, which suggested that recycling of glutathione increased in lung and decreased in liver. Injection of tumour necrosis factor reversed this effect. 9. The restoration of glutathione concentrations in liver after an inflammatory challenge is closely associated with an enhanced rate of synthesis and increased recycling. The former is impaired when inadequate sulphur amino acid is consumed before the challenge. In lung, increased recycling of glutathione may help maintain concentrations when food intake is restricted, but not during inflammation.
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PMID:Dietary sulphur amino acid adequacy influences glutathione synthesis and glutathione-dependent enzymes during the inflammatory response to endotoxin and tumour necrosis factor-alpha in rats. 909 11

Whether the decrease in food intake that occurs at the onset of anorexia in tumor bearing (TB) rats is related to a change in the hypothalamic neuropeptide Y (NPY) system was tested by comparing NPY expression in sham operated Fischer Control and anorectic TB rats. Coronal cryocut sections of their fixed brain were processed by the peroxidase-antiperoxidase method with NPY polyclonal antibodies. NPY-immunoreactive fibers were widely distributed throughout the forebrain, but were most prominent in the hypothalamic paraventricular, suprachiasmatic, arcuate and periventricular nuclei. NPY-immunoreactive neurons were visualized in Control and anorectic TB rats in the preoptic region, the arcuate nucleus, and occasionally in the lateral hypothalamus. Semiquantitative image analysis showed a significant decrease in the NPY immunostaining in some hypothalamic nuclei of the anorectic TB rats, most prominently in the supraoptic nucleus, the parvocellular portion of the paraventricular nucleus, and, to a lesser extent, the suprachiasmatic and arcuate nuclei. No changes in NPY innervation were seen in the ventromedial nucleus and the lateral hypothalamus. The data support the hypothesis of an altered hypothalamic NPY system at the onset of anorexia in TB rats and also reveal the hypothalamic nuclei through which NPY influences food intake.
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PMID:Decreased NPY innervation of the hypothalamic nuclei in rats with cancer anorexia. 1253 82


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