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Biomedical subjects

M C Gelfand

Publications and source records attributed to M C Gelfand.

At least 55 records · Page 3Linked to original sources
PubMed1978

Biochemical correlates of reversal of hepatic coma coated with charcoal hemoperfusion.

Ten patients in stage IV hepatic encephalopathy who had not responded to conventional therapy for at least 48 hrs were treated with one or more 4 hr periods of hemoperfusion. Nine (90%) awoke, and 4 (40%) are alive to date, the survivors having acutely toxic and infective hepatic lesions. Biochemical changes that occurred were a reduction in blood ammonia of 23%, a rise in the ratio of branched chain to aromatic amino acids in blood (1.08 +/- 0.3 to 1.3 +/- 0.4), and cerebrospinal fluid (0.26 +/- 0.02 to 0.32 to 0.03), and a rise in cerebrospinal fluid cAMP from 2.3 +/- 0.7 ng/ml to 3.4 +/- 1.29 ng/ml with hemoperfusion. Administration of platelets and fresh frozen plasma restored the reduction of platelet counts of 29% towards pretreatment values.

Adolescent↗
PubMed1977

Treatment of severe drug overdosage with charcoal hemoperfusion.

Mortality from severe poisoning remains excessively high in patients managed conservatively. In this report, charcoal hemoperfusion was used as a therapeutic aid to active drug removal in 10 patients (9 of whom were in Grade IV coma) intoxicated with a variety of drugs and a further 3 patients poisoned with the highly lethal herbicide, paraquat. All 10 patients who ingested drugs recovered. One of the 3 patients ingesting paraquat survived. The hemoperfusion treatments were associated with demonstrated drug removal. Complications associated with hemoperfusion were minor. Decreases in platelet levels were observed but were not accompanied by clinically important bleeding. The technique of hemoperfusion is simple and provides a therapeutic aid in the care of the severely poisoned patient.

Adolescent↗
PubMed1977

Localization of receptors for activated complement on visceral epithelial cells of the human renal glomerulus.

Receptors for activated C3 have recently been demonstrated to be present in glomeruli of normal human kidneys. In the present communication, the precise location of these receptors within the renal corpuscle was studied with scanning electron microscopy. By this technique, the glomerular complement receptor (GCR) was found to be located on the visceral epithelial cell of the renal corpusle. This epithelial cell location was confirmed by comparison of in vitro GCR activity with the location of immunoglobulin and C3 deposited in vivo. Renal tissues in which Ig and C3 had been deposited in vivo diffusely in subepithelial loci had no in vitro GCR activity. Renal biopsies not showing Ig or C3 deposition or biopsies with Ig and C3 in the mesangium retained GCR activity. These results further confirm an important role for GCR in the trapping and deposition of C3 in some forms of immunologically mediated renal disease.

Binding Sites↗
PubMed1976

The glomerular complement receptor in immunologically mediated renal glomerular injury.

We examined 25 renal-biopsy specimens to determine whether there is a relation between immunologically mediated renal diseases and the activity of complement receptors that selectively bind antigen-antibody complexes containing activated third component of complement (C3b). These receptors have been termed glomerular complement receptors. Renal lesions associated with in vivo deposition were associated with a loss of receptor sites as demonstrated by reduced or absent in vitro binding of C3b-coated test reagents by glomerular complement receptor. These findings suggest that binding of complement containing immune complexes to glomerular complement receptors in human subjects may participate in the immunopathologic processes of certain immune-complex-mediated renal diseases.

Antibody Specificity↗
PubMed1976

Treatment of digitalis intoxication by charcoal hemoperfusion (CHP).

In the present communication, we demonstrate the removal of digoxin both in vitro and in vivo from digoxin intoxicated dogs by use of hemoperfusion over activated charcoal. In vitro drug removal was 33 ml/min at mean blood flow rates of 160 ml/min. By 30 mins of in vitro perfusion 51% of drug was removed from the reservoir and by 2 1/2 hrs 83%. In vivo clearance in dogs was 55 ml/min at blood flow rates of 150 ml/min. In view of the poor success that has been encountered in the treatment of digoxin intoxication with other modalities, charcoal hemoperfusion may represent an effective method of rapid digoxin removal from blood.

Animals↗
PubMed1975

Geophagia. A cause of life-threatening hyperkalemia in patients with chronic renal failure.

Geophagia has been associated with life-threatening hyperkalemia in five patients with chronic renal failure. All five patients were black and had been born in the southeastern United States. Four had had frequent hyperkalemia requiring at least one hospitalization, and two had had hyperkalemia with serum potassium concentration as high as 9.8 mEq/liter, resulting in cardiac arrest in one and paralysis, disorientation, and cardiac arrythmia in the other. Since riverbed clay contains as much as 100 mEq of potassium in 100 gm of clay, much of which is exchangeable at acid pH, the mechanism of geophagia-induced hyperkalemia appears to be the absorption of potassium released from clay after ingestion. After discontinuing geophagia, no new hyperkalemic episodes occurred in these patients.

Adult↗
PubMed1975

A receptor for the third component of complement in the human renal glomerulus.

In the course of studying the nature of mononuclear cellular infiltrates in tissue sections of human kidney it was noted that indicator sheep erythrocytes densely coated with the third component of complement (C3) specifically adhered to all of the glomeruli in the tissue sections. The deposition of complement (C) within the glomerulus is a feature of many immunologically related renal diseases (1,2), yet the precise mechanism by which C is deposited remains unexplained. We feel that this observation, suggesting the presence of a receptor for C, is, therefore, of particular interest.

Animals↗
PubMed1975

Prolongation of allograft survival in mice by administration of anti-Thy 1 serum. I. Mediation by in vivo activation of regulatory T cells.

A single 0.5-ml dose of anti-Thy 1.2 serum raised in AKR (H-2k, Thy 1.1) mice by immunization with C3H (H-2k, Thy 1.2) thymocytes prolonged mean graft survival (MGS) of C57BL/L (H-2b, Thy 1.2) skin on BALB/c (H-2d, Thy, 1.2) mice from 9.2 to 13.0 days (p less than 0.01). Absorption of anti-Thy 1.2 serum with C3H but not AKR brain removed this activity. MGS was prolonged by anti-Thy 1.2 serum given as long as 2 weeks before grafting. Four separately raised anti-Thy 1.2 preparations prolonged MGS, one to a dilution of 1:128. Anti-Thy 1.1 serum prolonged MGS on AKR mice but not on BALB/c mice. Thymectomy 3 weeks or more before graft placement or treatment of BALB/c mice with anti-lymphocyte serum (ALS) diminished the effectiveness of anti-Thy 1.2 serum. Furthermore, infusion of 25 times 10(6) spleen cells from BALB/c mice given anti-Thy 1.2 serum prolonged MGS on syngeneic recipients to 15.6 days whereas spleen cells from mice given no treatment or ALS had no effect. Thymocytes from anti-Thy 1.2 serum treated donors were ineffective in prolonging MGS on transfer. Transfer or serum from anti-Thy 1.2 serum-treated mice also had no effect. The transfer of graft prolongation with lymphoid cells from anti-Thy 1 serum treated mice suggests anti-Thy 1 serum may prolong MGS by activating suppressor T cells.

Animals↗
PubMed1975

Lack of B lymphocyte depletion from murine spleen cell populations by a human gamma-globulin, anti-human gamma-globulin column system.

It has been reported previously that enriched populations of mouse thymus-dependent (T) lymphocytes could be prepared by the use of a column procedure that is believed to remove selectively cells with receptors for antigen-antibody complexes. In our hands, this procedure does not selectively remove B lymphocytes but rather masks the surface immunoglobulin. Analysis of the column-passed cells revealed an apparent decrease in the percentage of immunoglobulin-bearing cells but little decrease in either the percentage of complement receptor lymphocytes or the mitogenic response to lipopolysaccharide. Furthermore, rabbit immunoglobulin could be detected on the surface of 35 to 45% of the cells emerging from the columns prepared with rabbit anti-human gamma-globulin (HGG). After overnight incubation, 30 to 40% of the emerging cells reexpressed mouse immunoglobulin on their surfaces. Adsorption of the antisera used to make the columns with mouse gamma-globulin (MGG) diminished the depleting capacity of the columns. We conclude from these observations that antibodies in the anti-HGG sera, cross-reactive with mouse immunoglobulin, account for the spacious depletion of B lymphocytes observed when cells are passed over these antigen-antibody complex columns.

Animals↗
PubMed1974

Ontogeny of B lymphocytes. II. Relative rates of appearance of lymphocytes bearing surface immunoglobulin and complement receptors.

Many bursa-equivalent (B) lymphocytes of adult mice bear surface Ig and receptors for C3. The frequency of Ig-bearing cells increases rapidly immediately after birth, but these cells lack complement (C) receptors. Lymphocytes bearing C receptors are not found in the spleens of BALB/c, DBA/2, and C57BL/6 mice until 2 wk of age and do not attain substantial numbers until 3-4 wk of age. In AKR mice, a lag between appearance of Ig-bearing and complement receptor lymphocytes (CRL) is also observed but it is of much shorter duration. AKR mice have a frequency of CRL at 2 wk of age of 28% in comparison to a frequency of 4.8% for DBA/2 mice. The difference in frequency between young and adult mice and between "low" and "high CRL" strains cannot be explained by a nonspecific inability to form rosettes as similar results are obtained with soluble antigen-antibody-complement complexes. Analysis of CRL frequency in (AKR x DBA/2)F(1) mice and F(1) x parental backcross progeny suggests that two independent genes control the rate of appearance of CRL. Furthermore, the genetic difference in the ontogeny of CRL is recapitulated in the repopulation of the B-lymphocyte line in adult-irradiated mice restored with syngeneic bone marrow. Thus, the "CRL genes" described here appear to control B-cell differentiation throughout life.

Age Factors↗