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Journal articles on the topic 'E J (Enos John)'

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Published: 4 June 2021

Last updated: 12 February 2022

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1

Raphael, D. D. "J. S. Mill's Proof of the Principle of Utility." Utilitas 6, no. 1 (May 1994): 55–63. http://dx.doi.org/10.1017/s0953820800001321.

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In the introductory chapter of his essay on Utilitarianism, John Stuart Mill says his aim is to contribute towards the understanding of utilitarianism and towards ‘such proof as it is susceptible of’. He immediately adds that ‘this cannot be proof in the ordinary and popular meaning of the term’ because ‘ultimate ends are not amenable to direct proof’. A proof that something is good has to show that it is ‘a means to something admitted to be good without proof’. But, he goes on, this does not imply that a formula of ultimate ends can only be accepted on ‘blind impulse, or arbitrary choice’. It can be rationally discussed and subjected to proof in a wider sense of that word. ‘Considerations may be presented capable of determining the intellect either to give or withhold its assent to the doctrine; and this is equivalent to proof.’

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2

Russell, Julian. "The last students at the Scots College, Douai." Innes Review 58, no. 2 (November 2007): 222–25. http://dx.doi.org/10.3366/e0020157x07000091.

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The register of the Scots College, Douai, was printed in Records of the Scots Colleges I, New Spalding Club (Aberdeen, 1906).1 It ends in 1772, but does not contain the names of the secular students after 1765, when the Jesuits were expelled from France. The rector, John Riddoch, S. J., and his students moved to Dinant, taking the register with them, and it is the Dinant register that is printed. The college at Douai re-opened with a secular priest, Robert Grant, as rector, but no register survives for the period from 1765 until the final closure in 1793.2

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3

Kinzer, Bruce L. "The 1870 Education Bill and the Method of J. S. Mill's Later Politics." Albion 29, no. 2 (1997): 223–45. http://dx.doi.org/10.2307/4051811.

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The last fourteen years of John Stuart Mill's life (1859-1873), which followed the death of Harriet Taylor, possessed a hefty political content. They saw the publication of his essays on parliamentary reform and Considerations on Representative Government, his impassioned identification with the North in the American Civil War, the eventful parliamentary career sandwiched between the Westminster elections of 1865 and 1868, and a final phase of activity associated with causes such as women's suffrage and land tenure reform. When Mill acted politically he usually did so with strong feeling, but in his search to give deeply held principles practical effect he understood the need for dispassionate adaptation of means to ends. Both the feeling and the adaptation are evident in his treatment of the elementary education question in 1870, a treatment that vividly illustrates how Mill operated during the decade and a half before his death.Of the host of legislation Gladstone's first administration proposed, only one item, the 1870 Education Bill, elicited a congregation of public responses from Mill. Of course, Mill's political activity in the several years following his defeat at Westminster in autumn 1868 was not confined to the adoption of a stance on ministerial measures. With respect to women's suffrage and land reform Mill was not about to wait on any government, and his conspicuous connections with the National Society for Women's Suffrage and the Land Tenure Reform Association attracted notice at the time and have been the subject of comment since. Moreover, during his last years Mill continued to cultivate his contacts in the world of London working-class radicalism, particularly with George Odger, William Randal Cremer, and George Howell. Whereas Mill's parliamentary career has been explored in some detail, the political character of his post-Westminster years has received less attention.

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4

JOHANSSON, S. RYAN. "Death at the opposite ends of the Eurasian continent: mortality trends in Taiwan and the Netherlands, 1850-1945 - Edited by Theo Engelen, John R. Shepherd, and Wen-shan Yang." Economic History Review 65, no. 3 (July 2, 2012): 1191–92. http://dx.doi.org/10.1111/j.1468-0289.2011.00644_17.x.

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5

Holdsworth, Kevin. "Radiant Days: Writings by Enos Mills ed. by John Dotson." Western American Literature 30, no. 2 (1995): 214–15. http://dx.doi.org/10.1353/wal.1995.0046.

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6

Ali, Md Monsur, Srinivas A. Kandadai, and Yingfu Li. "Characterization of pH3DZ1 — An RNA-cleaving deoxyribozyme with optimal activity at pH 3." Canadian Journal of Chemistry 85, no. 4 (April 1, 2007): 261–73. http://dx.doi.org/10.1139/v07-017.

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We previously described a cis-acting RNA-cleaving deoxyribozyme known as pH3DZ1 that exhibits optimal catalytic activity at pH 3.0 (Zhongjie Liu, Shirley H. Mei, John D. Brennan, and Yingfu Li. J. Am. Chem. Soc. 125, 7539 (2003)). This DNA catalyst was made of a 99-nucleotide (nt) catalytic domain covalently linked to a 23-nt DNA–RNA chimeric substrate containing a single ribonucleotide as the cleavage site. In the present work, we conducted an extensive sequence examination of this deoxyribozyme via nucleotide truncation and reselection experiments, with a goal to minimize its size and identify the nucleotides that are crucial to its catalytic function. A trans-acting deoxyribozyme that can process an external substrate was also successfully designed. Stretches of 30 and 17 nucleotides from the 5′ and 3′ ends of the trans catalyst, respectively, were found to be completely dispensable; in contrast, few nucleotides could be deleted internally without producing a detrimental effect. The reselection experiment led to the discovery of 7 and 5 absolutely conserved nucleotides located at the 5′ and 3′ ends of the minimized catalyst, respectively, separated by a 31-nt element in which 14 highly conserved nucleotides were scattered among 17 variable nucleotides. The shortened deoxyribozyme and the original catalyst showed a similar pH profile with the optimal activity at pH 3; however, the minimized deoxyribozyme still exhibited strong catalytic activity at pH 2.5, while the full-length catalyst was barely active at this pH. Finally, it was found that this deoxyribozyme generated two cleavage fragments, one with 2′,3′-cyclic phosphate and the other with 5′-OH.Key words: DNA, deoxyribozyme, RNA cleavage, in vitro selection, catalysis.

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7

Lee, Gregory S., Matthew B. Neiditch, Richard R. Sinden, and David B. Roth. "Targeted Transposition by the V(D)J Recombinase." Molecular and Cellular Biology 22, no. 7 (April 1, 2002): 2068–77. http://dx.doi.org/10.1128/mcb.22.7.2068-2077.2002.

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ABSTRACT Cleavage by the V(D)J recombinase at a pair of recombination signal sequences creates two coding ends and two signal ends. The RAG proteins can integrate these signal ends, without sequence specificity, into an unrelated target DNA molecule. Here we demonstrate that such transposition events are greatly stimulated by—and specifically targeted to—hairpins and other distorted DNA structures. The mechanism of target selection by the RAG proteins thus appears to involve recognition of distorted DNA. These data also suggest a novel mechanism for the formation of alternative recombination products termed hybrid joints, in which a signal end is joined to a hairpin coding end. We suggest that hybrid joints may arise by transposition in vivo and propose a new model to account for some recurrent chromosome translocations found in human lymphomas. According to this model, transposition can join antigen receptor loci to partner sites that lack recombination signal sequence elements but bear particular structural features. The RAG proteins are capable of mediating all necessary breakage and joining events on both partner chromosomes; thus, the V(D)J recombinase may be far more culpable for oncogenic translocations than has been suspected.

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8

Förstermann, Ulrich, and Huige Li. "Therapeutic effect of enhancing endothelial nitric oxide synthase (eNOS) expression and preventing eNOS uncoupling." British Journal of Pharmacology 164, no. 2 (August 22, 2011): 213–23. http://dx.doi.org/10.1111/j.1476-5381.2010.01196.x.

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9

Igarashi, Junsuke, Sylvie G. Bernier, and Thomas Michel. "Sphingosine 1-Phosphate and Activation of Endothelial Nitric-oxide Synthase." Journal of Biological Chemistry 276, no. 15 (January 17, 2001): 12420–26. http://dx.doi.org/10.1074/jbc.m008375200.

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Sphingosine 1-phosphate (S1P) is a platelet-derived sphingolipid that elicits numerous biological responses in endothelial cells mediated by a family of G protein-coupled EDG receptors. Stimulation of EDG receptors by S1P has been shown to activate the endothelial isoform of nitric-oxide synthase (eNOS) in heterologous expression systems (Igarashi, J., and Michel, T. (2000)J. Biol. Chem.275, 32363–32370). However, the signaling pathways that modulate eNOS regulation by S1P/EDG in vascular endothelial cells remain less well understood. We now report that S1P treatment of bovine aortic endothelial cells (BAEC) acutely increases eNOS enzyme activity; the EC50for S1P activation of eNOS is ∼10 nm. The magnitude of eNOS activation by S1P in BAEC is equivalent to that elicited by the agonist bradykinin. S1P treatment activates Akt, a protein kinase implicated in phosphorylation of eNOS. S1P treatment of BAEC leads to eNOS phosphorylation at Ser1179, a residue phosphorylated by Akt; an eNOS mutant in which this Akt phosphorylation site is inactivated shows attenuated S1P-induced eNOS activation. S1P-induced activation both of Akt and of eNOS is inhibited by pertussis toxin, by the phosphoinositide 3-kinase inhibitor wortmannin, and by the intracellular calcium chelator BAPTA (1,2-bis(aminophenoxy)ethane-N,N,N′,N′-tetraacetic acid). By contrast to S1P, activation of G protein-coupled bradykinin B2 receptors neither activates kinase Akt nor promotes Ser1179eNOS phosphorylation despite robustly activating eNOS enzyme activity. Understanding the differential regulation of protein kinase pathways by S1P and bradykinin may lead to the identification of new points for eNOS regulation in vascular endothelial cells.

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10

Yin, Bu, Velibor Savic, Marisa M. Juntilla, Andrea L. Bredemeyer, Katherine S. Yang-Iott, Beth A. Helmink, Gary A. Koretzky, Barry P. Sleckman, and Craig H. Bassing. "Histone H2AX stabilizes broken DNA strands to suppress chromosome breaks and translocations during V(D)J recombination." Journal of Experimental Medicine 206, no. 12 (November 2, 2009): 2625–39. http://dx.doi.org/10.1084/jem.20091320.

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The H2AX core histone variant is phosphorylated in chromatin around DNA double strand breaks (DSBs) and functions through unknown mechanisms to suppress antigen receptor locus translocations during V(D)J recombination. Formation of chromosomal coding joins and suppression of translocations involves the ataxia telangiectasia mutated and DNA-dependent protein kinase catalytic subunit serine/threonine kinases, each of which phosphorylates H2AX along cleaved antigen receptor loci. Using Abelson transformed pre–B cell lines, we find that H2AX is not required for coding join formation within chromosomal V(D)J recombination substrates. Yet we show that H2AX is phosphorylated along cleaved Igκ DNA strands and prevents their separation in G1 phase cells and their progression into chromosome breaks and translocations after cellular proliferation. We also show that H2AX prevents chromosome breaks emanating from unrepaired RAG endonuclease-generated TCR-α/δ locus coding ends in primary thymocytes. Our data indicate that histone H2AX suppresses translocations during V(D)J recombination by creating chromatin modifications that stabilize disrupted antigen receptor locus DNA strands to prevent their irreversible dissociation. We propose that such H2AX-dependent mechanisms could function at additional chromosomal locations to facilitate the joining of DNA ends generated by other types of DSBs.

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11

Wada, Yoshihisa, Reina Umeno, Hajime Nagasu, Megumi Kondo, Atsuyuki Tokuyama, Hiroyuki Kadoya, Kengo Kidokoro, et al. "Endothelial Dysfunction Accelerates Impairment of Mitochondrial Function in Ageing Kidneys via Inflammasome Activation." International Journal of Molecular Sciences 22, no. 17 (August 27, 2021): 9269. http://dx.doi.org/10.3390/ijms22179269.

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Chronic kidney disease is a common problem in the elderly and is associated with increased mortality. We have reported on the role of nitric oxide, which is generated from endothelial nitric oxide synthase (eNOS), in the progression of aged kidneys. To elucidate the role of endothelial dysfunction and the lack of an eNOS-NO pathway in ageing kidneys, we conducted experiments using eNOS and ASC-deficient mice. C57B/6 J mice (wild type (WT)), eNOS knockout (eNOS KO), and ASC knockout (ASC KO) mice were used in the present study. Then, eNOS/ASC double-knockout (eNOS/ASC DKO) mice were generated by crossing eNOS KO and ASC KO mice. These mice were sacrificed at 17−19 months old. The Masson positive area and the KIM-1 positive area tended to increase in eNOS KO mice, compared with WT mice, but not eNOS/ASC DKO mice. The COX-positive area was significantly reduced in eNOS KO mice, compared with WT and eNOS/ASC DKO mice. To determine whether inflammasomes were activated in infiltrating macrophages, the double staining of IL-18 and F4/80 was performed. IL-18 and F4/80 were found to be co-localised in the tubulointerstitial areas. Inflammasomes play a pivotal role in inflammaging in ageing kidneys. Furthermore, inflammasome activation may accelerate cellular senescence via mitochondrial dysfunction. The importance of endothelial function as a regulatory mechanism suggests that protection of endothelial function may be a potential therapeutic target.

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12

Ortiz, Pablo A., Nancy J. Hong, and Jeffrey L. Garvin. "Luminal flow induces eNOS activation and translocation in the rat thick ascending limb. II. Role of PI3-kinase and Hsp90." American Journal of Physiology-Renal Physiology 287, no. 2 (August 2004): F281—F288. http://dx.doi.org/10.1152/ajprenal.00383.2003.

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Endothelial nitric oxide synthase (eNOS) regulates NaCl absorption by the thick ascending limb of the loop of Henle (THAL). We found that augmenting luminal flow induces eNOS activation and translocation to the apical membrane of THALs (Ortiz PA, Hong NJ, and Garvin JL. Am J Physiol Renal Physiol 287: F274–F280, 2004). In other cells, eNOS activation by shear stress is mediated by phosphatidylinositol 3-OH kinase (PI3)-kinase. We hypothesized that luminal flow induces eNOS activation via PI3-kinase. Pretreatment of THALs with wortmannin, a PI3-kinase inhibitor, significantly reduced flow-induced nitric oxide (NO) release by 75% (from 53.6 ± 6 to 13.2 ± 5.7 pA/mm). Increasing luminal flow from 0 to 20 nl/min induced eNOS translocation to the apical membrane, whereas in the presence of wortmannin eNOS translocation was prevented (basolateral = 32 ± 2%, middle = 38 ± 1%, apical = 30 ± 1%, n = 5, not significant vs. no flow). We next studied which PI3-kinase product mediates eNOS translocation. Addition of PI( 3 , 4 , 5 )P3 (5 μM) in the absence of flow increased NO levels ( P < 0.05) and induced eNOS translocation to the apical membrane (from 40 ± 4 to 60 ± 2% of total eNOS, n = 6, P < 0.05). Incubation with PI( 3 , 4 )P2 or PI( 4 , 5 )P2 did not change eNOS localization. We next tested whether heat shock protein (Hsp)90 is involved in eNOS translocation. The Hsp90 inhibitor geldanamycin blocked flow-induced eNOS translocation to the apical membrane ( n = 6). Flow also induced translocation of Hsp90 to the apical membrane (from 35 ± 2 to 57 ± 2%; P < 0.05) in a PI3-kinase-dependent manner. We conclude that luminal flow induces eNOS translocation and activation in the THAL via PI3-kinase and that Hsp90 is involved in eNOS translocation to the apical membrane.

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13

Liang, Zhuoyi, Vipul Kumar, Marie Le Bouteiller, Jeffrey Zurita, Josefin Kenrick, Sherry G. Lin, Jiangman Lou, et al. "Ku70 suppresses alternative end joining in G1-arrested progenitor B cells." Proceedings of the National Academy of Sciences 118, no. 21 (May 18, 2021): e2103630118. http://dx.doi.org/10.1073/pnas.2103630118.

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Classical nonhomologous end joining (C-NHEJ) repairs DNA double-strand breaks (DSBs) throughout interphase but predominates in G1 phase when homologous recombination is unavailable. Complexes containing the Ku70/80 (“Ku”) and XRCC4/ligase IV (Lig4) core C-NHEJ factors are required, respectively, for sensing and joining DSBs. While XRCC4/Lig4 are absolutely required for joining RAG1/2 endonuclease (“RAG”)-initiated DSBs during V(D)J recombination in G1-phase progenitor lymphocytes, cycling cells deficient for XRCC4/Lig4 also can join chromosomal DSBs by alternative end-joining (A-EJ) pathways. Restriction of V(D)J recombination by XRCC4/Lig4-mediated joining has been attributed to RAG shepherding V(D)J DSBs exclusively into the C-NHEJ pathway. Here, we report that A-EJ of DSB ends generated by RAG1/2, Cas9:gRNA, and Zinc finger endonucleases in Lig4-deficient G1-arrested progenitor B cell lines is suppressed by Ku. Thus, while diverse DSBs remain largely as free broken ends in Lig4-deficient G1-arrested progenitor B cells, deletion of Ku70 increases DSB rejoining and translocation levels to those observed in Ku70-deficient counterparts. Correspondingly, while RAG-initiated V(D)J DSB joining is abrogated in Lig4-deficient G1-arrested progenitor B cell lines, joining of RAG-generated DSBs in Ku70-deficient and Ku70/Lig4 double-deficient lines occurs through a translocation-like A-EJ mechanism. Thus, in G1-arrested, Lig4-deficient progenitor B cells are functionally end-joining suppressed due to Ku-dependent blockage of A-EJ, potentially in association with G1-phase down-regulation of Lig1. Finally, we suggest that differential impacts of Ku deficiency versus Lig4 deficiency on V(D)J recombination, neuronal apoptosis, and embryonic development results from Ku-mediated inhibition of A-EJ in the G1 cell cycle phase in Lig4-deficient developing lymphocyte and neuronal cells.

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14

Kotsoni, Eleni, Denis Mareschal, Gergely Csibra, and Mark H. Johnson. "Common-onset Visual Masking in Infancy: Behavioral and Electrophysiological Evidence." Journal of Cognitive Neuroscience 18, no. 6 (June 2006): 966–73. http://dx.doi.org/10.1162/jocn.2006.18.6.966.

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Common-onset visual masking (COVM) occurs when a mask and a target have common onset but delayed offset, with the mask persisting beyond the duration of the target [Di Lollo, V., Enns, J. T., & Rensink, R. A. Competition for consciousness among visual events: The psychophysics of reentrant visual events. Journal of Experimental Psychology: General, 129, 481–507, 2000]. We report the first behavioral and electrophysiological evidence of COVM in infants. An initial behavioral study included a familiarization phase during which a visual pattern (the target) surrounded by four black dots (the mask) was flashed 15 times to the infant. In the “unmasked” condition, the mask disappeared with the target. In the “masked” condition, the mask remained on the screen after deletion of the target for a further 93 msec. During the test phase, the familiar target pattern was paired with a new pattern. Infants in the unmasked condition showed a significant familiarity preference, suggesting that they had encoded the target during familiarization, whereas those in the masked condition showed no preference, suggesting that they had not encoded the target during familiarization. In the second experiment, high-density event-related potentials were used to investigate the electrophysiological pattern of activity that accompanies COVM. Six-month-old infants viewed both masked and unmasked conditions. Electrophysiological data indicated that over posterior channels the masked condition elicited a larger amplitude positive wave around 300 msec after stimulus onset than trials in the unmasked condition.

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15

Kalivendi, Shasi V., Srigiridhar Kotamraju, Hongtao Zhao, Joy Joseph, and B. Kalyanaraman. "Doxorubicin-induced Apoptosis Is Associated with Increased Transcription of Endothelial Nitric-oxide Synthase." Journal of Biological Chemistry 276, no. 50 (September 28, 2001): 47266–76. http://dx.doi.org/10.1074/jbc.m106829200.

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The clinical efficacy of the antitumor antibiotic drug doxorubicin (DOX) is severely limited by its dose-limiting cardiotoxicity in cancer patients. DOX-induced generation of reactive oxygen species was proposed to be a major mechanism of its cardiotoxicity. Previously, we showed that DOX undergoes a reductive activation at the reductase domain of endothelial nitric-oxide synthase (eNOS) forming the semiquinone and superoxide (Vásquez-Vivar, J., Martasek, P., Hogg, N., Masters, B. S. S., Pritchard, K. A., Jr., and Kalyanaraman, B. (1997)Biochemistry36, 11293–11297). In this report, we provide evidence for DOX-induced increase in eNOS transcription and protein expression in bovine aortic endothelial cells (BAEC). We propose that DOX-induced hydrogen peroxide formation is responsible for the increased transcription of eNOS. BAEC treated with antisense eNOS oligonucleotide inhibits DOX-induced endothelial apoptosis. Treatment with antioxidants restored the levels of antiapoptotic proteins (Hsp70 and Bcl-2) in DOX-treated BAEC. DOX-induced intracellular oxidative stress, as measured by oxidation of dichlorodihydrofluorescein diacetate to dichlorofluorescein and hydroethidium to ethidium, was inhibited by antisense eNOS oligonucleotide and antioxidant treatment. Furthermore, antiapoptotic antioxidants (e.g.FeTBAP, ebselen, and α-phenyl-tert-butyl nitrone) inhibited DOX-induced eNOS transcription. We conclude that DOX-induced apoptosis is linked to the redox activation of DOX by eNOS.

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16

Ortiz, P. A., and J. L. Garvin. "Trafficking and activation of eNOS in epithelial cells." Acta Physiologica Scandinavica 179, no. 2 (September 19, 2003): 107–14. http://dx.doi.org/10.1046/j.1365-201x.2003.01207.x.

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17

Casey, Darren P., Kenichi Ueda, Lauren Wegman-Points, and Gary L. Pierce. "Muscle contraction induced arterial shear stress increases endothelial nitric oxide synthase phosphorylation in humans." American Journal of Physiology-Heart and Circulatory Physiology 313, no. 4 (October 1, 2017): H854—H859. http://dx.doi.org/10.1152/ajpheart.00282.2017.

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We determined if local increases in brachial artery shear during repetitive muscle contractions induce changes in protein expression of endothelial nitric oxide synthase (eNOS) and/or phosphorylated (p-)eNOS at Ser1177, the primary activation site on eNOS, in endothelial cells (ECs) of humans. Seven young male subjects (25 ± 1 yr) performed 20 separate bouts (3 min each) of rhythmic forearm exercise at 20% of maximum over a 2-h period. Each bout of exercise was separated by 3 min of rest. An additional six male subjects (24 ± 1 yr) served as time controls (no exercise). ECs were freshly isolated from the brachial artery using sterile J-wires through an arterial catheter at baseline and again after the 2-h exercise or time control period. Expression of eNOS or p-eNOS Ser1177 in ECs was determined via immunofluorescence. Brachial artery mean shear rate was elevated compared with baseline and the time control group throughout the 2-h exercise protocol ( P < 0.001). p-eNOS Ser1177 expression was increased 57% in ECs in the exercise group [0.06 ± 0.01 vs. 0.10 ± 0.02 arbitrary units (au), P = 0.02] but not in the time control group (0.08 ± 0.01 vs. 0.07 ± 0.01 au, P = 0.72). In contrast, total eNOS expression did not change in either the exercise (0.13 ± 0.04 vs. 0.12 ± 0.03 au) or time control (0.12 ± 0.03 vs. 0.11 ± 0.03 au) group ( P > 0.05 for both). Our novel results suggest that elevations in brachial artery shear increase eNOS Ser1177 phosphorylation in the absence of changes in total eNOS in ECs of young healthy male subjects, suggesting that this model is sufficient to alter posttranslational modification of eNOS activity in vivo in humans. NEW & NOTEWORTHY Elevations in brachial artery shear in response to forearm exercise increased endothelial nitric oxide synthase Ser1177 phosphorylation in brachial artery endothelial cells of healthy humans. Our present study provides the first evidence in humans that muscle contraction-induced increases in conduit arterial shear lead to in vivo posttranslational modification of endothelial nitric oxide synthase activity in endothelial cells.

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18

Loeser, John D. "John J. Bonica." PAIN 158, no. 10 (October 2017): 1845–46. http://dx.doi.org/10.1097/j.pain.0000000000000962.

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19

Linton, Otha W., Brad Short, and Shawn Farley. "John J. Curry." Radiology 279, no. 2 (May 2016): 655. http://dx.doi.org/10.1148/radiol.2016154039.

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20

Shine, Keith P. "John J. Barnett." Weather 66, no. 1 (December 24, 2010): 27. http://dx.doi.org/10.1002/wea.738.

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21

Partin, Clyde. "John J. Osborn." Clinical Cardiology 21, no. 1 (January 1998): 66–68. http://dx.doi.org/10.1002/clc.4960210114.

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22

Martin, Ron, Roy Ringo, and Lee Teng. "John J. Livingood." Physics Today 40, no. 7 (July 1987): 90. http://dx.doi.org/10.1063/1.2820129.

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23

Meny, Geralyn M. "John J. Moulds." Immunohematology 27, no. 4 (2020): 117. http://dx.doi.org/10.21307/immunohematology-2019-184.

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24

Linda Wang. "John J. Cawley." C&EN Global Enterprise 99, no. 5 (February 8, 2021): 36. http://dx.doi.org/10.1021/cen-09905-obits3.

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25

NASEEM, K. M. "eNOS, iNOS or no NOS, that is the question." Journal of Thrombosis and Haemostasis 6, no. 8 (August 2008): 1373–75. http://dx.doi.org/10.1111/j.1538-7836.2008.03035.x.

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26

Dikalova, Anna, Judy L. Aschner, Mark R. Kaplowitz, Marshall Summar, and Candice D. Fike. "Tetrahydrobiopterin oral therapy recouples eNOS and ameliorates chronic hypoxia-induced pulmonary hypertension in newborn pigs." American Journal of Physiology-Lung Cellular and Molecular Physiology 311, no. 4 (October 1, 2016): L743—L753. http://dx.doi.org/10.1152/ajplung.00238.2016.

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We previously showed that newborn piglets who develop pulmonary hypertension during exposure to chronic hypoxia have diminished pulmonary vascular nitric oxide (NO) production and evidence of endothelial NO synthase (eNOS) uncoupling (Fike CD, Dikalova A, Kaplowitz MR, Cunningham G, Summar M, Aschner JL. Am J Respir Cell Mol Biol 53: 255–264, 2015). Tetrahydrobiopterin (BH4) is a cofactor that promotes eNOS coupling. Current clinical strategies typically invoke initiating treatment after the diagnosis of pulmonary hypertension, rather than prophylactically. The major purpose of this study was to determine whether starting treatment with an oral BH4 compound, sapropterin dihydrochloride (sapropterin), after the onset of pulmonary hypertension would recouple eNOS in the pulmonary vasculature and ameliorate disease progression in chronically hypoxic piglets. Normoxic (control) and hypoxic piglets were studied. Some hypoxic piglets received oral sapropterin starting on day 3 of hypoxia and continued throughout an additional 7 days of hypoxic exposure. Catheters were placed for hemodynamic measurements, and pulmonary arteries were dissected to assess eNOS dimer-to-monomer ratios (a measure of eNOS coupling), NO production, and superoxide (O2·−) generation. Although higher than in normoxic controls, pulmonary vascular resistance was lower in sapropterin-treated hypoxic piglets than in untreated hypoxic piglets. Consistent with eNOS recoupling, eNOS dimer-to-monomer ratios and NO production were greater and O2·− generation was less in pulmonary arteries from sapropterin-treated than untreated hypoxic animals. When started after disease onset, oral sapropterin treatment inhibits chronic hypoxia-induced pulmonary hypertension at least in part by recoupling eNOS in the pulmonary vasculature of newborn piglets. Rescue treatment with sapropterin may be an effective strategy to inhibit further development of pulmonary hypertension in newborn infants suffering from chronic cardiopulmonary conditions associated with episodes of prolonged hypoxia.

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27

Martinelli, Roberta, Matthew Gegg, Rebecca Longbottom, Peter Adamson, Patric Turowski, and John Greenwood. "ICAM-1–mediated Endothelial Nitric Oxide Synthase Activation via Calcium and AMP-activated Protein Kinase Is Required for Transendothelial Lymphocyte Migration." Molecular Biology of the Cell 20, no. 3 (February 2009): 995–1005. http://dx.doi.org/10.1091/mbc.e08-06-0636.

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As a gatekeeper of leukocyte trafficking the vasculature fulfills an essential immune function. We have recently shown that paracellular transendothelial lymphocyte migration is controlled by intercellular adhesion molecule 1 (ICAM-1)-mediated vascular endothelial cadherin (VEC) phosphorylation [Turowski et al., J. Cell Sci. 121, 29–37 (2008)]. Here we show that endothelial nitric oxide synthase (eNOS) is a critical regulator of this pathway. ICAM-1 stimulated eNOS by a mechanism that was clearly distinct from that utilized by insulin. In particular, phosphorylation of eNOS on S1177 in response to ICAM-1 activation was regulated by src family protein kinase, rho GTPase, Ca2+, CaMKK, and AMPK, but not Akt/PI3K. Functional neutralization of any component of this pathway or its downstream effector guanylyl cyclase significantly reduced lymphocyte diapedesis across the endothelial monolayer. In turn, activation of NO signaling promoted lymphocyte transmigration. The eNOS signaling pathway was required for T-cell transmigration across primary rat and human microvascular endothelial cells and also when shear flow was applied, suggesting that this pathway is ubiquitously used. These data reveal a novel and essential role of eNOS in basic immune function and provide a key link in the molecular network governing endothelial cell compliance to diapedesis.

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28

Zanoni, Thomas A., L. J. Dorr, and B. Sergios D. BioLlania. "John J. Wurdack Festschrift." Brittonia 50, no. 1 (January 1998): 18. http://dx.doi.org/10.2307/2807712.

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29

Becker, James M. "JOHN J. BYRNE, MD." Transactions of the ... Meeting of the American Surgical Association 123, &NA; (2005): 322–23. http://dx.doi.org/10.1097/00153307-200501230-00038.

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30

Keller, John J. "Chair: John J. Keller." Proceedings of the ASIL Annual Meeting 88 (1994): 271. http://dx.doi.org/10.1017/s0272503700082173.

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31

Loeser, John D. "John J. Bonica, MD." Journal of Musculoskeletal Pain 1, no. 1 (January 1993): 9–12. http://dx.doi.org/10.1300/j094v01n01_02.

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32

ZWANGER, JEROME. "John J. Magovern, M.D." Radiology 166, no. 2 (February 1988): 583. http://dx.doi.org/10.1148/radiology.166.2.583-b.

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33

Douglas, J. D. M. "John A J Macleod." BMJ 339, oct20 3 (October 20, 2009): b4296. http://dx.doi.org/10.1136/bmj.b4296.

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34

Ward Casscells, S. "John J. Joyce, M.D." Arthroscopy: The Journal of Arthroscopic & Related Surgery 7, no. 2 (June 1991): 252–53. http://dx.doi.org/10.1016/0749-8063(91)90117-g.

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35

Nesher, Nachum, Inna Frolkis, Doron Schwartz, Tamara Chernichovski, Sharon Levi, Yael Pri-Paz, Gil Chernin, et al. "l-Arginine improves endothelial function, independently of arginine uptake, in aortas from chronic renal failure female rats." American Journal of Physiology-Renal Physiology 306, no. 4 (February 15, 2014): F449—F456. http://dx.doi.org/10.1152/ajprenal.00457.2013.

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Endothelial cell dysfunction (ECD) is a common feature of chronic renal failure (CRF). Defective nitric oxide (NO) generation due to decreased endothelial nitric oxide synthase (eNOS) activity is a crucial parameter characterizing ECD. Decreased activity of cationic amino acid transporter-1 (CAT-1), the selective arginine transporter of eNOS, has been shown to inhibit eNOS in uremia. Recently, we failed to demonstrate a decrease in glomerular arginine transport in uremic female rats (Schwartz IF, Grupper A, Soetendorp H, Hillel O, Laron I, Chernichovski T, Ingbir M, Shtabski A, Weinstein T, Chernin G, Shashar M, Hershkoviz R, Schwartz D. Am J Physiol Renal Physiol 303: F396–F404, 2012). The current experiments were designed to determine whether sexual dimorphism which characterizes glomerular arginine transport system in uremia involves the systemic vasculature as well and to assess the effect of l-arginine in such conditions. Contractile and vasodilatory responses, ultrastructural changes, and measures of the l-arginine-NO system were performed in thoracic aortas of female rats subjected to ⅚ nephrectomy. The contractile response to KCl was significantly reduced, and acetylcholine-induced vasodilation was significantly impaired in aortas from CRF dames compared with healthy rats. Both of these findings were prevented by the administration of arginine in the drinking water. The decrease in both cGMP generation, a measure of eNOS activity, and aortic eNOS and phosphorylated eNOS abundance observed in CRF rats was completely abolished by l-arginine, while arginine transport and CAT-1 protein were unchanged in all experimental groups. Arginine decreased both serum levels of advanced glycation end products and the asymmetrical dimethylarginine/arginine ratio and restored the endothelial ultrastructure in CRF rats. In conclusion. arginine administration has a profound beneficial effect on ECD, independently of cellular arginine uptake, in CRF female rats.

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Gruber, H.-J., C. Bernecker, A. Lechner, S. Weiss, M. Wallner-Blazek, A. Meinitzer, G. Höbarth, et al. "Increased nitric oxide stress is associated with migraine." Cephalalgia 30, no. 4 (September 1, 2009): 486–92. http://dx.doi.org/10.1111/j.1468-2982.2009.01964.x.

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Nitric oxide (NO) has been implicated in migraine attacks, but the role of NO in migraine remains unclear. We here hypothesize that increased NO in the headache-free period is associated with migraine. One hundred and thirty probands participated in this study. Various parameters of the NO pathway, such as nitrate, nitrite, arginine, citrulline, nitrosylated proteins, asymmetric dimethylarginine, symmetrical dimethylarginine, expression of endothelial nitric oxide synthase (eNOS) and inducible nitric oxide synthase and two polymorphisms of eNOS were investigated. We found significant increased nitrate and decreased nitrite levels in migraineurs in the headache-free period. Nitrate and nitrite levels showed a significant inverse correlation. Logistic regression revealed an odds ratio of 3.6 for migraine. Other parameters of the NO pathway were neither altered in migraineurs nor correlated with nitrate. We show here that migraine patients suffer under sustained increased nitrosative stress in the headache-free period, which is associated with a 3.6-fold higher risk for migraine.

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37

Mackie, J. "John Richardson." BMJ 326, no. 7379 (January 4, 2003): 54j—54. http://dx.doi.org/10.1136/bmj.326.7379.54/j.

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38

RAKHIT, AMIT, COLIN T. MAGUIRE, HIROKO WAKIMOTO, JOSEF GEHRMANN, GORDON K. LI, RALPH A. KELLY, THOMAS MICHEL, and CHARLES I. BERUL. "In Vivo Electrophysiologic Studies in Endothelial Nitric Oxide Synthase (eNOS)-Deficient Mice." Journal of Cardiovascular Electrophysiology 12, no. 11 (November 2001): 1295–301. http://dx.doi.org/10.1046/j.1540-8167.2001.01295.x.

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39

Lee, Y. H., and G. G. Song. "Associations between eNOS polymorphisms and susceptibility to Behcet’s disease: a meta-analysis." Journal of the European Academy of Dermatology and Venereology 26, no. 10 (September 29, 2011): 1266–71. http://dx.doi.org/10.1111/j.1468-3083.2011.04280.x.

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40

Lee, Yung‐Chin, Shu‐Pin Huang, Chia‐Chu Liu, Yi‐Hsin Yang, Hsin‐Chih Yeh, Wei‐Ming Li, Wen‐Jeng Wu, et al. "The Association of eNOS G894T Polymorphism with Metabolic Syndrome and Erectile Dysfunction." Journal of Sexual Medicine 9, no. 3 (March 2012): 837–43. http://dx.doi.org/10.1111/j.1743-6109.2011.02588.x.

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41

Hermans, Michel P., Sylvie A. Ahn, and Michel F. Rousseau. "eNOS [Glu298Asp] polymorphism, erectile function and ocular pressure in type 2 diabetes." European Journal of Clinical Investigation 42, no. 7 (January 7, 2012): 729–37. http://dx.doi.org/10.1111/j.1365-2362.2011.02638.x.

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42

Hefler, Lukas A., Clemens B. Tempfer, Rene M. Moreno, William E. O'Brien, and Anthony R. Gregg. "Endothelial-derived nitric oxide and angiotensinogen: blood pressure and metabolism during mouse pregnancy." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 280, no. 1 (January 1, 2001): R174—R182. http://dx.doi.org/10.1152/ajpregu.2001.280.1.r174.

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The regulation of blood pressure during pregnancy involves several biological pathways. Candidate genes implicated in hypertensive diseases during pregnancy include those of the renin-angiotensin system and nitric oxide synthase (NOS). We evaluated blood pressure and metabolic characteristics during pregnancy in mutant mice. These included mice with a null mutation in the endothelial NOS (eNOS) gene ( Nos3−/− ), four copies of the angiotensinogen gene ( Agt2/2 ), and mutations in both genes [four copies of Agt and heterozygous deficient for eNOS (Agt2/2Nos3+/− ), four copies of Agt and homozygous deficient for eNOS ( Agt2/2Nos3−/− )]. Blood pressure measurements of nulliparous females from mutant strains were compared with two common laboratory strains C57Bl6/J and SV129 throughout their first pregnancy. Serum and urine analysis for the evaluation of renal and liver physiology were measured in the prepregnant state and during the third trimester of pregnancy. Throughout pregnancy blood pressures in all mutant strains were higher compared with controls. Agt2/2Nos3−/− showed the highest blood pressures and C57Bl6/J the lowest. Control mice, but not mutant mice, showed a second trimester decline in blood pressure. No immediate differences were noted regarding behavioral characteristics, renal or liver function parameters. Mice deficient for eNOS, mice with overexpression of Agt, and mice with mutations in both genes demonstrated higher blood pressure throughout pregnancy. There was no evidence of renal dysfunction, liver dysfunction, or hemolysis among any of the strains studied. We conclude that Nos3 and Agt are important genes in the regulation of blood pressure during pregnancy.

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43

Bossman, David M. "John J. Pilch, 1937–2016." Biblical Theology Bulletin: Journal of Bible and Culture 47, no. 2 (April 24, 2017): 66. http://dx.doi.org/10.1177/0146107917697900.

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44

Blackmore, Stephen, Keith Ferguson, Scott Russell, and Alexandra Wortley. "John J. Skvarla (1935–2014)." Grana 54, no. 3 (June 16, 2015): 167–73. http://dx.doi.org/10.1080/00173134.2015.1048990.

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45

Helmstaedt, Herb. "Tribute to John J. Gurney." Lithos 112 (November 2009): xx. http://dx.doi.org/10.1016/j.lithos.2009.10.002.

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46

Zimet, Carl N. "John J. Conger (1921-2006)." American Psychologist 62, no. 1 (2007): 48–49. http://dx.doi.org/10.1037/0003-066x.62.1.48.

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47

&NA;, &NA;. "Interview: John J. Costanzi, MD." Family & Community Health 11, no. 2 (August 1988): 81–82. http://dx.doi.org/10.1097/00003727-198808000-00011.

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48

Gal, Susan. "John J. Gumperz's Discourse Strategies." Journal of Linguistic Anthropology 23, no. 3 (December 2013): 115–26. http://dx.doi.org/10.1111/jola.12023.

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49

Cohn, Lawrence H. "JOHN J. COLLINS, JR., MD." Transactions of the ... Meeting of the American Surgical Association 128 (2010): 335–36. http://dx.doi.org/10.1097/01.sla.0000391119.10502.44.

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50

Griswold, A. "Profile of John J. Eppig." Proceedings of the National Academy of Sciences 110, no. 39 (September 5, 2013): 15506–8. http://dx.doi.org/10.1073/pnas.1315016110.

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