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Biomedical subjects

B Michel

Publications and source records attributed to B Michel.

At least 19 recordsLinked to original sources
PubMed1979

Electroencephalography in brain edema (127 cases of brain tumor investigated by cranial computerized tomography).

Cranial computerized tomography (CCT) in permitting visualization of cerebral edema in live patients, allows for the first time valid studies concerning the role of reactional edema in the generation of EEG abnormalities related to expanding processes. The authors analyze the results of EEG and CCT in 127 patients presenting cerebral tumor(s), 84 of which were accompanied by reactional edema. The study leads to the conclusion (also demonstrated by certain animal work) that edema per se is only rarely responsible (9.5%) for the EEG abnormalities.

Brain Edema↗
PubMed1979

Electroencephalographic cranial computerized tomographic correlations in brain abscess.

The authors studied 19 cases of brain abscess. The investigation included one or more EEG records from 13 patients and one or more cranial computerized tomograms in all cases. In this work the two techniques were associated to establish the diagnosis of cerebral abscess. The EEG is almost always abnormal and pronounced EEG disturbances are, in most cases, sufficient for indicating a diagnosis of a space-occupying process. On the other hand, EEG patterns suggestive of brain abscess were detected in only 38% of the patients. In brain abscess, CCT is of considerable value since the existence of 'suppurative' images was demonstrated in all cases and of these, 70% were characteristic. The association of these two techniques is thus extremely useful in the diagnosis of cerebral abscess, to follow its evolution and to detect postoperative relapse or to evaluate the efficiency of medical management alone.

Adolescent↗
PubMed1979

Appearance of "pemphigus acantholysis factor" in human skin cultured with pemphigus antibody.

These studies deal with the mechanism of pemphigus IgG-induced epidermal acantholysis. When normal human skin was culted with defined medium containing IgG from pemphigus serum, extensive epidermal acantholysis developed and heat-labile proteolytic enzyme(s) were recovered in the culture medium. The enzyme(s) displayed maximal activity at pH 6.5 when a 3H-amino acid-labeled, insoluble epidermal cell material was used as substrate. The enzyme activity increased during the first 3 days of culture and the appearance of maximal activity coincided with the time of onset of acantholysis. Acantholysis did not occur in control cultures incubated with normal IgG and the enzyme did not appear in the medium or in aqueous extracts of cultured tissues. The enzyme(s) is probably not of lysosomal origin because low pH-active proteases characteristic of these organelles remained within the cells. The effects of puromycin on appearance of enzyme activity, acantholysis and cell viability was studied. At cytotoxic concentrations, the appearance of the enzyme(s) and acantholysis were prevented, whereas at less toxic concentrations enzyme activity and acantholysis were not prevented. Because inhibition of protein synthetic rates by puromycin could not be dissociated from the cytotoxic effects, it is uncertain whether enzyme appearance and acantholysis were dependent upon living tissue or on specific protein synthesis. After pemphigus IgG was removed from the conditioned medium by DEAE cellulose and affinity column chromatography, the remaining material contained enzyme activity and caused acantholysis in fresh skin explants. Similar activities were not present in normal IgG-containing conditioned medium or unfractionated epidermal extracts from normal skin. These data indicate that when the pemphigus IgG autoantibody interacts with epidermal cell surface antigens, the cell responds by synthesis or activation of a non-IgG "pemphigus acantholysis factor" (PAF) which may be a nonlysosomal proteolytic enzyme. It is suggested that PAF causes loss of adhesion between keratinocytes and ultimately produces the characteristic acantholytic cells of pemphigus.

Acantholysis↗
PubMed1979

Corticosteroids, aurothioglucose and soybean trypsin inhibitor do not prevent pemphigus antibody-induced acantholysis in vitro.

Hydrocortisone, triamcinolone acetonide, aurothioglucose and soybean trypsin inhibitor were added to normal human skin explants cultured with IgG from pemphigus serum to determine if acantholysis could be prevented. At the therapeutic concentrations used none of these compounds prevented binding of the autoantibody to the epidermal target cells, and none prevented acantholysis. These experiments support the concepts that the pemphigus antibody alone is responsible for producing the acantholytic lesions of pemphigus, that the therapeutic effectiveness of steroids and gold salts is probably due to their ability to reduce serum autoantibody titres and that pemphigus acantholysis is probably not caused by a serine proteinase.

Acantholysis↗
PubMed1979

Effects of levamisole in Sézary syndrome. Apparent acceleration of disease.

2 patients with Sézary syndrome were treated with levamisole. Both patients had clinical and hematological evidence of acceleration of their disease and ultimately died, although 1 patient had improvement in skin test reactivity. We suggest that levamisole be used with caution, if at all, in patients with T-lymphocyte malignancies.

Adult↗
PubMed1979

[Pathogenesis of psoriasis].

Psoriasis is basically an excessive proliferation of the epiderm. This state results mainly from an imbalance in the cyclical nucleotides linked mainly to anomalies of the keratinocyte membranes. The membrane change is due to antibodies whose production may be dependent upon a deficit of a T-lymphocyte sub-population. This deficit may be considered the result of the penetration of virus agent with the help of multiple genetic factors. The various link of this pathogenic chain may be modified by numerous external factors which, by causing a worsening in a pre-existing imbalance, brings about the appearance of lesions.

Antibody Formation↗
PubMed1979

Status report of 376 mycosis fungoides patients at 4 years: Mycosis Fungoides Cooperative Group.

The frequency and prognostic importance of various characteristics of patients registered by the Mycosis Fungoides Cooperative Group between November 1974 and December 1977 are reported. Variables which were considered include demographic and historical factors, symptoms, extent of disease, and other physical findings. A staging system which is based on the extent of skin involvement and the number of nodal sites clinically involved is described. Finally, a description of therapeutic results to date for patients randomized into Mycosis Fungoides Cooperative Group protocols is presented.

Adult↗
PubMed1979

Management of necrotizing vasculitis with colchicine. Improvement in patients with cutaneous lesions and Behcet's syndrome.

Six patients with necrotizing vasculitis were treated with oral colchicine as part of an open study. Four patients with cutaneous vasculitis and normal levels of serum complement and one patient with vasculitis associated with Behcet's syndrome demonstrated clinical improvement while receiving colchicine. One patient with cryoglobulinemia, hypocomplementemia, and cutaneous vasculitis showed no response to colchicine therapy. In three patients, clinical improvement persisted after its withdrawal. Colchicine may be effective in controlling cutaneous necrotizing vasculitis and Behcet's syndrome through its effect on polymorphnuclear leukocyte function.

Administration, Oral↗
PubMed1978

Pemphigus antibody interaction with human epidermal cells in culture.

The mechanism of pemphigus acantholysis has been studied with an in vitro system. Freshly prepared human skin epidermal cells were incubated in F-10 medium which contained the immunoglobulin G fraction from either pemphigus serum or normal human serum. During 18-h incubation periods, the pemphigus antibody became bound to the surface of the epidermal cells, caused the destruction of 75% of the viable cells as compared to only 14% in the normal immunoglobulin G controls (trypan blue exclusion), prevented the accumulation of newly synthesized proteins by nearly 60% as determined by radioactive tracer studies, and caused a dramatic shift in distribution of the newly synthesized proteins from an insoluble cell-associated fraction to an extracellular soluble fraction. These effects on the accumulation and partitioning of newly synthesized proteins were antibody concentration-dependent. Kinetic studies showed that at a fixed pemphigus antibody concentration the inhibition of protein accumulation preceded solubilization by about 1 h, at which time rapid solubilization of up to 70% of the insoluble cellular material occurred. Several lines of evidence suggested that this phenomenon was caused by enzymatic activity. Epidermal extracts solubilized a prepared substrate of radioactivity labeled insoluble epidermal cell material. This activity was heat labile and pH dependent, with pH optima ranging from 4.5 to 6.5. Enzymes with pH optima between 6 and 6.5 were recovered in the culture medium after a 2-day incubation of pure, intact epidermis with the pemphigus antibody. We proposed the following hypothesis to account for pemphigus acantholysis. The pemphigus antibody reacts with the epidermal cell surface and produces such a severe disturbance that the integrity of the cell surface is lost. As a result of these primary perturbations, the cell is killed and during the process, responds by release or activiation of soluble hydrolytic enzymes. This autolytic process results in the characteristic acantholysis of pemphigus.

Acantholysis↗
PubMed1978

Epidermal acantholysis induced in vitro by pemphigus autoantibody. An ultrastructural study.

Suprabasilar acantholysis can be produced in organ culture of normal human skin in the presence of pemphigus IgG autoantibody. We have examined this in vitro system by electron microscopy. The earliest ultrastructural changes at 12 hours included widening of the intercellular spaces and disruption of the intercellular cement substance in the nondesmosomal areas. After 24 to 48 hours in culture, the tonofilaments retracted from the cell periphery, desmosomes were lost, and extensive cell surface digitation occurred. By 72 hours, isolated cells without noticeable desmosomes were seen in the suprabasilar areas, whereas basal cells, with intact hemidesmosomes, remained attached to the basal lamina. Control cultures which were grown in the presence of normal IgG or F-10 medium alone did not manifest these changes. The ultrastructural features support the conclusion that the acantholysis produced in this system is similar and probably identical to that of naturally occurring pemphigus.

Acantholysis↗
PubMed1977

Skin basement membrane immunofluorescence in rheumatoid arthritis: lack of diagnostic correlation.

Thirty-nine patients with rheumatoid arthritis were studied for the presence of skin basement membrane immunofluorescence. Punch biopsies from normal sun-exposed skin of the forearm were negative for basement membrane immunofluorescence in all cases, except one which was read as questionable. No correlation with serum antinuclear antibody or lupus erythematosus cells was observed. Skin immunofluorescence studies are helpful in differential diagnosis when patients with a clinical picture of rheumatoid arthritis present with serum antinuclear antibodies and lupus erythematosus cells. Positive basement membrane immunofluorescence is strong evidence of systemic lupus erythematosus.

Adolescent↗
PubMed1977

An organ culture model for the study of pemphigus acantholysis.

An in vitro model for the study of pemphigus acantholysis has been developed. The histological changes of pemphigus vulgaris were reproduced in vitro in organ culture by growing normal human skin in the presence of pemphigus vulgaris or pemphigus foliaceus sera. At 24 h a suprabasilar split was noted and at 72 h extensive suprabasilar acantholysis developed. Direct immunofluorescent tests demonstrated that pemphigus antibody became bound to the epidermal intercellular space antigen(s) during the first 6-12 h. As acantholysis increased the presence of tissue-fixed antibody decreased. The fixation of the pemphigus antibody to the skin prior to the development of acantholysis provides strong evidence for the pathogenetic role of this antibody in the production of acantholysis. The data suggest that complement is not required in this model for the production of the acantholytic changes of pemphigus since heating the serum for 30 min at 56 degrees C did not destroy the acantholytic activity and no complement (C3) could be detected by DIF of organ culture explants.

Acantholysis↗
PubMed1977

Factors influencing small bowel changes in dermatitis herpetiformis.

Factors influencing small bowel morphology in dermatitis herpetiformis (DH) were investigated by comparing patients with DH and normal small bowel biopsies to patients with DH and abnormal small bowel biopsies. The mean age of 18 patients with morphological changes in small bowel (38 years) was significantly lower (P less than 0-001) than the mean age of nine patients with normal bowel mucosa (60 years). HLA typing confirmed the high frequency of HLA-B8 in DH (64%) but HLA-B8 was unrelated to the presence or severity of small bowel lesions. Four patients had diarrhoea with progressive weight loss or abdominal cramps subsequently responsive to gluten withdrawal. In this subgroup serum levels of IgG and IgM were significantly lower than in patients with normal small bowel mucosa. Small bowel involvement appeared to be independent of the duration and severity of skin disease, and the deposition of immunoglobulin and complement (C3) in the dermal papillae of skin adjacent to skin lesions.

Adult↗