141 research outputs found
Two World Visions: Emanating Circles or Spiral Evolution?
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Properties of a‐SiGe:H thin films: correlation between photosensitivity and density of states
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Ten Simple Rules for Leading a Many-Author Non-Empirical Paper
No full textMany-author non-empirical papers include recommendations or consensus statements, catalogs of ideas, roadmaps for future research, calls to action, or “how to” articles. These papers have great potential to change the conversation or address unmet needs within research communities. Large, diverse authorship teams can create valuable resources that no individual co-author could create independently. Achieving these goals, however, requires a very different approach than researchers typically use to prepare papers with fewer authors. A small team of lead writers typically leads the content generation and writing processes. Many co-authors collaborate to create content and provide feedback throughout the writing process. Lead writers face many challenges, including defining the content and structure of the paper, coordinating complex logistics, preparing themselves and co-authors for a unique writing experience, and managing high-volume feedback. Here, we outline ten simple rules for leading a many-author non-empirical paper. These rules guide readers through the content generation and writing processes and highlight practical solutions to common challenges. While these rules were developed by preparing non-empirical papers with at least 30 authors, some rules may apply to research papers, or non-empirical papers with fewer authors. Lead writers can also use our companion paper, which shares ten simple rules for being a co-author on a many-author non-empirical paper, to prepare co-authors for an efficient and effective collaborative process
Effects of subinhibitory concentrations of antimicrobial agents on escherichia coli O157:H7 Shiga toxin release and role of the SOS response
No full textTreatment of Escherichia coli O157:H7 by certain antimicrobial agents often exacerbates the patient's condition by increasing either the release of preformed Shiga toxins (Stx) upon cell lysis or their production through the SOS response-triggered induction of Stx-producing prophages. Recommended subinhibitory concentrations (sub-MICs) of azithromycin (AZI), gentamicin (GEN), imipenem (IMI), and rifampicin (RIF) were evaluated in comparison to norfloxacin (NOR), an SOS-inducer, to assess the role of the SOS response in Stx release. Relative expression of recA (SOS-inducer), Q (late antitermination gene of Stx-producing prophage), stx1, and stx2 genes was assessed at two sub-MICs of the antimicrobials for two different strains of E. coli O157:H7 using reverse transcription-real-time polymerase chain reaction. Both strains at the two sub-MICs were also subjected to Western blotting for LexA protein expression and to reverse passive latex agglutination for Stx detection. For both strains at both sub-MICs, NOR and AZI caused SOS-induced Stx production (high recA, Q, and stx2 gene expression and high Stx2 production), so they should be avoided in E. coli O157:H7 treatment; however, sub-MICs of RIF and IMI induced Stx2 production in an SOS-independent manner except for one strain at the first twofold dilution below MIC of RIF where Stx2 production decreased. Moreover, GEN caused somewhat increased Stx2 production due to its mode of action rather than any effect on gene expression. The choice of antimicrobial therapy should rely on the antimicrobial mode of action, its concentration, and on the nature of the strain. © 2013, Mary Ann Liebert, Inc.Ahmad A, 2006, CURR MICROBIOL, V53, P324, DOI 10.1007-s00284-006-0089-3; [CLSI] Clinical and Laboratory Standards Institute, 2009, M07A8 CLSI; Foster PL, 2005, MUTAT RES-FUND MOL M, V569, P3, DOI 10.1016-j.mrfmmm.2004.07.017; Foti JJ, 2010, HDB CELL SIGNALING, P2127, DOI 10.1016-B978-0-12-374145-5.00258-8; Galkin VE, 2009, J MOL BIOL, V385, P779, DOI 10.1016-j.jmb.2008.10.081; Grif K, 1998, EUR J CLIN MICROBIOL, V17, P761, DOI 10.1007-s100960050181; Herold S, 2005, ANTIMICROB AGENTS CH, V49, P931, DOI 10.1128-AAC.49.3.931-944.2005; Janion C, 2008, INT J BIOL SCI, V4, P338; Jinneman KC, 2003, APPL ENVIRON MICROB, V69, P6327, DOI 10.1128-AEM.69.10.6327-6333.2003; Kadurugamuwa JL, 1997, J ANTIMICROB CHEMOTH, V40, P615, DOI 10.1093-jac-40.5.615; Kanbar A., 2003, J APPL RES, V3, P137; Kimmitt PT, 2000, EMERG INFECT DIS, V6, P458; Kolling GL, 1999, APPL ENVIRON MICROB, V65, P1843; Lee JH, 2009, J MICROBIOL BIOTECHN, V19, P1238, DOI 10.4014-jmb.0903.03006; LeJeune JT, 2004, EMERG INFECT DIS, V10, P1482; Livak KJ, 2001, METHODS, V25, P402, DOI 10.1006-meth.2001.1262; Los JM, 2009, MICROB PATHOGENESIS, V47, P289, DOI 10.1016-j.micpath.2009.09.006; Matsushiro A, 1999, J BACTERIOL, V181, P2257; McGannon CM, 2010, ANTIMICROB AGENTS CH, V54, P3790, DOI 10.1128-AAC.01783-09; Mead PS, 1998, LANCET, V352, P1207, DOI 10.1016-S0140-6736(98)01267-7; Mohsin M, 2010, FOODBORNE PATHOG DIS, V7, P85, DOI 10.1089-fpd.2009.0311; Ohara T, 2002, ANTIMICROB AGENTS CH, V46, P3478, DOI 10.1128-AAC.46.11.3478-3483.2002; Panos GZ, 2006, ALIMENT PHARM THER, V24, P731, DOI 10.1111-j.1365-2036.2006.03036.x; Pedersen MG, 2008, J CLIN MICROBIOL, V46, P2987, DOI 10.1128-JCM.00871-08; Rahal EA, 2011, INT J ANTIMICROB AG, V37, P135, DOI 10.1016-j.ijantimicag.2010.10.009; Rahal EA, 2011, ANN CLIN MICROB ANTI, V10, DOI 10.1186-1476-0711-10-34; Rokney A, 2008, MOL MICROBIOL, V68, P29, DOI 10.1111-j.1365-2958.2008.06119.x; Shilpakala SR, 2009, MOL BIOL REP, V36, P1937, DOI 10.1007-s11033-008-9402-5; Shimizu T, 2009, INFECT IMMUN, V77, P2813, DOI 10.1128-IAI.00060-09; Stohl EA, 2003, J BIOL CHEM, V278, P2278, DOI 10.1074-jbc.M210496200; Wegrzyn A, 1998, FEBS LETT, V440, P172, DOI 10.1016-S0014-5793(98)01449-5; Wong CS, 2000, NEW ENGL J MED, V342, P1930, DOI 10.1056-NEJM200006293422601; YARNELL WS, 1992, CELL, V69, P1181, DOI 10.1016-0092-8674(92)90639-T; Zhang QS, 2009, J INFECT DIS, V199, P486, DOI 10.1086-59650914
University Technology Buyers, A Glimpse Into Their Thoughts?
Get PDFThe university technology licensing research phenomena has mostly been addressed from seller (university) point of view while the technology buyer (licensee) has mostly been ignored. This paper reverses this research trend and addresses the university technology licensing phenomenon from the buyers’ perspectives. To explore the criteria most crucial to the university technology licensing decision making process, the author undertook a national survey addressing the most influential technology licensing executive in the US. In addition, the survey also addresses several questions about the licensing of university technologies, and shed insights on why some university technologies get licensed while many others do not
The impact of prophylactic antiviral agents and statin administration on graft longevity in kidney allograft recipients
No full textContext: In an earlier study, we compared the duration of kidney graft survival between two groups of recipients; one on triple (cyclosporine, prednisone and mycophenolate mofetil) and the other on quadruple (cyclosporine, prednisone, mycophenolate mofetil, and sirolimus) immunosuppressive therapy. Objective: The aim of this study was to examine the impact of antiviral and statin therapy on graft longevity. Materials and methods: One hundred five kidney allograft recipients were preoperatively assessed for serological markers of infection with various viral agents. All patients were on a prophylactic antiviral regimen of acyclovir and gancyclovir. Seventeen patients were on a statin. Patients were monitored for viral infections and graft rejection or loss for period of 3 years posttransplantation. Results: We detected a high preoperative prevalence rate of IgG immunoglobulins versus the latency-establishing Herpesviridae viruses. Two patients who were preoperatively IgG positive for CMV had cytomegalovirus disease after transplantation. One patient who was preoperatively IgG positive for VZV had shingles after the surgery. No other confirmed viral infections were reported. Thirteen of 88 patients (14.77percent) whose treatment regimen did not include a statin suffered a rejection episode or lost the graft whereas 1 of 17 patients (5.88percent) on a statin had a rejection episode. Conclusions: The low rate of viral infections observed in our study population supports the utility of prophylactic administration of antiviral agents to transplant recipients. However, statins seem to have a protective effect on graft longevity (odds ratio [OR]0.361, 95percent confidence interval [CI]0.044-2.957). © 2012 Informa Healthcare USA, Inc.Abdelnoor AM, 2009, IMMUNOPHARM IMMUNOT, V31, P83, DOI 10.1080-08923970802365123; Abdelnoor A.M., 1985, LEB SCI B, V1, P115; Asher Jordan, 2007, J Clin Hypertens (Greenwich), V9, P622, DOI 10.1111-j.1524-6175.2007.06639.x; Brennan DC, 2001, J AM SOC NEPHROL, V12, P848; Chade AR, 2005, HYPERTENSION, V45, P1042, DOI 10.1161-01.HYP.0000167121.14254.a0; CHAKRABARTI R, 1991, J BIOL CHEM, V266, P12216; CUTTS JL, 1990, J CELL PHYSIOL, V145, P244, DOI 10.1002-jcp.1041450208; Davis CL., 1999, ATLAS DIS KIDNEY, P103; El-Haibi C, 2006, IMMUNOPHARM IMMUNOT, V28, P459, DOI 10.1080-08923970600928056; ENDO A, 1976, FEBS LETT, V72, P323, DOI 10.1016-0014-5793(76)80996-9; Fellstrom B, 2000, TRANSPLANTATION, V70, pSS51; Gomez E, 2005, TRANSPLANT P, V37, P3760, DOI 10.1016-j.transproceed.2005.08.058; HO M, 1994, TRANSPLANT P, V26, P7; Istvan ES, 2001, SCIENCE, V292, P1160, DOI 10.1126-science.1059344; Katznelson S, 1998, J HEART LUNG TRANSPL, V17, P335; Kleemann R, 2004, BLOOD, V103, P4188, DOI 10.1182-blood-2003-10-3791; Kothe H, 2000, CIRCULATION, V101, P1760; Kwak B, 2000, NAT MED, V6, P1399; Liu L, 1999, J BIOL CHEM, V274, P33334, DOI 10.1074-jbc.274.47.33334; Palaniswamy C, 2010, AM J THER, V17, P75, DOI 10.1097-MJT.0b013e31819cdc86; Rahal E.A., 2011, ISRN IMMUNOLOGY; Reinke P, 1999, Transpl Infect Dis, V1, P157, DOI 10.1034-j.1399-3062.1999.010304.x; REYES J, 1992, TRANSPLANT P, V24, P1249; Romano M, 2000, LAB INVEST, V80, P1095, DOI 10.1038-labinvest.3780115; ROOK AH, 1988, REV INFECT DIS, V10, pS460; Rosenson RS, 1999, LANCET, V353, P983, DOI 10.1016-S0140-6736(98)05917-0; Rudich SM, 1998, TRANSPLANT P, V30, P992, DOI 10.1016-S0041-1345(98)00123-7; Seale H, 2006, CLIN VACCINE IMMUNOL, V13, P1181, DOI 10.1128-CVI.00203-06; Sia IG, 2000, CLIN MICROBIOL REV, V13, P83; Staras SAS, 2006, CLIN INFECT DIS, V43, P1143, DOI 10.1086-508173; Wang HR, 2005, CLIN CHIM ACTA, V353, P53, DOI 10.1016-j.cccn.2004.10.007; Weber C, 1997, J AM COLL CARDIOL, V30, P1212, DOI 10.1016-S0735-1097(97)00324-0; WEBER C, 1995, CELL BIOCHEM FUNCT, V13, P273, DOI 10.1002-cbf.290130408; Weikert BC, 2008, CLIN J AM SOC NEPHRO, V3, pS76, DOI 10.2215-CJN.029007070
Between Oral Tradition and Narrative Voice The Survival of Ancestral Speech in Allah n’est pasobligéby Ahmadou Kourouma
No full textThis article examines how ancestral speech is embedded in the novelistic writing of Allah n’est pas obligéby Ahmadou Kourouma, particularly through the voice of the narrator, Birahima. The author uses this speech to weave a link between oral tradition and the violent realities of the contemporary world, especially civil war in Africa. Through the character of Birahima, the author highlights the resilience of popular speech, inherited from ancestral wisdom, which serves both as a vehicle of memory and as a form of social critique in a context of dehumanization.
The article explores the multiple forms of orality present in the novel, such as hybrid language, Malinké proverbs, myths, and popular maxims, which become tools of cultural resistance against colonial and postcolonial oppression. Birahima’s speech embodies this oral tradition while also revealing the rift between ancient wisdom and contemporary barbarism, especially through the effects of war. Furthermore, orality becomes a means of identity reappropriation, allowing characters to resist cultural erasure caused by colonization and its impact on African society.
Finally, the study demonstrates that orality, far from being a mere survival of the past, constitutes a “living memory”, a poetics of resistance capable of preserving identity and criticizing contemporary injustices. Kourouma’s novel fits within an African literary tradition where ancestral speech, even when fragmented and wounded, persists as an agent of change and a means of cultural affirmation.Cet article étudie la manière dont la parole ancestrale s’inscrit dans l’écriture romanesque de Allah n’est pas obligé d’Ahmadou Kourouma, en particulier à travers la voix du narrateur, Birahima. L’auteur utilise cette parole pour tisser un lien entre la tradition orale et les réalités violentes du monde contemporain, en particulier la guerre civile en Afrique. À travers le personnage de Birahima, l’auteur met en lumière la résilience de la parole populaire, héritée de la sagesse ancestrale, qui sert à la fois de vecteur de mémoire et de critique sociale dans un contexte de déshumanisation.
L’article expose les multiples formes de l’oralité présentes dans le roman, telles que la langue hybride, les proverbes malinkés, les mythes et les maximes populaires, qui deviennent des outils de résistance culturelle face à l’oppression coloniale et postcoloniale. La parole de Birahima incarne cette tradition oralisée, tout en mettant en évidence la fracture entre la sagesse ancienne et la barbarie contemporaine, notamment à travers les effets de la guerre. En outre, l’oralité devient un moyen de réappropriation identitaire, permettant aux personnages de résister à l’effacement culturel lié à la colonisation et à ses effets sur la société africaine.
Enfin, l’étude démontre que l’oralité, loin d’être une simple survivance du passé, constitue une « mémoire vivante », une poétique de la résistance capable de préserver l’identité et de critiquer les injustices contemporaines. Le roman s’inscrit dans une tradition littéraire africaine où la parole ancestrale, même fragmentée et blessée, persiste comme un agent de changement et un moyen d’affirmation culturelle
Serum C-reactive protein and complement proteins in patients with acute myocardial infarction
No full textC-reactive protein (CRP) and complement proteins levels were determined in 20 patients with acute myocardial infarction (AMI) and 20 controls. Blood was obtained from all subjects at admission, 6 hr and 12 hr later. Serum CRP levels were determined by ELISA and complement proteins by radial immunodiffusion. A statistically significant elevation of the mean CRP level was obtained at 12 hr postadmission. The mean complement proteins levels were 16-49percent higher in AMI patients than the controls. It appeared that the alternate pathway was activated initially, followed by activation of the classical pathway. The increased levels of CRP and complement proteins are suggestive of their involvement in AMI. Copyright © 2005 Taylor and Francis Inc.BAUMANN H, 1994, IMMUNOL TODAY, V15, P74, DOI 10.1016-0167-5699(94)90137-6; Chakraborti T, 2000, CELL SIGNAL, V12, P607, DOI 10.1016-S0898-6568(00)00111-X; DEWINTER RJ, 1995, CIRCULATION, V92, P3401; Feucht HE, 2003, AM J TRANSPLANT, V3, P646, DOI 10.1034-j.1600-6143.2003.00171.x; Griselli M, 1999, J EXP MED, V190, P1733, DOI 10.1084-jem.190.12.1733; Hecke F, 1997, CRIT CARE MED, V25, P2015, DOI 10.1097-00003246-199712000-00019; Lagrand WK, 1997, CIRCULATION, V95, P97; LANGLOIS PF, 1988, ATHEROSCLEROSIS, V70, P95, DOI 10.1016-0021-9150(88)90103-7; Laufer J, 2001, MOL IMMUNOL, V38, P221, DOI 10.1016-S0161-5890(01)00044-X; LIUZZO G, 1994, NEW ENGL J MED, V331, P417, DOI 10.1056-NEJM199408183310701; MOLLNES TE, 1988, COMPLEMENT INFLAMMAT, V5, P33; Monsinjon T, 2001, FUND CLIN PHARMACOL, V15, P293, DOI 10.1046-j.1472-8206.2001.00040.x; Ortmann C, 2000, INT J LEGAL MED, V113, P215, DOI 10.1007-s004149900094; PINKARD RN, 1975, J CLIN INVEST, V56, P740; STAHMER S, MYOCARDIAL INFARCTIO; STEEL DM, 1994, IMMUNOL TODAY, V15, P81, DOI 10.1016-0167-5699(94)90138-4; Suzuki K, 2001, CIRCULATION, V104, P1308; Zhang A, 2002, DIABETES, V51, P349941
Effect of atorvastatin on antibody, interleukin-4 and gamma-interferon production in mice immunized with egg albumin
No full textThree-hydroxy-3-methylglutaryl CoA reductase inhibitors, also known as statins, are widely used as the drug of choice for the treatment of hyperlipidemia. However, actions beyond that of simply lowering cholesterol levels have been reported. This study aims at evaluating the effect of atorvastatin on antibody interleukin-4 and γ-interferon production in mice immunized with egg albumin. Antibody levels were determined by an enzyme linked immunosorbent assay and cytokine transcripts by reverse transcriptase- polymerase chain reaction. Results indicated that repeated daily doses of 40 mg-Kg body weight of atorvastatin following immunization suppressed the antibody response in mice to egg albumin. Moreover, a decline in interleukin-4 and γ-interferon transcripts was observed. Copyright © Informa Healthcare.Blum CB, 2001, TRANSPLANTATION, V72, P751, DOI 10.1097-00007890-200108270-00037; Chung HK, 2002, EXP MOL MED, V34, P451; Favre N, 1997, J IMMUNOL METHODS, V204, P57, DOI 10.1016-S0022-1759(97)00033-1; Fellstrom B, 2000, TRANSPLANTATION S, V70, P51; *GENTR SYST, 2003, PUR RNA PUR KIT QUAN; Hakamada-Taguchi R, 2003, CIRC RES, V93, P948, DOI 10.1161-01.RES.0000101298.76864.14; He X, 2004, TRANSPLANT P, V36, P1321, DOI 10.1016-j.transproceed.2004.04.084; Kwak B, 2000, NAT MED, V6, P1399; Lennernas H, 1997, CLIN PHARMACOKINET, V32, P403; Leung BP, 2003, J IMMUNOL, V170, P1524; Mach F, 2004, CIRCULATION, V109, P15, DOI 10.1161-01.CIR.0000129502.10459.fe; McKay A, 2004, J IMMUNOL, V172, P2903; Mulhaupt F, 2003, CARDIOVASC RES, V59, P755, DOI 10.1016-S0008-6363(03)00515-7; *PFIZ IREL PHARM, LIP AT CALC TABL; Sayegh MH, 1998, NEW ENGL J MED, V338, P1813; Stancu C, 2001, J CELL MOL MED, V5, P378, DOI 10.1111-j.1582-4934.2001.tb00172.x; Terasaki PI, 2005, TRANSPLANTATION, V80, P1194, DOI 10.1097-01.tp.0000174338.97313.5a; VOET D, 1995, BIOCHEMISTRY-US, P662; WOFSY D, 1985, J IMMUNOL, V135, P1698; Youssef S, 2002, NATURE, V420, P78, DOI 10.1038-nature0115822
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