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Query: UMLS:C0155339 (Brown)
 12,436 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. The aim of this study was to determine the nitrogen balance and the performance of laying hens fed on diets with a protein content lower than the diets currently used in commercial practice but with adequate concentrations of lysine, sulphur amino acids, tryptophan and threonine. 2. Ninety-six Hy-Line Brown hens, 24 weeks old, were divided into 3 groups of 8 replicates and received, for 16 weeks, diets formulated to have 3 different protein concentrations: 170 (control), 150 and 130 g/kg CP and the same energy content. For each protein concentration, the contents of lysine, methionine, methionine+cystine, tryptophan and threonine were maintained at minimum requirement concentrations by supplying synthetic amino acids. 3. In the first half of the trial, egg production and egg weight were similar in all groups. From the 9th week onwards group 150 CP laid heavier eggs and had a slightly lower egg deposition and total mass. Food conversion ratio was best in the control group. 4. Nitrogen intake was related to the protein concentration of the diet, the food intake being almost the same in the 3 experimental groups. Faecal nitrogen content significantly and linearly decreased with reduction in dietary protein content and was about 50% of the intake. Considering the nitrogen faecal/intake ratio, the 150 CP group showed better nitrogen utilisation at each sampling time.
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PMID:Nitrogen retention and performance of brown laying hens on diets with different protein content and constant concentration of amino acids and energy. 1142 31

Four trypsin inhibitor homologs, the first known from Dendroaspis angusticeps venom, were characterized using a combination of gel filtration, cation exchange, reverse-phase liquid chromatography, Edman degradation and mass spectrometry. The four toxins comprise two 57 residue and two 59 residue isoforms. The long toxins possess a Lys-Gln N-terminal extension lacked by the short toxins. The only other structural difference is an Arg/His replacement at position 55. The long Arg55 variant is identical to trypsin inhibitor E from the venom of Dendroaspis polylepis. The name epsilon-dendrotoxin is suggested so as to follow the nomenclature of Benishin, C.G., Sorensen, R.G., Brown, W.E., Krueger, B.K., Blaustein, M.P., 1988. Four polypeptide components of green mamba venom selectively block certain potassium channels in rat brain synaptosomes. Mol. Pharmacol. 34, 152-159. Among snake venom protease inhibitors, the epsilon-dendrotoxins are structurally most like the delta-dendrotoxins, with which they share only 64% of their residues. In addition, the epsilon-dendrotoxins display hydropathy profiles more like those of the alpha- and delta-dendrotoxins, than those of the trypsin inhibitors from snake venoms. Given the strong protease inhibitory activity of trypsin inhibitor E and the recently demonstrated weak K(+) channel inhibitory activity of two of these variants (Tytgat, J., Vandenberghe, I., Ulens, C., Van Beeumen, J., 2001. New polypeptide components purified from mamba venom. FEBS Lett. 491, 217-221), the epsilon-dendrotoxins represent structural and functional intermediates between the facilitatory toxins and the protease inhibitors.
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PMID:Primary structures of four trypsin inhibitor E homologs from venom of Dendroaspis angusticeps: structure-function comparisons with other dendrotoxin homologs. 1171 Nov 27

In this study, 151 (18.6%) of 814 ceca obtained during in-line processing of 28 broiler (Hybro G, Avian, Arbor acres, and Cobb breeds) and 5 layer (Ross, Tetra SL, Isa Brown, and Brown Nick breeds) flocks in Turkey were found to be contaminated with four different Salmonella serovars. Only Salmonella enterica subsp. enterica Serovar Enteritidis (Salmonella Enteritidis) was recovered from layer birds, whereas Salmonella Enteritidis (81.5%). Salmonella Agona (7.6%), Salmonella Thompson (10.1%), and Salmonella Sarajane (0.8%) were isolated from broiler birds. Isolations of Salmonella Agona and Salmonella Thompson from poultry are reported for the first time in Turkey. The isolation of Salmonella Sarajane from chickens is the first report in the world. The standard method of National Poultry Improvement Plan, U.S. Department of Agriculture, was used to detect Salmonella from chicken cecal samples. Primary and delayed secondary enrichments (PE and DSE) were done in tetrathionate-Hajna broth (TTHB). Two different agar media, xylose lysine tergitol 4 (XLT4) and brilliant green with novobiocin (BGN) were used to observe, and compared for their isolation and selective differentiation of, Salmonella-suspected colonies. Isolated salmonellae were then biotyped and serotyped. Ninety-one and 151 salmonellae were isolated with XLT4 agar after PE and DSE, respectively. From the same samples, BGN agar was able to detect only 50 and 131 Salmonella after PE and DSE, respectively. The isolation rate with XLT4 was 11.2% (P < 0.01) with PE, and this rate increased to 18.6% after DSE. Also, the PE isolation rate (11.2%) with XLT4 agar was significantly higher (P < 0.01) than PE with BGN agar (6.1%). Salmonella was isolated from 39.3% (11 of 28) of the broiler flocks and from 60.0% (3 of 5) of the layers. The detection sensitivity of the isolation method was determined as 1 CFU g(-1) experimentally. These data demonstrate the presence of Salmonella Enteritidis, Salmonella Thompson, Salmonella Agona, and Salmonella Sarajane in chicken flocks in Turkey.
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PMID:Prevalence of Salmonella serovars in chickens in Turkey. 1172 69

The heterodimeric CGRP receptor requires co-expression of calcitonin receptor-like receptor (CRLR) and an accessory protein called receptor activity-modifying protein (RAMP) 1 (McLatchie, L. M., Fraser, N. J., Main, M. J., Wise, A., Brown, J., Thompson, N., Solari, R., Lee, M. G., and Foord, S. M. (1998) Nature 393, 333-339). Several non-peptide CGRP receptor antagonists have been shown to exhibit marked species selectivity, with >100-fold higher affinities for the human CGRP receptor than for receptors from other species (Doods, H., Hallermayer, G., Wu, D., Entzeroth, M., Rudolf, K., Engel, W., and Eberlein, W. (2000) Br. J. Pharmacol. 129, 420-423; Edvinsson, L., Sams, A., Jansen-Olesen, I., Tajti, J., Kane, S. A., Rutledge, R. Z., Koblan, K. S., Hill, R. G., and Longmore, J. (2001) Eur. J. Pharmacol. 415, 39-44). This observation provided an opportunity to map the determinants of receptor affinity exhibited by BIBN4096BS and the truncated analogs, Compounds 1 and 2. All three compounds exhibited higher affinity for the human receptor, human CRLR/human RAMP1, than for the rat receptor, rat CRLR/rat RAMP1. We have now demonstrated that this species selectivity was directed exclusively by RAMP1. By generating recombinant human/rat CRLR/RAMP1 receptors, we demonstrated that co-expression of human CRLR with rat RAMP1 produced rat receptor pharmacology, and vice versa. Moreover, with rat/human RAMP1 chimeras and site-directed mutants, we have identified a single amino acid at position 74 of RAMP1 that modulates the affinity of small molecule antagonists for CRLR/RAMP1. Replacement of lysine 74 in rat RAMP1 with tryptophan (the homologous amino acid in the human receptor) resulted in a > or =100-fold increase in antagonist affinities, similar to the K(i) values for the human receptor. These observations suggest that important determinants of small molecule antagonist affinity for the CGRP receptor reside within the extracellular region of RAMP1 and provide evidence that this receptor accessory protein may participate in antagonist binding.
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PMID:Receptor activity-modifying protein 1 determines the species selectivity of non-peptide CGRP receptor antagonists. 1184 13

1. IL-13 is an important mediator in inflammatory diseases such as asthma. IL-13 is mainly produced by T cells. However, signalling pathways leading to induction of this cytokine are not well-characterized. We analysed the regulation of IL-13 in human peripheral blood mononuclear cells and CD4(+) T cells. 2. Cyclosporine (CsA) and FK-506 inhibited IL-13 synthesis, when cells were stimulated by TPA/ionomycin. However, stimulation by alpha-CD3/alpha-CD28 led to an enhanced IL-13 synthesis. 3. NF-kappa B inhibitor N-tosyl-L-lysine chloromethylketone (TLCK) inhibited IL-13 synthesis more effectively after TPA/ionomycin stimulation. After alpha-CD3/alpha-CD28 stimulation, only 300 microM TLCK inhibited IL-13 synthesis. Dexamethasone inhibited IL-13 equally effective after alpha-CD3/alpha-CD28 and TPA/ionomycin stimulation. 4. p38 MAPK inhibitor SB203580 inhibited IL-13 synthesis only partially. MEK inhibitor U0126 inhibited TPA/ionomycin induced IL-13 synthesis very effectively, whereas alpha-CD3/alpha-CD28 stimulated IL-13 induction was resistant to this drug. 5. These results were confirmed in purified CD4(+) T cells. In difference to PBMCs alpha-CD3/alpha-CD28 stimulated IL-13 synthesis was effectively inhibited by CsA, FK-506 and U0126. 6. Therefore U0126 was tested in an animal model of allergic asthma. We could demonstrate for the first time that inhibition of the MEK - ERK cascade is a therapeutic option for asthma. Intraperitoneal administration of 10 mg kg(-1) U0126 reduced lung eosinophilia in ovalbumin-challenged Brown Norway rats by 44%. 7. These results demonstrate that different signalling pathways are involved in regulating IL-13 synthesis in primary human T cells. Characterizing highly potent inhibitors of IL-13 synthesis can be exploited to identify new drugs to treat immunological diseases such as asthma.
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PMID:Regulation of IL-13 synthesis in human lymphocytes: implications for asthma therapy. 1195 94

Chronic cellular inflammation and airway wall remodeling with subepithelial fibrosis and airway smooth muscle thickening are features of chronic asthma. We determined the role of nitric oxide in the pathogenesis of allergen-induced airway cell proliferation and inflammation by studying the effects of a relatively selective prodrug inhibitor of nitric-oxide synthase type 2 (NOS2), L-N6-(1-iminoethyl)-lysine-5-tetrazole amide (SC-51). Brown-Norway rats were sensitized to ovalbumin and were exposed to ovalbumin aerosol every 3rd day on six occasions and were treated orally with either vehicle or SC-51 (10 mg. kg(-1); 12 doses). We measured inflammatory cell accumulation in the airways and proliferation of cells by incorporation of bromodeoxyuridine. There was an increase in the total number of airway smooth muscle cells expressing bromodeoxyuridine from 1.3% of airway smooth muscle cells in saline exposed to 5.4% after allergen-exposure (P < 0.001) and airway epithelial cells from 3.3 cells/mm basement membrane to 9.6 after allergen-exposure (P < 0.001). SC-51 had no effect on airway smooth muscle or epithelial cell proliferation. SC-51 attenuated the allergen-induced increase in major basic protein (MBP+) eosinophil (P < 0.05) and CD4+ T-cell (P < 0.05) accumulation. We conclude that nitric oxide derived during allergic inflammation is involved in the expression of eosinophilic inflammation and not in epithelial or airway smooth muscle cell DNA synthesis induced by chronic allergen exposure.
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PMID:Role of nitric oxide in chronic allergen-induced airway cell proliferation and inflammation. 1249 May 71

The mechanism(s) of bradykinin-induced bronchoconstriction was investigated in the Brown Norway (BN) rat model of allergic asthma. Bronchoconstrictor responses to i.v. bradykinin in BN rats were maximally augmented 24 h following challenge with allergen and declined at later time points. Histological evaluation of the inflammatory status of the lungs after ovalbumin (OA) challenge showed a marked inflammatory response, which was maximal at 24 h and declined thereafter. However, pretreatment with budesonide did not inhibit the augmented bronchoconstrictor response to bradykinin 24 h after allergen challenge. The selective B1 receptor agonist, Lys-[desArg9]-BK had no bronchoconstrictor effects, whereas the selective B2 receptor antagonist, HOE 140, abolished the response to bradykinin in OA-challenged animals. The augmented response to bradykinin was not affected by methysergide, indomethacin, disodium cromoglycate, iralukast, the 5-lipoxygenase inhibitor, CGS8515, or the NK2 receptor antagonist, SR48968. It was, however, partially inhibited by atropine both in saline- and OA-challenged animals. Pretreatment with captopril and thiorphan markedly potentiated responses to bradykinin both in saline- and OA-challenged animals. Thus, augmentation of the bronchoconstrictor response to bradykinin occurs in actively sensitised BN rats 24 h after challenge with OA and is associated with marked pulmonary inflammation. The response is entirely B2 receptor mediated and approximately 50% of the response is cholinergic. However, mast cell activation, the products of the cyclooxygenase or 5-lipoxygenase pathways and tachykinins are not involved. Peptidase inhibition mimics the effect of allergen challenge on the bronchoconstrictor response to bradykinin and it remains possible that the mechanism of the augmented response to bradykinin following allergen challenge involves downregulation of peptidase activity as a consequence of the inflammatory response.
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PMID:Airway hyperresponsiveness to bradykinin induced by allergen challenge in actively sensitised Brown Norway rats. 1472 5

We report the cloning and initial characterization of the genes encoding DGAT2 (diacylglycerol transferase 2), MOGAT1 and MOGAT2 (monoacylglycerol transferases 1 and 2) in domestic cattle (Bos taurus). The three closely related genes belong to a gene family with at least eight members in mammals and are candidate genes for quantitative traits related to dietary fat uptake, lipid synthesis and storage. MOGAT2 and DGAT2 form a tandem and were mapped to bovine chromosome (BTA) 15q25-->q26 by fluorescence in situ hybridization. MOGAT1 was localized to BTA 2q43-->q44. The three genes were investigated for polymorphisms that might be associated with breeding values for milk fat percentage in the dairy breeds German Holstein, German Simmental and German Brown. All the detected polymorphisms were located outside exons or, with one exception, were silent. In MOGAT1, a missense mutation in exon 4 was found that causes a non-conservative substitution of cysteine170 (uncharged, hydrophobic) by lysine (positively charged, hydrophilic). However, allele frequency estimates from pooled DNA samples revealed no significant association of the observed polymorphisms with breeding values for milk fat percentage. A comparative analysis of chromosomal locations and exon-intron structure of the known members of the DGAT2/MOGAT gene family in humans, rodents and cattle indicates an ancient tandem duplication of the ancestor gene combined with an intron gain (or loss) in one copy. Further members of the family may have arisen by duplications of this gene tandem via two rounds of interchromosomal or genome duplications as well as further local (single) gene duplication and loss events.
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PMID:Genomic organization of the DGAT2/MOGAT gene family in cattle (Bos taurus) and other mammals. 1497 Jun 77

To gain insight into the anti-ageing mechanisms of caloric restriction (CR), liver mitochondria were isolated from male Brown-Norway rats of different ages (fully fed control and CR) and various specific markers of non-enzymatic protein modification (by oxidative, glyco- and lipoxidative-reactions) were measured by GC/MS and Western blotting. A membrane peroxidizability index (PI) was calculated from the fatty acid profiles. Between 6 and 18 months of age, there were significant decreases in the concentration of all markers of damage in mitochondria from both the fully fed and CR groups. In contrast, between the ages of 18 and 28 months, there were significant increases in the concentrations of all markers of damage. In mitochondria from both fully fed and CR groups, there were significant increases in N-epsilon (Nepsilon)-(carboxymethyl)lysine (CML) and N-epsilon-(malondialdehyde)lysine (MDAL) between 6 and 28 months of age. In general, damage tended to be lower in mitochondria from CR animals, but the effects were not significant, except for the concentration of N-epsilon-(carboxymethyl)lysine at 28 months of age. PI increased steadily and significantly with age in fully fed animals, whilst CR induced a significant decrease in this index at 28 months of age. It is concluded that for male rats of the Brown-Norway strain, and mitochondria from liver (i) old (but not mature) age is associated with an increased membrane PI and protein oxidative damage and (ii) CR does not lead to a general reversion in age-related protein damage, but it does prevent the age-induced increase in PI very late in life.
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PMID:Effect of ageing and caloric restriction on specific markers of protein oxidative damage and membrane peroxidizability in rat liver mitochondria. 1533 10

N(alpha)-Palmitoyl-L-lysyl-L-lysine-ethyl ester dihydrochloride (PLL) has antimicrobial properties and may be useful as a food preservative. This study was conducted to see if PLL can inhibit growth and synthesis of aflatoxin by Aspergillus parasiticus. Growth of mold and accumulation of aflatoxins were monitored for up to 15 days. To compare these data with those of a known inhibitor of aflatoxin synthesis, dichlorvos was added to media, and mold growth and aflatoxin accumulation were monitored. The kinetic model of Brown and Vass that correlates growth and formation of secondary metabolites was applied to results of this study, and values for maturation time (t(m)) and aflatoxin accumulation rate constant (alpha) were calculated. Values of t(m) decreased when cultures contained PLL, whereas presence of dichlorvos resulted in a considerable increase. The lag phase of mold growth increased in the presence of PLL. The values of alpha increased with an increasing amount (up to 300 ppm) of PLL in media. Higher concentrations of PLL decreased the value of alpha. All levels of dichlorvos tested decreased the value of alpha. The aflatoxin accumulation rate constant (alpha) as a function of concentration of additive (C) followed the general equation: \documentclass{article}\pagestyle{empty}\begin{document}$$\alpha = \frac{{\alpha _m C\exp (- {C \mathord{\left/ {\vphantom {C {K_i }}} \right. \kern-\nulldelimiterspace} {K_i }})}}{{C + K_a }}$$\end{document} where alpha(m), K(a), and K(i) are constants.
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PMID:Kinetics of aflatoxin biosynthesis by Aspergillus parasiticus in the presence of N(alpha)-palmitoyl-L-lysyl-L-lysine-ethyl ester dihydrochloride or dichlorvos. 1854 85


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