[The electroencephalogram in meningococcal cerebrospinal meningitis. (Apropos of 72 cases)].
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Biomedical subjects
Publications and source records attributed to A Fournier.
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To assess myocardial electric potentials late after Kawasaki disease (KD) we measured signal-averaged electrocardiography (SAECG) and QT dispersion parameters. Thirteen patients with persistent coronary aneurysm (group I), 12 with late resolution of the aneurysm (>3 months) (group II), and 13 with early resolution (group III) were studied 7.9 +/- 3.9, 6.7 +/- 3.9, and 7.2 +/- 3.6 years after the initial diagnosis (p = NS). In group I, myocardial infarction occurred in one patient during the acute illness, and coronary thrombosis in another; all except two patients had giant aneurysm (n = 8) and/or stenosis (n = 7). At 40-Hz high-pass filter SAECG, terminal 40-msec root mean square amplitude (RMS40) was significantly lower in group I versus II and III (64.1 +/- 40.8 microV, 79.9 +/- 47.2 microV, and 115 +/- 65.4 microV, respectively; p <0.05). Global QT dispersion was significantly greater in group I versus III (52 +/- 11 msec and 37 +/- 11 msec, respectively; p <0.05), but not in comparison to group II (45 +/- 13 msec). The same trend was present for rate-corrected QT dispersion, without reaching statistical significance (84.0 +/- 34, 71.5 +/- 31, and 61.8 +/- 21 respectively). Both depolarization and repolarization parameters are altered in patients with persistent coronary artery aneurysms long-term after KD. This may represent risk factors for developing ventricular arrhythmia in a growing population.
The congenital form of junctional ectopic tachycardia has never been reported during the prenatal period. We describe a case in which the diagnosis could be ascertained in utero with the superior vena cava/ascending aorta Doppler approach. The diagnosis was based on the evidence of ventricular tachycardia with atrioventricular (AV) dissociation and the simultaneous occurrence of atrial and ventricular contractions during an episode of tachycardia with 1:1 AV relationship.
Responses of various preparations of guinea pig and rat airways to synthetic porcine neuropeptide Y were analysed in vitro. NPY in doses up to 10(-6) M, induced a dose dependent contraction in trachea, bronchi and lung parenchymal strips of the guinea pig but did not have any effect in similar preparations obtained from the rat. In guinea pig airways the contractile responses to NPY were small in size and characterized by a slow onset and a long duration. This effect of the peptide was not dependent on pre-junctional nerve stimulation but rather mediated through the secondary generation of cyclooxygenase products. It is concluded that NPY may contribute per se to regulating the resting tone of guinea pig airways.
A conformational study of the C-terminal fragment 21-28 of vasoactive intestinal peptide (VIP) was carried out by high resolution NMR spectroscopy. All spectral data were recorded with a Brüker 400 MHz spectrometer. The correct assignment of peaks was determined by specific homonuclear decoupling and by titration. The chemical shifts of amide protons were measured as a function of temperature in order to detect the presence of intramolecular hydrogen bonds. A tridimensional structure is proposed for the peptide.
VIP and related fragments were prepared by the solid-phase method. The peptides were assembled on a benzhydrylamine resin and couplings of the Boc-amino acids were carried out by the symmetrical anhydride method. Cleavage was achieved by treatment with liquid HF and purification was accomplished by successive steps of cation exchange, partition and semi-preparative high pressure liquid chromatography. The biological activities were evaluated in vitro in the rabbit perfused heart and in vivo on the rat blood pressure. Structural studies were performed by high resolution (400 MHz) 1H-NMR spectroscopy and circular dichroism. The results show that among all the fragments tested, only VIP2-28 retains significant biological activity. The fragments 1-14 and 15-28, which are devoid of activity, were found to be inactive as antagonists. VIP and some of the fragments tend to adopt the helical structure, as demonstrated by spectroscopic techniques.
In order to examine whether the truncated fragments of hCGRP, hCGRP(8-37) or hCGRP(12-37), behave as competitive CGRP receptor antagonists in the vascular system of the rat, systemic blood pressure was continually monitored in pentobarbital-anesthetized Sprague-Dawley rats. The IV administration of 7.9-527 pmol hCGRP/rat caused dose-related reductions in mean arterial blood pressure that lasted, depending on the dose, about 3-10 min. In contrast, hCGRP fragments 8-37 or 12-37 proved inactive up to 60,000 pmol/rat. Pretreatment with either 10 or 30 nmol hCGRP(8-37) or 20 or 90 nmol hCGRP(12-37)/rat reduced the magnitude of the CGRP-induced hypotensive responses caused by 79 pmol hCGRP/rat; pretreatment with 10 nmol of the hCGRP fragments displaced about 3-fold the hCGRP as well as the [Cys(ACM)2.7]hCGRP dose-response curve to the right in a parallel fashion. The specificity of hCGRP(8-37) as a CGRP receptor antagonist was documented by the finding that it did not antagonize the hypotensive responses induced with bradykinin, histamine or substance P.