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Journal articles on the topic 'Reduction pathway'

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Published: 4 June 2021
Last updated: 8 February 2022

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1

TSERNG, Kou-Yi, Shiow-Jen JIN, and Lin-Su CHEN. "Reduction pathway of cis-5 unsaturated fatty acids in intact rat-liver and rat-heart mitochondria: assessment with stable-isotype-labelled substrates." Biochemical Journal 313, no. 2 (1996): 581–88. http://dx.doi.org/10.1042/bj3130581.

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Besides the conventional isomerase-mediated pathway, unsaturated fatty acids with odd-numbered double bonds are also metabolized by reduction pathways with NADPH as cofactor. The relative contributions of these pathways were measured in intact rat-liver and rat-heart mitochondria with a novel stable isotope tracer technique. A mixture of equal amounts of unlabelled cis-5-enoyl-CoA and 13C4-labelled acyl-CoA of equal chain lengths was incubated with mitochondria. The isotope distribution of 3-hydroxy fatty acids produced from the first cycle of β-oxidation was analysed with selected ion monitoring by gas chromatograph-mass spectrometer. 3-Hydroxy fatty acids produced from the reduction pathway of unsaturated fatty acids were unlabelled (m+0) whereas those produced from saturated fatty acids were labelled (m+4). The m+0 content serves to indicate the extent of reduction pathway. Rotenone treatment was used to switch the pathway completely to reduction. The extent of m+0 enrichment in untreated mitochondria normalized to the m+0 enrichment of rotenone-treated mitochondria was the percentage of reduction pathway. With this technique, cis-4-decenoate was found to be metabolized completely by the reduction pathway in both liver and heart mitochondria. cis-5-Dodecenoate was metabolized essentially by the reduction pathway in liver mitochondria, but only to 75% in heart mitochondria. When the chain length was extended to cis-5-tetradecenoate, the reduction pathway in liver mitochondria decreased to 86% and that in heart mitochondria to 65%. The effects of carnitine, clofibrate and other conditions on the reduction pathway were also studied. Enrichments of the label on saturated fatty acids and 3-hydroxy fatty acids indicated that the major pathway of reduction was not by the direct reduction of the cis-5 double bond. Instead, it is most probably by a pathway that does not involve forming a reduced saturated fatty acid first.
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2

BRADLEY, A. S., W. D. LEAVITT, and D. T. JOHNSTON. "Revisiting the dissimilatory sulfate reduction pathway." Geobiology 9, no. 5 (2011): 446–57. http://dx.doi.org/10.1111/j.1472-4669.2011.00292.x.

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3

Brown, S. B., J. A. Holroyd, D. I. Vernon, Y. K. Shim, and K. M. Smith. "The biosynthesis of the chromophore of phycocyanin. Pathway of reduction of biliverdin to phycocyanobilin." Biochemical Journal 261, no. 1 (1989): 259–63. http://dx.doi.org/10.1042/bj2610259.

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The later stages in the pathway of biosynthesis of phycocyanobilin, the chromophore of phycocyanin, were studied by using radiolabelled intermediates. Three possible pathways from biliverdin IX-alpha to phycocyanobilin were considered. 14C-labelled samples of key intermediates in two of the pathways, 3-vinyl-18-ethyl biliverdin IX-alpha and 3-ethyl-18-vinyl biliverdin IX-alpha, were synthesized chemically and were administered to cultures of Cyanidium caldarium that were actively synthesizing photosynthetic pigments in the light. Neither of these two compounds was apparently incorporated into the phycobiliprotein chromophore, suggesting that two of the three pathways were not operative. By elimination, the results imply that the third possible pathway, which involves phytochromobilin, the chromophore of phytochrome, represents the route for biosynthesis of phycocyanobilin. Unfortunately, since 14C-labelled phytochromobilin is not available, no direct proof of this pathway could be obtained. However, if correct, the present interpretation represents a unified pathway for biosynthesis of all plant bilins, via the intermediacy of phytochromobilin.
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4

Muthukrishnan, A., S. Al-Ismail, G. Bertelli, and P. Browne. "MRONJ risk reduction pathway - 360 degree survey." British Dental Journal 222, no. 5 (2017): 386–90. http://dx.doi.org/10.1038/sj.bdj.2017.225.

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5

Zhu, Hongjie, and Lexin Li. "Biological pathway selection through nonlinear dimension reduction." Biostatistics 12, no. 3 (2011): 429–44. http://dx.doi.org/10.1093/biostatistics/kxq081.

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6

Peattie, Ken, and Sue Peattie. "Social marketing: A pathway to consumption reduction?" Journal of Business Research 62, no. 2 (2009): 260–68. http://dx.doi.org/10.1016/j.jbusres.2008.01.033.

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7

Hickman, Gareth, Su Thrift, and Chénelle Taylor. "Case study illustrations of a psychological treatment pathway in a secure intellectual disability service." Journal of Intellectual Disabilities and Offending Behaviour 9, no. 2 (2018): 102–14. http://dx.doi.org/10.1108/jidob-02-2018-0002.

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PurposeThe purpose of this paper is to describe in detail the treatment pathway utilised in a male medium and low secure intellectual disability (ID) service. Over the preceding five years, service users have followed the outlined treatment pathway. The current paper offers case study material to illustrate the care pathway.Design/methodology/approachThe treatment pathway is described and two case examples are provided, illustrating participation in the pathway. Evaluative data are provided on length of hospitalisation, direction of pathway at discharge and risk reduction as assessed by the HCR-20, SVR-20 and HONOS Secure measures.FindingsThe case examples provided document the assessment and treatment of two male offenders with ID, outlining their treatment pathways, subsequent reductions in assessed risk and their successful community discharge.Originality/valueA comprehensive treatment pathway is outlined together with the theoretical rationale, with illustrative case examples.
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8

Toktarova, Alla, Ida Karlsson, Johan Rootzén, Lisa Göransson, Mikael Odenberger, and Filip Johnsson. "Pathways for Low-Carbon Transition of the Steel Industry—A Swedish Case Study." Energies 13, no. 15 (2020): 3840. http://dx.doi.org/10.3390/en13153840.

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The concept of techno-economic pathways is used to investigate the potential implementation of CO2 abatement measures over time towards zero-emission steelmaking in Sweden. The following mitigation measures are investigated and combined in three pathways: top gas recycling blast furnace (TGRBF); carbon capture and storage (CCS); substitution of pulverized coal injection (PCI) with biomass; hydrogen direct reduction of iron ore (H-DR); and electric arc furnace (EAF), where fossil fuels are replaced with biomass. The results show that CCS in combination with biomass substitution in the blast furnace and a replacement primary steel production plant with EAF with biomass (Pathway 1) yield CO2 emission reductions of 83% in 2045 compared to CO2 emissions with current steel process configurations. Electrification of the primary steel production in terms of H-DR/EAF process (Pathway 2), could result in almost fossil-free steel production, and Sweden could achieve a 10% reduction in total CO2 emissions. Finally, (Pathway 3) we show that increased production of hot briquetted iron pellets (HBI), could lead to decarbonization of the steel industry outside Sweden, assuming that the exported HBI will be converted via EAF and the receiving country has a decarbonized power sector.
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9

Roth, EF Jr, S. Schulman, J. Vanderberg, and J. Olson. "Pathways for the reduction of oxidized glutathione in the Plasmodium falciparum-infected erythrocyte: can parasite enzymes replace host red cell glucose-6-phosphate dehydrogenase?" Blood 67, no. 3 (1986): 827–30. http://dx.doi.org/10.1182/blood.v67.3.827.827.

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Abstract Plasmodium falciparum-infected human red cells possess at least two pathways for the generation of reduced nicotinamide adenine dinucleotide phosphate (NADPH): (1) the glucose-6-phosphate dehydrogenase (G6PD) pathway and (2) the glutamate dehydrogenase (GD) pathway using glutamate as a substrate. Uninfected erythrocytes lack the GD pathway. The NADPH generated can be used to reduce oxidized glutathione (GSSG), which accumulates in the presence of an oxidative stress. In red cell G6PD deficiency, this pathway is reduced or absent, and the host cells as well as the parasites within them are vulnerable to oxidant stress. In view of the presence of the GD pathway in parasitized red cells and the recent description of a parasite-derived G6PD enzyme, we have asked whether the pathways for the reduction of GSSG provided by the parasite can substitute for the host G6PD in red cells deficient in G6PD activity. We have devised a functional assay in which the reduction rate of GSSG is monitored in the presence of buffered infected or control red cell lysates and substrates. Infected G6PD-deficient erythrocytes were obtained from in vitro cultures after a single prior growth cycle of the parasites in G6PD deficient cells to eliminate contaminating normal red cells. The results show that only parasitized red cells can reduce GSSG via the GD pathway. In parasitized G6PD Mediterranean red cells (completely G6PD-deficient), there is a detectable GSSG reduction via the G6PD pathway, not found in uninfected lysates from the same individual. In G6PD A- (African type, featuring partial deficiency), a small increment in the G6PD-dependent reduction of GSSG can also be detected. However, when compared to G6PD normal red cells, the activities from the parasite-derived pathways are small and could not be considered substitutes for normal host enzyme activity. It is concluded that while the plasmodium provides additional pathways for the generation of NADPH that may serve its own metabolic needs, the host red cells and hence the parasite itself remain vulnerable to oxidant stress.
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10

Roth, EF Jr, S. Schulman, J. Vanderberg, and J. Olson. "Pathways for the reduction of oxidized glutathione in the Plasmodium falciparum-infected erythrocyte: can parasite enzymes replace host red cell glucose-6-phosphate dehydrogenase?" Blood 67, no. 3 (1986): 827–30. http://dx.doi.org/10.1182/blood.v67.3.827.bloodjournal673827.

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Plasmodium falciparum-infected human red cells possess at least two pathways for the generation of reduced nicotinamide adenine dinucleotide phosphate (NADPH): (1) the glucose-6-phosphate dehydrogenase (G6PD) pathway and (2) the glutamate dehydrogenase (GD) pathway using glutamate as a substrate. Uninfected erythrocytes lack the GD pathway. The NADPH generated can be used to reduce oxidized glutathione (GSSG), which accumulates in the presence of an oxidative stress. In red cell G6PD deficiency, this pathway is reduced or absent, and the host cells as well as the parasites within them are vulnerable to oxidant stress. In view of the presence of the GD pathway in parasitized red cells and the recent description of a parasite-derived G6PD enzyme, we have asked whether the pathways for the reduction of GSSG provided by the parasite can substitute for the host G6PD in red cells deficient in G6PD activity. We have devised a functional assay in which the reduction rate of GSSG is monitored in the presence of buffered infected or control red cell lysates and substrates. Infected G6PD-deficient erythrocytes were obtained from in vitro cultures after a single prior growth cycle of the parasites in G6PD deficient cells to eliminate contaminating normal red cells. The results show that only parasitized red cells can reduce GSSG via the GD pathway. In parasitized G6PD Mediterranean red cells (completely G6PD-deficient), there is a detectable GSSG reduction via the G6PD pathway, not found in uninfected lysates from the same individual. In G6PD A- (African type, featuring partial deficiency), a small increment in the G6PD-dependent reduction of GSSG can also be detected. However, when compared to G6PD normal red cells, the activities from the parasite-derived pathways are small and could not be considered substitutes for normal host enzyme activity. It is concluded that while the plasmodium provides additional pathways for the generation of NADPH that may serve its own metabolic needs, the host red cells and hence the parasite itself remain vulnerable to oxidant stress.
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11

Gamboa, Antonio, Baptiste Farbos, Philippe Aurel, Gérard L. Vignoles, and Jean-Marc Leyssale. "Mechanism of strength reduction along the graphenization pathway." Science Advances 1, no. 10 (2015): e1501009. http://dx.doi.org/10.1126/sciadv.1501009.

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Even though polycrystalline graphene has shown a surprisingly high tensile strength, the influence of inherent grain boundaries on such property remains unclear. We study the fracture properties of a series of polycrystalline graphene models of increasing thermodynamic stability, as obtained from a long molecular dynamics simulation at an elevated temperature. All of the models show the typical and well-documented brittle fracture behavior of polycrystalline graphene; however, a clear decrease in all fracture properties is observed with increasing annealing time. The remarkably high fracture properties obtained for the most disordered (less annealed) structures arise from the formation of many nonpropagating prefracture cracks, significantly retarding failure. The stability of these reversible cracks is due to the nonlocal character of load transfer after a bond rupture in very disordered systems. It results in an insufficient strain level on neighboring bonds to promote fracture propagation. Although polycrystallinity seems to be an unavoidable feature of chemically synthesized graphenes, these results suggest that targeting highly disordered states might be a convenient way to obtain improved mechanical properties.
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12

Kattel, Shyam, and Guofeng Wang. "Reaction Pathway for Oxygen Reduction on FeN4Embedded Graphene." Journal of Physical Chemistry Letters 5, no. 3 (2014): 452–56. http://dx.doi.org/10.1021/jz402717r.

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13

Zhang, Qiurong, Xiaolei Liu, Hongyan Meng, Sijin Liu, and Chengdong Zhang. "Reduction pathway-dependent cytotoxicity of reduced graphene oxide." Environmental Science: Nano 5, no. 6 (2018): 1361–71. http://dx.doi.org/10.1039/c8en00242h.

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14

Roy, Anindita, Biplab Debnath, Ramkrishna Sahoo, Teresa Aditya, and Tarasankar Pal. "Micelle confined mechanistic pathway for 4-nitrophenol reduction." Journal of Colloid and Interface Science 493 (May 2017): 288–94. http://dx.doi.org/10.1016/j.jcis.2017.01.045.

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15

Okabe, Toru H., and Donald R. Sadoway. "Metallothermic reduction as an electronically mediated reaction." Journal of Materials Research 13, no. 12 (1998): 3372–77. http://dx.doi.org/10.1557/jmr.1998.0459.

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The commonly held view that metallothermic reduction is strictly a chemical reaction and that the process is rate limited by mass transfer has been found to be incomplete. In a study of the production of tantalum powder by the reaction of K2TaF7 with sodium, it has been shown that there are two dominant kinetic pathways, both involving electron transfer. Furthermore, the overall rate of reaction is limited by electron transport between the reactants. This indicates that metallothermic reduction is an “electronically mediated reaction” (EMR). Experiments found that the location of the tantalum deposit and its morphology are governed by the reaction pathway.
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16

Zhou, Li, Xiliang Zhang, Tianyu Qi, Jiankun He, and Xiaohu Luo. "Regional disaggregation of China's national carbon intensity reduction target by reduction pathway analysis." Energy for Sustainable Development 23 (December 2014): 25–31. http://dx.doi.org/10.1016/j.esd.2014.07.003.

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17

Manulis, Shulamit, Anat Haviv-Chesner, Maria T. Brandl, Steve E. Lindow, and Isaac Barash. "Differential Involvement of Indole-3-Acetic Acid Biosynthetic Pathways in Pathogenicity and Epiphytic Fitness of Erwinia herbicola pv. gypsophilae." Molecular Plant-Microbe Interactions® 11, no. 7 (1998): 634–42. http://dx.doi.org/10.1094/mpmi.1998.11.7.634.

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Erwinia herbicola pv. gypsophilae (Ehg), which induces galls on Gypsophila paniculata, harbors two major pathways for indole-3-acetic acid (IAA) synthesis, the indole-3-acetamide (IAM) and indole-3-pyruvate (IPyA) routes, as well as cytokinin biosynthetic genes. Mutants were generated in which the various biosynthetic routes were disrupted separately or jointly in order to assess the contribution of IAA of various origins and cytokinins to pathogenicity and epiphytic fitness. Inactivation of the IAM pathway or cytokinin biosynthesis caused the largest reduction in gall size. Inactivation of the IPyA pathway caused a minor, nonsignificant decrease in pathogenicity. No further reduction in gall size was observed by the simultaneous inactivation of both IAA pathways only or in combination with that of cytokinin production. However, inactivation of the IPyA pathway caused a 14-fold reduction in the population of Ehg on bean plants. Inactivation of the IAM pathway or cytokinin production did not affect epiphytic fitness. While the apparent transcriptional activity of iaaM-inaZ fusion increased slightly in cells of Ehg on bean and gypsophila leaves, compared with that in culture, very high levels of induction were observed in cells injected into gypsophila stems. In contrast, moderate levels of induction of ipdC-inaZ in Ehg were observed on leaves of these plants and in gypsophila stems, when compared with that in culture. These results suggest that the IAM pathway is involved primarily in gall formation and support the main contribution of the IpyA pathway to the epiphytic fitness of this bacterial species.
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18

MURATA, Kenji, Hiroyuki OGURA, Takashi OGAWA, Yasoshi ITO, and Tamotsu SHIROGAMI. "Oxygen Reduction on Meniscus Electrode in Molten Carbonates VI. Temperature Dependency of Reduction Pathway." Denki Kagaku oyobi Kogyo Butsuri Kagaku 65, no. 5 (1997): 379–83. http://dx.doi.org/10.5796/kogyobutsurikagaku.65.379.

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19

Sarkar, Anjana, Eduardo Gracia-Espino, Thomas Wågberg, et al. "Photocatalytic reduction of CO2 with H2O over modified TiO2 nanofibers: Understanding the reduction pathway." Nano Research 9, no. 7 (2016): 1956–68. http://dx.doi.org/10.1007/s12274-016-1087-9.

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20

Chechik, Gal, Michael J. Anderson, Omer Bar-Yosef, Eric D. Young, Naftali Tishby, and Israel Nelken. "Reduction of Information Redundancy in the Ascending Auditory Pathway." Neuron 51, no. 3 (2006): 359–68. http://dx.doi.org/10.1016/j.neuron.2006.06.030.

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21

Massy, Z. A., W. F. Keane, and B. L. Kasiske. "Inhibition of the mevalonate pathway: benefits beyond cholesterol reduction?" Lancet 347, no. 8994 (1996): 102–3. http://dx.doi.org/10.1016/s0140-6736(96)90217-2.

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22

Yu, Yu-Han, and Pei C. Chiu. "Kinetics and Pathway of Vinyl Fluoride Reduction over Rhodium." Environmental Science & Technology Letters 1, no. 11 (2014): 448–52. http://dx.doi.org/10.1021/ez500291g.

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23

Lipshutz, Bruce, Ching-Tien Lee, and Benjamin Taft. "A Conjugate Reduction Pathway to Chiral Silanes Using CuH." Synthesis 2007, no. 20 (2007): 3257–60. http://dx.doi.org/10.1055/s-2007-983830.

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24

Nomura, Kota, Tadashi Mizoguchi, and Hitoshi Tamiaki. "Regioselective Reduction Pathway of Geranylgeranyl Moiety in Chlorophyll Biosynthesis." Biophysical Journal 106, no. 2 (2014): 182a—183a. http://dx.doi.org/10.1016/j.bpj.2013.11.1032.

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25

Idaka, Eiichi, Toshihiko Ogawa, and Hiroyuki Horitsu. "Oxidative pathway after reduction of p-aminoazobenzene byPseudomonas cepacia." Bulletin of Environmental Contamination and Toxicology 39, no. 1 (1987): 108–13. http://dx.doi.org/10.1007/bf01691797.

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26

Muthukrishnan, Azhagumuthu, Yuta Nabae, and Takeo Ohsaka. "Role of iron in the reduction of H2O2 intermediate during the oxygen reduction reaction on iron-containing polyimide-based electrocatalysts." RSC Advances 6, no. 5 (2016): 3774–77. http://dx.doi.org/10.1039/c5ra23162k.

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The role of Fe in Fe–N–C catalysts is to catalyze the reduction of the H<sub>2</sub>O<sub>2</sub> intermediate of the peroxide pathway of the oxygen reduction reaction (ORR). The results demonstrate that the ORR of Fe–N–C catalysts follows the two-site peroxide pathway.
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27

Ha, Sook S., Inyoung Kim, Yue Wang, and Jianhua Xuan. "Applications of Different Weighting Schemes to Improve Pathway-Based Analysis." Comparative and Functional Genomics 2011 (2011): 1–15. http://dx.doi.org/10.1155/2011/463645.

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Conventionally, pathway-based analysis assumes that genes in a pathway equally contribute to a biological function, thus assigning uniform weight to genes. However, this assumption has been proved incorrect, and applying uniform weight in the pathway analysis may not be an appropriate approach for the tasks like molecular classification of diseases, as genes in a functional group may have different predicting power. Hence, we propose to use different weights to genes in pathway-based analysis and devise four weighting schemes. We applied them in two existing pathway analysis methods using both real and simulated gene expression data for pathways. Among all schemes, random weighting scheme, which generates random weights and selects optimal weights minimizing an objective function, performs best in terms ofPvalue or error rate reduction. Weighting changes pathway scoring and brings up some new significant pathways, leading to the detection of disease-related genes that are missed under uniform weight.
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Wallin, R., S. D. Patrick, and L. F. Martin. "Vitamin K1 reduction in human liver. Location of the coumarin-drug-insensitive enzyme." Biochemical Journal 260, no. 3 (1989): 879–84. http://dx.doi.org/10.1042/bj2600879.

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The antidotal effect of vitamin K in overcoming poisoning by coumarin anticoagulant drugs is mediated by a vitamin K-reducing enzyme of the endoplasmic reticulum [Wallin &amp; Martin (1987) Biochem. J. 241, 389-396]. With microsomes obtained from human liver biopsies, we have investigated the localization and the transverse orientation of this enzyme in the endoplasmic reticulum and compared its orientation to that of the other enzymes of the vitamin K-dependent carboxylation system. All enzymes were protected by the microsomal membrane and thus appear to have a luminal orientation in the endoplasmic reticulum, consistent with their role in the vitamin K-dependent modification of secretory glycoproteins. Separation of rough and smooth microsomes showed that vitamin K-dependent carboxylase activity was 6-fold higher in rough than in smooth microsomes. Vitamin K1 reduction by the coumarin-drug-sensitive (pathway I) and -insensitive (pathway II) enzymes of the vitamin K-dependent carboxylation system was the same in rough and smooth microsomes. The data suggest a close association between the pathway I and II enzymes in the endoplasmic reticulum. These pathways may be partial reactions of multienzyme complex which carries out the various activities associated with the vitamin K-dependent carboxylation system.
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Tserng, K. Y., and S. J. Jin. "Oxidation of cis-5-unsaturated fatty acids in intact rat liver mitochondria: the operation of reduction pathways." Biochemical Journal 308, no. 1 (1995): 39–44. http://dx.doi.org/10.1042/bj3080039.

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The metabolism of cis-5 unsaturated fatty acids was studied in intact rat liver mitochondria to assess the operation of a reduction pathway. By using direct quantification of metabolites with a capillary-column gas chromatography, 3-hydroxydodecanoate was identified among other metabolites when cis-5-dodecenoate was metabolized in intact rat liver mitochondria. The formation of 3-hydroxydodecanoate supports the existence of a reduction pathway in the metabolism of cis-5-unsaturated fatty acids. This metabolite cannot be produced from the conventional isomerase-mediated pathway. However, the data also indicated the possible operation of the conventional isomerase-mediated pathway in intact rat liver mitochondria. The reduction pathway appears to account for at least 61% of the pathway for cis-5-dodecenoate. This reduction pathway was likely to proceed from the dehydrogenation to trans-2,cis-5-dodecadienoyl-CoA, which was isomerized to delta 3, delta 5-dodecadienoyl-CoA, then to trans-2,trans-4-dodecadienoate. The reduction was mediated by 2,4-dienoyl-CoA reductase by the conversion of trans-2,trans-4-dodecadienoyl-CoA into trans-3-dodecenoyl-CoA. However, direct reduction of the cis-5 double bond was also shown to be operating, although to a lesser extent.
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Uko, Nne E., Osman F. Güner, Diane F. Matesic, and J. Phillip Bowen. "Akt Pathway Inhibitors." Current Topics in Medicinal Chemistry 20, no. 10 (2020): 883–900. http://dx.doi.org/10.2174/1568026620666200224101808.

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Cancer is a devastating disease that has plagued humans from ancient times to this day. After decades of slow research progress, promising drug development, and the identification of new targets, the war on cancer was launched, in 1972. The P13K/Akt pathway is a growth-regulating cellular signaling pathway, which in many human cancers is over-activated. Studies have demonstrated that a decrease in Akt activity by Akt inhibitors is associated with a reduction in tumor cell proliferation. There have been several promising drug candidates that have been studied, including but not limited to ipatasertib (RG7440), 1; afuresertib (GSK2110183), 2; uprosertib (GSK2141795), 3; capivasertib (AZD5363), 4; which reportedly bind to the ATP active site and inhibit Akt activity, thus exerting cytotoxic and antiproliferative activities against human cancer cells. For most of the compounds discussed in this review, data from preclinical studies in various cancers suggest a mechanistic basis involving hyperactivated Akt signaling. Allosteric inhibitors are also known to alter the activity of kinases. Perifosine (KRX- 0401), 5, an alkylphospholipid, is known as the first allosteric Akt inhibitor to enter clinical development and is mechanistically characterized as a PH-domain dependent inhibitor, non-competitive with ATP. This results in a reduction in Akt enzymatic and cellular activities. Other small molecule (MK- 2206, 6, PHT-427, Akti-1/2) inhibitors with a similar mechanism of action, alter Akt activity through the suppression of cell growth mediated by the inhibition of Akt membrane localization and subsequent activation. The natural product solenopsin has been identified as an inhibitor of Akt. A few promising solenopsin derivatives have emerged through pharmacophore modeling, energy-based calculations, and property predictions.
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Rogina, Blanka, Kavitha Kannan, Dushyant Mishra, et al. "The Effects of INDY on Fly Metabolism." Innovation in Aging 4, Supplement_1 (2020): 737. http://dx.doi.org/10.1093/geroni/igaa057.2622.

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Abstract The Indy (I’m not dead yet) gene encodes a plasma membrane citrate transporter in Drosophila. INDY reduction affects metabolism and extends longevity of flies and worms. In flies, INDY is predominantly expressed in the midgut, fat body and oenocytes, tissues with a key role in metabolism. We hypothesize that INDY reduction in the midgut regulates citrate levels leading to metabolic changes that preserve intestinal stem cell (ISC) homeostasis and slows aging by modifying Insulin/Insulin-like signaling (IIS), which is a key nutrient sensing pathway. Our second goal was to examine the role of JAK/STAT signaling pathway, which activates epithelial renewal in the gut, in response to aging-related stressors. We hypothesize that Indy reduction has effects on the microbiome, preventing bacterial overgrowth and altering community diversity, leading to extended longevity in a JAK/STAT-mediated fashion. Our data suggest that effects of Indy reduction is mediated by reduced IIS and JAK/STAT pathways
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32

Lin, Shih-Chieh Aaron, Yi-Hung Liu, Shie-Ming Peng, and Shiuh-Tzung Liu. "Diruthenium complex catalyzed reduction of nitroarenes-investigation of reaction pathway." Molecular Catalysis 466 (April 2019): 46–51. http://dx.doi.org/10.1016/j.mcat.2019.01.005.

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33

Oh, Seok-Young, Daniel K. Cha, Byung J. Kim, and Pei C. Chiu. "Reduction of Nitroglycerin with Elemental Iron: Pathway, Kinetics, and Mechanisms." Environmental Science & Technology 38, no. 13 (2004): 3723–30. http://dx.doi.org/10.1021/es0354667.

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34

Suzuki, Yoshinori, Yoshihiro Kitatsuji, Toshihiko Ohnuki, and Seiya Tsujimura. "Flavin mononucleotide mediated electron pathway for microbial U(vi) reduction." Physical Chemistry Chemical Physics 12, no. 34 (2010): 10081. http://dx.doi.org/10.1039/c0cp00339e.

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35

Yao, Yao, Hui Li, Haijiang Wang, and Minhua Shao. "(Invited) Nitrogen Electrochemical Reduction Reaction Pathway on Noble Metallic Surfaces." ECS Meeting Abstracts MA2020-01, no. 41 (2020): 1812. http://dx.doi.org/10.1149/ma2020-01411812mtgabs.

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Woods, Stephen C. "The Endocannabinoid System: Novel Pathway for Cardiometabolic Risk-Factor Reduction." Journal of the American Academy of Physician Assistants 20, no. 11 (2007): 7–10. http://dx.doi.org/10.1097/01720610-200711000-00005.

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Woods, Stephen C. "The Endocannabinoid System: Novel Pathway for Cardiometabolic Risk-Factor Reduction." Journal of the American Academy of Physician Assistants 20, no. 11 (2007): 7–10. http://dx.doi.org/10.1097/01720610-200711010-00004.

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Zheng, Huzhi, Qinlong Wang, Yijuan Long, Haijie Zhang, Xiaoxiao Huang, and Rui Zhu. "Enhancing the luminescence of carbon dots with a reduction pathway." Chemical Communications 47, no. 38 (2011): 10650. http://dx.doi.org/10.1039/c1cc14741b.

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Karamad, Mohammadreza, Heine A. Hansen, Jan Rossmeisl, and Jens K. Nørskov. "Mechanistic Pathway in the Electrochemical Reduction of CO2 on RuO2." ACS Catalysis 5, no. 7 (2015): 4075–81. http://dx.doi.org/10.1021/cs501542n.

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Scott, Jennifer, Sandro Gambarotta, Ilia Korobkov, and Peter H. M. Budzelaar. "Reduction of (Diiminopyridine)iron: Evidence for a Noncationic Polymerization Pathway?" Organometallics 24, no. 26 (2005): 6298–300. http://dx.doi.org/10.1021/om0507833.

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Kong, Liangliang, and Neil M. Price. "A reduction‐dependent copper uptake pathway in an oceanic diatom." Limnology and Oceanography 65, no. 3 (2019): 601–11. http://dx.doi.org/10.1002/lno.11329.

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Modesto, Jennifer L., Anna Hull, Andrea Y. Angstadt, et al. "NNK reduction pathway gene polymorphisms and risk of lung cancer." Molecular Carcinogenesis 54, S1 (2014): E94—E102. http://dx.doi.org/10.1002/mc.22187.

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Barraza, Román A., Jay W. McLaren, and Eric M. Poeschla. "Prostaglandin Pathway Gene Therapy for Sustained Reduction of Intraocular Pressure." Molecular Therapy 18, no. 3 (2010): 491–501. http://dx.doi.org/10.1038/mt.2009.278.

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Knapp, Kurtis G., and James R. Swartz. "Evidence for an additional disulfide reduction pathway in Escherichia coli." Journal of Bioscience and Bioengineering 103, no. 4 (2007): 373–76. http://dx.doi.org/10.1263/jbb.103.373.

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Greenland, Philip, Scott Grundy, Richard C. Pasternak, and Claude Lenfant. "Problems on the Pathway From Risk Assessment to Risk Reduction." Circulation 97, no. 18 (1998): 1761–62. http://dx.doi.org/10.1161/01.cir.97.18.1761.

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Ito, Yasushi, Shinji Sato, Takamasa Ohashi, Shinsuke Nakayama, Kaoru Shimokata, and Hiroaki Kume. "Reduction of airway anion secretion via CFTR in sphingomyelin pathway." Biochemical and Biophysical Research Communications 324, no. 2 (2004): 901–8. http://dx.doi.org/10.1016/j.bbrc.2004.09.134.

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Hornafius, Katherine Y., and J. Scott Hornafius. "Carbon negative oil: A pathway for CO2 emission reduction goals." International Journal of Greenhouse Gas Control 37 (June 2015): 492–503. http://dx.doi.org/10.1016/j.ijggc.2015.04.007.

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Welander, Paula V., and William W. Metcalf. "Mutagenesis of the C1 Oxidation Pathway in Methanosarcina barkeri: New Insights into the Mtr/Mer Bypass Pathway." Journal of Bacteriology 190, no. 6 (2008): 1928–36. http://dx.doi.org/10.1128/jb.01424-07.

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ABSTRACT A series of Methanosarcina barkeri mutants lacking the genes encoding the enzymes involved in the C1 oxidation/reduction pathway were constructed. Mutants lacking the methyl-tetrahydromethanopterin (H4MPT):coenzyme M (CoM) methyltransferase-encoding operon (Δmtr), the methylene-H4MPT reductase-encoding gene (Δmer), the methylene-H4MPT dehydrogenase-encoding gene (Δmtd), and the formyl-methanofuran:H4MPT formyl-transferase-encoding gene (Δftr) all failed to grow using either methanol or H2/CO2 as a growth substrate, indicating that there is an absolute requirement for the C1 oxidation/reduction pathway for hydrogenotrophic and methylotrophic methanogenesis. The mutants also failed to grow on acetate, and we suggest that this was due to an inability to generate the reducing equivalents needed for biosynthetic reactions. Despite their lack of growth on methanol, the Δmtr and Δmer mutants were capable of producing methane from this substrate, whereas the Δmtd and Δftr mutants were not. Thus, there is an Mtr/Mer bypass pathway that allows oxidation of methanol to the level of methylene-H4MPT in M. barkeri. The data further suggested that formaldehyde may be an intermediate in this bypass; however, no methanol dehydrogenase activity was found in Δmtr cell extracts, nor was there an obligate role for the formaldehyde-activating enzyme (Fae), which has been shown to catalyze the condensation of formaldehyde and H4MPT in vitro. Both the Δmer and Δmtr mutants were able to grow on a combination of methanol plus acetate, but they did so by metabolic pathways that are clearly distinct from each other and from previously characterized methanogenic pathways.
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Uzark, K., C. Frederick, JJ Lamberti, et al. "Changing practice patterns for children with heart disease: a clinical pathway approach." American Journal of Critical Care 7, no. 2 (1998): 101–5. http://dx.doi.org/10.4037/ajcc1998.7.2.101.

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BACKGROUND: Pediatric cardiac care is costly and requires extensive resources. We studied the effect of clinical pathways on practice patterns and patient care outcomes in infants and children hospitalized for cardiac surgery. METHODS: In consecutive patients admitted for selected cardiac surgical procedures before (n = 69) and after (n = 173) implementation of clinical pathways, outcomes including hospital length of stay, days in the ICU, time to extubation, ordering of blood studies, costs, and readmissions were compared. Data were analyzed for each of five cardiac surgical procedures: repair of an atrial septal defect, repair of a ventricular septal defect, division of a patent ductus arteriosus, repair of tetralogy of Fallot, and neonatal arterial switch operation to correct transposition of the great arteries. RESULTS: A significant reduction in length of hospital stay, including days in the ICU (decreased 1 to 2 days per admission), was achieved after the clinical pathway was implemented. Reductions in average duration of mechanical ventilation ranged from 28% for repair of a ventricular septal defect to 63% for repair of tetralogy of Fallot. The number of blood studies ordered decreased 20% to 30%. A significant reduction in hospital costs for each procedure, ranging from 16% to 29%, was also achieved with no adverse effects on patients' outcomes. CONCLUSIONS: Use of clinical pathways with children hospitalized for cardiac surgery can shorten length of stay in the hospital, reduce use of resources, and improve cost-effectiveness with beneficial outcomes for patients.
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Manski, Thomas J., Charles S. Ha worth, Bertrand J. Duval-Arnould, and Elisabeth J. Rushing. "Optic pathway glioma infiltrating into somatostatinergic pathways in a young boy with gigantism." Journal of Neurosurgery 81, no. 4 (1994): 595–600. http://dx.doi.org/10.3171/jns.1994.81.4.0595.

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✓ The authors report gigantism in a 16-month-old boy with an extensive optic pathway glioma infiltrating into somatostatinergic pathways, as revealed by magnetic resonance imaging and immunocytochemical studies. Stereotactic biopsies of areas showing hyperintense signal abnormalities on T2-weighted images in and adjacent to the involved visual pathways provided rarely obtained histological correlation of such areas. The patient received chemotherapy, which resulted in reduction of size and signal intensity of the tumor and stabilization of vision and growth velocity.
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