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USE OF IL-6 IN THE PREPARATION OF PHARMACEUTICAL COMPOSITIONS FOR TREATING AND PREVENTING LIVER INJURY
The new and less toxic protease inhibitor saquinavir–NO maintains anti-HIV-1 properties in vitro indistinguishable from those of the parental compound saquinavir
EDAP a member of TNF ligand superfamily is able to induce macrophage-granulocyte cross-talk.
Going Beyond Counting First Authors in Author Co-citation Analysis
The present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
Increased levels of IFN-GAMMA soluble receptors in human amniotic fluid and urine at midgestation and correlation with the TNF-ALPHA soluble receptors
The new and less toxic protease inhibitor saquinavir-NO maintains anti-HIV-1 properties in vitro indistinguishable from those of the parental compound saquinavir.
Acute haemodynamic effects of IL-6 treatment in vivo: Involvement of vagus nerve in NO-mediated negative inotropism
Interleukin-6 (IL-6) reduces myocardial haemodynamics. However, the intrinsic mechanisms of IL-6 effects are not known. We
hypothesized that nitric oxide (NO) synthesised by neuronal synthase (nNOS) can be the molecular mediator of IL-6-mediated
cardiac effects. Thus, we investigated in vivo after IL-6 acute administration: (1) the role of NO pathway; (2) the importance of NO
derived from nNOS located in intracardiac vagal ganglion in the anterior surface of the left ventricle.
SpragueeDawley (SD) rats (225e250 g) were anaesthetized (sodium pentobarbital 30 mg/kg intraperitoneally administered) and
ventilated. The effects of a single IL-6 bolus (100 mg/kg intravenously administered) were studied in four experimental groups: (a)
IL-6 (nZ6), (b) IL-6 plus 30 mg/kg of L-NAME (an eNOS and nNOS inhibitor; nZ6), (c) IL-6 plus 25 mg/kg of 7-NI (a specific
nNOS inhibitor; nZ6), (d) IL-6 plus vagal resection (nZ6).
We evaluated the following parameters: mean aortic pressure (MAP), left ventricular end systolic pressure (LVESP), left
ventricular positive peak dP/dt (PP dP/dt). Data are expressed as meanGsem. IL-6 caused a transient but significant reduction of
MAP (21.8% of basal: p!0.05), LVESP (from 130G4.2 to 1056.5 mmHg: p!0.05) and PP dP/dt (from 5390G158 to
4400G223 mmHg/s, p!0.02). Concomitant treatment with L-NAME or 7-NI totally abolished IL-6 effects. Vagal resection
significantly reduced the haemodynamic effects (MAP: 10% of basal: pZns; LVEDS: from 125G7.3 to 117G6.8 mmHg,
p!0.05; PP dP/dt from 5500G150 to 5000G143 mmHg/s, p!0.05).
We conclude that acute administration of IL-6 caused transient but significant cardiac negative inotropism. IL-6 haemodynamic
effects are partly due to NO synthesised by nNOS located in vagal left ventricular ganglia.
2005 Elsevier Ltd. All rights reserved
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