35 results on '"Eells, J."'
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2. Women taking action: Multisession learning circles, storytelling, and an ecosystem of relationships for conservation
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Shenk, L., primary, Eells, J., additional, and Almitra, W., additional
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- 2023
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3. Open Embeddings of Certain Banach Manifolds
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Eells, J. and Elworthy, K. D.
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- 1970
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4. RWD174 Real World Treatment Usage of Biologic and Targeted Synthetic Disease-Modifying Anti-Rheumatic Drugs in US Patients with Psoriatic Arthritis: Persistence, Factors Associated with Non-Persistence, and Dosing Patterns
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Welby, S., Song, J., Lu, C., Pilipczuk, O., Willems, D., Beaty, S., Eells, J., and Feudjo Tepie, M.
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- 2023
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5. Do women farmland owners count in agricultural conservation? A review of research on women farmland owners in the United States
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Eells, J. C., primary and Soulis, J., additional
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- 2013
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6. Maps help landowners think beyond human scale
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Eells, J., primary, Dahlstrom, M. F., additional, and Ritland, R., additional
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- 2012
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7. One size does not fit all: Customizing conservation to a changing demographic
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Wells, B., primary and Eells, J., additional
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- 2011
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8. The geometry of harmonic maps, by Y. Xin. Pp. 248. 1996. DM138. ISBN 3-7643-3820-2 (Birkhäuser).
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Eells, J., primary
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- 1997
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9. Mitochondria-Mediated Cell Injury1.
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Wallace, K. B., Eells, J. T., Madeira, V. M. C., Cortopassi, G., and Jones, D. P.
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MITOCHONDRIA ,ADENOSINE triphosphate ,OXIDIZING agents ,ELECTROPHILES ,HOMEOSTASIS - Abstract
Mitochondria have long been known to participate in the process of cell injury associated with metabolic failure. Only recently, however, have we come to appreciate the role of mitochondria as primary intracellular targets in the initiation of cell dysfunction. In addition to ATP synthesis, mitochondria are also critical to modulation of cell redox status, osmotic regulation, pH control, and cytosolic calcium homeostasis and cell signaling. Mitochondria are susceptible to damage by oxidants, electrophiles, and lipophilic cations and weak acids. Chemical-induced mitochondrial dysfunction may be manifested as diverse bioenergetic disorders and considerable effort is required to distinguish between mechanisms involving critical mitochondrial targets and those in which mitochondrial dysfunction is secondary and plays only a modulatory role in cell injury. The following paragraphs review a few important examples of chemical-induced cytotoxic responses that are manifested as interference with mitochondrial metabolism and bioenergetics, gene regulation, or signal transduction in the form of apoptosis and altered cell cycle control. Greater understanding of the molecular mechanisms of mitochondrial bioenergetics, ion regulation, and genetics will lead to numerous additional examples of mitochondria-mediated cell injury, revealing important new insight regarding the prediction, prevention, diagnosis, and treatment of chemical-induced toxic tissue injury. [ABSTRACT FROM AUTHOR]
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- 1997
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10. The Geometry of Harmonic Maps Y. Xin
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Eells, J.
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- 1997
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11. Role of hepatic tetrahydrofolate in the species difference in methanol toxicity.
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Black, K A, Eells, J T, Noker, P E, Hawtrey, C A, and Tephly, T R
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The susceptibility of various species to methanol toxicity is inversely related to the rate of tetrahydrofolate (H4folate)-dependent formate oxidation to carbon dioxide. Thus, the levels of various folate derivatives and folate-dependent enzyme activities present in the livers of monkeys, which are sensitive to methanol, and rats, which are not, were compared in order to investigate the biochemical basis of this species difference. Hepatic H4folate levels in monkeys were 60% of those in rats, and formylated-H4folate derivatives were 2-fold higher in monkeys than in rats. No significant difference between monkeys and rats in the levels of total hepatic folate or 5-methyl-H4folate was observed. The activities of formyl-H4folate synthetase (EC 6.3.4.3) and formyl-H4folate dehydrogenase (EC 1.5.1.6) were 4- and 2-fold higher, respectively, in monkeys than in rats. There was no significant difference between monkeys and rats in methionine synthetase activity (EC 2.1.1.13). Dihydrofolate reductase activity (EC 1.5.1.3) in monkeys was 20% of that in rats. 5,10-Methylene-H4folate reductase (NADPH) activity (EC 1.1.1.171) in monkeys was 40% and 25% of that in rats when the rates of the forward and reverse reactions, respectively, were compared. Serine hydroxymethyltransferase activity (EC 2.1.2.1) was 2-fold higher in monkeys than in rats. The differences in the activities of methylene-H4folate reductase and serine hydroxymethyl-transferase between monkeys and rats may have contributed to the difference in hepatic H4folate levels. The 40% lower level of hepatic H4folate in monkeys, as compared to rats, relates well to the 50% lower maximal rate of formate oxidation in monkeys. Thus, the species difference in susceptibility to methanol may be explained by the difference in the level of hepatic H4folate.
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- 1985
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12. Twistorial construction of harmonic maps
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Eells, J and Salamon, Simon
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- 1985
13. The diffeomorphism group of a compact Riemann surface
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Earle, C. J. and Eells, J.
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- 1967
14. Gene and noncoding RNA regulation underlying photoreceptor protection: Microarray study of dietary antioxidant saffron and photobiomodulation in rat retina
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Natoli R, Zhu Y, Krisztina Valter, Bisti S, Eells J, and Stone J
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RNA, Untranslated ,Cell Death ,Light ,Reverse Transcriptase Polymerase Chain Reaction ,Gene Expression Profiling ,Reproducibility of Results ,Crocus ,Antioxidants ,Retina ,Diet ,Rats ,Rats, Sprague-Dawley ,Gene Expression Regulation ,Cytoprotection ,Animals ,Cluster Analysis ,Immunologic Factors ,Research Article ,Oligonucleotide Array Sequence Analysis ,Photoreceptor Cells, Vertebrate - Abstract
Purpose To identify the genes and noncoding RNAs (ncRNAs) involved in the neuroprotective actions of a dietary antioxidant (saffron) and of photobiomodulation (PBM). Methods We used a previously published assay of photoreceptor damage, in which albino Sprague Dawley rats raised in dim cyclic illumination (12 h 5 lux, 12 h darkness) were challenged by 24 h exposure to bright (1,000 lux) light. Experimental groups were protected against light damage by pretreatment with dietary saffron (1 mg/kg/day for 21 days) or PBM (9 J/cm2 at the eye, daily for 5 days). RNA from one eye of four animals in each of the six experimental groups (control, light damage [LD], saffron, PBM, saffronLD, and PBMLD) was hybridized to Affymetrix rat genome ST arrays. Quantitative real-time PCR analysis of 14 selected genes was used to validate the microarray results. Results LD caused the regulation of 175 entities (genes and ncRNAs) beyond criterion levels (p2). PBM pretreatment reduced the expression of 126 of these 175 LD-regulated entities below criterion; saffron pretreatment reduced the expression of 53 entities (50 in common with PBM). In addition, PBM pretreatment regulated the expression of 67 entities not regulated by LD, while saffron pretreatment regulated 122 entities not regulated by LD (48 in common with PBM). PBM and saffron, given without LD, regulated genes and ncRNAs beyond criterion levels, but in lesser numbers than during their protective action. A high proportion of the entities regulated by LD (>90%) were known genes. By contrast, ncRNAs were prominent among the entities regulated by PBM and saffron in their neuroprotective roles (73% and 62%, respectively). Conclusions Given alone, saffron and (more prominently) PBM both regulated significant numbers of genes and ncRNAs. Given before retinal exposure to damaging light, thus while exerting their neuroprotective action, they regulated much larger numbers of entities, among which ncRNAs were prominent. Further, the downregulation of known genes and of ncRNAs was prominent in the protective actions of both neuroprotectants. These comparisons provide an overview of gene expression induced by two neuroprotectants and provide a basis for the more focused study of their mechanisms.
15. Restrictions on harmonic maps of surfaces
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Eells, J., primary and Wood, J.C., additional
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- 1976
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16. Harmonic maps from surfaces to complex projective spaces
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Eells, J, primary and Wood, C, additional
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- 1983
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17. The diffeomorphism group of a compact Riemann surface
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Earle, C. J., primary and Eells, J., additional
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- 1967
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18. Book Review: The geometry of harmonic maps
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Eells, J.
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- 1997
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19. Comparative Effectiveness of Bimekizumab and Risankizumab in Patients with Psoriatic Arthritis at 52 Weeks Assessed Using a Matching-Adjusted Indirect Comparison.
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Mease PJ, Warren RB, Nash P, Grouin JM, Lyris N, Willems D, Taieb V, Eells J, and McInnes IB
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Introduction: The relative efficacy of bimekizumab and risankizumab in patients with PsA who were biologic disease-modifying anti-rheumatic drug naïve (bDMARD naïve) or with previous inadequate response or intolerance to tumor necrosis factor inhibitors (TNFi-IR) was assessed at 52 weeks (Wk52) using matching-adjusted indirect comparisons (MAIC)., Methods: Relevant trials were systematically identified. For patients who were bDMARD naïve, individual patient data (IPD) from BE OPTIMAL (NCT03895203; N = 431) were matched with summary data from KEEPsAKE-1 (NCT03675308; N = 483). For patients who were TNFi-IR, IPD from BE COMPLETE (NCT03896581; N = 267) were matched with summary data from the TNFi-IR patient subgroup in KEEPsAKE-2 (NCT03671148; N = 106). To adjust for cross-trial differences, patients from the bimekizumab trials were re-weighted to match the baseline characteristics of patients in the risankizumab trials. Adjustment variables were selected based on expert consensus (n = 5) and adherence to established MAIC guidelines. Recalculated bimekizumab Wk52 outcomes for American College of Rheumatology (ACR) 20/50/70 response criteria and minimal disease activity (MDA) index (non-responder imputation) were compared with risankizumab outcomes via non-placebo-adjusted comparisons., Results: In patients who were bDMARD naïve, bimekizumab had a significantly greater likelihood of response than risankizumab at Wk52 for ACR50 (odds ratio [95% confidence interval]: 1.52 [1.11, 2.09]) and ACR70 (1.80 [1.29, 2.51]). In patients who were TNFi-IR, bimekizumab had a significantly greater likelihood of response than risankizumab at Wk52 for ACR20 (1.78 [1.08, 2.96]), ACR50 (3.05 [1.74, 5.32]), ACR70 (3.69 [1.82, 7.46]), and MDA (2.43 [1.37, 4.32])., Conclusions: Using MAIC, bimekizumab demonstrated a greater likelihood of efficacy in most ACR and MDA outcomes than risankizumab in patients with PsA who were bDMARD naïve and TNFi-IR at Wk52., Trial Registration: NCT03895203, NCT03896581, NCT03675308, NCT03671148., (© 2024. The Author(s).)
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- 2024
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20. Comparative Effectiveness of Bimekizumab and Ustekinumab in Patients with Psoriatic Arthritis at 52 Weeks Assessed Using a Matching-Adjusted Indirect Comparison.
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Mease PJ, Warren RB, Nash P, Grouin JM, Lyris N, Taieb V, Eells J, and McInnes IB
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Introduction: A matching-adjusted indirect comparison (MAIC) was conducted to assess the relative efficacy at 52 weeks (Wk52) of bimekizumab 160 mg every 4 weeks (Q4W) and ustekinumab 45 or 90 mg every 12 weeks (Q12W) in patients with psoriatic arthritis (PsA) who were biologic disease-modifying anti-rheumatic drug naïve (bDMARD naïve) or who had a previous inadequate response or an intolerance to tumor necrosis factor inhibitors (TNFi-IR)., Methods: Relevant trials were systematically identified. Individual patient data from the bimekizumab trials BE OPTIMAL (NCT03895203; N = 431) and BE COMPLETE (NCT03896581; N = 267) were matched with summary data on patients receiving ustekinumab in the PSUMMIT 1 trial (NCT01009086; 45 mg, N = 205; 90 mg; N = 204) and a subgroup of TNFi-IR patients receiving ustekinumab in the PSUMMIT 2 trial (NCT01077362; 45 mg, N = 60; 90 mg, N = 58), respectively. Patients from the bimekizumab trials were re-weighted using propensity scores to match the baseline characteristics of the ustekinumab trial patients. Adjustment variables were selected based on expert consensus (n = 5) and adherence to established MAIC guidelines. Non-placebo-adjusted comparisons of recalculated bimekizumab and ustekinumab outcomes for the American College of Rheumatology (ACR) 20/50/70 response criteria (non-responder imputation) were analyzed., Results: In patients who were bDMARD naïve, bimekizumab had a greater likelihood of response than ustekinumab at Wk52 for ACR20 (odds ratio [95% confidence interval] 45 mg: 2.14 [1.35, 3.40]; 90 mg: 1.98 [1.24, 3.16]), ACR50 (45 mg: 2.74 [1.75, 4.29]; 90 mg: 2.29 [1.48, 3.55]), and ACR70 (45 mg: 3.33 [2.04, 5.46]; 90 mg: 3.05 [1.89, 4.91]). In patients who were TNFi-IR, bimekizumab had a greater likelihood of response than ustekinumab at Wk52 for ACR20 (45 mg: 4.17 [2.13, 8.16]; 90 mg: 4.19 [2.07, 8.49]), ACR50 (45 mg: 5.00 [2.26, 11.05]; 90 mg: 3.86 [1.70, 8.79]), and ACR70 (45 mg: 9.85 [2.79, 34.79]; 90 mg: 6.29 [1.98, 20.04])., Conclusions: Using MAIC, bimekizumab showed greater efficacy than ustekinumab in achieving all ACR responses in patients with PsA who were bDMARD naïve and TNFi-IR at Wk52., Trial Registration: NCT03895203, NCT03896581, NCT01009086, NCT01077362., (© 2024. The Author(s).)
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- 2024
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21. Comparative Effectiveness of Bimekizumab and Secukinumab in Patients with Psoriatic Arthritis at 52 Weeks Using a Matching-Adjusted Indirect Comparison.
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Mease PJ, Warren RB, Nash P, Grouin JM, Lyris N, Willems D, Taieb V, Eells J, and McInnes IB
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Introduction: Matching-adjusted indirect comparisons (MAICs) were used to compare the efficacy of bimekizumab and secukinumab 150 mg and 300 mg at 52 weeks for the treatment of psoriatic arthritis (PsA) in patients who were biologic disease-modifying anti-rheumatic drug-naïve (bDMARD-naïve) or with previous inadequate response or intolerance to tumor necrosis factor inhibitors (TNFi-IR)., Methods: Relevant trials were systematically identified. Individual patient data from bimekizumab randomized controlled trials, BE OPTIMAL (N = 431) and BE COMPLETE (N = 267), were matched to aggregate data from bDMARD-naïve and TNFi-IR patient subgroups from FUTURE 2 using secukinumab 150 mg and 300 mg doses (bDMARD-naïve: N = 63/37; TNFi-IR: N = 67/33). To adjust for cross-trial differences, patients from the bimekizumab trials were re-weighted using propensity scores to match the baseline characteristics of patients in the secukinumab trials. Unanchored comparisons of recalculated bimekizumab and secukinumab 52-week non-responder imputation outcomes for 20/50/70% improvement in American College of Rheumatology score (ACR20/50/70) and minimal disease activity (MDA) index were analyzed., Results: In patients who were bDMARD-naïve, bimekizumab had a greater likelihood of ACR70 response than secukinumab 150 mg (odds ratio [95% confidence interval] 2.39 [1.26, 4.53]; p = 0.008) and secukinumab 300 mg (2.03 [1.11, 3.72]; p = 0.021) at 52 weeks. In patients who were TNFi-IR, bimekizumab had a greater likelihood of response compared to secukinumab 150 mg for ACR20 (3.50 [1.64-7.49]; p = 0.001), ACR50 (3.32 [1.41, 7.80]; p = 0.006), ACR70 (2.95 [1.08, 8.07]; p = 0.035) and MDA (3.52 [1.38, 8.99]; p = 0.009), and a greater likelihood of response compared to secukinumab 300 mg for ACR50 (2.44 [1.06, 5.65]; p = 0.037) and MDA (2.92 [1.20, 7.09]; p = 0.018) at 52 weeks., Conclusion: In this MAIC analysis, the efficacy of bimekizumab, as demonstrated by the likelihood of ACR20/50/70 and MDA response at 52 weeks, was greater or comparable to secukinumab 150 mg and 300 mg for patients with PsA who were bDMARD-naïve and TNFi-IR., Trial Registration Numbers: NCT03895203, NCT03896581, NCT04009499, NCT01752634, NCT01989468, NCT02294227, NCT02404350., (© 2024. The Author(s).)
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- 2024
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22. Comparative Effectiveness of Bimekizumab and Guselkumab in Patients with Psoriatic Arthritis at 52 Weeks Assessed Using a Matching-Adjusted Indirect Comparison.
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Warren RB, McInnes IB, Nash P, Grouin JM, Lyris N, Willems D, Taieb V, Eells J, and Mease PJ
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Introduction: Matching-adjusted indirect comparisons (MAIC) were used to assess the relative efficacy of bimekizumab 160 mg every 4 weeks (Q4W) compared to guselkumab 100 mg Q4W or every 8 weeks (Q8W) at 48/52 weeks in patients with psoriatic arthritis (PsA) who were biologic disease-modifying antirheumatic drug-naïve (bDMARD-naïve) or with previous inadequate response or intolerance to tumor necrosis factor inhibitors (TNFi-IR)., Methods: Relevant trials were identified as part of a systematic literature review. For patients who were bDMARD-naïve, individual patient data (IPD) from BE OPTIMAL (N = 431) was matched to summary data from DISCOVER-2 (Q4W, n = 245; Q8W, n = 248). For patients who were TNFi-IR, IPD from BE COMPLETE (n = 267) and summary data from COSMOS (Q8W, N = 189). Trial populations were re-weighted using propensity scores. Unanchored comparisons of recalculated bimekizumab and guselkumab 48- or 52-week non-responder imputation outcomes for 20/50/70% improvement in American College of Rheumatology score (ACR20/50/70) and minimal disease activity (MDA) index were analyzed., Results: In patients who were bDMARD-naïve, bimekizumab was associated with a greater likelihood of ACR50 (odds ratio [95% confidence interval] 1.62 [1.07, 2.44]; p = 0.021), ACR70 (2.20 [1.43, 3.38]; p < 0.001), and MDA (1.82 [1.20, 2.76]; p = 0.005) compared to guselkumab Q4W at week 52. Bimekizumab also had a greater likelihood of ACR70 response (2.08 [1.34, 3.22]; p = 0.001) and MDA (2.07 [1.35, 3.17]; p < 0.001) compared to guselkumab Q8W at week 52. In patients who were TNFi-IR, bimekizumab had a greater likelihood in achieving all evaluated outcomes compared to guselkumab Q8W at week 48/52 (ACR20, 1.77 [1.15, 2.72]; p = 0.010; ACR50, 1.56 [1.03, 2.36]; p = 0.037; ACR70, 1.66 [1.05, 2.61]; p = 0.028; and MDA, 1.95 [1.27, 3.02]; p = 0.003)., Conclusions: According to MAICs, bimekizumab demonstrated greater or comparable efficacy on ACR50/70 and MDA outcomes than guselkumab in patients with PsA who were bDMARD-naïve and TNFi-IR at week 48/52. Bimekizumab had a more favorable likelihood than guselkumab in achieving more stringent treatment outcomes., Trial Registrations: NCT03895203, NCT03896581, NCT04009499, NCT03158285, NCT03796858., (© 2024. The Author(s).)
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- 2024
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23. Effect of bimekizumab on symptoms and impact of disease in patients with psoriatic arthritis over 3 years: results from BE ACTIVE.
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Mease PJ, Asahina A, Gladman DD, Tanaka Y, Tillett W, Ink B, Assudani D, de la Loge C, Coarse J, Eells J, and Gossec L
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- Humans, Male, Middle Aged, Female, Quality of Life, Fatigue drug therapy, Fatigue etiology, Double-Blind Method, Pain, Treatment Outcome, Arthritis, Psoriatic diagnosis
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Objectives: Evaluate effects of long-term bimekizumab treatment on patient-reported outcome (PRO) measures, symptoms and the impact of PsA on patients., Methods: Patients with active PsA were enrolled into BE ACTIVE, a 48-week randomised controlled trial (NCT02969525). After Week 48, patients could enter a 104-week open-label extension (NCT03347110), receiving bimekizumab 160 mg every four weeks. PRO measures assessed included arthritis pain visual analogue scale (VAS), PsA Impact of Disease (PsAID)-9, 36-Item Short Form Survey (SF-36) and HAQ-Disability Index (HAQ-DI). Results were analysed as mean (S.E.M.) changes from baseline (CfB) from Week 0 to the end of the open-label extension (3 years) and as percentage of patients reaching patient-acceptable symptom state (PASS) for global impact (PsAID-9 total score ≤4) and normal function (HAQ-DI total score <0.5). Non-responder imputation was applied to missing binary outcomes., Results: In 206 patients (mean age 49.3 years, 51.0% male), completion rate was high; 161 (78.2%) patients completed Week 152. Bimekizumab treatment was associated with long-term sustained improvements in pain [arthritis pain VAS CfB; Week 48: -29.9 (1.9); Week 152: -32.0 (1.9)] and fatigue [PsAID-9 fatigue CfB; -2.4 (0.2); -2.7 (0.2)]. High percentages of patients achieved acceptable symptom state (PsAID-9 PASS: 75.2%; 65.0%) and normalised function (HAQ-DI <0.5: 49.0%; 46.1%). Improvements in patient global assessment and SF-36 Physical Component Summary were also sustained., Conclusions: Bimekizumab treatment was associated with long-term sustained improvements in pain and fatigue, reducing overall impact of PsA on patients. Physical function and quality of life improved up to 3 years., Trial Registration: ClinicalTrials.gov, https://clinicaltrials.gov, NCT02969525, NCT03347110., (© The Author(s) 2022. Published by Oxford University Press on behalf of the British Society for Rheumatology.)
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- 2023
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24. Acquired Resilience: An Evolved System of Tissue Protection in Mammals.
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Stone J, Mitrofanis J, Johnstone DM, Falsini B, Bisti S, Adam P, Nuevo AB, George-Weinstein M, Mason R, and Eells J
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This review brings together observations on the stress-induced regulation of resilience mechanisms in body tissues. It is argued that the stresses that induce tissue resilience in mammals arise from everyday sources: sunlight, food, lack of food, hypoxia and physical stresses. At low levels, these stresses induce an organised protective response in probably all tissues; and, at some higher level, cause tissue destruction. This pattern of response to stress is well known to toxicologists, who have termed it hormesis. The phenotypes of resilience are diverse and reports of stress-induced resilience are to be found in journals of neuroscience, sports medicine, cancer, healthy ageing, dementia, parkinsonism, ophthalmology and more. This diversity makes the proposing of a general concept of induced resilience a significant task, which this review attempts. We suggest that a system of stress-induced tissue resilience has evolved to enhance the survival of animals. By analogy with acquired immunity, we term this system 'acquired resilience'. Evidence is reviewed that acquired resilience, like acquired immunity, fades with age. This fading is, we suggest, a major component of ageing. Understanding of acquired resilience may, we argue, open pathways for the maintenance of good health in the later decades of human life., Competing Interests: Declaration of Conflicting Interests: The author(s) declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: J.S. is a director of CSCM Pty Ltd. R.M. has received consultancy fees over the past 3 years from Australian Doctor Eduction. M.G.W. is coinventor on the patent: Compositions and Methods for the Treatment of Lens Fibrotic Disease WO2010065920 A1, licensed by Genisphere, LLC. S.B. holds a nonremunerative relationship with Hortus Novus s.r.l.
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- 2018
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25. Optical imaging of mitochondrial redox state in rodent model of retinitis pigmentosa.
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Maleki S, Gopalakrishnan S, Ghanian Z, Sepehr R, Schmitt H, Eells J, and Ranji M
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- Analysis of Variance, Animals, Disease Models, Animal, Mitochondria pathology, NAD metabolism, Oxidation-Reduction, Oxidative Stress physiology, Rats, Rats, Sprague-Dawley, Rats, Transgenic, Retinitis Pigmentosa pathology, Image Processing, Computer-Assisted methods, Mitochondria metabolism, Optical Imaging methods, Retinitis Pigmentosa metabolism
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Oxidative stress (OS) and mitochondrial dysfunction contribute to photoreceptor cell loss in retinal degenerative disorders. The metabolic state of the retina in a rodent model of retinitis pigmentosa (RP) was investigated using a cryo-fluorescence imaging technique. The mitochondrial metabolic coenzymes nicotinamide adenine dinucleotide (NADH) and flavin adenine dinucleotide (FAD) are autofluorescent and can be monitored without exogenous labels using optical techniques. The cryo-fluorescence redox imaging technique provides a quantitative assessment of the metabolism. More specifically, the ratio of the fluorescence intensity of these fluorophores (NADH/FAD), the NADH redox ratio (RR), is a marker of the metabolic state of the tissue. The NADH RR and retinal function were examined in an established rodent model of RP, the P23H rat compared to that of nondystrophic Sprague-Dawley (SD) rats. The NADH RR mean values were 1.11 ± 0.03 in the SD normal and 0.841 ± 0.01 in the P23H retina, indicating increased OS in the P23H retina. Electroretinographic data revealed a significant reduction in photoreceptor function in P23H animals compared to SD nozrmal rats. Thus, cryo-fluorescence redox imaging was used as a quantitative marker of OS in eyes from transgenic rats and demonstrated that alterations in the oxidative state of eyes occur during the early stages of RP.
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- 2013
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26. Photobiomodulation protects the retina from light-induced photoreceptor degeneration.
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Albarracin R, Eells J, and Valter K
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- Animals, Calcium-Binding Proteins metabolism, Ciliary Neurotrophic Factor metabolism, Electroretinography, Fibroblast Growth Factor 2 genetics, Fibroblast Growth Factor 2 metabolism, Fluorescent Antibody Technique, Indirect, Glial Fibrillary Acidic Protein genetics, Glial Fibrillary Acidic Protein metabolism, Immunomodulation, Microfilament Proteins metabolism, Radiation Injuries, Experimental etiology, Radiation Injuries, Experimental metabolism, Rats, Rats, Sprague-Dawley, Retina metabolism, Retinal Degeneration etiology, Retinal Degeneration metabolism, Reverse Transcriptase Polymerase Chain Reaction, Stress, Physiological, Infrared Rays, Light adverse effects, Phototherapy, Radiation Injuries, Experimental therapy, Retina radiation effects, Retinal Degeneration therapy
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Purpose: In this study, the hypothesis that near-infrared (NIR) light treatment (photobiomodulation) attenuates bright-light damage in the albino rat retina was tested., Methods: Young adult Sprague-Dawley (SD) albino rats were raised in dim (5 lux), cyclic light and then exposed to bright (1000 lux), continuous light for 24 hours. The animals were treated with 670-nm light (9 J/cm(2)) in an LED array before, during, or after exposure to light. The retinas were examined for function, structural changes, cell loss, and markers of stress and inflammation at 1 week and 1 month after exposure to damaging white light., Results: Bright light caused photoreceptor-specific cell death in control retinas. Significant upregulation of stress and neuroprotective factors and the presence of activated microglia were also noted after light-induced damage. Photobiomodulation profoundly attenuated histopathologic alterations in all three treatment groups. NIR treatment also abolished microglial invasion of the retina and significantly reduced the presence of stress and neuroprotectant molecules. Bright-light-induced reductions in photoreceptor function were significantly ameliorated by photobiomodulation in animals treated before and during exposure to damaging light. Photoreceptor function was initially reduced in animals treated after bright-light-induced damage, but recovered by 1 month after exposure., Conclusions: NIR photobiomodulation is protective against bright-light-induced retinal degeneration, even when NIR treatment is applied after exposure to light. This protective effect appears to involve a reduction of cell death and inflammation. Photobiomodulation has the potential to become an important treatment modality for the prevention or treatment of light-induced stress in the retina. More generally, it could be beneficial in the prevention and treatment of retinal conditions involving inflammatory mechanisms.
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- 2011
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27. Gene and noncoding RNA regulation underlying photoreceptor protection: microarray study of dietary antioxidant saffron and photobiomodulation in rat retina.
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Natoli R, Zhu Y, Valter K, Bisti S, Eells J, and Stone J
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- Animals, Cell Death drug effects, Cluster Analysis, Crocus chemistry, Cytoprotection drug effects, Cytoprotection radiation effects, Diet, Gene Expression Profiling, Gene Expression Regulation radiation effects, Immunologic Factors pharmacology, Photoreceptor Cells, Vertebrate drug effects, Photoreceptor Cells, Vertebrate metabolism, Photoreceptor Cells, Vertebrate radiation effects, Rats, Rats, Sprague-Dawley, Reproducibility of Results, Retina drug effects, Retina radiation effects, Reverse Transcriptase Polymerase Chain Reaction, Antioxidants pharmacology, Gene Expression Regulation drug effects, Light, Oligonucleotide Array Sequence Analysis, Photoreceptor Cells, Vertebrate cytology, RNA, Untranslated genetics, Retina metabolism
- Abstract
Purpose: To identify the genes and noncoding RNAs (ncRNAs) involved in the neuroprotective actions of a dietary antioxidant (saffron) and of photobiomodulation (PBM)., Methods: We used a previously published assay of photoreceptor damage, in which albino Sprague Dawley rats raised in dim cyclic illumination (12 h 5 lux, 12 h darkness) were challenged by 24 h exposure to bright (1,000 lux) light. Experimental groups were protected against light damage by pretreatment with dietary saffron (1 mg/kg/day for 21 days) or PBM (9 J/cm(2) at the eye, daily for 5 days). RNA from one eye of four animals in each of the six experimental groups (control, light damage [LD], saffron, PBM, saffronLD, and PBMLD) was hybridized to Affymetrix rat genome ST arrays. Quantitative real-time PCR analysis of 14 selected genes was used to validate the microarray results., Results: LD caused the regulation of 175 entities (genes and ncRNAs) beyond criterion levels (p<0.05 in comparison with controls, fold-change >2). PBM pretreatment reduced the expression of 126 of these 175 LD-regulated entities below criterion; saffron pretreatment reduced the expression of 53 entities (50 in common with PBM). In addition, PBM pretreatment regulated the expression of 67 entities not regulated by LD, while saffron pretreatment regulated 122 entities not regulated by LD (48 in common with PBM). PBM and saffron, given without LD, regulated genes and ncRNAs beyond criterion levels, but in lesser numbers than during their protective action. A high proportion of the entities regulated by LD (>90%) were known genes. By contrast, ncRNAs were prominent among the entities regulated by PBM and saffron in their neuroprotective roles (73% and 62%, respectively)., Conclusions: Given alone, saffron and (more prominently) PBM both regulated significant numbers of genes and ncRNAs. Given before retinal exposure to damaging light, thus while exerting their neuroprotective action, they regulated much larger numbers of entities, among which ncRNAs were prominent. Further, the downregulation of known genes and of ncRNAs was prominent in the protective actions of both neuroprotectants. These comparisons provide an overview of gene expression induced by two neuroprotectants and provide a basis for the more focused study of their mechanisms.
- Published
- 2010
28. Differential recovery of retinal function after mitochondrial inhibition by methanol intoxication.
- Author
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Seme MT, Summerfelt P, Neitz J, Eells JT, and Henry MM
- Subjects
- Adenosine Diphosphate metabolism, Adenosine Triphosphate metabolism, Animals, Electroretinography, Formates metabolism, Glutathione metabolism, Male, Mitochondria metabolism, Rats, Rats, Long-Evans, Retina drug effects, Retina metabolism, Retina pathology, Methanol toxicity, Mitochondria drug effects, Retina physiology
- Abstract
Purpose: The authors' laboratory has previously documented formate-induced retinal toxicity in a rodent model of methanol intoxication. These studies determined functional, bioenergetic, and structural recovery of the retina after methanol intoxication., Methods: Rats were intoxicated with methanol, and retinal function was assessed by electroretinography 72 hours after the initial dose of methanol and after a 72-hour recovery period. Retinal energy metabolites, glutathione (GSH) concentrations, and histology were determined at the same time points., Results: Both rod-dominated and UV-cone-mediated electroretinogram responses were profoundly attenuated in methanol-intoxicated rats. In rats allowed to recover from methanol intoxication, there was significant, although incomplete, recovery of rod-dominated retinal function. However, there was no demonstrable improvement in UV-cone-mediated responses. Retinal adenosine triphosphate (ATP), adenosine diphosphate (ADP), and GSH concentrations were significantly reduced after intoxication. Although retinal energy metabolites returned to control values after the recovery period, retinal GSH remained significantly depleted. Histopathologic changes were apparent in the photoreceptors after methanol intoxication, with evidence of inner segment swelling and mitochondrial disruption. In animals allowed to recover from methanol intoxication, there was no evidence of histopathology at the light microscopic level; however, ultrastructural studies revealed subtle photoreceptor mitochondrial alterations., Conclusions: These findings support the hypothesis that formate inhibits retinal mitochondrial function and increases oxidative stress. They also provide evidence for a differential sensitivity of photoreceptors to the cytotoxic actions of formic acid, with a partial recovery of rod-dominated responses and no recovery of UV-cone-mediated responses.
- Published
- 2001
29. Increased mitochondrial K(ATP) channel activity during chronic myocardial hypoxia: is cardioprotection mediated by improved bioenergetics?
- Author
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Eells JT, Henry MM, Gross GJ, and Baker JE
- Subjects
- Adaptation, Physiological drug effects, Adenosine Triphosphate metabolism, Animals, Animals, Newborn, Benzopyrans pharmacology, Cell Hypoxia physiology, Chronic Disease, Cytoprotection physiology, Decanoic Acids pharmacology, Dihydropyridines pharmacology, Energy Metabolism drug effects, Energy Metabolism physiology, Glyburide pharmacology, Heart Ventricles metabolism, Hemodynamics drug effects, Hydroxy Acids pharmacology, In Vitro Techniques, Membrane Potentials drug effects, Mitochondria, Heart drug effects, Potassium Channel Blockers, Potassium Channels agonists, Rabbits, Hypoxia metabolism, Mitochondria, Heart metabolism, Myocardial Ischemia metabolism, Myocardium metabolism, Potassium Channels metabolism
- Abstract
Increased resistance to myocardial ischemia in chronically hypoxic immature rabbit hearts is associated with activation of ATP-sensitive K(+) (K(ATP)) channels. We determined whether chronic hypoxia from birth alters the function of the mitochondrial K(ATP) channel. The K(ATP) channel opener bimakalim (1 micromol/L) increased postischemic recovery of left ventricular developed pressure in isolated normoxic (FIO(2)=0.21) hearts to values (42+/-4% to 67+/-5% ) not different from those of hypoxic controls but did not alter postischemic recovery of developed pressure in isolated chronically hypoxic (FIO(2)=0.12) hearts (69+/-5% to 72+/-5%). Conversely, the K(ATP) channel blockers glibenclamide (1 micromol/L) and 5-hydroxydecanoate (5-HD, 300 micromol/L) attenuated the cardioprotective effect of hypoxia but had no effect on postischemic recovery of function in normoxic hearts. ATP synthesis rates in hypoxic heart mitochondria (3.92+/-0.23 micromol ATP. min(-1). mg mitochondrial protein(-1)) were significantly greater than rates in normoxic hearts (2.95+/-0.08 micromol ATP. min(-1). mg mitochondrial protein(-1)). Bimakalim (1 micromol/L) decreased the rate of ATP synthesis in normoxic heart mitochondria consistent with mitochondrial K(ATP) channel activation and mitochondrial depolarization. The effect of bimakalim on ATP synthesis was antagonized by the K(ATP) channel blockers glibenclamide (1 micromol/L) and 5-HD (300 micromol/L) in normoxic heart mitochondria, whereas glibenclamide and 5-HD alone had no effect. In hypoxic heart mitochondria, the rate of ATP synthesis was not affected by bimakalim but was attenuated by glibenclamide and 5-HD. We conclude that mitochondrial K(ATP) channels are activated in chronically hypoxic rabbit hearts and implicate activation of this channel in the improved mitochondrial bioenergetics and cardioprotection observed.
- Published
- 2000
- Full Text
- View/download PDF
30. Ischemic preconditioning in rats: role of mitochondrial K(ATP) channel in preservation of mitochondrial function.
- Author
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Fryer RM, Eells JT, Hsu AK, Henry MM, and Gross GJ
- Subjects
- Adenosine Triphosphate biosynthesis, Adenosine Triphosphate metabolism, Animals, Decanoic Acids pharmacology, Diazoxide pharmacology, Hemodynamics drug effects, Hydroxy Acids pharmacology, Male, Membrane Proteins antagonists & inhibitors, Mitochondria, Heart metabolism, Myocardial Infarction pathology, Myocardium metabolism, Osmolar Concentration, Potassium Channels, Rats, Rats, Wistar, Ischemic Preconditioning, Myocardial, Membrane Proteins physiology, Mitochondria, Heart physiology
- Abstract
We examined the role of the sarcolemmal and mitochondrial K(ATP) channels in a rat model of ischemic preconditioning (IPC). Infarct size was expressed as a percentage of the area at risk (IS/AAR). IPC significantly reduced infarct size (7 +/- 1%) versus control (56 +/- 1%). The sarcolemmal K(ATP) channel-selective antagonist HMR-1098 administered before IPC did not significantly attenuate cardioprotection. However, pretreatment with the mitochondrial K(ATP) channel-selective antagonist 5-hydroxydecanoic acid (5-HD) 5 min before IPC partially abolished cardioprotection (40 +/- 1%). Diazoxide (10 mg/kg iv) also reduced IS/AAR (36.2 +/- 4.8%), but this effect was abolished by 5-HD. As an index of mitochondrial bioenergetic function, the rate of ATP synthesis in the AAR was examined. Untreated animals synthesized ATP at 2.12 +/- 0.30 micromol x min(-1) x mg mitochondrial protein(-1). Rats subjected to ischemia-reperfusion synthesized ATP at 0.67 +/- 0.06 micromol x min(-1) x mg mitochondrial protein(-1). IPC significantly increased ATP synthesis to 1.86 +/- 0.23 micromol x min(-1) x mg mitochondrial protein(-1). However, when 5-HD was administered before IPC, the preservation of ATP synthesis was attenuated (1.18 +/- 0.15 micromol x min(-1) x mg mitochondrial protein(-1)). These data are consistent with the notion that inhibition of mitochondrial K(ATP) channels attenuates IPC by reducing IPC-induced protection of mitochondrial function.
- Published
- 2000
- Full Text
- View/download PDF
31. Opioid-induced second window of cardioprotection: potential role of mitochondrial KATP channels.
- Author
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Fryer RM, Hsu AK, Eells JT, Nagase H, and Gross GJ
- Subjects
- Analgesics pharmacology, Animals, Benzylidene Compounds pharmacology, Blood Pressure, Coronary Circulation, Glyburide pharmacology, Hypoglycemic Agents pharmacology, Ischemic Preconditioning, Myocardial, Male, Myocardial Infarction drug therapy, Myocardial Infarction physiopathology, Myocardial Ischemia drug therapy, Myocardial Reperfusion Injury drug therapy, Myocardium chemistry, Naltrexone analogs & derivatives, Naltrexone pharmacology, Narcotic Antagonists pharmacology, Quinolines pharmacology, Rats, Rats, Wistar, Mitochondria chemistry, Myocardial Ischemia physiopathology, Myocardial Reperfusion Injury physiopathology, Potassium Channels physiology, Receptors, Opioid, delta physiology
- Abstract
Opioids have been previously shown to confer short-term cardioprotection against a prolonged ischemic insult. Therefore, the present study was designed to determine whether opioids can induce a delayed or "second window" of cardioprotection and to assess the potential involvement of the mitochondrial KATP channel. All rats were subjected to 30 minutes of ischemia and 2 hours of reperfusion (I/R). Control animals, injected with saline 24 hours before I/R, elicited an infarct size/area at risk (IS/AAR) of 62.9+/-3.4. TAN-67, a delta1-opioid receptor agonist, was administered 10 or 30 mg/kg IP 12, 24, 48, or 72 hours before I/R. TAN-67 (10 mg/kg) 12- or 24-hour pretreatment did not significantly reduce IS/AAR (62.1+/-6.3 and 43.3+/-7.3, respectively). Similarly, 12-hour pretreatment with TAN-67 (30 mg/kg) did not reduce IS/AAR (60.0+/-5.6); however, 24-hour pretreatment significantly reduced IS/AAR (34.5+/-5.9). Forty-eight-hour pretreatment with TAN-67 maximally reduced IS/AAR (29.2+/-7.0), and opioid-induced cardioprotection was lost after 72-hour pretreatment (61.7+/-3.8). TAN-67-induced cardioprotection could be abolished by pretreatment with the selective delta1-opioid receptor antagonist 7-benzylidenenaltrexone, BNTX, administered either 30 minutes before TAN-67 given 48 hours before I/R or 10 minutes before I/R in rats previously treated for 48 hours with TAN-67 (59.6+/-3.1 and 58.7+/-3.5, respectively). The involvement of the KATP channel was investigated with 2 inhibitors: glibenclamide, a nonselective KATP channel inhibitor, and 5-hydroxydecanoic acid, selective for the mitochondrial KATP channel in rabbits. Glibenclamide, administered 30 minutes before I/R in 48-hour TAN-67-pretreated rats, completely abolished cardioprotection (60. 4+/-3.2). Similarly, 5-hydroxydecanoic acid, administered 5 minutes before I/R in rats pretreated 48 hours previously with TAN-67, completely abolished cardioprotection (57.8+/-2.5). These results suggest that delta1-opioid receptor stimulation, 24 to 48 hours before an ischemic insult, produces a delayed cardioprotective effect that is possibly the result of mitochondrial KATP channel activation.
- Published
- 1999
- Full Text
- View/download PDF
32. In time of grief.
- Author
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Eells J
- Published
- 1977
- Full Text
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33. A VARIATIONAL METHOD IN THE THEORY OF HARMONIC INTEGRALS.
- Author
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Morrey CB and Eells J
- Published
- 1955
- Full Text
- View/download PDF
34. ON SUBMANIFOLDS OF CERTAIN FUNCTION SPACES.
- Author
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Eells J
- Published
- 1959
- Full Text
- View/download PDF
35. GEOMETRIC ASPECTS OF CURRENTS AND DISTRIBUTIONS.
- Author
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Eells J
- Published
- 1955
- Full Text
- View/download PDF
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