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Journal articles on the topic 'Deoxycholic acid'

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Published: 4 June 2021
Last updated: 1 February 2022

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1

Rose, Paul T. "Deoxycholic Acid." Dermatologic Surgery 43, no. 4 (April 2017): 609–10. http://dx.doi.org/10.1097/dss.0000000000001065.

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2

&NA;. "Deoxycholic acid/phosphatidylcholine." Reactions Weekly &NA;, no. 1331 (December 2010): 15. http://dx.doi.org/10.2165/00128415-201013310-00047.

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3

&NA;. "Deoxycholic acid/phosphatidylcholine." Reactions Weekly &NA;, no. 1426 (November 2012): 20. http://dx.doi.org/10.2165/00128415-201214260-00068.

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4

van Faassen, Arendina, Thomas Ochsenkühn, Saskia Houterman, Elisabeth M. C. van der Ploeg, Bas H. Bueno-de-Mesquita, Marga C. Ocké, Ekkehard Bayerdörffer, and Ruud A. Janknegt. "Plasma deoxycholic acid is related to deoxycholic acid in faecal water." Cancer Letters 114, no. 1-2 (March 1997): 293–94. http://dx.doi.org/10.1016/s0304-3835(97)04683-1.

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5

Mishra, Satyendra, and Sejal Patel. "Design, Synthesis, and Anti-bacterial Activity of Novel Deoxycholic Acid- Amino Alcohol Conjugates." Medicinal Chemistry 16, no. 3 (April 17, 2020): 385–91. http://dx.doi.org/10.2174/1573406415666190206231002.

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Background: Numerous synthetic bile acid derivatives have been recognized for their various biological activities. Among these, bile acid amides have emerged as an attractive antibacterial agent. We herein illustrate the synthesis and antibacterial evaluation of deoxycholic acidamino alcohols conjugates. Objective: Design and Synthesis of novel deoxycholic acid-amino alcohol conjugates to investigate their antibacterial activity against E. coli and S. aureus. Methods: Novel deoxycholic acid-amino alcohol conjugates were synthesized, from conjugation of deoxycholic acid-NHS ester with amino alcohols. Various amino alcohols moieties were appended to the C24 position of deoxycholic acid to yield deoxycholic acid-amino alcohol conjugates. All the synthesized compounds were characterized by 1H NMR, 13C NMR, IR and massspectroscopy. The entire synthesized deoxycholic acid-amino alcohol conjugates were evaluated for their antibacterial activity against E. coli and S. aureus using the broth dilution method. Results: The outcome illustrated that some of the novel deoxycholic acid-amino alcohol conjugates exhibited enhanced anti-bacterial activities. Amongst them, deoxycholic acid-amino alcohol conjugate containing (-R)-2-aminocyclohexanol (1) demonstrated promising efficacy against both strains S. aureus ATCC 25923 (MIC 15 μg/mL) and E. coli ATCC 25922 (MIC 45 μg/mL) and was identified as a lead molecule. Conclusion: Numbers of novel deoxycholic acid-amino alcohol conjugates were synthesized and their antimicrobial activities provided useful information that the potency was strongly depending on the structures of deoxycholic acid-amino alcohol conjugates.
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Kren, B. T., C. M. Rodrigues, K. D. Setchell, and C. J. Steer. "Posttranscriptional regulation of mRNA levels in rat liver associated with deoxycholic acid feeding." American Journal of Physiology-Gastrointestinal and Liver Physiology 269, no. 6 (December 1, 1995): G961—G973. http://dx.doi.org/10.1152/ajpgi.1995.269.6.g961.

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We investigated the effects of bile acid feeding on the mRNA levels and transcriptional activity of genes involved in various facets of hepatic cell function. Rats were maintained for 10 days on standard diet supplemented with combinations of 1 and 0.4% deoxycholic acid and ursodeoxycholic acid. Significant reductions in mRNA levels for liver fatty acid binding protein, albumin, the asialoglycoprotein receptor, connexins 32 and 26, and cytochromes P-450IIB1 and P-450IIE1 were associated with 1% deoxycholic acid feeding. Conversely, the 1% deoxycholic acid-fed animals exhibited increased mRNA levels for cholesterol 7 alpha-hydroxylase, 3-hydroxy-3-methylglutaryl-CoA reductase, multidrug resistance, procollagens, extracellular matrix, protooncogenes, tumor suppressors, and cyclins. The 0.4% deoxycholic acid-fed animals exhibited increased mRNA levels for c-jun, H-ras, p53, cyclins D1 and D3, fibronectin, and procollagens alpha 1(I) and alpha 1(III). Transcriptional rate changes could not account for the observed changes in steady-state mRNA levels. Ursodeoxycholic acid feeding had no significant effect on gene expression and almost completely inhibited the changes associated with 1% deoxycholic acid when coadministered. The results indicate that dietary ingestion of deoxycholic acid profoundly affects hepatic gene expression in the rat, and regulation occurs primarily at the posttranscriptional level.
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7

Watchmaker, Jacqueline, Daniel J. Callaghan, and Jeffrey S. Dover. "Deoxycholic Acid in Aesthetic Medicine." Advances in Cosmetic Surgery 3, no. 1 (June 2020): 77–87. http://dx.doi.org/10.1016/j.yacs.2020.01.009.

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8

Sachdev, Divya, Tarana Mohammadi, and Sabrina G. Fabi. "Deoxycholic Acid–Induced Skin Necrosis." Dermatologic Surgery 44, no. 7 (July 2018): 1037–39. http://dx.doi.org/10.1097/dss.0000000000001384.

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9

Montes, José Raúl, Elizabeth Santos, and Annirudha Chillar. "Jowl Reduction With Deoxycholic Acid." Dermatologic Surgery 46, no. 1 (January 2020): 78–85. http://dx.doi.org/10.1097/dss.0000000000001869.

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10

Veysey, M. J., L. A. Thomas, A. I. Mallet, P. J. Jenkins, G. M. Besser, J. A. H. Wass, G. M. Murphy, and R. H. Dowling. "Prolonged large bowel transit increases serum deoxycholic acid: a risk factor for octreotide induced gallstones." Gut 44, no. 5 (May 1, 1999): 675–81. http://dx.doi.org/10.1136/gut.44.5.675.

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BACKGROUNDTreatment of acromegaly with octreotide increases the proportion of deoxycholic acid in, and the cholesterol saturation of, bile and induces the formation of gallstones. Prolongation of intestinal transit has been proposed as the mechanism for the increase in the proportion of deoxycholic acid in bile.AIMSTo study the effects of octreotide on intestinal transit in acromegalic patients during octreotide treatment, and to examine the relation between intestinal transit and bile acid composition in fasting serum.METHODSMouth to caecum and large bowel transit times, and the proportion of deoxycholic acid in fasting serum were measured in non-acromegalic controls, acromegalic patients untreated with octreotide, acromegalics on long term octreotide, and patients with simple constipation. Intestinal transit and the proportion of deoxycholic acid were compared in acromegalic patients before and during octreotide.RESULTSAcromegalics untreated with octreotide had longer mouth to caecum and large bowel transit times than controls. Intestinal transit was further prolonged by chronic octreotide treatment. There were significant linear relations between large bowel transit time and the proportion of deoxycholic acid in the total, conjugated, and unconjugated fractions of fasting serum.CONCLUSIONSThese data support the hypothesis that, by prolonging large bowel transit, octreotide increases the proportion of deoxycholic acid in fasting serum (and, by implication, in bile) and thereby the risk of gallstone formation.
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11

Campbell, Nigel B., Craig G. Ruaux, Donnie E. Shifflett, Jöerg M. Steiner, David A. Williams, and Anthony T. Blikslager. "Physiological concentrations of bile salts inhibit recovery of ischemic-injured porcine ileum." American Journal of Physiology-Gastrointestinal and Liver Physiology 287, no. 2 (August 2004): G399—G407. http://dx.doi.org/10.1152/ajpgi.00310.2003.

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We have previously shown rapid in vitro recovery of barrier function in porcine ischemic-injured ileal mucosa, attributable principally to reductions in paracellular permeability. However, these experiments did not take into account the effects of luminal contents, such as bile salts. Therefore, the objective of this study was to evaluate the role of physiological concentrations of deoxycholic acid in recovery of mucosal barrier function. Porcine ileum was subjected to 45 min of ischemia, after which mucosa was mounted in Ussing chambers and exposed to varying concentrations of deoxycholic acid. The ischemic episode resulted in significant reductions in transepithelial electrical resistance (TER), which recovered to control levels of TER within 120 min, associated with significant reductions in mucosal-to-serosal 3H-labeled mannitol flux. However, treatment of ischemic-injured tissues with 10−5 M deoxycholic acid significantly inhibited recovery of TER with significant increases in mucosal-to-serosal 3H-labeled mannitol flux, whereas 10−6 M deoxycholic acid had no effect. Histological evaluation at 120 min revealed complete restitution regardless of treatment, indicating that the breakdown in barrier function was due to changes in paracellular permeability. Similar effects were noted with the application of 10−5 M taurodeoxycholic acid, and the effects of deoxycholic acid were reversed with application of the Ca2+-mobilizing agent thapsigargin. Deoxycholic acid at physiological concentrations significantly impairs recovery of epithelial barrier function by an effect on paracellular pathways, and these effects appear to be Ca2+ dependent.
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12

Lalić-Popović, Mladena, Velibor Vasović, Boris Milijašević, Svetlana Goločorbin-Kon, Hani Al-Salami, and Momir Mikov. "Deoxycholic Acid as a Modifier of the Permeation of Gliclazide through the Blood Brain Barrier of a Rat." Journal of Diabetes Research 2013 (2013): 1–8. http://dx.doi.org/10.1155/2013/598603.

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Major problem for diabetic patients represents damage of blood vessels and the oxidative stress of the brain cells due to increased concentration of free radicals and poor nutrition of brain cells. Gliclazide has antioxidative properties and poor blood brain barrier (BBB) penetration. Bile acids are known for their hypoglycemic effect and as promoters of drug penetration across biological membranes. Accordingly, the aim of this study is to investigate whether the bile acid (deoxycholic acid) can change the permeation of gliclazide, through the blood brain barrier of a rat model type-1 diabetes. Twenty-four male Wistar rats were randomly allocated to four groups, of which, two were given alloxan intraperitoneally (100 mg/kg) to induce diabetes. One diabetic group and one healthy group were given a bolus gliclazide intra-arterially (20 mg/kg), while the other two groups apart from gliclazide got deoxycholic acid (4 mg/kg) subcutaneously. Blood samples were collected 30, 60, 150, and 240 seconds after dose, brain tissues were immediately excised and blood glucose and gliclazide concentrations were measured. Penetration of gliclazide in groups without deoxycholic acid pretreatment was increased in diabetic animals compared to healthy animals. Also in both, the healthy and diabetic animals, deoxycholic acid increased the permeation of gliclazide through that in BBB.
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13

Limmatvapirat, S., K. Yamaguchi, E. Yonemochi, T. Oguchi, and K. Yamamoto. "A 1:1 Deoxycholic Acid–Salicylic Acid Complex." Acta Crystallographica Section C Crystal Structure Communications 53, no. 6 (June 15, 1997): 803–5. http://dx.doi.org/10.1107/s0108270197000899.

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14

Xiao, Linxia, Endian Yu, Hanlin Yue, and Qingyong Li. "Enhanced Liver Targeting of Camptothecin via Conjugation with Deoxycholic Acid." Molecules 24, no. 6 (March 26, 2019): 1179. http://dx.doi.org/10.3390/molecules24061179.

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Camptothecin (CPT) shows potent anticancer activity through inhibition of topoisomerase I. However, its water insolubility and severe toxicity limit its clinical application. Coupling with bile acid moieties is a promising method for liver-targeted drug delivery, which takes advantage of the bile acid receptors on hepatocytes. In this study, we evaluated the potential liver targeting and stability of a deoxycholic acid-CPT conjugate (G2). The competitive inhibition of antitumor activity experiment based on bile acid transporters was performed using the MTT method. The effects of deoxycholic acid on uptake of G2 and CPT were assessed in 2D and 3D HepG2 cell models. The stability of G2 and CPT was evaluated in vitro (in simulated gastric fluid, simulated intestinal fluid, and fresh rat plasma). Finally, biodistribution of G2 and CPT was investigated in Kunming mice following oral administration. The results showed that deoxycholic acid pretreatment could significantly reduce the antitumor activity and cellular uptake of G2 in HepG2 cells, but had no distinct effects on CPT. Meanwhile, G2 exhibited better stability compared with CPT. More importantly, biodistribution study in mice demonstrated that the liver targeting index of G2 increased 1.67-fold than that of CPT. Overall, the study suggests that conjugation with deoxycholic acid is a feasible method to achieve liver targeting delivery of CPT.
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15

Veysey, Martin J., Linzi A. Thomas, Anthony I. Mallet, Paul J. Jenkins, G. Michael Besser, Gerard M. Murphy, and R. Hermon Dowling. "Colonic transit influences deoxycholic acid kinetics." Gastroenterology 121, no. 4 (October 2001): 812–22. http://dx.doi.org/10.1053/gast.2001.28015.

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16

Bhatti, Zabeer, Jaswinder Virk, and Devamohan Sivalingam. "Submental Abscess After Deoxycholic Acid Injection." American Journal of Therapeutics 25, no. 2 (2018): e285-e286. http://dx.doi.org/10.1097/mjt.0000000000000514.

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17

McKay, Cather, Cynthia Price, and Lisa Pruett. "Vascular Injury After Deoxycholic Acid Injection." Dermatologic Surgery 45, no. 2 (February 2019): 306–9. http://dx.doi.org/10.1097/dss.0000000000001550.

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18

Pham, Christine T., Alfred Lee, Calvin T. Sung, Franchesca Choi, Margit Juhasz, and Natasha A. Mesinkovska. "Adverse Events of Injectable Deoxycholic Acid." Dermatologic Surgery 46, no. 7 (July 2020): 942–49. http://dx.doi.org/10.1097/dss.0000000000002318.

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19

Hussar, Daniel A., and Jerry Rachel George. "Brivaracetam, lumacaftor/ivacaftor, and deoxycholic acid." Journal of the American Pharmacists Association 56, no. 4 (July 2016): 474–77. http://dx.doi.org/10.1016/j.japh.2016.06.001.

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20

Wang, Yun-Cang, Zhi-Qiang Wang, Yong Yuan, Tao Ren, Peng-Zhi Ni, and Long-Qi Chen. "Notch Signaling Pathway Is Inhibited in the Development of Barrett’s Esophagus: An In Vivo and In Vitro Study." Canadian Journal of Gastroenterology and Hepatology 2018 (2018): 1–11. http://dx.doi.org/10.1155/2018/4149317.

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Objective. To explore the role of Notch signaling in the development of Barrett’s esophagus. Methods. Patients with esophagectomy and gastric interposition were recruited as a human model of gastroesophageal reflux disease. The expressions of Notch signaling genes in normal esophagus from surgical specimen and columnar metaplasia in the esophageal remnant after esophagectomy were evaluated by real time quantitative Polymerase Chain Reaction (RT-qPCR) and immunohistochemistry (IHC). For in vitro experiments, Het-1A cells were treated with hydrochloric acid, deoxycholic acid, mixture of hydrochloric acid and deoxycholic acid, or Notch1-siRNA, and expressions of Notch1, Hes1, MUC2, and K13 were evaluated via RT-qPCR and western blot. Results. Samples were obtained from 36 patients with columnar metaplasia in the esophageal remnant. Both IHC and RT-qPCR indicated that Notch1 and Hes1 expressions were significantly higher in normal esophagus than that in metaplasia. Hydrochloric acid and deoxycholic acid suppressed Notch1, Hes1, and K13 expressions, in concert with increasing MUC2 expressions. Notch inhibition by Notch1-siRNA contributed to the downregulation of Notch1, Hes1, and K13 expressions, whereas MUC2 expression was enhanced. Conclusions. Both hydrochloric acid and deoxycholic acid could suppress Notch signaling pathway in esophageal epithelial cells, and inhibited Notch signaling has important functions in the development of Barrett’s esophagus.
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21

Stellaard, F., G. Paumgartner, G. P. van Berge Henegouwen, and S. D. van der Werf. "Determination of deoxycholic acid pool size and input rate using [24-13C]deoxycholic acid and serum sampling." Journal of Lipid Research 27, no. 11 (May 1990): 1222–25. http://dx.doi.org/10.1016/s0022-2275(20)38758-7.

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22

Reddy, Sheela, T. A. B. Sanders, R. W. Owen, and M. H. Thompson. "Faecal pH, bile acid and sterol concentrations in premenopausal Indian and white vegetarians compared with white omnivores." British Journal of Nutrition 79, no. 6 (June 1998): 495–500. http://dx.doi.org/10.1079/bjn19980087.

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Faecal bulk, pH, water content, the concentrations of neutral sterols and bile acids and dietary intakes were measured in twenty-two Indian vegetarian, twenty-two white omnivorous and eighteen white vegetarian premenopausal women. Faecal bulk and water content were greater and pH lower in the Indian vegetarians. Total faecal animal sterol and coprostanol concentrations expressed on a dry-weight basis were lower in the vegetarians compared with the omnivores. The faecal sterol concentrations were correlated with dietary cholesterol intake. Primary bile acids were detected in six Indian vegetarians, two white vegetarians and two white omnivores; secondary bile acids were detected in all the white omnivore and vegetarian subjects but not in two of the Indian vegetarians. Total faecal free bile acid and conjugated bile acid concentrations were lower in the white vegetarians compared with the omnivores. Faecal lithocholic acid concentrations were lower in both Indian and white vegetarians. The lithocholic: deoxycholic acid ratio and coprostanol: total animal sterols ratio were significantly lower in the Indian vegetarians compared with the omnivores. Both ratios were positively correlated with faecal pH. Stepwise multiple regression analyses were undertaken in order to identify which nutrients influenced faecal pH, lithocholic and deoxycholic acid concentrations. The intakes of starch and dietary fibre were negatively associated with faecal concentrations of lithocholic and deoxycholic acid. Starch intake alone was negatively associated with faecal pH. The results of this study confirm that diets high in dietary fibre decrease faecal bile acid concentrations and suggest that the complex carbohydrates present in Indian vegetarian diets influence faecal pH and inhibit the degradation of faecal steroids.
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23

Chen, Mei, AXiaojun Ye, Jingxi Wei, Ruihua Wang, and Karen Poon. "Deoxycholic Acid Upregulates the Reprogramming Factors KFL4 and OCT4 Through the IL-6/STAT3 Pathway in Esophageal Adenocarcinoma Cells." Technology in Cancer Research & Treatment 19 (January 1, 2020): 153303382094530. http://dx.doi.org/10.1177/1533033820945302.

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Cancer stem cells, a special subgroup of cancer cells, have self-renewal capabilities and multidirectional potential, which may be reprogrammed from the dedifferentiation of cancer cells, contributing to the failure of clinical treatments. Esophageal adenocarcinoma grows in an inflammatory environment stimulated by deoxycholic acid, an important component of gastroesophageal reflux content, contributing to the transformation of esophageal squamous epithelium to the precancerous lesions of esophageal adenocarcinoma, that is, Barrett esophagus. In the present study, deoxycholic acid was used to investigate whether it could induce the expression of reprogramming factors Krüppel-like factor, OCT4, and Nanog; the transformation to cancer stem cells in esophageal adenocarcinoma; and the involvement of the interleukin-6/signal transduction and activation of transcription 3 inflammatory signaling pathway. OE33 cells were treated with deoxycholic acid (250 μM) for 0 hour, 3 hours, 6 hours, and 12 hours before evaluating the messenger RNA expression of Krüppel-like factor, OCT4, Nanog, interleukin-6, and Bcl-xL by reverse transcription-quantitative polymerase chain reaction. Interleukin-6 protein was detected by enzyme linked immunosorbent assay, while signal transduction and activation of transcription 3, phosphorylated signal transduction and activation of transcription 3, Krüppel-like factor, and OCT4 were detected by Western blot. Signal transduction and activation of transcription 3 small interfering RNA and human recombinant interleukin-6 were used to treat OE33 cells and to detect their effects on Krüppel-like factor, OCT4, Nanog, CD44, hypoxia-inducible factor 1-α, and Bcl-xL expression. Results showed that deoxycholic acid promotes the expression of reprogramming factors Krüppel-like factor and OCT4, which are regulated by the interleukin-6/signal transduction and activation of transcription 3 signaling pathway. Deoxycholic acid has a malignancy-inducing effect on the transformation of esophageal adenocarcinoma stem cells, improving the antiapoptotic ability of tumors, and increasing the malignancy of esophageal adenocarcinoma. Deactivating the regulatory signaling pathway of interleukin-6/signal transduction and activation of transcription 3 and neutralizing deoxycholic acid may be novel targets for improving the clinical efficacy of esophageal adenocarcinoma therapy.
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24

Hoppe, Hans-Wolfgang, and Peter Welzel. "A synthesis of bufalin from deoxycholic acid." Tetrahedron Letters 27, no. 22 (January 1986): 2459–62. http://dx.doi.org/10.1016/s0040-4039(00)84555-4.

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Cataldo, Franco, Pietro Ragni, Aldo Rosati, and Ornella Ursini. "Inclusion polymerization of isoprene in deoxycholic acid." Radiation Physics and Chemistry 78, no. 5 (May 2009): 338–44. http://dx.doi.org/10.1016/j.radphyschem.2009.01.008.

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26

Koivukorpi, Juha, and Erkki Kolehmainen. "Novel deoxycholic acid alkylamide-phenylurea-derived organogelators." Tetrahedron Letters 51, no. 8 (February 2010): 1199–201. http://dx.doi.org/10.1016/j.tetlet.2009.12.101.

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27

Nair, Vijay, and Jaya Prabhakaran. "Novel Crown Ethers From 7-Deoxycholic Acid." Synthetic Communications 24, no. 4 (February 1, 1996): 697–702. http://dx.doi.org/10.1080/00397919608003668.

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Nair, Vijay, and Jaya Prabhakaran. "Novel crown ethers from 7-deoxycholic acid." Synthetic Communications 26, no. 4 (February 1996): 697–702. http://dx.doi.org/10.1080/00397919608086743.

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29

MIYATA, M., and K. SADA. "ChemInform Abstract: Deoxycholic Acid and Related Hosts." ChemInform 28, no. 2 (August 4, 2010): no. http://dx.doi.org/10.1002/chin.199702319.

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30

Grady, Brittany, Fernanda Porphirio, and Cameron Rokhsar. "Submental Alopecia at Deoxycholic Acid Injection Site." Dermatologic Surgery 43, no. 8 (August 2017): 1105–8. http://dx.doi.org/10.1097/dss.0000000000001085.

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Jegasothy, S. Manjula. "Deoxycholic Acid Injections for Bra-Line Lipolysis." Dermatologic Surgery 44, no. 5 (May 2018): 757–60. http://dx.doi.org/10.1097/dss.0000000000001311.

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32

Humphrey, Shannon, Priya Femmer, Katie Beleznay, and Jean D. A. Carruthers. "Deoxycholic Acid for Submental Fullness and More." Dermatologic Surgery 45, no. 4 (April 2019): 624–27. http://dx.doi.org/10.1097/dss.0000000000001652.

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Patel, Jigar, Roshni Ranjit-Reeves, and Julie Woodward. "Recurrent Xanthelasmas Treated With Intralesional Deoxycholic Acid." Dermatologic Surgery 46, no. 6 (June 2020): 847–48. http://dx.doi.org/10.1097/dss.0000000000001936.

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34

Dayan, Steven H., Shannon Humphrey, Derek H. Jones, Paul F. Lizzul, Todd M. Gross, Karen Stauffer, and Frederick C. Beddingfield. "Overview of ATX-101 (Deoxycholic Acid Injection)." Dermatologic Surgery 42 (November 2016): S263—S270. http://dx.doi.org/10.1097/dss.0000000000000870.

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Terzić, Nataša, Dejan Opsenica, Dragana Milić, Bernard Tinant, Kirsten S. Smith, Wilbur K. Milhous, and Bogdan A. Šolaja. "Deoxycholic Acid-Derived Tetraoxane Antimalarials and Antiproliferatives1." Journal of Medicinal Chemistry 50, no. 21 (October 2007): 5118–27. http://dx.doi.org/10.1021/jm070684m.

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36

Nagengast, Fokko M., Ivo P. Van Munser, Jan M. J. I. Salemans, and Sjoerd D. J. van der Werf. "Deoxycholic acid metabolism in patients with adenomas." Gastroenterology 105, no. 3 (September 1993): 955–56. http://dx.doi.org/10.1016/0016-5085(93)90930-b.

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Májer, Ferenc, Ruchika Sharma, Claire Mullins, Luke Keogh, Sinead Phipps, Shane Duggan, Dermot Kelleher, et al. "New highly toxic bile acids derived from deoxycholic acid, chenodeoxycholic acid and lithocholic acid." Bioorganic & Medicinal Chemistry 22, no. 1 (January 2014): 256–68. http://dx.doi.org/10.1016/j.bmc.2013.11.029.

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Shi, Yanyan, Ying Wei, Ting Zhang, Jing Zhang, Ye Wang, and Shigang Ding. "Deoxycholic Acid Could Induce Apoptosis and Trigger Gastric Carcinogenesis on Gastric Epithelial Cells by Quantitative Proteomic Analysis." Gastroenterology Research and Practice 2016 (2016): 1–10. http://dx.doi.org/10.1155/2016/9638963.

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Background.Pathologic duodenogastric reflux can induce or aggravate gastritis because of the presence of bile acids. Bile reflux has been generally considered to be associated with intestinal metaplasia and gastric cancer. However, the pathogenic mechanisms of the effects of bile acids on gastric mucosa are still unknown.Methods.To explore the mechanisms by which bile acids induce gastric mucosal lesions, we examined cell apoptosis in the gastric epithelial cell line GES-1 and investigated the changes in protein profiles of GES-1 cells in response to a bile acid deoxycholic acid using a proteomics approach. Changes in the profiles of the differently expressed proteins were analyzed using the DAVID and STRING programs.Results.We found apoptosis was significantly induced in GES-1 cells by deoxycholic acid. Using liquid chromatographic/tandem mass spectrometric (LC-MS/MS) methods, 134 upregulated proteins and 214 downregulated proteins were identified in the bile acid treated GES-1 cells. Bioinformatics analysis revealed the interactions and signaling networks of these differentially expressed proteins.Conclusion.These findings may improve the understanding of the molecular mechanisms underlying the pathogenicity of bile acids on gastric mucosa.
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Leppik, R. A., and D. J. Sinden. "Pseudomonas μtant strains that accumulate androstane and seco-androstane intermediates from bile acids." Biochemical Journal 243, no. 1 (April 1, 1987): 15–21. http://dx.doi.org/10.1042/bj2430015.

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Transposon mutant strains which were affected in bile acid catabolism were isolated from four Pseudomonas spp. Two of the mutant groups isolated were found to accumulate 12 alpha-hydroxyandrosta-1,4-diene-3,17-dione as the major product from deoxycholic acid. Strains in one of these two groups were able to grow on steroids such as chenodeoxycholic acid, which lacks a 12 alpha-hydroxy function, whereas the one member of the second group could not. With chenodeoxycholic acid, this latter strain accumulated a yellow muconic-like derivative, tentatively identified as 3,7-dihydroxy-5,9,17-trioxo-4(5),9(10)-disecoandrosta-1(10)2 -dien-4-oic acid. Members of two further mutant groups accumulated either 12 beta-hydroxyandrosta-1,4-diene-3,17-dione or 3,12 beta-dihydroxy-9(10)-secoandrosta-1,3,5(10)-triene-9,17-dione as the major product from deoxycholic acid. The relationship between the catabolism of m- and p-cresol, 3-ethylphenol and the bile acids was also examined.
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Kuhajda, Ksenija, Stanko Cvjeticanin, Evgenija Djurendic, Marija Sakac, Katarina Penov-Gasi, Vesna Kojic, and Gordana Bogdanovic. "Synthesis and cytotoxic activity of a series of bile acid derivatives." Chemical Industry 63, no. 4 (2009): 313–18. http://dx.doi.org/10.2298/hemind0904313k.

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The new conjugates of selected bile acids (hyocholic (2), deoxycholic (3), hyodeoxycholic (4) and 12-ketocholic (5) acids) with ethyl 11-aminoundecanoate 7, 8, 11, and 13 were synthesized. The conjugation reaction was carried out in ethyl acetate in the presence of N-ethoxycarbonyl-2-ethoxy-1,2-dihydroquinoline (EEDQ) and triethylamine. Under the same experimental conditions, the conjugation reaction involving ethyl 6-aminohexanoate resulted in formation of a conjugate 9 only in the case of deoxycholic acid (3) in addition to the unexpected ethyl ester 10. In the case of the other bile acids (cholic (1), hyodeoxycholic (4) and 12-ketocholic (5) acids) only an unexpected ester formation took place giving esters 6, 12, and 14. Cytotoxic activity against four tumor cell lines (human breast adenocarcinoma ER-, MDA-MB-231; breast adenocarcinoma ER+, MCF-7; cervix epiteloid carcinoma, HeLa S-3; and prostate cancer, PC-3) was evaluated. Conjugate 8 showed strong activity against HeLa S-3 and conjugate 11 for PC-3. Ethyl ester of 12-ketocholic acid 14 showed very strong antiproliferative activity against MCF-7 and HeLa S-3.
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41

Yan, Tingting, Nana Yan, Hong Wang, Tomoki Yagai, Yuhong Luo, Shogo Takahashi, Min Zhao, et al. "FXR-Deoxycholic Acid-TNF-α Axis Modulates Acetaminophen-Induced Hepatotoxicity." Toxicological Sciences 181, no. 2 (February 28, 2021): 273–84. http://dx.doi.org/10.1093/toxsci/kfab027.

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Abstract The idiosyncratic characteristics and severity of acetaminophen (APAP) overdose-induced hepatotoxicity render identifying the predisposing factors and mechanisms of APAP-induced liver toxicity necessary and urgent. Farnesoid X receptor (FXR) controls bile acid homeostasis and modulates the progression of various liver diseases. Although global FXR deficiency in mice enhances APAP intoxication, the mechanism remains elusive. In this study, an increased sensitivity to APAP-induced toxicity was found in global Fxr-null (Fxr−/−) mice, but was not observed in hepatocyte-specific or macrophage-specific Fxr-null mice, suggesting that global FXR deficiency enhances APAP hepatotoxicity via disruption of systematic bile acid homeostasis. Indeed, more bile acid accumulation was found in global Fxr−/− mice, while 2% cholestyramine diet feeding decreased serum bile acids and alleviated APAP hepatotoxicity in global Fxr−/− mice, suggesting that bile acid accumulation contributes to APAP toxicity. Bile acids were suspected to induce macrophage to release tumor necrosis factor-α (TNF-α), which is known to enhance the APAP hepatotoxicity. In vitro, deoxycholic acid (DCA), a secondary bile acid metabolite, significantly induced Tnfa mRNA and dose-dependently enhanced TNF-α release from macrophage, while the same dose of DCA did not directly potentiate APAP toxicity in cultured primary hepatocytes. In vivo, DCA enhanced TNF-α release and potentiated APAP toxicity, both of which were abolished by the specific TNF-α antagonist infliximab. These results reveal an FXR-DCA-TNF-α axis that potentiates APAP hepatotoxicity, which could guide the clinical safe use of APAP.
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42

Liu, Li, Wenxiao Dong, Sinan Wang, Yujie Zhang, Tianyu Liu, Runxiang Xie, Bangmao Wang, and Hailong Cao. "Deoxycholic acid disrupts the intestinal mucosal barrier and promotes intestinal tumorigenesis." Food & Function 9, no. 11 (2018): 5588–97. http://dx.doi.org/10.1039/c8fo01143e.

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43

Mroz, Magdalena S., Natalia K. Lajczak, Bridie J. Goggins, Simon Keely, and Stephen J. Keely. "The bile acids, deoxycholic acid and ursodeoxycholic acid, regulate colonic epithelial wound healing." American Journal of Physiology-Gastrointestinal and Liver Physiology 314, no. 3 (March 1, 2018): G378—G387. http://dx.doi.org/10.1152/ajpgi.00435.2016.

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The intestinal epithelium constitutes an innate barrier which, upon injury, undergoes self-repair processes known as restitution. Although bile acids are known as important regulators of epithelial function in health and disease, their effects on wound healing processes are not yet clear. Here we set out to investigate the effects of the colonic bile acids, deoxycholic acid (DCA) and ursodeoxycholic acid (UDCA), on epithelial restitution. Wound healing in T84 cell monolayers grown on transparent, permeable supports was assessed over 48 h with or without bile acids. Cell migration was measured in Boyden chambers. mRNA and protein expression were measured by RT-PCR and Western blotting. DCA (50–150 µM) significantly inhibited wound closure in cultured epithelial monolayers and attenuated cell migration in Boyden chamber assays. DCA also induced nuclear accumulation of the farnesoid X receptor (FXR), whereas an FXR agonist, GW4064 (10 µM), inhibited wound closure. Both DCA and GW4064 attenuated the expression of CFTR Cl− channels, whereas inhibition of CFTR activity with either CFTR-inh-172 (10 µM) or GlyH-101 (25 µM) also prevented wound healing. Promoter/reporter assays revealed that FXR-induced downregulation of CFTR is mediated at the transcriptional level. In contrast, UDCA (50–150 µM) enhanced wound healing in vitro and prevented the effects of DCA. Finally, DCA inhibited and UDCA promoted mucosal healing in an in vivo mouse model. In conclusion, these studies suggest bile acids are important regulators of epithelial wound healing and are therefore good targets for development of new drugs to modulate intestinal barrier function in disease treatment. NEW & NOTEWORTHY The secondary bile acid, deoxycholic acid, inhibits colonic epithelial wound healing, an effect which appears to be mediated by activation of the nuclear bile acid receptor, FXR, with subsequent downregulation of CFTR expression and activity. In contrast, ursodeoxycholic acid promotes wound healing, suggesting it may provide an alternative approach to prevent the losses of barrier function that are associated with mucosal inflammation in IBD patients.
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44

Chung, Hyewon, Jin-Woo Park, Dai-Hyun Kim, Soo-Hong Seo, Kyoung-Ah Kim, Woo-Shun Lee, and Ji-Young Park. "Safety, Tolerability, Pharmacokinetics, and Pharmacodynamics of Cholic Acid (MT921) after a Subcutaneous Injection in the Submental Area to Humans." Pharmaceuticals 14, no. 8 (August 23, 2021): 830. http://dx.doi.org/10.3390/ph14080830.

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This study aimed to explore pharmacokinetics, pharmacodynamics, and safety/tolerability of MT921, an injectable cholic acid, after a single subcutaneous administration to healthy volunteers. A randomized, double-blinded, placebo-controlled, single dose-ascending phase 1 study enrolled 24 subjects who were assigned to three groups (60 mg, 120 mg, and 150 mg) of MT921. Blood samples were obtained for a 24-h period before and after injecting MT921 to the submental fat area. Plasma concentrations of cholic acid and deoxycholic acid were determined for pharmacokinetic analysis. Levels of free fatty acid, triglyceride, and total cholesterol were measured for pharmacodynamic analysis. Safety and tolerability were assessed until 21 days post-dose. While systemic exposure to cholic acid tended to increase as the MT921 dose increased, pharmacokinetic profiles of deoxycholic acid were similar among dose groups without showing significant changes. Pharmacodynamic profiles were comparable when measured at baseline and post-dose. The most frequent adverse events were injection site pain and edema. All adverse drug reactions resolved without treatment. MT921 appeared to be well-tolerated after an injection to the submental area at a dose up to 150 mg. Systemic exposure to cholic acid increased as the dose increased. Blood lipid profiles and deoxycholic acid levels were not affected by MT921 treatment.
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45

Diallo, Alpha O., Claude Meyer, and Nguyen Van-Thanh. "Article." Canadian Journal of Chemistry 77, no. 1 (January 1, 1999): 122–29. http://dx.doi.org/10.1139/v98-224.

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The frequencies of the O-D stretching vibrations of CH3COOD have been measured in the liquid and vapour phases and in the form of molecular associations with deoxycholic acid and cholesterol. The spectra confirm that the vapour phase is a mixture of monomeric and dimeric forms at room temperature. The vibrational assignment made for the gaseous phase is used in conjunction with prior data available on the monomeric O-D stretching frequencies in solutions to explain the spectroscopic behaviour of the molecular complexes. The pattern of frequency shifts suggests that deuterium bonding links the cholesterol and CH3COOD in the hydrophilic regions and that the self association of the heavy acid is limited to the dimeric species in the complex with deoxycholic acid. Extra absorption bands observed in the spectral region characteristic of the deuterium bond vibrations are tentatively considered to arise from O-D groups in different local environments with different vibrational energies compared with the D-bonded species. Further evidence for steroid-CH3COOD interactions is obtained from a study of the O-H and CbetaO stretching vibrations of the compounds.Key words: acetic acid-d, complexation with deoxycholic acid and cholesterol, infrared spectroscopy.
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46

Kosuge, Tomoo, Tomoe Beppu, Takao Kodama, Koh Hidai, and Yasuo Idezuki. "Serum bile acid profile in thyroid dysfunction and effect of medical treatment." Clinical Science 73, no. 4 (October 1, 1987): 425–29. http://dx.doi.org/10.1042/cs0730425.

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1. Serum non-esterified bile acid profile was examined in patients with thyroid dysfunction. Sixteen hyperthyroid patients, six hypothyroid patients, nine patients taking thyroid or antithyroid drugs and 26 healthy controls were studied. The medicated patients were euthyroid when serum samples were collected. Bile acid concentration was determined by the simplified microassay method involving mass fragmentation spectrometry. 2. The sum of the concentrations of the individual bile acids was not significantly different among the four groups. However, the composition of bile acid reflected the thyroid function. The most prominent bile acid was deoxycholic acid in the hypothyroid patients and chenodeoxycholic acid in the hyperthyroid patients. The serum bile acid profile of medically treated patients was similar to that of normal cpntrols. The ratio of the sum of deoxycholic and cholic acid to that of lithocholic and chenodeoxycholic acid was found to be a good indicator of thyroid function, while the ratio of cholic acid to chenodeoxycholic acid correlated poorly with it. 3. The characteristic effect of thyroid hormone on the serum bile acid composition in man was the shift from the ‘family’ of cholic acid to that of chenodeoxycholic acid. This is in agreement with experimental results in the rat, and suggests a specific action of thyroid hormone on the hydroxylating enzymes involved in the conversion of cholesterol into bile acids.
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47

Kollerov, V. V., T. G. Lobastova, D. Monti, N. O. Deshcherevskaya, E. E. Ferrandi, G. Fronza, S. Riva, and M. V. Donova. "Deoxycholic acid transformations catalyzed by selected filamentous fungi." Steroids 107 (March 2016): 20–29. http://dx.doi.org/10.1016/j.steroids.2015.12.015.

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48

Duret, Guillaume, and Anne H. Delcour. "Deoxycholic Acid BlocksVibrio choleraeOmpT but Not OmpU Porin." Journal of Biological Chemistry 281, no. 29 (May 2, 2006): 19899–905. http://dx.doi.org/10.1074/jbc.m602426200.

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49

Jean-Louis, Samira, Sandeep Akare, M. Ahad Ali, Eugene A. Mash, Emmanuelle Meuillet, and Jesse D. Martinez. "Deoxycholic Acid Induces Intracellular Signaling through Membrane Perturbations." Journal of Biological Chemistry 281, no. 21 (March 17, 2006): 14948–60. http://dx.doi.org/10.1074/jbc.m506710200.

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50

Raufman, Jean-Pierre, Ying Chen, Piotr Zimniak, and Kunrong Cheng. "Deoxycholic Acid Conjugates Are Muscarinic Cholinergic Receptor Antagonists." Pharmacology 65, no. 4 (2002): 215–21. http://dx.doi.org/10.1159/000064347.

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