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[PMID]: 29204974
[Au] Autor:Beslon V; Moreau P; Maruani A; Maisonneuve H; Giraudeau B; Fournier JP
[Ad] Address:Département de médecine générale, Université de Nantes, 1, rue Gaston Veil, 44035, Nantes, France.
[Ti] Title:Effects of Discontinuation of Urate-Lowering Therapy: A Systematic Review.
[So] Source:J Gen Intern Med;33(3):358-366, 2018 Mar.
[Is] ISSN:1525-1497
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND: Urate-lowering therapy (ULT) is associated with low rates of adherence, leading to a potential risk of relapse of gouty arthritis, tophi, or urolithiasis. Our main aim was to identify the recurrence of gouty arthritis, tophi, or urolithiasis after discontinuation of ULT. Secondary aims included an assessment of ULT reintroduction rates and factors associated with relapse. METHODS: We conducted a systematic literature review of clinical studies investigating the effect of discontinuing any ULT (allopurinol, febuxostat, probenecid, sulfinpyrazone, benzbromarone) in adults on long-term therapy. We searched The Cochrane Central Register of Controlled Trials, MEDLINE, EMBASE, Science Citation Index, and ClinicalTrials.gov from inception to March 2016. Conference abstracts of the ACR/ARHP and EULAR annual conferences were hand-searched. Study quality was assessed using the first eight items of the methodological index for non-randomized studies (MINORS) tool. The review protocol is registered with PROSPERO (CRD42016042048). RESULTS: A total of 4640 articles were identified, eight of which were ultimately included. Most of these studies predated 2000. MINORS scores ranged from 5 to 10 out of a possible 16. Mean follow-up duration after discontinuation ranged from 12 to 96 months. Five studies focused on discontinuation of ULT in gouty arthritis and tophi, two in urolithiasis, and one in asymptomatic hyperuricemia. Relapse rates were high in gout (36-81%) and lower in urolithiasis (15%). Relapses occurred 1-4.5 years after ULT discontinuation. In one study, a low serum urate level before and after ULT discontinuation was associated with lower gout recurrence. DISCUSSION: Relapse of gout is common although delayed after discontinuation of ULT. Short-term prognosis after ULT discontinuation appears favorable if the serum urate level was low before ULT discontinuation. The results of this review are limited by the paucity of existing studies and their low quality. Further comparative studies should consider larger primary care populations and discontinuation of febuxostat.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:In-Data-Review
[do] DOI:10.1007/s11606-017-4233-5

  2 / 1171 MEDLINE  
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[PMID]: 29164598
[Au] Autor:Domith I; Socodato R; Portugal CC; Munis AF; Duarte-Silva AT; Paes-de-Carvalho R
[Ad] Address:Program of Neurosciences, Fluminense Federal University.
[Ti] Title:Vitamin C modulates glutamate transport and NMDA receptor function in the retina.
[So] Source:J Neurochem;, 2017 Nov 21.
[Is] ISSN:1471-4159
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Vitamin C (in the reduced form ascorbate or in the oxidized form dehydroascorbate) is implicated in signaling events throughout the central nervous system (CNS). In the retina, a high-affinity transport system for ascorbate has been described and glutamatergic signaling has been reported to control ascorbate release. Here we investigated the modulatory role played by vitamin C upon glutamate uptake and N-methyl-D-aspartate (NMDA) receptor activation in cultured retinal cells or in intact retinal tissue using biochemical and imaging techniques. We show that both forms of vitamin C, ascorbate or dehydroascorbate, promote an accumulation of extracellular glutamate by a mechanism involving the inhibition of glutamate uptake. This inhibition correlates with the finding that ascorbate promotes a decrease in cell surface levels of the neuronal glutamate transporter excitatory amino acid transporter 3 (EAAT3) in retinal neuronal cultures. Interestingly, vitamin C is prone to increase the activity of NMDA receptors but also promotes a decrease of glutamate-stimulated ( H) MK801 binding and decreases cell membrane content of NMDA receptor glutamate ionotropic receptor subunit 1 (GluN1) subunits. Both compounds were also able to increase cAMP response element-binding protein (CREB) phosphorylation in neuronal nuclei in a glutamate receptor and calcium/calmodulin kinase-dependent manner. Moreover, the effect of ascorbate is not blocked by sulfinpyrazone and then does not depend on its uptake by retinal cells. Overall, these data indicate a novel molecular and functional target for vitamin C impacting on glutamate signaling in retinal neurons. This article is protected by copyright. All rights reserved.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1711
[Cu] Class update date: 171122
[Lr] Last revision date:171122
[St] Status:Publisher
[do] DOI:10.1111/jnc.14260

  3 / 1171 MEDLINE  
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[PMID]: 28386072
[Au] Autor:Tan PK; Liu S; Gunic E; Miner JN
[Ad] Address:Department of Biology, Ardea Biosciences, Inc. (A member of the AstraZeneca Group), San Diego, CA, USA. ptphiltan@gmail.com.
[Ti] Title:Discovery and characterization of verinurad, a potent and specific inhibitor of URAT1 for the treatment of hyperuricemia and gout.
[So] Source:Sci Rep;7(1):665, 2017 Apr 06.
[Is] ISSN:2045-2322
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Gout is caused by elevated serum urate levels, which can be treated using inhibitors of the uric acid transporter, URAT1. Here, we characterize verinurad (RDEA3170), which is currently under evaluation for gout therapy. Verinurad specifically inhibits URAT1 with a potency of 25 nM. High affinity inhibition of uric acid transport requires URAT1 residues Cys-32, Ser-35, Phe-365 and Ile-481. Unlike other available uricosuric agents, the requirement for Cys-32 is unique to verinurad. Two of these residues, Ser-35 and Phe-365, are also important for urate transport kinetics. A URAT1 binding assay using radiolabeled verinurad revealed that distinct URAT1 inhibitors benzbromarone, sulfinpyrazone and probenecid all inhibit verinurad binding via a competitive mechanism. However, mutations made within the predicted transporter substrate channel differentially altered the potency for individual URAT1 inhibitors. Overall, our results suggest that URAT1 inhibitors bind to a common site in the core of the transporter and sterically hinder the transit of uric acid through the substrate channel, albeit with vastly different potencies and with differential interactions with specific URAT1 amino acids.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1704
[Cu] Class update date: 170516
[Lr] Last revision date:170516
[St] Status:In-Data-Review
[do] DOI:10.1038/s41598-017-00706-7

  4 / 1171 MEDLINE  
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[PMID]: 28040245
[Au] Autor:Rai SK; Aviña-Zubieta JA; McCormick N; De Vera MA; Shojania K; Sayre EC; Choi HK
[Ad] Address:Arthritis Research Canada, Vancouver, British Columbia, Canada; Department of Experimental Medicine, University of British Columbia, Vancouver, British Columbia, Canada.
[Ti] Title:The rising prevalence and incidence of gout in British Columbia, Canada: Population-based trends from 2000 to 2012.
[So] Source:Semin Arthritis Rheum;46(4):451-456, 2017 Feb.
[Is] ISSN:1532-866X
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:OBJECTIVES: Gout is increasingly recognized as the most common form of inflammatory arthritis worldwide; however, no Canadian data on the disease burden of gout are available. We estimated the prevalence, incidence, prescription patterns, and comorbidity burden of gout in an entire Canadian province [British Columbia (BC)] over the last decade. METHODS: We utilized PopulationData BC, a province-wide database, to estimate temporal trends in the prevalence and incidence of gout from 2000 to 2012, as well as according to age category. Annual estimates were age-sex-standardized using 2012 as the reference. We also examined annual trends in prescription patterns of common gout medications and assessed the comorbidity burden among gout patients in 2012. RESULTS: The 2012 prevalence of gout was 3.8% among the overall population, and the incidence rate was 2.9 per 1000 person-years. Both gout prevalence and incidence increased substantially over the study period. This burden additionally increased according to age category, affecting over 8% of those ages 60-69 years in 2012. Approximately 22% of gout patients received a prescription for urate-lowering therapy (ULT), which remained stable over the study period, while colchicine and oral glucocorticoid use both increased modestly. By 2012, 72%, 52%, and 18% of prevalent gout patients had been diagnosed with hypertension, hyperlipidemia, and diabetes, respectively. CONCLUSIONS: The burden of gout in BC, Canada, is substantial, and both the prevalence and incidence have increased over the past decade, while prescription of ULT remains low. These data support the need to improve gout prevention and care.
[Mh] MeSH terms primary: Gout/epidemiology
[Mh] MeSH terms secundary: Aged
Allopurinol/therapeutic use
Anti-Inflammatory Agents, Non-Steroidal/therapeutic use
British Columbia/epidemiology
Colchicine/therapeutic use
Comorbidity
Diabetes Mellitus/epidemiology
Febuxostat/therapeutic use
Female
Glucocorticoids/therapeutic use
Gout/drug therapy
Gout Suppressants/therapeutic use
Humans
Hyperlipidemias/epidemiology
Hypertension/epidemiology
Incidence
Male
Middle Aged
Population Growth
Prevalence
Probenecid/therapeutic use
Sulfinpyrazone/therapeutic use
Uricosuric Agents/therapeutic use
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Anti-Inflammatory Agents, Non-Steroidal); 0 (Glucocorticoids); 0 (Gout Suppressants); 0 (Uricosuric Agents); 101V0R1N2E (Febuxostat); 63CZ7GJN5I (Allopurinol); PO572Z7917 (Probenecid); SML2Y3J35T (Colchicine); V6OFU47K3W (Sulfinpyrazone)
[Em] Entry month:1711
[Cu] Class update date: 171107
[Lr] Last revision date:171107
[Js] Journal subset:IM
[Da] Date of entry for processing:170102
[St] Status:MEDLINE

  5 / 1171 MEDLINE  
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[PMID]: 27786405
[Au] Autor:Li X; Zhu B; Gao X; Liang P
[Ad] Address:Department of Entomology, China Agricultural University, Beijing, P.R. China.
[Ti] Title:Over-expression of UDP-glycosyltransferase gene UGT2B17 is involved in chlorantraniliprole resistance in Plutella xylostella (L.).
[So] Source:Pest Manag Sci;73(7):1402-1409, 2017 Jul.
[Is] ISSN:1526-4998
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: UDP-glycosyltransferases (UGTs) are phase II detoxification enzymes widely distributed within living organisms. Their involvement in the biotransformation of various lipophilic endogenous compounds and phytoalexins in insects has been documented. However, the roles of this enzyme family in insecticide resistance have rarely been reported. Here, the functions of UGTs in chlorantraniliprole resistance in Plutella xylostella were investigated. RESULTS: Treatment with sulfinpyrazone and 5-nitrouracil (both inhibitors of UGT enzymes) significantly increased the toxicity of chlorantraniliprole against the third instar larvae of P. xylostella. Among the 23 UGT transcripts examined, only UGT2B17 was found to be over-expressed (with a range from 30.7- to 77.3-fold) in all four chlorantraniliprole-resistant populations compared to the susceptible one (CHS). The knock-down of UGT2B17 by RNA interference (RNAi) dramatically increased the toxicity of chlorantraniliprole by 27.4% and 29.8% in the CHS and CHR (resistant) populations, respectively. In contrast, exposure to phenobarbital significantly increased the relative expression of UGT2B17 while decreasing the toxicity of chlorantraniliprole to the larvae by 14.0%. CONCLUSION: UGT2B17 is involved in the detoxification of chlorantraniliprole, and its over-expression may play an important role in chlorantraniliprole resistance in P. xylostella. These results shed some light upon and further our understanding of the mechanisms of diamide insecticide resistance in insects. © 2016 Society of Chemical Industry.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1610
[Cu] Class update date: 170608
[Lr] Last revision date:170608
[St] Status:In-Process
[do] DOI:10.1002/ps.4469

  6 / 1171 MEDLINE  
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[PMID]: 27289558
[Au] Autor:Tanner NC; da Silva AF
[Ad] Address:Department of Vascular Surgery, Wrexham Maelor Hospital, Wrexham LL13 7TD, UK. Electronic address: Nicolatanner@doctors.org.uk.
[Ti] Title:Medical Adjuvant Treatment to Improve the Patency of Arteriovenous Fistulae and Grafts: A Systematic Review and Meta-analysis.
[So] Source:Eur J Vasc Endovasc Surg;52(2):243-52, 2016 Aug.
[Is] ISSN:1532-2165
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: Many patients using haemodialysis for end-stage renal disease (ESRD) require arteriovenous fistulae (AVF) or grafts. Patency can be variable, and this systematic review aimed to determine the effects of adjuvant drug treatment on the patency of AVFs and grafts. METHODS: The Cochrane Peripheral Vascular Diseases Group searched the Specialised Register and CENTRAL for all randomised controlled trials (RCTs) investigating the effect of active drug versus placebo on patency. The primary outcome was fistula or graft patency rate. The odds ratio (OR) was used as the measure of effect for each outcome. If several trials assessed the same adjuvant therapy then a meta-analysis was conducted using a Mantel-Haenszel model. RESULTS: Fifteen trials were deemed suitable for inclusion, investigating nine drug treatments in 2,230 participants. Overall, the quality of evidence was low. Three trials compared ticlopidine (a platelet aggregation inhibitor) versus placebo and favoured active treatment (OR 0.45, 95% CI 0.25 to 0.82; p = .009). Three RCTs assessed aspirin versus placebo and did not show a statistical benefit (OR 0.40, 95% CI 0.07-2.25; p = .30). Two trials compared clopidogrel with placebo. The overall result did not favour treatment (OR 0.40, 95% CI 0.13 to 1.19; p = .10). Three trials evaluated human type-I pancreatic elastase but did not provide evidence of improved patency (OR 0.75, 95% CI 0.42-1.32; p = .31). Finally, two RCTs assessed fish oil and did not favour treatment (OR 0.24, 95% CI 0.03-1.95; p = .18). Single trials comparing dipyridamole alone, dipyridamole plus aspirin, and sulfinpyrazone against placebo favoured active treatment but a meta-analysis could not be undertaken. Finally, a single trial of warfarin versus placebo found warfarin resulted in increased complications and worse patency rates. CONCLUSION: This systematic review has not demonstrated a beneficial effect for any adjuvant treatment to increase the patency of AVF or grafts in the short term, except ticlopidine which has been taken off the market.
[Mh] MeSH terms primary: Arteriovenous Shunt, Surgical/methods
Vascular Grafting/methods
Vascular Patency
[Mh] MeSH terms secundary: Anticoagulants/therapeutic use
Chemotherapy, Adjuvant/methods
Hematologic Agents/therapeutic use
Humans
Platelet Aggregation Inhibitors/therapeutic use
Vascular Patency/drug effects
[Pt] Publication type:JOURNAL ARTICLE; META-ANALYSIS; REVIEW
[Nm] Name of substance:0 (Anticoagulants); 0 (Hematologic Agents); 0 (Platelet Aggregation Inhibitors)
[Em] Entry month:1612
[Cu] Class update date: 161230
[Lr] Last revision date:161230
[Js] Journal subset:IM
[Da] Date of entry for processing:160613
[St] Status:MEDLINE

  7 / 1171 MEDLINE  
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[PMID]: 26826239
[Au] Autor:Sasidharan Nair V; Song MH; Oh KI
[Ad] Address:Department of Pathology, Hallym University College of Medicine, Chuncheon, Gangwon-Do 200-702, Korea.
[Ti] Title:Vitamin C Facilitates Demethylation of the Foxp3 Enhancer in a Tet-Dependent Manner.
[So] Source:J Immunol;196(5):2119-31, 2016 Mar 01.
[Is] ISSN:1550-6606
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Demethylation of CpG motifs in the Foxp3 intronic element, conserved noncoding sequence 2 (CNS2), is indispensable for the stable expression of Foxp3 in regulatory T cells (Tregs). In this study, we found that vitamin C induces CNS2 demethylation in Tregs in a ten-eleven-translocation 2 (Tet2)-dependent manner. The CpG motifs of CNS2 in Tregs generated in vitro by TGF-ß (iTregs), which were methylated originally, became demethylated after vitamin C treatment. The conversion of 5-methylcytosin into 5-hydroxymethylcytosin was more efficient, and the methyl group from the CpG motifs of Foxp3 CNS2 was erased rapidly in iTregs treated with vitamin C. The effect of vitamin C disappeared in Tet2(-/-) iTregs. Furthermore, CNS2 in peripheral Tregs in vivo, which were demethylated originally, became methylated after treatment with a sodium-dependent vitamin C transporter inhibitor, sulfinpyrazone. Finally, CNS2 demethylation in thymic Tregs was also impaired in Tet2(-/-) mice, but not in wild type mice, when they were treated with sulfinpyrazone. Collectively, vitamin C was required for the CNS2 demethylation mediated by Tet proteins, which was essential for Foxp3 expression. Our findings indicate that environmental factors, such as nutrients, could bring about changes in immune homeostasis through epigenetic mechanisms.
[Mh] MeSH terms primary: Ascorbic Acid/pharmacology
DNA Methylation/drug effects
Forkhead Transcription Factors/genetics
Gene Expression Regulation/drug effects
T-Lymphocytes, Regulatory/drug effects
T-Lymphocytes, Regulatory/immunology
[Mh] MeSH terms secundary: Adoptive Transfer
Animals
Cell Separation
CpG Islands/genetics
CpG Islands/immunology
DNA-Directed DNA Polymerase/genetics
DNA-Directed DNA Polymerase/immunology
Flow Cytometry
Forkhead Transcription Factors/biosynthesis
Forkhead Transcription Factors/immunology
Gene Expression Regulation/immunology
Immunoprecipitation
Mice
Mice, Inbred C57BL
Mice, Transgenic
Oligonucleotide Array Sequence Analysis
Reverse Transcriptase Polymerase Chain Reaction
Transfection
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Name of substance:0 (Forkhead Transcription Factors); 0 (Foxp3 protein, mouse); EC 2.7.7.- (Tet DNA polymerase); EC 2.7.7.7 (DNA-Directed DNA Polymerase); PQ6CK8PD0R (Ascorbic Acid)
[Em] Entry month:1608
[Cu] Class update date: 160220
[Lr] Last revision date:160220
[Js] Journal subset:AIM; IM
[Da] Date of entry for processing:160131
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1502352

  8 / 1171 MEDLINE  
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[PMID]: 26742828
[Au] Autor:Mohamed SK; Younes SH; Abdel-Raheem EM; Horton PN; Akkurt M; Glidewell C
[Ad] Address:Chemistry and Environmental Division, Manchester Metropolitan University, Manchester M1 5GD, England.
[Ti] Title:Triclinic and monoclinic polymorphs of meso-(E,E)-1,1'-[1,2-bis(4-chlorophenyl)ethane-1,2-diyl]bis(phenyldiazene): the high-yield synthesis of an unexpected product, concomitant polymorphism and configurational disorder.
[So] Source:Acta Crystallogr C Struct Chem;72(Pt 1):57-62, 2016 Jan.
[Is] ISSN:2053-2296
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Pyrazolidine-3,5-diones and their derivatives exhibit a wide range of biological activities. Seeking to explore the effect of combining a hydrocarbyl ring substituent, as present in sulfinpyrazone (used to treat gout), with a chlorinated aryl ring, as present in muzolimine (a diuretic), we explored the reaction between 1-phenylpyrazolidine-3,5-dione and 4-chlorobenzaldehyde under mildly basic conditions in the expectation of producing the simple condensation product 4-(4-chlorobenzylidene)-1-phenylpyrazolidine-3,5-dione. However, the reaction product proved to be meso-(E,E)-1,1'-[1,2-bis(4-chlorophenyl)ethane-1,2-diyl]bis(phenyldiazene), C26H20Cl2N4, and a tentative mechanism is proposed. Crystallization from ethanol produces two concomitant polymorphs, i.e. a triclinic form, (I), in the space group P-1, and a monoclinic form, (II), in the space group C2/c. In both polymorphs, the molecules lie across centres of inversion, but in (II), the molecules are subject to whole-molecule disorder equivalent to configurational disorder with occupancies of 0.6021 (19) and 0.3979 (19). There are no hydrogen bonds in the crystal structure of polymorph (I), but the molecules of polymorph (II) are linked by C-H...π(arene) hydrogen bonds into complex chains, which are further linked into sheets by C-H...N interactions.
[Mh] MeSH terms primary: Imines/chemical synthesis
[Mh] MeSH terms secundary: Biological Phenomena
Crystallization
Crystallography, X-Ray
Hydrogen Bonding
Imines/chemistry
Models, Molecular
Molecular Structure
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Name of substance:0 (1,1'-(1,2-bis(4-chlorophenyl)ethane-1,2-diyl)bis(phenyldiazene)); 0 (Imines); 931-55-5 (phenyldiazene)
[Em] Entry month:1606
[Cu] Class update date: 161126
[Lr] Last revision date:161126
[Js] Journal subset:IM
[Da] Date of entry for processing:160109
[St] Status:MEDLINE
[do] DOI:10.1107/S2053229615023578

  9 / 1171 MEDLINE  
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[PMID]: 26340060
[Au] Autor:May JM; Qu ZC
[Ad] Address:Department of Medicine, Vanderbilt University School of Medicine, Nashville, TN.
[Ti] Title:Ascorbic acid efflux from human brain microvascular pericytes: role of re-uptake.
[So] Source:Biofactors;41(5):330-8, 2015 Sep-Oct.
[Is] ISSN:1872-8081
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Microvascular pericytes take up ascorbic acid on the ascorbate transporter SVCT2. Intracellular ascorbate then protects the cells against apoptosis induced by culture at diabetic glucose concentrations. To investigate whether pericytes might also provide ascorbate to the underlying endothelial cells, we studied ascorbate efflux from human pericytes. When loaded with ascorbate to intracellular concentrations of 0.8-1.0 mM, almost two-thirds of intracellular ascorbate effluxed from the cells over 2 H. This efflux was opposed by ascorbate re-uptake from the medium, since preventing re-uptake by destroying extracellular ascorbate with ascorbate oxidase increased ascorbate loss even further. Ascorbate re-uptake occurred on the SVCT2, since its blockade by replacing medium sodium with choline, by the SVCT2 inhibitor sulfinpyrazone, or by extracellular ascorbate accelerated ascorbate loss from the cells. This was supported by finding that net efflux of radiolabeled ascorbate was increased by unlabeled extracellular ascorbate with a half-maximal effect in the range of the high affinity Km of the SVCT2. Intracellular ascorbate did not inhibit its efflux. To assess the mechanism of ascorbate efflux, known inhibitors of volume-regulated anion channels (VRACs) were tested. These potently inhibited ascorbate transport into cells on the SVCT2, but not its efflux. An exception was the anion transport inhibitor DIDS, which, despite inhibition of ascorbate uptake, also inhibited net efflux at 25-50 µM. These results suggest that ascorbate efflux from vascular pericytes occurs on a DIDS-inhibitable transporter or channel different from VRACs. Further, ascorbate efflux is opposed by re-uptake of ascorbate on the SVCT2, providing a potential regulatory mechanism.
[Mh] MeSH terms primary: Ascorbic Acid/metabolism
Brain/cytology
Pericytes/metabolism
[Mh] MeSH terms secundary: Cells, Cultured
Humans
Sodium-Coupled Vitamin C Transporters/metabolism
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Name of substance:0 (Sodium-Coupled Vitamin C Transporters); PQ6CK8PD0R (Ascorbic Acid)
[Em] Entry month:1609
[Cu] Class update date: 161019
[Lr] Last revision date:161019
[Js] Journal subset:IM
[Da] Date of entry for processing:150905
[St] Status:MEDLINE
[do] DOI:10.1002/biof.1227

  10 / 1171 MEDLINE  
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[PMID]: 26086788
[Au] Autor:Shiozawa A; Cloutier M; Heroux J; Guerin A; Wu EQ; Jackson R
[Ad] Address:a a Takeda Pharmaceuticals International Inc. , Deerfield , IL , USA.
[Ti] Title:Real-world treatment patterns of gout patients treated with colchicine or other common treatments for gout in acute care settings: a retrospective chart review study.
[So] Source:Curr Med Res Opin;31(8):1611-20, 2015 Aug.
[Is] ISSN:1473-4877
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:OBJECTIVE: To describe real-world treatment patterns of patients receiving colchicine or other treatments during a gout-related emergency room or acute care facility (ER/ACF) visit. METHODS: An online physician-administered questionnaire was used to collect chart data on 500 patients with a gout-related ER/ACF visit after 16 October 2009; 250 patients receiving colchicine (Colchicine Cohort) and 250 receiving NSAIDs, systemic corticosteroids, narcotics, allopurinol, febuxostat, pegloticase, probenecid, or sulfinpyrazone (Other Cohort). Patient characteristics and treatment received/prescribed during the ER/ACF visit (Period 1 [P1]), at discharge (P2), and at the first follow-up visit (P3) are reported. RESULTS: A total of 45 rheumatologists and 63 primary care physicians participated in the study. Patient mean age was 51 years and 74.8% were male. The most common treatments in the Other Cohort were NSAIDs (59.6%), systemic corticosteroids (45.2%), and narcotics (33.6%). The 500 patients contributed 307 distinct treatment patterns from P1 to P3. Of the 20.6% patients not prescribed a treatment in P2, 60.2% were restarted on a treatment in P3. Of the 78.6% treated patients in P2, 27.0% had a treatment adjustment (dose increase, treatment add-on, or initiation of a different gout-related treatment - not with a urate lowering therapy only) in P3; for 72.6% of these patients, physicians justified the treatment adjustment by inadequacy of the treatment for maintenance therapy, insufficient dosage, or inadequate response. In the Colchicine Cohort, 60.8% of patients were prescribed colchicine consistently from P1 to P3, while 26.8% and 17.7% of patients in the Other Cohort were prescribed consistently NSAIDs and systemic corticosteroids from P1 to P3, respectively. LIMITATIONS: Specific nature of the acute gout-related symptoms or potential attack/flare during the ER/ACF visit was not recorded. CONCLUSION: Real-world clinical practice reveals a substantial number of distinct treatment patterns and frequent treatment adjustments by treating physicians for patients with a gout-related ER/ACF visit.
[Mh] MeSH terms primary: Colchicine/therapeutic use
Gout Suppressants/therapeutic use
Gout/drug therapy
[Mh] MeSH terms secundary: Adrenal Cortex Hormones/therapeutic use
Adult
Aged
Female
Humans
Male
Middle Aged
Retrospective Studies
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Name of substance:0 (Adrenal Cortex Hormones); 0 (Gout Suppressants); SML2Y3J35T (Colchicine)
[Em] Entry month:1604
[Cu] Class update date: 150826
[Lr] Last revision date:150826
[Js] Journal subset:IM
[Da] Date of entry for processing:150619
[St] Status:MEDLINE
[do] DOI:10.1185/03007995.2015.1062750


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BIREME/PAHO/WHO - Latin American and Caribbean Center on Health Sciences Information