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Journal articles on the topic 'Propionate'

Author: Grafiati

Published: 4 June 2021

Last updated: 29 January 2023

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1

Mirnaya, T. A., G. G. Yaremchuk, and S. V. Volkov. "Phase Diagrams of Binary Systems of Some Alkali Propionates." Zeitschrift für Naturforschung A 48, no. 10 (October 1, 1993): 995–99. http://dx.doi.org/10.1515/zna-1993-1006.

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Abstract The phase diagrams of the binary systems sodium-potassium, sodium-caesium, and potassium-caesium propionates have been investigated by differential thermal analysis and hot-stage polarization microscopy. Smectic liquid crystals in the systems with sodium propionate have been discovered. Liquid crystal formation in binaries of two non-mesomorphic components is explained by latent mesomorphism which is shown to be inherent to both sodium and potassium propionate.

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2

Deacon, Glen B., Peter C. Junk, Winnie W. Lee, Maria Forsyth, and Jun Wang. "Rare earth 3-(4′-hydroxyphenyl)propionate complexes." New Journal of Chemistry 39, no. 10 (2015): 7688–95. http://dx.doi.org/10.1039/c5nj00787a.

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Structural variation of lanthanoid 3-(4′-hydroxyphenyl)propionates and investigation of the anti-corrosion properties of lanthanum 3-(4′-hydroxyphenyl)propionate are presented, highlighting lanthanoid contraction and the importance of the –CHCH− structural unit of 4-hydroxycinnamates in corrosion mitigation.

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3

Sebastiani, Federico, Chiara Baroni, Gaurav Patil, Andrea Dali, Maurizio Becucci, Stefan Hofbauer, and Giulietta Smulevich. "The Role of the Hydrogen Bond Network in Maintaining Heme Pocket Stability and Protein Function Specificity of C. diphtheriae Coproheme Decarboxylase." Biomolecules 13, no. 2 (January 25, 2023): 235. http://dx.doi.org/10.3390/biom13020235.

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Monoderm bacteria accumulate heme b via the coproporphyrin-dependent biosynthesis pathway. In the final step, in the presence of two molecules of H2O2, the propionate groups of coproheme at positions 2 and 4 are decarboxylated to form vinyl groups by coproheme decarboxylase (ChdC), in a stepwise process. Decarboxylation of propionate 2 produces an intermediate that rotates by 90° inside the protein pocket, bringing propionate 4 near the catalytic tyrosine, to allow the second decarboxylation step. The active site of ChdCs is stabilized by an extensive H-bond network involving water molecules, specific amino acid residues, and the propionate groups of the porphyrin. To evaluate the role of these H-bonds in the pocket stability and enzyme functionality, we characterized, via resonance Raman and electronic absorption spectroscopies, single and double mutants of the actinobacterial pathogen Corynebacterium diphtheriae ChdC complexed with coproheme and heme b. The selective elimination of the H-bond interactions between propionates 2, 4, 6, and 7 and the polar residues of the pocket allowed us to establish the role of each H-bond in the catalytic reaction and to follow the changes in the interactions from the substrate to the product.

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4

Hayashi, Takashi, Hideaki Sato, Takashi Matsuo, Takaaki Matsuda, Yutaka Hitomi, and Yoshio Hisaeda. "Enhancement of enzymatic activity for myoglobins by modification of heme-propionate side chains." Journal of Porphyrins and Phthalocyanines 08, no. 03 (March 2004): 255–64. http://dx.doi.org/10.1142/s1088424604000246.

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The modification of myoglobin is an attractive process not only for understanding its molecular mechanism but also for engineering the protein function. The strategy of myoglobin functionalization can be divided into at least two approaches: site-directed mutagenesis and reconstitution with a non-natural prosthetic group. The former method enables us to mainly modulate the physiological function, while the latter has the advantage of introducing a new function on the protein. Particularly, replacement of the native hemin with an artificially created hemin having hydrophobic moieties at the terminal of the heme-propionate side chains serves as an appropriate substrate-binding site near the heme pocket, and consequently enhances the peroxidase and peroxygenase activities for the reconstituted myoglobin. In addition, the incorporation of the synthetic hemin bearing modified heme-propionates into an appropriate apomyoglobin mutant drastically enhances the peroxidase activity. In contrast, to convert myoglobin into a cytochrome P450 enzyme, a flavin moiety as an electron transfer mediator was introduced at the terminal of the heme-propionate side chain. The flavomyoglobin catalyzes the deformylation of 2-phenylpropanal in the presence of NADH under aerobic conditions through the peroxoanion formation from the oxygenated species. In addition, modification of the heme-propionate side chains has an significant influence on regulating the reactivity of the horseradish peroxidase. Furthermore, the heme-propionate side chain can form a metal binding site with a carboxylate residue in the heme pocket. These studies indicate that modification of the heme-propionate side chains can be a new and effective way to engineer functions for the hemoproteins.

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5

&NA;. "Fluticasone propionate." Reactions Weekly &NA;, no. 1379 (November 2011): 19. http://dx.doi.org/10.2165/00128415-201113790-00068.

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6

&NA;. "Fluticasone propionate." Reactions Weekly &NA;, no. 1384 (January 2012): 27. http://dx.doi.org/10.2165/00128415-201213840-00108.

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7

&NA;. "Fluticasone propionate." Reactions Weekly &NA;, no. 708 (July 1998): 6. http://dx.doi.org/10.2165/00128415-199807080-00015.

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8

&NA;. "Fluticasone propionate." Reactions Weekly &NA;, no. 730 (December 1998): 7. http://dx.doi.org/10.2165/00128415-199807300-00023.

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9

&NA;. "Fluticasone propionate." Reactions Weekly &NA;, no. 731 (December 1998): 7. http://dx.doi.org/10.2165/00128415-199807310-00019.

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10

&NA;. "Fluticasone propionate." Reactions Weekly &NA;, no. 742 (March 1999): 8–9. http://dx.doi.org/10.2165/00128415-199907420-00021.

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11

&NA;. "Fluticasone propionate." Reactions Weekly &NA;, no. 758 (July 1999): 8. http://dx.doi.org/10.2165/00128415-199907580-00023.

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&NA;. "Fluticasone propionate." Reactions Weekly &NA;, no. 767 (September 1999): 7. http://dx.doi.org/10.2165/00128415-199907670-00021.

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13

&NA;. "Fluticasone propionate." Reactions Weekly &NA;, no. 1164 (August 2007): 14. http://dx.doi.org/10.2165/00128415-200711640-00039.

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14

&NA;. "Fluticasone propionate." Inpharma Weekly &NA;, no. 1210 (October 1999): 18. http://dx.doi.org/10.2165/00128413-199912100-00042.

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&NA;. "Fluticasone propionate." Inpharma Weekly &NA;, no. 1213 (November 1999): 19. http://dx.doi.org/10.2165/00128413-199912130-00037.

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16

&NA;. "Fluticasone propionate." Reactions Weekly &NA;, no. 1365 (August 2011): 21. http://dx.doi.org/10.2165/00128415-201113650-00072.

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17

&NA;. "Fluticasone propionate." Reactions Weekly &NA;, no. 1368 (September 2011): 20. http://dx.doi.org/10.2165/00128415-201113680-00072.

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18

&NA;. "Fluticasone propionate." Reactions Weekly &NA;, no. 771 (October 1999): 9. http://dx.doi.org/10.2165/00128415-199907710-00024.

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19

&NA;. "Fluticasone propionate." Reactions Weekly &NA;, no. 817 (September 2000): 7. http://dx.doi.org/10.2165/00128415-200008170-00016.

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20

&NA;. "Fluticasone propionate." Reactions Weekly &NA;, no. 848 (April 2001): 6. http://dx.doi.org/10.2165/00128415-200108480-00012.

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21

&NA;. "Fluticasone propionate." Reactions Weekly &NA;, no. 1207 (June 2008): 20–21. http://dx.doi.org/10.2165/00128415-200812070-00059.

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22

&NA;. "Fluticasone propionate." Reactions Weekly &NA;, no. 1211 (July 2008): 17. http://dx.doi.org/10.2165/00128415-200812110-00052.

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&NA;. "Fluticasone propionate." Reactions Weekly &NA;, no. 1223 (October 2008): 14. http://dx.doi.org/10.2165/00128415-200812230-00044.

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24

&NA;. "Fluticasone propionate." Reactions Weekly &NA;, no. 901 (May 2002): 10. http://dx.doi.org/10.2165/00128415-200209010-00030.

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25

&NA;. "Fluticasone propionate." Reactions Weekly &NA;, no. 911 (July 2002): 9. http://dx.doi.org/10.2165/00128415-200209110-00026.

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26

&NA;. "Fluticasone propionate." Reactions Weekly &NA;, no. 935/936 (January 2003): 8. http://dx.doi.org/10.2165/00128415-200309350-00027.

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27

&NA;. "Fluticasone propionate." Reactions Weekly &NA;, no. 940 (March 2003): 8. http://dx.doi.org/10.2165/00128415-200309400-00022.

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28

&NA;. "Fluticasone propionate." Reactions Weekly &NA;, no. 1268 (September 2009): 17. http://dx.doi.org/10.2165/00128415-200912680-00052.

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29

&NA;. "Fluticasone propionate." Reactions Weekly &NA;, no. 1240 (February 2009): 21–22. http://dx.doi.org/10.2165/00128415-200912400-00065.

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30

&NA;. "Fluticasone propionate." Reactions Weekly &NA;, no. 1325 (October 2010): 16–17. http://dx.doi.org/10.2165/00128415-201013250-00054.

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31

Hopkins, S. J. "Fluticasone propionate." Drugs of Today 28, no. 2 (1992): 89. http://dx.doi.org/10.1358/dot.1992.28.2.205216.

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32

&NA;. "Fluticasone propionate." Reactions Weekly &NA;, no. 966 (August 2003): 10. http://dx.doi.org/10.2165/00128415-200309660-00027.

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&NA;. "Fluticasone propionate." Reactions Weekly &NA;, no. 993 (March 2004): 9. http://dx.doi.org/10.2165/00128415-200409930-00023.

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34

&NA;. "Fluticasone propionate." Reactions Weekly &NA;, no. 1308 (July 2010): 18. http://dx.doi.org/10.2165/00128415-201013080-00049.

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35

&NA;. "Fluticasone propionate." Reactions Weekly &NA;, no. 1071 (October 2005): 8. http://dx.doi.org/10.2165/00128415-200510710-00022.

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36

&NA;. "Fluticasone propionate." Reactions Weekly &NA;, no. 1330 (December 2010): 21. http://dx.doi.org/10.2165/00128415-201013300-00068.

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37

&NA;. "Fluticasone propionate." Reactions Weekly &NA;, no. 1331 (December 2010): 16–17. http://dx.doi.org/10.2165/00128415-201013310-00051.

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38

&NA;. "Fluticasone propionate." Reactions Weekly &NA;, no. 1340 (February 2011): 22. http://dx.doi.org/10.2165/00128415-201113400-00073.

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39

&NA;. "Fluticasone propionate." Reactions Weekly &NA;, no. 1340 (February 2011): 22. http://dx.doi.org/10.2165/00128415-201113400-00075.

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40

&NA;. "Fluticasone propionate." Reactions Weekly &NA;, no. 1350 (May 2011): 24. http://dx.doi.org/10.2165/00128415-201113500-00074.

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41

Pieters, Willem R., Koo K. Wilson, Heather C. E. Smith, Johannes J. Tamminga, and Seema Sondhi. "Salmeterol/Fluticasone Propionate versus Fluticasone Propionate Plus Montelukast." Treatments in Respiratory Medicine 4, no. 2 (2005): 129–38. http://dx.doi.org/10.2165/00151829-200504020-00007.

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42

Walter, John H., Geoffrey N. Thompson, James V. Leonard, Clive S. Heatherington, and Kim Bartlett. "Measurement of propionate turnover in vivo using sodium [2H5]propionate and sodium [13C]propionate." Clinica Chimica Acta 182, no. 2 (June 1989): 141–50. http://dx.doi.org/10.1016/0009-8981(89)90073-9.

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43

Thompson, G. N., J. H. Walter, J. L. Bresson, G. C. Ford, S. L. Lyonnet, R. A. Chalmers, J. M. Saudubray, J. V. Leonard, and D. Halliday. "Sources of propionate in inborn errors of propionate metabolism." Metabolism 39, no. 11 (November 1990): 1133–37. http://dx.doi.org/10.1016/0026-0495(90)90084-p.

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44

Morland, Cecilie, Anne-Sofie Frøland, Mi Nguyen Pettersen, Jon Storm-Mathisen, Vidar Gundersen, Frode Rise, and Bjørnar Hassel. "Propionate enters GABAergic neurons, inhibits GABA transaminase, causes GABA accumulation and lethargy in a model of propionic acidemia." Biochemical Journal 475, no. 4 (February 16, 2018): 749–58. http://dx.doi.org/10.1042/bcj20170814.

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Propionic acidemia is the accumulation of propionate in blood due to dysfunction of propionyl-CoA carboxylase. The condition causes lethargy and striatal degeneration with motor impairment in humans. How propionate exerts its toxic effect is unclear. Here, we show that intravenous administration of propionate causes dose-dependent propionate accumulation in the brain and transient lethargy in mice. Propionate, an inhibitor of histone deacetylase, entered GABAergic neurons, as could be seen from increased neuronal histone H4 acetylation in the striatum and neocortex. Propionate caused an increase in GABA (γ-amino butyric acid) levels in the brain, suggesting inhibition of GABA breakdown. In vitro propionate inhibited GABA transaminase with a Ki of ∼1 mmol/l. In isolated nerve endings, propionate caused increased release of GABA to the extracellular fluid. In vivo, propionate reduced cerebral glucose metabolism in both striatum and neocortex. We conclude that propionate-induced inhibition of GABA transaminase causes accumulation of GABA in the brain, leading to increased extracellular GABA concentration, which inhibits neuronal activity and causes lethargy. Propionate-mediated inhibition of neuronal GABA transaminase, an enzyme of the inner mitochondrial membrane, indicates entry of propionate into neuronal mitochondria. However, previous work has shown that neurons are unable to metabolize propionate oxidatively, leading us to conclude that propionyl-CoA synthetase is probably absent from neuronal mitochondria. Propionate-induced inhibition of energy metabolism in GABAergic neurons may render the striatum, in which >90% of the neurons are GABAergic, particularly vulnerable to degeneration in propionic acidemia.

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45

LIU, Q., C. WANG, G. GUO, W. Z. YANG, K. H. DONG, Y. X. HUANG, X. M. YANG, and D. C. HE. "Effects of calcium propionate on rumen fermentation, urinary excretion of purine derivatives and feed digestibility in steers." Journal of Agricultural Science 147, no. 2 (January 23, 2009): 201–9. http://dx.doi.org/10.1017/s0021859609008429.

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SUMMARYThe objective of the current study was to evaluate the effects of calcium propionate supplementation on rumen fermentation, urinary excretion of purine derivatives (PD) and feed digestibility in the total gastrointestinal tract of steers. Eight ruminally cannulated Simmental steers (462±14 kg) were used in a replicated 4×4 Latin square arrangement of treatments with experimental periods of 21 days. The treatments were: control (without calcium propionate), LCaP (calcium propionate – low), MCaP (calcium propionate – medium) and HCaP (calcium propionate – high) with 100, 200 and 300 g calcium propionate per steer per day. Diet consisted of 0·60 maize stover and 0·40 concentrate (dry matter (DM) basis). DM intake (average 9 kg/day) was restricted to a maximum of 0·90 ofad libitumintake. Ruminal pH (range of 6·7–6·5) linearly (P<0·003) and quadratically (P<0·005) decreased, and total volatile fatty acid (VFA) concentration (range of 64·4–67·1 mm) tended (P<0·087) to increase linearly with rising calcium propionate supplementation. Ratio of acetate to propionate fell linearly (P<0·006) and quadratically (P<0·008) from 3·5 to 2·6 as calcium propionate supplementation increased due to the additional propionate supplementation.In situruminal neutral detergent fibre (NDF) degradation of maize stover and crude protein (CP) degradability of concentrate mix were improved with increasing concentration of calcium propionate. Urinary excretion of PD was linearly (P<0·032) and quadratically (P<0·048) increased with greater calcium propionate supplementation (72, 74, 77 and 76 mmol/day for control, LCaP, MCaP and HCaP, respectively). Similarly, digestibilities of organic matter (OM), NDF and CP in the total tract were also linearly and quadratically improved with increasing calcium propionate. The results indicate that the calcium propionate supplementation potentially improves rumen fermentation and feed digestion in beef cattle. It is speculated that calcium propionate stimulates the digestive microorganisms or enzymes in a dose-dependent manner. In the experimental conditions of the current trial, the optimum calcium propionate dose was about 200 g calcium propionate per steer per day.

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46

Tam, N. F. Y., G. L. W. Leung, and Y. S. Wong. "The effects of external carbon loading on nitrogen removal in sequencing batch reactors." Water Science and Technology 30, no. 6 (September 1, 1994): 73–81. http://dx.doi.org/10.2166/wst.1994.0254.

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A bench-scale study was undertaken to examine the effects of easily biodegradable organic carbon substrate on denitrification reaction and overall nitrogen removal from domestic wastewater under a modified sequencing batch reactor (SBR) system. The operation strategy of the SBR consisted of 0.75 h FILL, 8 h REACT separated into 4 h aerobic, 3 h anoxic and 1 h aerobic stages, 1.5 h SETTLE, 1 h DRAW and 0.75 h IDLE. Methanol, sodium acetate and sodium propionate, at the concentrations equivalent to theoretical COD values of 50, 100 and 150 mg O2 1−1 were used as the external carbon sources and added to the reactors prior to the anoxic stage. The study reveals that 4 h aerobic stage was sufficient to nitrify more than 98% NH4+-N and carbon addition caused slightly more nitrification than the control. Addition of sodium propionate at a low concentration (50 mg O2 1−1) significantly enhanced the denitrification process, the nitrate content in this reactor dropped to 3 mg 1−1 (89% reduction) at the end of the anoxic stage. Among the three substrate added at low dose, sodium propionate was the most effective carbon source, followed by acetate and the least effective one was methanol. When the carbon substrate were added at the doses of 100 and 150 mg O2 1−1, the denitrification rates of the acetate reactors recorded at the first hour of the anoxic stage were similar to those of the propionate's and significantly higher than the methanol reactors. When high dose (150 mg O2 1−1) of acetate or propionate was used, 95% reduction in wastewater NOx-N was found after 1 h anoxic stage while 3 h anoxic stage was required when the carbon dose was at 100 mg O2 1−1, indicating that addition of external carbon substrate at large quantity could shorten the denitrification time. However, the final effluent discharged from reactors treated with high dose of acetate and propionate contained more than 20 mg 1−1 BOD5 which might cause a contamination problem. Therefore, addition of sodium acetate or propionate at the concentration equivalent to theoretical COD values of 100 mg O2 1−1 appeared to be the most economical and reliable option.

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47

&NA;. "Fluticasone propionate/mometasone." Reactions Weekly &NA;, no. 1384 (January 2012): 27. http://dx.doi.org/10.2165/00128415-201213840-00107.

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48

&NA;. "Salmeterol/fluticasone propionate." Reactions Weekly &NA;, no. 1392 (March 2012): 40–41. http://dx.doi.org/10.2165/00128415-201213920-00135.

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49

&NA;. "Beclomethasone/fluticasone propionate." Reactions Weekly &NA;, no. 744 (March 1999): 6. http://dx.doi.org/10.2165/00128415-199907440-00013.

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50

&NA;. "Fluticasone propionate abuse." Reactions Weekly &NA;, no. 747 (April 1999): 7. http://dx.doi.org/10.2165/00128415-199907470-00017.

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