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Biomedical subjects

A Bernard

Publications and source records attributed to A Bernard.

At least 631 records · Page 35Linked to original sources
PubMed1978

Some chronic lymphocytic leukemia cells bearing surface immunoglobulins share determinants with T cells.

One set of antigens is common to some chronic lymphocytic leukemia (CLL) cells bearing surface immunoglobulins (Ig) and normal T cells. Proliferating cells from thirty-eight patients were studied with four antisera recognizing normal human T but not B cells. These antisera were raised in rabbits against (a) Sezary cells, (b) blood lymphocytes from a patient with sex-linked agammaglobulinemia, (c) T lymphoblasts and (d) thymus cells. In four CLL cases, the cells expressed the receptor for sheep erythrocytes and lacked surface Ig. Cells from thirty-four CLL cases bore monoclonal surface Ig and did not bind sheep erythrocytes. Twelve out of these thirty-four cases of CLL had cells which were lysed by one or, more frequently, by the four anti-human T cell xenoantisera. By absorption experiments, one set of at least three antigens common to the cells of some of these CLL and T cells was defined. Depending on the patient, the cells can either carry one, some or all of the antigens of this set. However, it was also demonstrated by absorption that these cells lacked antigens particular to the T cell lineage, while the cells from T CLL cases carried both sets of antigens.

Animals↗
PubMed1978

alpha 1-antitrypsin in cadmium toxicity: an evaluation of its suggested role.

Chowdhury and Louria [1] reported that cadmium could reduce in vitro the concentration and the trypsin inhibitory capacity of plasma alpha 1-antitrypsin. They suggested that this could explain the emphysema observed in some workers exposed to cadmium. Using the same experimental approach as these authors, we could not reproduce their observations. Furthermore, in vivo results obtained on workers excessively exposed to cadmium during more than 20 years and exhibiting obvious signs of chronic cadmium intoxication did not reveal a decrease in the concentration and the activity of plasma alpha 1-antitrypsin.

Cadmium Poisoning↗
PubMed1978

Experimental confirmation in rats of the mixed type proteinuria observed in workers exposed to cadmium.

Recently we have reported that the proteinuria developed by workers exposed to cadmium was characterized by an increased excretion of high and low molecular weight proteins. These observations were confirmed experimentally. Female rats which were injected intraperitoneally with CdCl2 (1 mg Cd2+/kg) 5 times a week developed after 2 months of treatment a proteinuria qualitatively similar to that observed in workers exposed to cadmium. The analysis of this proteinuria by electrophoresis and gel filtration revealed an increased excretion of low and high molecular weight proteins. This animal study, which confirms previous observations on man, strengthens our hypothesis that the cadmium-induced proteinuria, classically considered as a tubular type proteinuria, is in fact a mixed type proteinuria, involving not only the tubule but also the glomerulus.

Animals↗
PubMed1978

Investigations of factors influencing exposure and response to lead, mercury, and cadmium in man and in animals.

The susceptibility of the heme biosynthetic pathway to lead, as reflected by increased free erythrocyte porphyrin (FEP) concentration, is in humans as well as in rats in the order of young greater than or equal to female greater than male. The difference between adult male and female rats can be explained at least partially by the interaction of estradiol and progesterone with the FEP response to lead; the hormonal influence on FEP does not seem to be mediated through changes in plasma iron. The classical "tubular type" proteinuria in workers chronically exposed to cadmium has two not necessarily concomitant components, namely, a tubular type and a glomerular type component characterized by increased excretion of low and high molecular weight proteins, respectivley. No synergistic effect of cadmium and lead on the proteinuria of workers simultaneously exposed to both metals was observed. Mercury (most likely methylmercury) is freely transferred from the mother to the fetus; there is only a slight placental barrier for lead and a rather strong one for cadmium. Compared to maternal blood, placenta does not accumulate lead or mercury but concentrates cadmium about 10-fold.

Age Factors↗
PubMed1978

Urinary excretion of beta2-microglobulin and other proteins in workers exposed to cadmium, lead or mercury.

For the range of exposure to heavy metals sustained by the different groups of workers, a significant increase in the urinary excretion of low and/or high molecular weight proteins was found in the workers exposed to cadmium or to lead + cadmium, but no in those exposed to lead only and those exposed to mercury. Our observations suggest that the classical "tubular" proteinuria induced by cadmium has two not necessarily concomitant components : a "tubular type" component with increased excretion of low molecular weight proteins and a "glomerular type" component with increased excretion of high molecular weight proteins.

Beta-Globulins↗
PubMed1977

[Percutaneous puncture of a hydatid cyst of the kidney].

The authors stress the value of percutaneous puncture in the case of hydatid cyst of the kidney, making possible opaque cystography -- the findings of which are characteristic, and cytological study of the fluid obtained. In addition, they report the safety of this method of investigation.

Biopsy, Needle↗
PubMed1976

[Vascularization of the anal canal].

The arterial blood supply of the anal canal derives from the superior, middle and inferior rectal arteries, whose branches reach the anal submucosa. Three main arterial trunks in the right anterior, right posterior and left lateral positions can be isolated below the pectinate line. They come, for the most important part, from the superior rectal artery. On the course of the anal submucosal venous plexus are fusiform, saccular or serpiginous dilatations confined to the lower half of the anal canal. This plexus is mainly tributary of the superior rectal vein to the portal system and secondly, of the middle and inferior rectal veins and the lateral sacral veins to the inferior vena cava. Arterio-venous direct communications have been demonstrated by serial section and by radiography of cadaveric specimens and by selective inferior mesenteric arteriography in patients. The erectile property of the anal submucosa as suggested by large vascular spaces, arterio-venous shunts and glomic systems may function in the erectile mechanism.

Anal Canal↗
PubMed1976

Leukocyte-derived complement inhibitor. IV. The functional properties of C1 bound to erythrocytes pretreated with leukocyte culture supernatant.

E, pretreated with leukocyte cultures supernatant (ES), binds C1 through C1q; ES and EIgM that bind the same amount of C1 as measured in a hemolytic assay have the same uptake of 125I-C1q; ESC1q and EIgMC1q, carrying the same number of molecules of CUq per cell, have the same uptake of CUr and CUs; soluble immune compleses prevent the binding of C1 and C1q to ES. The activity of C1 bound to ES is impaired; ESC1 can react with C4 but not with C2. The C4 turnover and the C1 ING turnover by ESC1 are reduced so that ES-bound C1 is protected from destruction by C1 ING. These modifications are fully reversed when C1 is transferred from ES to EA:C1 recovers its ability to react with C2, and C1 INH. Thus the C1s activity can be modulated inside the C1 molecular complex upon binding of C1q to a lymphocyte product. In addition, the 125I-C1q uptake is proportional to the amount of IgM hemolysin used to sensitize E; it has, however, an exponential relationship to the amount of IgG or S used to sensitize E. The ratio of 125I-C1q uptake towhole C1 uptake measured in a hemolytic assay is lowerthan 2. This indicates that one molecule of IgM is sufficient to bind one molecule of C1q on E, that several molecules of IgG or S are required to bind one molecule of C1q, and that one molecule of C1q is sufficient to create a lytic site on E.

Animals↗
PubMed1975

Complement inhibitor(s) released by leukocytes. I. Pretreatment of sheep erythrocytes with supernatants of mouse spleen and thymus cells inhibit whole complement activity and C2 utilization.

Sheep erythrocytes pretreated with supernatants of mouse spleen or thymus cells become resistant to lysis by guinea pig complement. The inhibitory activity (IA) reduces the utilization of C2 by EAC14. Because IA binds to the surface of sheep erythrocytes and does not inhibit C1 irreversibly, it is probably a hitherto undescribed inhibitor of complement.

Animals↗