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Biomedical subjects

M Kessler

Publications and source records attributed to M Kessler.

At least 307 records · Page 17Linked to original sources
PubMed1989

[Berger's disease or primary IgA nephropathy in children].

Primary IgA mesangial nephropathy was first described in adults by Berger, and has been increasingly recognized in children. IgA nephropathy is a frequent type of glomerulonephritis in 3 to 15 year-old children in France. Clinical features and outcome have been defined and the progression to renal failure is possible. The pathogeny of IgA nephropathy remains unclear and is under multifactorial control and, at present, no satisfactory specific treatment is available.

Acute Kidney Injury↗
PubMed1988

Transcription termination in animal viruses and cells.

Three experimental systems: isolated nuclei, cell-free reactions and whole cells were used for defining and characterizing cis and trans elements which regulate the block of transcription elongation in animal viruses and cells. In addition we have presented models for transcription termination within and at the end of a gene, which are consistent with the available information on the transcription bubble propagated during transcription elongation and can explain the modes of transcription termination described for various eukaryotic genes.

Adenoviruses, Human↗
PubMed1988

[Joint complications in patients with chronic renal failure hemodialyzed for over 10 years. 40 cases].

A retrospective study of 40 patients with chronic renal failure who underwent haemodialysis for more than 10 years (mean: 153 months) showed that 18 patients (45 p. 100) had arthralgia in the shoulders, hands, wrists and knees, 13 (32 p. 100) had carpal tunnel syndrome requiring surgery, and 20 (50 p. 100) were found to have bone cavities in the humeral head, external supra-acetabular region, carpus and patella. Aluminium overload was present in 47 p. 100 of the patients, and amyloid deposits were found in 10 of the 12 patient operated upon for carpal tunnel syndrome. This study confirms the frequency in patients under long-term haemodialysis of an articular pathological entity consisting of arthralgia, carpal tunnel syndrome, juxta-articular bone cavities and amyloid deposits which are now known to be made of beta 2-microglobulin. The initial lesion seems to affect the synovial membrane; it appears to be facilitated by age and is often associated with aluminium overload. The mechanism(s) responsible for amyloid deposits remain (s) to be elucidated.

Adolescent↗
PubMed1988

[Current pathogenetic data on mesangial glomerulonephritis with immunoglobulin A deposits].

The pathogenesis of mesangial immunoglobulin A nephropathies was elucidated through the analysis of their clinical features and investigation of their biological characteristics. An alteration of the mucosal immune system is currently considered chiefly responsible for these diseases. A dysregulation of other compartments of the immune system is likely to enhance this abnormality and/or contribute to the persistence of immune complexes. Little is known, however, about the etiology of these renal diseases, and their treatment remains palliative or preventive.

Glomerular Mesangium↗
PubMed1988

IgA nephropathy and alcoholic liver cirrhosis. A prospective necropsy study.

The incidence of mesangial IgA nephropathy (mIgAN) was investigated in a series of patients with alcoholic liver cirrhosis (ALC). Biologic parameters classically reported in IgAN were assessed in 98 patients, namely hematuria, proteinuria, and serum IgA. An immunohistologic study of the liver and kidney was performed in 33 patients who died during the study. Renal data were compared with those obtained in a matched necropsic series of controls. This study confirmed a global elevation of serum IgA levels in ALC. A possible hepatic origin of these immunoglobulins was supported by the observation of plasma cells in portal spaces in 68% of the patients. Biologic signs of renal disease consistent with mIgAN were observed in 16% of the patients; IgAN was diagnosed in 18% of patients with ALC and 10% of the controls. These data suggest that the incidence of mIgAN in ALC is not different than in the general population.

Adult↗
PubMed1988

Septicemia due to Yersinia enterocolitica in a long-term hemodialysis patient after a single desferrioxamine administration.

A long-term hemodialysis male patient was known to have systemic iron overload due to regular blood transfusions. As he was suspected to have aluminum overload, he received a single intravenous administration of desferrioxamine (that supported the hypothesis). Four days later, he became highly febrile with no focus of infection on physical examination. All blood cultures yielded Yersinia enterocolitica. The aim of this case report is to recall the potential risk of Yersinia sepsis in iron overload patients treated with desferrioxamine, even for a short time. The diagnosis should be suspected even in the absence of digestive symptoms, leading to immediate desferrioxamine withdrawal and antibiotic therapy.

Deferoxamine↗
PubMed1988

Effects of thiol-reagents on [3H]alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid binding to rat telencephalic membranes.

The binding of [3H]alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid ([3H]AMPA), a ligand for the quisqualate subtype of excitatory amino acid receptors, was measured after chemical modifications of rat brain synaptic membranes. Treatment with oxidizing or thiol-alkylating agents did not modify [3H]AMPA binding, whereas treatment with several sulfhydryl reagents produced marked increases in binding. The involvement of free sulfhydryl groups in the regulation of the properties of [3H]AMPA binding sites was suggested by the specificity of p-chloromercuribenzoic acid (PCMB), its sulfonate analog p-chloromercuriphenyl-sulfonic acid (PCMBS), and HgCl2, plus the reversal of their effects after reduction with dithiothreitol. Pretreatment of synaptic membranes with the oxidizing agent 5,5'-dithiobis(2-nitrobenzoic acid) or the alkylating agent N-ethylmaleimide did not significantly affect [3H]AMPA binding but markedly reduced the enhancing effect of PCMBS. On the other hand, the increase in [3H]AMPA binding produced by PCMBS was not prevented by treatment with agonists such as quisqualate or L-glutamate and was produced equally well in resealed postsynaptic membranes with both lipophilic or nonlipophilic SH-reagents. Using filtration assays, two types of binding sites could be detected with high and low affinity for [3H]AMPA. Treatment with SH-reagents produced an increase in the Bmax for the high affinity component and a decrease in the Bmax for the low affinity component, accompanied by an increase in its affinity for the ligand. Using centrifugation assays, the same two types of sites could be detected under control conditions but treatment with SH-reagents produced an increase in affinity of the large component that prevented the analytical differentiation of the two sites. Treatment with SH-reagents also increased the binding of [3H] glutamate to the N-methyl-D-aspartate receptors but did not modify the binding of [3H]kainate to the kainate receptors or the strychnine-insensitive [3H]glycine binding. These results suggest that free sulfhydryl groups allosterically modulate the affinity of the quisqualate subtype of excitatory amino acid receptors and also indicate that different types of glutamate receptors might be differentially affected by chemical modification.

Allosteric Regulation↗