Search PubMed⌕ Search

Biomedical subjects

C Vial

Publications and source records attributed to C Vial.

143 records · Page 8Linked to original sources
PubMed1978

Regional myocardial energetics during brief periods of coronary occlusion and reperfusion: Comparison with S-T segment changes.

In open-chest dogs transient occlusion of the left anterior descending coronary artery induced an immediate decline in the creatine phosphate content of the ischaemic area, a lesser decline of the ATP and total adenine nucleotide contents and a rise in S-T segments. Reperfusion after 15 min restored creatine phosphate level and intramyocardial electrograms to normal whereas ATP and total adenine nucleotide levels stayed down. None of these parameters were modified in the nonischaemic area during the experiments. This study shows that there is no close relationship between electrical and biochemical events during either ischaemia or reflow.

Adenine Nucleotides↗
PubMedDate not supplied

Adenine nucleotide content and regional function during ischemia and reperfusion in canine ventricular myocardium.

We have compared in open-chest dogs the evolution of adenine nucleotides and creatine phosphate to that of regional mechanical function during ischemia and reperfusion. Reperfusion restored normal value of creatine phosphate whereas adenine nucleotide level remained depressed. The percentage of systolic shortening, which after occlusion has a zero or negative value, increased to about 20% of control, after reperfusion similarly the pressure-length loop areas decreased to 14.9% of control during ischemia and increased to 39.3% of control during the early phase of the reperfusion period. No individual correlation was found between the ATP content and segmental function during ischemia or reperfusion, suggesting that a low level of ATP did not prevent some restoration of mechanical function. However, the ATP content measured at the end of the ischemic period was correlated with mechanical function measured 75 min after reperfusion, and thus ATP depletion could appear as an indicator of the severity of ischemic damage.

Adenine Nucleotides↗
PubMedDate not supplied

[Measurement of antiganglioside autoantibodies by immunodot-blot assay: clinical importance in peripheral neuropathies].

We retrospectively evaluated measurement data and clinical relevance of autoantibodies to gangliosides in peripheral neuropathies (PN). The IgG and IgM antiganglioside autoantibodies were determined by our own immunodot-blot assay on membrane and by enzyme-linked immunosorbent assay (Elisa) in sera of 1,342 patients with peripheral neuropathies. Anti-GM1 and anti-GD1b autoantibodies formed a part of the normal autoantibody repertoire and were common place in 12% of normal subjects and in 14% of disease control groups. Polyclonal IgM antiganglioside autoantibodies were detected in chronic PN, polyclonal IgG antiganglioside autoantibodies were detected in acute PN. Polyclonal IgM anti-GM1 and anti-GD1b autoantibodies were detected in 35 patients out of 48 with treatable multifocal motor neuropathy with persistent conduction blocks. These autoantibodies well discriminated between suspected motor peripheral neuropathies and motor neuron diseases (sensitivity 73%, specificity 83%, positive predictive value 60%, negative predictive value 91%). Monoclonal IgM autoantibodies reacted strongly with gangliosides in 15 patients out of 77 with M-IgM neuropathy (19%). M-IgM autoantibodies differed in their fine specificities with different principal target antigens as demonstrated with cross-reactivity. Such findings provide further evidence for a relationship between neurological syndromes and antiganglioside antibody profiles and also suggest that different gangliosides could be principal target antigens such as GM1, GD1b, GT1b, GD1a or GM2. Polyclonal IgG anti-GM1 and anti-GD1b autoantibodies were detected in 21 patients out of 22 with acute motor axonal Guillain-Barré syndrome with antecedent of infection by Campylobacter jejuni, polyclonal IgG anti-GQ1b autoantibodies in 9 patients out of 10 with Miller-Fisher syndrome. Detection of antiganglioside autoantibodies by immunodot-blot assay which is simple and quick in testing a large panel of gangliosides has become very important in the diagnosis and in the choose of expensive therapeutic strategies in chronic or acute autoimmune neuropathies.

Acute Disease↗
PubMedDate not supplied

[Monoclonal IgM autoantibody activity vis-à-vis glycoconjugates of peripheral nerves: apropos of 112 cases].

Serum IgM and IgG autoantibodies against carbohydrate epitopes on glycolipids and glycoproteins have been determined in a series of 112 neuropathies associated with monoclonal IgM (M-IgM) by different immunological techniques. The M-IgM anti-myelin sheath antibodies were determined by indirect immunofluorescence microscopy, the M-IgM anti-myelin associated glycoprotein (MAG) antibodies by western-blot analysis, the M-IgM anti-SGPG and SGLPG antibodies by immunodetection on thin-layer chromatography, the M-IgM anti-ganglioside GM3, GM2, GD3, GM1, GD1a, GD1b, GT1b, GQ1b and anti-sulfatide antibodies by immunodot-blot assay on membrane. Among the 112 M-IgM, 81 had autoantibody activity against nerve glycolipid antigens concentrated in peripheral nerve (72%). M-IgM bound strongly to myelin sheath in 34,5% of cases, to MAG in 38% of cases, to SGPG/SGLPG in 52% of cases, to gangliosides in 21.5% of cases and to sulfatide in 26 % of cases. Six M-IgM autoantibody activity profiles have been described in correlation with distinct clinical syndromes: - the M-IgM autoantibody activity profile against the carbohydrate epitope common to the glycolipids SGPG and SGLPG and myelin associated glycoprotein (MAG) in chronic demyelinating sensitive and sensorimotor peripheral neuropathies (58 patients, 52%); - the M-IgM autoantibody activity profile against immunodominant GM1 in demyelinating pure motor neuropathies (9 patients, 8%); - the M-IgM autoantibody activity profile against immunodominant disialosylgangliosides in chronic demyelinating sensitive ataxic neuropathies (8 patients, 7%); - the M-IgM autoantibody activity profile against immunodominant GM2 in demyelinating motor polyneuropathies (3 patients, 2.5%); - the M-IgM autoantibody activity profile against immunodominant GD1a in pure motor polyneuropathies (2 patients, 2%); - the M-IgM autoantibody activity profile against immunodominant GT1b and polysialosylgangliosides in one acute polyradiculoneuropathy (1%). The M-IgM recognized all gangliosides except GM1 and GM2. The neuropathies associated with IgM monoclonal gammopathy with autoreactive specificity form distinct syndromes. In 27.5% of cases, M-IgM had no identifiable activity autoantibodies.

Aged↗
PubMedDate not supplied

[Antiganglioside autoantibody profiles in Guillain-Barré syndrome].

We established anti-ganglioside antibody profiles in GBS and studied the frequency, fine specificity and clinical correlate. IgG and IgM antibodies to 8 gangliosides were tested by immunodot-blot in 249 consecutive patients with Guillain-Barré syndrome with large variability in clinical expression, referred to our laboratory over a 8-year period. IgG and IgM anti-GM1 antibodies were measured by Elisa. Thin-layer chromatography overlayed by serum was used to control positivity. 89/249 GBS (36%) had characteristic anti-ganglioside antibody profile. Isotypes were, IgG (62%), IgG + IgM (26%) and IgM (12%). Antecedent infections were found in 62% of GBS included more frequently Campylobacter jejuni and cytomegalovirus. Various autoantibody profiles were described with an immunodominant ganglioside. We detected 6 characteristic anti-ganglioside profiles with fine specificity and immunodominant ganglioside corresponding to 6 immuno-clinical variants of GBS: 1) anti-GM1 and GD1b IgG and IgG > IgM in the acute motor axonal neuropathy after Campylobacter jejuni infection in 41 GBS; 2) anti-GD1a IgG in 6 severe motor axonal GBS after Campylobacter jejuni infection; 3) selectively anti-GQ1b IgG in 17 typical Miller Fisher syndrome with areflexia, ataxia and ophthalmoplegia; 4) anti- GT1b ganglioside and polysialogangliosides IgG (n = 9) in two separate cranial nerve variants, ophthalmoplegic SGB and lower cranial nerve variants depending upon the presenting deficit; 5) anti-GD1b IgG in 5 pure ataxic sensory GBS (4%); 6) anti-GM2 IgM in 11 severe GBS with antecedent CMV infection (8%). 34 GBS (14%) had low levels of anti-GM1 and GD1b IgM antibodies which are not disease specific and may simply represent part of the naturally occurring autoantibody population or a secondary response to disease. 126 GBS (50%) had no antibodies, predominantly in classical form. Associations between isotype, fine specificity and clinical presentation permit the definition of homogeneous immuno-clinical variants. Various autoantibody profiles with diagnostic and prognostic value are easy to perform by immunodot blot in acute peripheral neuropathies.

Adolescent↗
PubMedDate not supplied

[Anti-GD1b IgG positive case of overlapping Ficher's and Guillain-Barré syndromes].

We describe a patient who developed overlapping sensory ataxic form of Guillain-Barré syndrome (GBS) and Miller Fisher syndrome (MFS) following Campylobacter jejuni infection. Two cerebrospinal fluid examinations shown albuminocytologic dissociation associated with Campylobacter jejuni infection after tongue pierced. He had high titers of monospecific anti-GD1b IgG antibody. Because of the rarety of this disorder the diagnostic was difficult. There is a close association of IgG anti-ganglioside GD1b antibodies in sensory ataxic GBS. The findings of the present study show that antibody to GD1b ganglioside is one of the immunological factors in the pathogenesis of sensory ataxic form of GBS, a rare specific immuno-clinical variant form of GBS with prominent sensory ataxia.

Adult↗
PubMedDate not supplied

[Screening for anti-glycolipid antibody profiles from patients with immune-mediated peripheral neuropathies by Dotzen Ganglio Profile Antibodies].

The presence of anti-glycolipid specific antibodies have been found to be associated with acute and chronic immune-mediated peripheral neuropathies. Recently a number of anti-glycolipid antibody assays have became commercially available. In this study we established specific anti-glycolipid antibody profiles in a series of sera by the Dotzen Ganglio Profile antibodies. This kit screens for the simultaneous detection of ten anti-glycolipid antibodies against GM3, GM2, GM1, GD3, GD1a, GD1b, GT1a, GT1b, GQ1b gangliosides and sulfatides of the IgM and IgG classes. Sera from 89 patients with acute and chronic neuropathies were selected in a well-characterized cohort of banked sera with anti-glycolipid antibody profiles identified by in-house immunodot assay. Serum from 52 clinical variants of Guillain-Barré syndrome with IgG autoantibody profiles and 37 chronic acquired peripheral neuropathy with IgM autoantibody profiles were tested. The assay correctly identified with good agreement 50 of 52 IgG antibody profiles and 32 of 37 IgM antibody profiles. The assay compared well with in-house immunodot assay. It is easy to screen 10 crossreacting glycolipid antibodies to establish specific antibody profiles to define different subgroups of immune-mediated peripheral neuropathies for classification and immune management.

Autoantibodies↗
PubMedDate not supplied

[Diagnostic value of autoantibodies to MAG by ELISA Bühlmann in 117 immune-mediated peripheral neuropathies associated with monoclonal IgM to SGPG/SGLPG].

The neuropathies associated with monoclonal IgM gammopathy reacted with glycoconjugated targets on a very antigenic epitope on the sulfated glucuronic glycolipids corresponding to SGPG and SGLPG (sulfoglucuronyl paragloboside and sulfoglucuronyl lactosaminyl paragloboside), myelin-associated glycoprotein (MAG) and sulfatide. Sometimes monoclonal IgM binds to a broad spectrum of gangliosides. The detection of targets of autoantibodies has considerable importance in the diagnosis and management of patients. It is not known whether the results of antibody tests are equally sensitive and specific for identification of involved auto-antigens. In this study we evaluated the results obtained using IgM reactivity against MAG by enzyme-linked immunosorbent assay (ELISA Bühlmann) with IgM reactivity against SGPG/SGLPG obtained by overlay thin-layer chromatography. We selected 117 patients with anti-SGPG/SGLPG monoclonal gammopathy and peripheral neuropathy and a control group of 102 peripheral neuropathies with 24 having IgM high titres of monoclonal IgM anti-ganglioside antibodies. The anti-MAG sensitivity was 0.97, specificity was 0.86. There is a crossreactivity between 8 (57%) monoclonal IgM antibodies anti-MAG and anti-ganglioside GM1 and 2 (28%) anti-disialylated gangliosides. These results indicate that in clinical practice, anti-MAG ELISA is useful for eliminating anti-MAG neuropathy, as well as for positive diagnosis for titres upper than 10,000 BTU. It is also alpha good test to appreciate clinical improvement after Rituximab treatment.

Antibodies, Monoclonal↗
PubMedDate not supplied

Myocardial protection with Hamburg oxygenated crystalloid cardioplegic solution for multiple coronary bypass and multivalvular replacement.

We evaluated myocardial protection with Hamburg oxygenated crystalloid cardioplegic solution in a double study. Part I was a prospective metabolic study, measuring myocardial adenosine triphosphate (ATP) and creatine phosphate (CP) contents before and after ischemia in 30 coronary bypass (CABG) patients. During ischemia, CP levels decreased significantly, whereas ATP did not. After 10 minute of reperfusion, mean ATP contents were 90% of preischemic values and CP levels increased to 85% of preischemic values. Spontaneous myocardial defibrillation was seen in 93.3% of patients. Part II included evaluation of early postischemic myocardial function in 228 patients, 48 with multiple valve replacement (MUVR) and 180 with CABG. Spontaneous myocardial defibrillation was seen in 90.3%. Cardiac index, measured before and 1 and 12 hours after surgery, increased significantly in the postischemic period (from 1.95 +/- 0.9 to 2.5 +/- 0.7 l/min m2 in MUVR, p 0.04; from 2.2 +/- 0.6 to 2.7 +/- 0.7 l/min/m2 in CABG, p 0.01). Myocardial infarction frequency was 3% among CABG patients, and unrelated to the number of distal anastomosis or to aortic cross-clamp time. Early postoperative mortality was 6.2% for MUVR and 0.5% for CABG. Thus, oxygenated cardioplegia with Hamburg solution preserves high-energy phosphate compounds and prevents ischemic injury, with excellent short-term clinical results.

Adenosine Triphosphate↗