Gotowe bibliografie tematyczne / Bile Acids

Gotowa bibliografia na temat „Bile Acids”

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Data publikacji: 4 czerwca 2021
Data aktualizacji: 29 lipca 2024

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Artykuły w czasopismach na temat "Bile Acids"

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Kritchevsky, D. "Bile acids". European Journal of Cancer Prevention 1 (październik 1991): 23–28. http://dx.doi.org/10.1097/00008469-199110002-00005.

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Patrick, Ping H., i William H. Elliott. "Bile acids". Journal of Chromatography A 347 (styczeń 1985): 155–62. http://dx.doi.org/10.1016/s0021-9673(01)95479-2.

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Abbott, David A., David E. Schlarman, Ping H. Patrick, Daniel M. Tal i William H. Elliott. "Bile acids". Analytical Biochemistry 146, nr 2 (maj 1985): 437–41. http://dx.doi.org/10.1016/0003-2697(85)90566-4.

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Mikov, Momir, i J. Paul Fawcett. "Bile acids". European Journal of Drug Metabolism and Pharmacokinetics 31, nr 3 (wrzesień 2006): 133–34. http://dx.doi.org/10.1007/bf03190709.

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KURAMOTO, Taiju, Junko MIYAMOTO, Masaki KONISHI, Takahiko HOSHITA, Takako MASUI i Mizuho UNE. "Bile Acids in Porcine Fetal Bile." Biological & Pharmaceutical Bulletin 23, nr 10 (2000): 1143–46. http://dx.doi.org/10.1248/bpb.23.1143.

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Paumgartner, Gustav. "Serum bile acids". Journal of Hepatology 2, nr 2 (styczeń 1986): 291–98. http://dx.doi.org/10.1016/s0168-8278(86)80088-5.

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Phillipson, Maggie. "Bile acids revisited". Food and Chemical Toxicology 25, nr 11 (listopad 1987): 881–82. http://dx.doi.org/10.1016/0278-6915(87)90274-2.

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Hamilton, James P., Guofeng Xie, Jean-Pierre Raufman, Susan Hogan, Terrance L. Griffin, Christine A. Packard, Dale A. Chatfield, Lee R. Hagey, Joseph H. Steinbach i Alan F. Hofmann. "Human cecal bile acids: concentration and spectrum". American Journal of Physiology-Gastrointestinal and Liver Physiology 293, nr 1 (lipiec 2007): G256—G263. http://dx.doi.org/10.1152/ajpgi.00027.2007.

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To obtain information on the concentration and spectrum of bile acids in human cecal content, samples were obtained from 19 persons who had died an unnatural death from causes such as trauma, homicide, suicide, or drug overdose. Bile acid concentration was measured via an enzymatic assay for 3α-hydroxy bile acids; bile acid classes were determined by electrospray ionization mass spectrometry and individual bile acids by gas chromatography mass spectrometry and liquid chromatography mass spectrometry. The 3α-hydroxy bile acid concentration (μmol bile acid/ml cecal content) was 0.4 ± 0.2 mM (mean ± SD); the total 3-hydroxy bile acid concentration was 0.6 ± 0.3 mM. The aqueous concentration of bile acids (supernatant after centrifugation) was identical, indicating that most bile acids were in solution. By liquid chromatography mass spectrometry, bile acids were mostly in unconjugated form (90 ± 9%, mean ± SD); sulfated, nonamidated bile acids were 7 ± 5%, and nonsulfated amidated bile acids (glycine or taurine conjugates) were 3 ± 7%. By gas chromatography mass spectrometry, 10 bile acids were identified: deoxycholic (34 ± 16%), lithocholic (26 ± 10%), and ursodeoxycholic (6 ± 9), as well as their primary bile acid precursors cholic (6 ± 9%) and chenodeoxycholic acid (7 ± 8%). In addition, 3β-hydroxy derivatives of some or all of these bile acids were present and averaged 27 ± 18% of total bile acids, indicating that 3β-hydroxy bile acids are normal constituents of cecal content. In the human cecum, deconjugation and dehydroxylation of bile acids are nearly complete, resulting in most bile acids being in unconjugated form at submicellar and subsecretory concentrations.
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Das, John B., Nicholas D. Poulos i G. Ghaus Ansari. "Biliary Lipid Composition and Bile Acid Profiles During and After Enteral Fast of Total Parenteral Nutrition in the Rabbit". Journal of Pediatric Gastroenterology and Nutrition 22, nr 1 (styczeń 1996): 85–91. http://dx.doi.org/10.1002/j.1536-4801.1996.tb01508.x.

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SummaryFeeding and fasting influence biliary lipid composition. With total parenteral nutrition (TPN), it is possible to study the effects of a long‐term “enteral fast” on biliary lipid composition without the metabolic illeffects on nutrient deprivation. We compared the lipid and bile acid (BA) contents of hepatic and gallbladder biles in rabbits on completion of a 14‐day regimen of TPN with those in rabbits returned to oral feeds for 6 weeks after a similar spell of TPN. Chow‐fed rabbits served as controls. With TPN, plasma phospholipid and cholesterol levels were elevated. Basal bile flow and the secretion of bile acids and phospholipids were decreased in the TPN and post‐TPN groups, while the cholesterol secretion rate was essentially unchanged. During TPN, the molar percent of cholesterol (relative to bile acids and phospholipid) in hepatic bile was increased. Biliary glycolithocholic acid (GLCA; as a percent of total conjugated BA) in hepatic bile increased from 1.7% (0.9% SEM) in the chow‐fed to 8.5% (1.5% SEM) during TPN. In TPN and post‐TPN groups, the gallbladder was enlarged to more than twice normal (chow‐fed) size, and contained a dark, mucoid bile (biliary sludge). In this bile, (a) there was a 2.5‐fold increase in bile acid concentration; and (b) the molar percent of cholesterol decreased while that of bile acids increased. TPN produced a state of functional cholestasis, which extended into the post‐TPN period. Gallbladder distension was the common denominator of the hepatobiliary dysfunction in the TPN and post‐TPN rabbits. With sequestration of bile acids in the gallbladder during and after TPN, the circulating bile acid pool was constricted, and the enterohepatic circulation impaired. As cholesterol secretion was low at all times, cholesterol supersaturation did not occur. The molar percent of cholesterol in gallbladder bile decreased, while that of bile acids increased; this suggests absorption of cholesterol by gallbladder mucosa. The increase in biliary GLCA probably resulted from bacterial biotransformation of glycochenodeoxycholic acid to lithocholic acid and its increased absorption from the cecum during TPN.
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Camilleri, Michael. "Bile acid detergency: permeability, inflammation, and effects of sulfation". American Journal of Physiology-Gastrointestinal and Liver Physiology 322, nr 5 (1.05.2022): G480—G488. http://dx.doi.org/10.1152/ajpgi.00011.2022.

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Bile acids are amphipathic, detergent molecules. The detergent effects of di-α-hydroxy-bile acids are relevant to several colonic diseases. The aims were to review the concentrations of bile acids reaching the human colon in health and disease, the molecular structure of bile acids that determine detergent functions and the relationship to human diseases (neuroendocrine tumors, microscopic colitis, active celiac disease, and ulcerative colitis, Crohn’s disease and ileal resection), the relationship to bacterial uptake into the mucosa, mucin depletion, and epithelial damage, the role of bile acids in mucosal inflammation and microscopic colitis, and the role of sulfation of bile salts in detoxification or prevention of the detergent effects of bile acids. The concentrations of bile acids reaching the human colon range from 2 to 10 mM; di-α-hydroxy bile acids are the only bile acids with detergent effects that include mucin depletion, mucosal damage, bacterial uptake, and microscopic inflammation that may be manifest in diseases associated with no overt inflammation of the mucosa, such as bile acid diarrhea, ileal diseases such as neuroendocrine tumors, ileal resection, and nonalcoholic steatohepatitis. Sulfation inactivates colonic secretion due to primary bile acids, but it may render secondary bile acids proinflammatory in the colon. Other evidence in preclinical models of inflammatory bowel disease (IBD) suggests reduced sulfation causes barrier dysfunction, inflammation, or carcinogenesis. These advances emphasize relevance and opportunities afforded by greater understanding of the chemistry and metabolism of bile acids, which stands to be further enhanced by research into the metabolic interactions of microbiota with bile acids.
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Rozprawy doktorskie na temat "Bile Acids"

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Li, Hai. "Bile acids enterohepatic circulation". [S.l. : Amsterdam : s.n.] ; Universiteit van Amsterdam [Host], 2005. http://dare.uva.nl/document/77982.

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Zhu, Xiao Xia. "Binding interactions of bile acids and bile pigments with amines". Thesis, McGill University, 1988. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=75846.

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The binding of selected bile acids and bile pigments by peptides and quaternary amines has been studied by adsorption and NMR experiments. Novel adsorbents with quaternized peptide-containing functional groups for bile acids have been prepared by solid phase peptide synthesis techniques. The adsorption studies, conducted in aqueous buffer solutions, show that these resins have an enhanced capacity, on a per active site basis, and improved specificity over cholestyramine and colestipol. The interaction between bile acid anions and the pendants is predominantly ionic linkage, although hydrophobic and other interactions are also important. An NMR study of the binding between bile acids and various ligands, including peptides, by the determination of carbon-13 spin-lattice relaxation times, confirms the ionic and hydrophobic interactions which occur cooperatively and simultaneously.
New adsorbents for bilirubin have been prepared by covalently coating a water-swellable polyamide resin with polypeptides. These resins have much higher capacities for bilirubin in aqueous buffer solution than cholestyramine and improved capacities over the resins with attached oligopeptide pendants. The binding behavior of the resin coated with poly- sc D-lysine is the same as that of poly- sc L-lysine. The amount of bilirubin adsorbed by these resins is directly proportional to the number of lysine residues on the resin, which is consistent with the formation of an ionic linkage. This is confirmed by a study of the interaction of bilirubin with an oligopeptide, sc L-lysyl- sc L-lysine, by measurements of proton and carbon-13 NMR spin-lattice relaxation times combined with nitrogen-15 NMR experiments. The $ sp{15}$N NMR spectra of bilirubin and some related bile pigments have also been assigned by two-dimensional $ sp{15}$N-$ sp1$H heteronuclear correlation experiments.
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Rao, Girish. "Enzyme electrode studies of bile acids". Thesis, Imperial College London, 1990. http://hdl.handle.net/10044/1/11881.

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Bradburn, David Michael. "Bile acids and short fatty acids in familial adenomatous polyposis". Thesis, University of Newcastle Upon Tyne, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.308760.

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Trusova, Tatyana. "Quantitative estimation of bile acid conjugates in human bile using HPLC /". Connect to online version, 1995. http://hdl.handle.net/1989/3555.

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Qian, Jiang. "Studies of Sulfur Reduction of Taurine and Taurine-Conjugated Bile Acids by Bile acid 7α-Dehydroxylating Bacteria". TopSCHOLAR®, 2000. http://digitalcommons.wku.edu/theses/694.

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Bile acids are C24 steroids that are derived in the liver from cholesterol and secreted into the intestinal lumen to aid in emulsification of dietary lipids and lipid-soluble vitamins. The indigenous intestinal microflora modify bile acids, producing up to 20 unique bile acid metabolites. The 7α-dehydroxylation of the bile acids is the most physiologically important bile acid biotransformation. All known intestinal bacteria capable of bile acid 7α-dehydroxylation are anaerobic, gram-positive rods of the genera Clostridium and Eubcicterium. Bile acid 7α-dehydroxylating bacteria often contain bile salt hydrolase, which hydrolyzes the peptide bond in taurine-conjugated bile acids to yield a free bile acid and taurine. Taurine is an organosulfonate containing a sulfite moiety. There have been no published reports indicating whether 7α-dehydroxylating bacteria can utilize taurine. Given that taurine and taurine-conjugated bile acids are found at great concentrations in the intestine, the ability to utilize the compound would confer a competitive advantage to these bacteria. In this study, the ability of 7α-dehydroxylating bacteria to dissimilate taurine and taurine-conjugated bile acids produce hydrogen sulfide was investigated. First, hydrogen sulfide produced by bile acid 7α-dehydroxylating bacteria cultured in tryptic soy broth and semi-defined media from taurine and taurine-conjugated bile acids was qualitatively detected by inclusion of ferric ammonium citrate in the media. The results obtained from trials utilizing anaerobic tryptic soy broth and from semi-defined medium were not consistent, suggesting that qualitative determination of sulfide by inclusion of ferric ammonium citrate is inconclusive. Then hydrogen sulfide produced by bile acid 7α-dehydroxylating bacteria cultured in modified semi-defined medium (not containing a reducing agent) over time in the presence or absence of taurine-conjugated bile acids was quantified using the methylene blue method. Sulfide concentrations in medium cultured with two different strains of bile acid 7α-dehydroxylating bacteria, Eubcicterium sp. 12708 and Clostridium sp. HD-17, in presence of 100 |j.M or 5 mM sulfonates were not significantly higher than those in the absence of sulfonate. In addition, the highest sulfide concentration determined from medium cultured with two different strains of bile acid 7α-dehydroxylating bacteria for a period of five days was not above backgroud level. These data demonstrated that these two bile acid 7α-dehydroxylating bacteria, Eubcicterium sp. 12708 and Clostridium sp. HD-17, are not capable of desulfonating taurine and taurineconjugated bile acids to produce hydrogen sulfide under the conditions tested.
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McNeilly, Alison Delamere. "The impact of bile acids on glucocorticoid metabolism". Thesis, University of Edinburgh, 2006. http://hdl.handle.net/1842/24968.

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The work in this thesis demonstrates that bile acids and their conjugates are competitive inhibitors of glucocorticoid metabolism by both 11β-HSD1 and 5β-reductase in liver. In vivo, in male Wistar rats, manipulation of hepatic bile acid concentrations by dietary supplementation with chenodeoxycholic acid (CDCA; 1% w/w) suppressed activities of hepatic 5β-reductase and 11βHSD1 activity and caused a reduction in total urinary (mainly 5β-reduced) glucocorticoid metabolites. In response to acute restraint stress bile acid treated animals showed a delay in return to basal corticosterone levels indicative of altered clearance. In addition, adrenal weight and lipid accumulation within the adrenal gland was reduced in bile acid treated animals. Stimulation of bile acid synthesis by cholestyramine (5% w/w) reduced hepatic 5β-reductase activity with animals excreting fewer urinary total (mainly 5β-reduced) glucocorticoid metabolites. Conversely, a reduction in hepatic bile acid content via administration of a fat-free diet, induced hepatic 5β-reductase activity accompanied by an increase in total, principally 5β-reduced, urinary metabolites. Animals fed the fat-free diet had larger adrenal glands, and suppressed circulating corticosterone, again suggesting altered HPA axis regulation. These findings were pursued in rats with bile duct ligation, a pathological model of elevated bile acids. In these animals, reduced activities of 5β-reductase and 11β-HSD1 were also identified. Lastly investigations were made of the impact of bile acids on the renin-angiotensin-aldosterone system (RAAS). Manipulations which increased bile acids concentrations were predicted to reduce the rate of aldosterone inactivation, since it too is a substrate for 5β-reductase. Treatments increasing bile acids were accompanied by a renin-independent increase in aldosterone and associated sodium retention.
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Leonard, Danièle. "Adsorption of bile acids by ion-exchange resins". Thesis, McGill University, 1989. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=74309.

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The interactions of cholestyramine with bile acids in aqueous buffer solutions were studied by in vitro adsorption experiments. Application of the Donnan theory, which is based on ion partitioning between two phases, indicates that the adsorption is an ion-exchange process--the bile acid anion displaces the chloride counter-ion of cholestyramine. Donnan considerations indicate that the bile acid in the resin phase exists in two forms, bound and unbound, but at higher Ceq the bound form is increasingly favoured. Since the concentrations of bound bile acid in the resin phase are above the critical micellar concentration, micelle-type ordering is occurring. It is also possible that the unbound bile acid in the resin phase aggregates to form "regular" micelles. The micellization promotes the partitioning of glycocholic acid into the resin phase, explaining the ability of cholestyramine to adsorb glycocholic acid significantly, in vitro.
Ion-exchange resins were prepared by solid phase peptide synthesis with active sites chosen to resemble those of cholestyramine. They were produced by coupling 4-(aminomethyl)benzoic acid, 4-aminophenylacetic acid or 4-(aminomethyl)phenylacetic acid to the backbone. The ion-exchange resins were prepared both as primary amines and in the quaternized form. The cholestyramine-like sorbents were synthesized with systematic changes in the structure, to determine which structural parts of cholestyramine are involved in the adsorption process. As compared to cholestyramine, both sets of resins were remarkably ineffective in adsorbing bile acids in vitro. It was found that the nature of the backbone determines the accessibility to the active site; that the resins with the methylene group positioned between the phenyl group and the amino group have higher adsorption capacity for glycocholic acid; and that quaternization increases the adsorption capacity. The two latter observations indicate the importance of the basicity of the active site. Therefore, in cholestyramine, the backbone is such that it permits the transfer of ionic species and the quaternary ammonium group is involved in the interaction with bile acids.
Computer modelling showed that the cholestyramine pendants are close to one another and are separated by benzene rings, thus leaving too little space between them to allow a bile acid molecule to interact with the benzene rings. Therefore, the bile acids must interact with the quaternary ammonium group, leaving the bile acid molecule inside the cavity where they interact with one another to form micelles. The possible modes of interactions of bile acids with the synthesized resins are more numerous since the pendants are not as close together. (Abstract shortened by UMI.)
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Zeck, Lisa. "Optimization of an immobilized enzyme system for conjugated bile acids /". Connect to online version, 1995. http://hdl.handle.net/1989/3548.

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Barker, Gillian M. "Bile acids and neutral sterols in familial adenomatous polyposis". Thesis, University of Aberdeen, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.308002.

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In familial adenomatous polyposis (FAP), inactivation of the APC gene is directly linked to the development of gastrointestinal polyps and cancer. It is likely that other epigenetic factors are involved in the malignant change of polyp to carcinoma. Previous studies have implied an abnormal bile acid profile, both in faeces and bile. In this study, using carefully matched control groups, extraction of bile acids from faeces and bile was performed and analysis was rigorously performed using Gas-liquid chromatography-Mass Spectrometry. No significant differences were found between the two groups in the profile of major bile acids. An increased faecal excretion of two minor bile acids, 5β-cholanoic acid-3α-ol-12-one and 5α-cholanoic acid-3α-ol-12-one and an increased level of 5β-cholanoic acid-3α-01-12-one in bile was found in patients with FAP. A difference in the faecal neutral sterol profile had also been suggested, but this study showed no significant difference between the two groups when matching controls are used. This study does not support the idea that there are significant differences in faecal bile acid, biliary bile acid or neutral sterol profiles between individuals with familial adenomatous polyposis and controls.
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Książki na temat "Bile Acids"

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Jenkins, Gareth J., i Laura Hardie, red. Bile Acids. Cambridge: Royal Society of Chemistry, 2008. http://dx.doi.org/10.1039/9781847558336.

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Tazuma, Susumu, i Hajime Takikawa, red. Bile Acids in Gastroenterology. Tokyo: Springer Japan, 2017. http://dx.doi.org/10.1007/978-4-431-56062-3.

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Henry, Danielsson, i Sjövall Jan, red. Sterols and bile acids. Amsterdam: Elsevier, 1985.

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M, Grundy Scott, red. Bile acids and atherosclerosis. New York: Raven Press, 1986.

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Galli, G., i E. Bosisio, red. Liver, Nutrition, and Bile Acids. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4615-9427-7.

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Fiorucci, Stefano, i Eleonora Distrutti, red. Bile Acids and Their Receptors. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-22005-1.

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NATO Advanced Study Institute on Liver, Nutrition, and Bile Acids (1983 Maratea, Italy). Liver, nutrition, and bile acids. New York: Plenum Press, 1985.

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Jenkins, Gareth. Bile acids: Toxicology and bioactivity. Cambridge: SC Pub., 2008.

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Riadh, Jazrawi, Northfield Tim i Zentler-Munro Patrick, red. Bile acids in health and disease: Update on cholesterol gallstones and bile acid diarrhoea. Dordrecht: Kluwer Academic, 1988.

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1949-, Hinze Willie L., red. Bile acid/salt surfactant systems. Stamford, Connecticut: JAI Press, 2000.

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Części książek na temat "Bile Acids"

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Soma, Toshiya, i Yutaka Shimada. "Bile Acids". W Encyclopedia of Cancer, 1–3. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27841-9_615-2.

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Soma, Toshiya, i Yutaka Shimada. "Bile Acids". W Encyclopedia of Cancer, 495–97. Berlin, Heidelberg: Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/978-3-662-46875-3_615.

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Gooch, Jan W. "Bile Acids". W Encyclopedic Dictionary of Polymers, 878. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-6247-8_13249.

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Amplatz, Benno, i Günter Fauler. "Bile Acids". W Encyclopedia of Lipidomics, 1–3. Dordrecht: Springer Netherlands, 2021. http://dx.doi.org/10.1007/978-94-007-7864-1_47-2.

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Amplatz, Benno, i Günter Fauler. "Bile Acids". W Encyclopedia of Lipidomics, 1–3. Dordrecht: Springer Netherlands, 2015. http://dx.doi.org/10.1007/978-94-007-7864-1_47-1.

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Soma, Toshiya, i Yutaka Shimada. "Bile Acids". W Encyclopedia of Cancer, 397–99. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_615.

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Murphy, G. M. "Serum Bile Acids". W The Bile Acids: Chemistry, Physiology, and Metabolism, 379–403. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4613-0901-7_10.

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Back, Peter. "Urinary Bile Acids". W The Bile Acids: Chemistry, Physiology, and Metabolism, 405–40. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4613-0901-7_11.

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Setchell, K. D. R., J. M. Street i J. Sjövall. "Fecal Bile Acids". W The Bile Acids: Chemistry, Physiology, and Metabolism, 441–570. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4613-0901-7_12.

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Takikawa, Hajime. "Metabolism of Bile Acids". W Bile Acids in Gastroenterology, 3–8. Tokyo: Springer Japan, 2017. http://dx.doi.org/10.1007/978-4-431-56062-3_1.

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Streszczenia konferencji na temat "Bile Acids"

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Castelli, Michelle, John Reiners, Jr. i David Kessel. "Promotion of PDT efficacy by bile acids". W Biomedical Optics 2003, redaktor David Kessel. SPIE, 2003. http://dx.doi.org/10.1117/12.473615.

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Zhang, Rongwei, Shuting Wei i Boris Mizaikoff. "Selective Recognition of Bile Acids by Molecular Imprints". W 2007 IEEE Sensors. IEEE, 2007. http://dx.doi.org/10.1109/icsens.2007.4388585.

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Urso, Andreacarola, Jose Perez-Zoghbi, Renu Nandakumar, Serge Cremers, Nigel Bunnett, Charles Emala i Frank D’Ovidio. "Aspirated bile acids affect lung immunity and function". W ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.pa3359.

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Joshi, Arnav, i Rajgopal Govindarajan. "Bile acids inhibit equilibrative adenosine transport during cholestasis". W ASPET 2024 Annual Meeting Abstract. American Society for Pharmacology and Experimental Therapeutics, 2024. http://dx.doi.org/10.1124/jpet.044.131351.

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Fangmann, D., C. Knappe, A. Zietzsch, DM Schulte, K. Türk, A. Franke i M. Laudes. "Bile acids as possible mediators of microbiome-host interaction". W Diabetes Kongress 2018 – 53. Jahrestagung der DDG. Georg Thieme Verlag KG, 2018. http://dx.doi.org/10.1055/s-0038-1641766.

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Bikmullina, Zarina, i Masanobu Yamamoto. "Bile acids as a geochemical tool: an analytical procedure". W Goldschmidt2023. France: European Association of Geochemistry, 2023. http://dx.doi.org/10.7185/gold2023.18707.

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Jean-Louis, Samira, i Jesse D. Martinez. "Membrane Perturbation by Bile Acids Causes Signal Transduction Through Caveolae". W Minority Trainee Research Forum, 2004. TheScientificWorld Ltd, 2004. http://dx.doi.org/10.1100/tsw.2004.167.

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Roesly, Heather B., Kimberly A. Hill, HwuDauRw Chen i Katerina Dvorak. "Abstract 3793: Bile acids and autophagy resistance in Barrett's esophagus". W Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-3793.

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Aliwa, BO, A. Horvath, J. Traub, N. Feldbacher i V. Stadlbauer-Köllner. "Gut Microbiome Dysbiosis, Bile acids, and Sarcopenia in Liver Cirrhosis". W 54. Jahrestagung & 31. Fortbildungskurs der Österreichischen Gesellschaft für Gastroenterologie & Hepatologie – ÖGGH (Hybrid Veranstaltung). Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0041-1734302.

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Afolabi, Bene Akromaa, Sandra Appiah, Azra Pachenari i Lucy Ghali. "Abstract B01: Impacts of inulin on bile acids induced colon cancer". W Abstracts: Third AACR International Conference on Frontiers in Basic Cancer Research - September 18-22, 2013; National Harbor, MD. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.fbcr13-b01.

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Raporty organizacyjne na temat "Bile Acids"

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yu, luyou, jinping yang, xi meng i yanhua lin. Effectiveness of the gut microbiota-bile acid pathway (BAS) in the treatment of Type 2 diabetes: A protocol for systematic review and meta analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, lipiec 2022. http://dx.doi.org/10.37766/inplasy2022.7.0117.

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Review question / Objective: To systematically evaluate the efficacy of the intestinal microbiome - bile acid pathway (BAS) in the treatment of T2DM. Condition being studied: Bile acids (BAs), an important component of bile, are also metabolites derived from cholesterol and promote intestinal absorption and transportation of dietary lipids . Studies have shown that bile acid receptor agonists can promote glP-1 secretion and improve glucose metabolism in preclinical mouse models of obesity and insulin resistance , which may become a new therapeutic target for Type 2 diabetes. However, no systematic review and meta-analysis has been found on the treatment of type 2 diabetes by intestinal microbiome - bile acid pathway. Therefore, we conducted a systematic review and meta-analysis to evaluate the safety and effectiveness of intestinal microbiome-bile acid pathway in the treatment of type 2 diabetes.
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Lyutakov, Ivan, Radislav Nakov, Borislav Vladimirov, Ventsislav Nakov, Anastas Dimov, Boyana Asenova, Milena Chetirska i in. Diagnostic Accuracy and Predictive Value of Serum Fibroblast Growth Factor 19 (FGF19) and Total Free Fecal Bile Acids as Biomarkers of Bile Acid Malabsorption in Patients with Chronic Diarrhea: a Pilot Study. "Prof. Marin Drinov" Publishing House of Bulgarian Academy of Sciences, grudzień 2020. http://dx.doi.org/10.7546/crabs.2020.12.16.

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Shapira, Roni, Judith Grizzle, Nachman Paster, Mark Pines i Chamindrani Mendis-Handagama. Novel Approach to Mycotoxin Detoxification in Farm Animals Using Probiotics Added to Feed Stuffs. United States Department of Agriculture, maj 2010. http://dx.doi.org/10.32747/2010.7592115.bard.

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T-2 toxin, a toxic product belongs to the trichothecene mycotoxins, attracts major interest because of its severe detrimental effects on the health of human and farm animals. The occurrence of trichothecenes contamination is global and they are very resistant to physical or chemical detoxification techniques. Trichothecenes are absorbed in the small intestine into the blood stream. The hypothesis of this project was to develop a protecting system using probiotic bacteria that will express trichothecene 3-O-acetyltransferase (Tri101) that convert T-2 to a less toxic intermediate to reduce ingested levels in-situ. The major obstacle that we had faced during the project is the absence of stable and efficient expression vectors in probiotics. Most of the project period was invested to screen and isolate strong promoter to express high amounts of the detoxify enzyme on one hand and to stabilize the expression vector on the other hand. In order to estimate the detoxification capacity of the isolated promoters we had developed two very sensitive bioassays.The first system was based on Saccharomyces cerevisiae cells expressing the green fluorescent protein (GFP). Human liver cells proliferation was used as the second bioassay system.Using both systems we were able to prove actual detoxification on living cells by probiotic bacteria expressing Tri101. The first step was the isolation of already discovered strong promoters from lactic acid bacteria, cloning them downstream the Tri101 gene and transformed vectors to E. coli, a lactic acid bacteria strain Lactococcuslactis MG1363, and a probiotic strain of Lactobacillus casei. All plasmid constructs transformed to L. casei were unstable. The promoter designated lacA found to be the most efficient in reducing T-2 from the growth media of E. coli and L. lactis. A prompter library was generated from L. casei in order to isolate authentic probiotic promoters. Seven promoters were isolated, cloned downstream Tri101, transformed to bacteria and their detoxification capability was compared. One of those prompters, designated P201 showed a relatively high efficiency in detoxification. Sequence analysis of the promoter region of P201 and another promoter, P41, revealed the consensus region recognized by the sigma factor. We further attempted to isolate an inducible, strong promoter by comparing the protein profiles of L. casei grown in the presence of 0.3% bile salt (mimicking intestine conditions). Six spots that were consistently overexpressed in the presence of bile salts were isolated and identified. Their promoter reigns are now under investigation and characterization.
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Zhou, Ting, Roni Shapira, Peter Pauls, Nachman Paster i Mark Pines. Biological Detoxification of the Mycotoxin Deoxynivalenol (DON) to Improve Safety of Animal Feed and Food. United States Department of Agriculture, lipiec 2010. http://dx.doi.org/10.32747/2010.7613885.bard.

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The trichothecene deoxynivalenol (DON, vomitoxin), one of the most common mycotoxin contaminants of grains, is produced by members of the Fusarium genus. DON poses a health risk to consumers and impairs livestock performance because it causes feed refusal, nausea, vomiting, diarrhea, hemolytic effects and cellular injury. The occurrence of trichothecenes contamination is global and they are very resistant to physical or chemical detoxification techniques. Trichothecenes are absorbed in the small intestine into the blood stream. The overall objective of this project was to develop a protecting system using probiotic bacteria that will express trichothecene 3-O-acetyltransferase (Tri101) that convert T-2 to a less toxic intermediate to reduce ingested levels in-situ. The major obstacle that we had faced during the project is the absence of stable and efficient expression vectors in probiotics. Most of the project period was invested to screen and isolate strong promoter to express high amounts of the detoxify enzyme on one hand and to stabilize the expression vector on the other hand. In order to estimate the detoxification capacity of the isolated promoters we had developed two very sensitive bioassays.The first system was based on Saccharomyces cerevisiae cells expressing the green fluorescent protein (GFP). Human liver cells proliferation was used as the second bioassay system.Using both systems we were able to prove actual detoxification on living cells by probiotic bacteria expressing Tri101. The first step was the isolation of already discovered strong promoters from lactic acid bacteria, cloning them downstream the Tri101 gene and transformed vectors to E. coli, a lactic acid bacteria strain Lactococcuslactis MG1363, and a probiotic strain of Lactobacillus casei. All plasmid constructs transformed to L. casei were unstable. The promoter designated lacA found to be the most efficient in reducing T-2 from the growth media of E. coli and L. lactis. A prompter library was generated from L. casei in order to isolate authentic probiotic promoters. Seven promoters were isolated, cloned downstream Tri101, transformed to bacteria and their detoxification capability was compared. One of those prompters, designated P201 showed a relatively high efficiency in detoxification. Sequence analysis of the promoter region of P201 and another promoter, P41, revealed the consensus region recognized by the sigma factor. We further attempted to isolate an inducible, strong promoter by comparing the protein profiles of L. casei grown in the presence of 0.3% bile salt (mimicking intestine conditions). Six spots that were consistently overexpressed in the presence of bile salts were isolated and identified. Their promoter reigns are now under investigation and characterization.
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MALDONADO, KARELYS, JUAN ESPINOZA, DANIELA ASTUDILLO i WILSON BRAVO. Fatigue and fracture resistance and survival of occlusal veneers of composite resin and ceramics blocks in posterior teeth with occlusal wear: A protocol for a systematic review. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, październik 2021. http://dx.doi.org/10.37766/inplasy2021.10.0036.

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Review question / Objective: The aim of this systematic review is to synthesize the scientific evidence that evaluates fatigue and fracture resistance, survival, and stress distribution, of composite resin CAD/CAM and ceramic CAD/CAM occlusal veneers in posterior teeth with severe occlusal wear. Condition being studied: Currently there is an increase in cases of dental wear, due to several factors such as: excessive consumption of carbonated drinks, a diet high in acids, gastric diseases, anorexia, bulimia, dental grinding, use of highly abrasive toothpastes, or a combination of these(9) (10) (11) (12); which affect the patient in several aspects: loss of vertical dimension, sensitivity due to the exposure of dentin, esthetics, affectation of the neuromuscular system(11) (13) (14). With the advent of minimally invasive dentistry, occlusal veneers have been found to be a valid option to rehabilitate this type of cases and thus avoid greater wear of the dental structure with full coverage restorations. Sometimes when performing a tabletop it is not necessary to perform any preparation, thus preserving the maximum amount of dental tissue(3) (6) (15). Due to the masticatory load either in patients without parafunction where the maximum masticatory force is approximately 424 N for women and 630 N for men or in those who present parafunction where the maximum bite force can vary from 780 to 1120N(7), it is necessary that the occlusal veneers support that load which makes indispensable a compilation of studies investigating both fatigue and fracture resistance and the survival rate of occlusal veneers in different materials and thicknesses.
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