PubMed Health⌕ Search

Biomedical subjects

C Adam

Publications and source records attributed to C Adam.

At least 109 records · Page 6Linked to original sources

Yellow fever in the Gambia, 1978--1979: entomological aspects and epidemiological correlations.

An entomological survey was conducted in the Gambia in January 1979, during the last phase of a yellow fever (YF) outbreak which began during the previous rainy season. In the dry conditions which prevailed in January, Aedes aegypti was the only YF vector present. Two YF virus strains were isolated from females of this mosquito species caught in a village of western Gambia, where active human cases were documented. The ae. aegypti breeding sites were exclusively of the domestic type. Larval indices varied greatly from place to place, but generally appeared to correlate with the incidence of disease. A better understanding of the conditions that prevailed at the onset and during the early phase of the epidemic will require further entomological investigations. Nevertheless, it appears probable that initial transmission as by sylvatic vectors such as the Ae. furcifer-taylori group and possibly others such as Ae. luteocephalus, Ae. metallicus, and Ae. vittatus. As the outbreak progressed, interhuman transmission by Ae. aegypti also occurred, and this mixed epidemiological pattern later gave way to transmission by Ae. aegypti only when sylvatic vector populations declined in the dry season. We speculate that a prolongation of the rainy season during 1976--1978 was important in the origin of the outbreak. The relationship of this epidemic to the established focus of sylvatic YF in southeastern Senegal is discussed. The Gambian outbreak is considered the result of a recent northwesterly extension of the YF Emergence Zone.

Aedes↗

The effect of exogenous interferon: acceleration of autoimmune and renal diseases in (NZB/W) F1 mice.

To determine the effect of prolonged administration of exogenous interferon on the autoimmune disease of NZB/W female mice, forty-four NZB/W mice received three injections per week of 6.4 x 10(4) interferon units from birth to 33 weeks, forty mice were injected with mock interferon and forty-eight mice were left untreated. In mice injected with interferon growth was delayed, survival was decreased, and the severity of the glomerulonephritis was enhanced. Interferon increased the titre of serum anti-ssDNA and anti-soluble nucleoprotein antibodies, but had no effect on the circulating immune complex load. These results suggest that interferon in some way affects local deposition of immune complexes within the glomerulus.

Animals↗

Dense deposit disease with rapidly progressive renal failure in a narcotic addict.

A girl aged 17 developed a nephrotic syndrome with renal insufficiency after narcotic abuse. Renal biopsy showed a diffuse glomerulonephritis with crescents and dense deposits within the glomerular basement membrane; glomerular C3 deposits were present without immunoglobulin. The serum complement profile was typical of activation via the alternative pathway, and tests for C3 nephritic factor were strongly positive. Terminal renal failure occurred within 6 months and required chronic hemodialysis. It is likely that the narcotics used or their contaminants were responsible for the renal damage, presumably by activating the complement system via the alternative pathway.

Adolescent↗

Circulating immune complexes and C3d in human parasitosis.

Using the Raji cell radioimmune assay, we found low levels of circulating immune complexes (IC) in a small percentage of patients with schistosomiasis and filariasis. C3d levels, measured by immunoprecipitation, were elevated in a large number of these patients, whereas complement levels were within normal limits. Proteinuria was not found in any of the 55 patients studied. Circulating IC or elevated C3d levels were not found in any of the 19 patients with hydatidosis. The increased C3d levels, apparently not related to circulating IC, may be due to direct complement activation by parasite antigens or to sequestered IC. The latter hypothesis appears more attractive because the highest levels of C3d were found in schistosomiasis whereas schistosome antigens were unable to activate complement in vitro.

Antigen-Antibody Complex↗

A study of the material inhibiting EAC-rosette formation in the sera of patients with nephropathies.

Significant levels of EAC-rosette inhibition compared to control subjects were found in the sera of patients with focal and segmental hyalinosis (FSH), membranoproliferative glomerulonephritis (MPGN) and extra-membranous glomerulonephritis (EGN). In patients with IgA disease, although some sera produced high levels of inhibition, the group as a whole did not differ significantly from the controls. Evidence was obtained suggesting that the rosette inhibitory activity was due to immune complexes (IC) bearing C3 rather than C3 fragments. Firstly, the inhibitory activity was precipitable by 4% PEG, a concentration which does not precipitate the C3 fragments. Secondly, the inhibitory activity was selectively removed from the PEG precipitates by an anti-human immunoglobulin G immunoabsorbent. Finally, since it had been suggested that in some instances an unknown serum factor could inhibit EAC-rosette formation and activation of the alternative pathway of complement, the latter was studied and found to be normal in all the sera studied. Taken together, these results suggest that the inhibition of EAC-rosette formation obtained with the sera of the patients studied was due to the presence in these sera of some material behaving as IC. No clear-cut association was, however, seen between rosette inhibition and the presence or absence of Ig or C3 deposits in the kidney.

Adult↗

"Topical nephropathy" and "tropical extramembranous glomerulonephritis" of unknown aetiology in Senegal.

A study of renal biopsy specimens obtained in Senegal from 24 children and six adults with nephrotic syndrome showed two unusual varieties of nephropathy--namely, an extramembranous glomerulonephritis associated with hypocomplementaemia (four cases), a combination previously described only in systemic lupus erythematosus, and a "tropical nephropathy" (16 cases). The latter, though lacking the diffuse glomerular deposits of immunoglobulin described in quartan malarial nephropathy (Q.M.N.), showed a curious progressive and segmental glomerulosclerosis, characterized by a "flaking" or fibrillary splitting of the glomerular capillary wall, seen in Q.M.N. Serological evidence of malaria was lacking in a third of the childhood cases.

Adult↗

Mechanisms of activation of the properdin system. Studies on properdin electrophoretic mobility in agarose activation of the alternative pathway.

The electrophoretic mobility of properdin in agarose with and without EDTA examined in sera from normal subjects and from patients with mesangiocapillary glomerulonephritis, systemic lupus erythematosus, rapidly progressive glomerulonephritis, mesangial IgG-IgA disease, minimal change glomerulonephritis and partial lipodystrophy. In 'EDTA agarose", the properdin arc of normal serum was always cathodal (gamma), whereas in non-EDTA agarose it was always (beta), indicating that agarose activated properdin with its consequent conversion from a cathodal to an anodal form. Using this change in the mobility of properdin to investigate activation of the properdin system, it was found that the lower the C3 concentration of diseased sera, the less able were they to support properdin conversion by non-EDTA agarose. This relationship we interpret as a manifestation of the requirement of an intact C3b feedback pathway for properdin activation. This view was supported experimentally by (i) decreasing ability of non-EDTA agarose to shift properdin mobility in normal serum as it was progressively depleted of components of the alternative pathway by cobra venom factor, C3 nehritic factor or Mg2+, and (ii) the inability of non-EDTA agarose to shift properdin in sera depleted of C3 or factor B, and in serum deficient in C3. The report of other workers that activated properdin causes generation of C3b, coupled with our finding that properdin activation depends on the C3b feedback, indicates that a system exists in which activation of the C3b feedback cycle allows activation of properdin, allowing in turn further amplification of the C3b feedback. That the anodal form of properdin may be a property of activated properdin was shown by our observations that properdin eluted from zymosan was anodal and activated, and that the properdin in the supernatant normal serum incubated with inulin was anodal.

Complement C3↗

[Medical treatment of Raynaud's syndrome].

The authors review the drug treatment of Raynaud's disease. Many substances have been used including nitrate derivatives, calcium antagonists, alpha blockers, angiotensin converting enzyme inhibitors, prostaglandin E1, E2 and I2, and ketanserin. The efficacy of these drugs is often partial and variable. The indications are discussed with respect to the clinical course and etiology of the Raynaud's phenomenon.

Connective Tissue Diseases↗

Correlations between magnetic resonance imaging-based hippocampal sclerosis and depth electrode investigation in epilepsy of the mesiotemporal lobe.

Quantitative analysis of hippocampal formations (HF) by magnetic resonance imaging (MRI) was correlated with depth electrode recordings in 18 patients with partial epilepsy. All had seizures of mesiotemporal origin. Electrodes explored three HF segments: amygdala and HF head and anterior and posterior HF body. Corresponding HF measurements were made on coronal MRI sequences, and atrophy was quantified by one global and three segmental indexes of asymmetry per patient. HF from which seizure originated showed global atrophy in 15 patients. Segmental analysis demonstrated discrete tissue damage in 1 patient; thus, 16 patients (88%) had significant hippocampal atrophy ipsilateral to the mesial focus. The existence of more pronounced atrophy in segments giving rise to ictal onset than in segments without ictal onset was not statistically significant. Nevertheless, in posterior HF, all segments (four) with seizure onset were atrophied and none of the nonatrophied posterior segments (four) were at seizure origin. These findings confirm that MRI-detected hippocampal atrophy is a powerful indicator of a mesiotemporal focus and strongly contributes to consideration of resective surgery without intracerebral EEG monitoring. Study of the distribution of maximal tissue damage may add some information, and help surgeons decide on the posterior extent of hippocampus removal. As illustrated by 3 patients who had multiple sites of seizure onset, however, the presence of this marker should not be interpreted systematically as evidence of pure mesiotemporal epilepsy.

Adolescent↗

Temporal and spatial characteristics of intracerebral seizure propagation: predictive value in surgery for temporal lobe epilepsy.

We examined the prognostic value of spatial and temporal characteristics of intracerebral propagation of seizures during temporal lobe epilepsy (TLE) surgery. Seven TLE patients resistant to standard anterotemporal lobectomy who had no known causes of resistance [e.g., extratemporal (ET), lesions, multifocal epilepsy] were matched with 7 seizure-free patients and 7 others who were almost seizure-free after operation. Intracerebral ictal propagation pathways were not different in the three groups. Propagation was multidirectional, most frequently to the frontal lobes and sometimes to the contralateral temporal lobe (CTL). ET propagation delays were significantly shorter in resistant patients than in markedly improved patients. The resistant group also had more frequent propagation delays < 1.0 s, but propagation times > 1.0 s were equally likely in all groups. The extent of ET propagation and frequency of focal onsets were not different among the groups. Results suggest that very short propagation times predict reduced efficacy of operation, and that long propagation times are not related to surgical success.

Electroencephalography↗