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Biomedical subjects

S Friedman

Publications and source records attributed to S Friedman.

At least 379 records · Page 21Linked to original sources
PubMed1984

Glomerular capillary wall function in human lupus nephritis.

Eighteen patients with nephrotic-range proteinuria due to lupus nephritis were evaluated with a differential solute clearance technique. Renal plasma flow was similar to that in 17 healthy volunteer controls (506 +/- 75 vs. 503 +/- 32 ml/min, P = NS), while oncotic pressure in pre- and postglomerular plasma was depressed by 9.2 and 17.3 mmHg, respectively. These findings are consistent with elevation of net ultrafiltration pressure and suggest that glomerular hypofiltration (51 +/- 9 vs. 103 +/- 8 ml/min, P less than 0.001) was due to a lowered glomerular ultrafiltration coefficient (Kf). In lupus nephritis the fractional clearance of smaller dextrans (radii less than 50 A) was depressed, while that of larger dextrans (radii greater than 50 A) was elevated. A pore model of solute transport, when applied to the dextran filtration data, revealed a subpopulation of large protein-permeable pores in lupus nephritis not present in controls. Moreover, the fraction of glomerular filtrate permeating these enlarged pores correlated directly with the respective fractional clearances of albumin (r = 0.71) and immunoglobulin G (r = 0.75) in individual patients. Immunosuppression in nine patients was associated with an increase of the filtration rate and filtration fraction. Conversely, fractional protein clearances and the area fraction of the glomerular membrane occupied by large pores decreased. We conclude that human immune glomerular inflammation is manifested by a reduction of Kf and increased glomerular porosity and that these membrane alterations are partially reversible.

Adult↗
PubMed1984

Nature of the renal injury following total renal ischemia in man.

The effects of total renal ischemia (TRI) of 15-87 min duration due to suprarenal clamping of the aorta were studied in 15 mannitol-treated patients undergoing abdominal aortic surgery. 15 patients undergoing similar surgery but requiring only infrarenal clamping served as controls. 1-2 h following TRI, GFR was reduced to only 39% of that in controls, 23 +/- 5 vs. 59 +/- 7 ml/min (P less than 0.001). This could not be ascribed to impaired renal plasma flow (RPF), which was mildly reduced to 331 +/- 71 and was not different from the value in controls, 407 +/- 66 ml/min. However, impaired PAH extraction (43 +/- 7%) and isosthenuria, not present in controls, suggest a primary role for tubular injury in lowering GFR at this time. 24 h following TRI, the GFR remained depressed below controls, 45 +/- 8 vs. 84 +/- 8 ml/min (P less than 0.005), while the transglomerular sieving of neutral dextrans was significantly enhanced (radius interval, 24-40 A). A theoretical analysis of transcapillary solute exchange revealed that these findings could be largely explained by a selective reduction of either RPF (-61%) or of transmembrane hydraulic pressure difference (-18%) below control values. Alternately, a combination of these two factors with changes of smaller magnitude could explain the findings. In contrast, a selective increase in oncotic pressure or decrease of the glomerular ultrafiltration coefficient could be excluded as a cause of hypofiltration 24 h after TRI. These observations lead us to suggest that the transient azotemia observed following TRI is due to a self-limited injury to the nephron that is identical to that seen in overt and sustained forms of acute renal failure.

Aged↗
PubMed1984

Cloned mouse mast cells derived from immunized lymph node cells and from foetal liver cells exhibit characteristics of bone marrow-derived mast cells containing chondroitin sulphate E proteoglycan.

Cloned mouse mast cells which were T cell growth-dependent were derived both from immunized lymph node and from foetal liver, and were found to be morphologically and biochemically similar to mast cells previously differentiated in vitro from mouse bone marrow (BMMC). These two T cell growth-dependent mouse mast cell clones were identical to the BMMC in their preferential synthesis of chondroitin sulphate E proteoglycan rather than heparin proteoglycan. The hydrodynamic size of the cell-associated proteoglycan from each of the three mast cell sources was 150,000-250,000 mol. wt.; and that of the covalently bound glycosaminoglycans was 13,000-25,000 mol. wt. Chondroitinase ABC digestion of the [35S]proteoglycans from both cloned mast cells, as well as the BMMC, yielded only two disaccharides which comigrated on ascending thin layer chromatography with delta Di-4S and delta Di-diSE standards, respectively. Quantification of the radioactivity in the enzyme digests revealed that one-sixth to one-half of the resulting disaccharides were disulphated, similar to that found in BMMC containing chondroitin sulphate E. When sensitized with monoclonal IgE, washed, and subsequently challenged with specific antigen, each of the two cloned mast cells generated more than 100 ng of leukotriene C4 (LTC4)/10(6) cells, but only 3-12 ng leukotriene B4 (LTB4)/10(6) cells, characteristics also observed for the BMMC. Based upon these observations, it is concluded that the cloned mast cells from lymph node and liver and the bone marrow-derived mast cell belong to a distinct subclass of mast cells. These mast cells have been designated E-mast cells (E-MC) in order to distinguish them from heparin-containing mast cells (H-MC).

Animals↗
PubMed1983

Predicting psychiatric admission from an emergency room. Psychiatric, psychosocial, and methodological factors.

The determinants of psychiatric hospitalization, especially nonspecific issues, have been studied extensively. The methodological problem of correlational non-cross-validated findings are seen as contributing to our uncertainties about the critical issues involved in the decision to admit. A cross-validated multiple regression analysis of determinants of hospitalization in an inner-city municipal hospital revealed two determinants of hospitalization: severity of schizophrenic symptoms and active suicidal and/or homicidal ideation. They accounted for one third of the variance without shrinkage. Quasi-experimental designs may be the most efficient means of studying the remaining unexplained variance.

Commitment of Persons with Psychiatric Disorders↗
PubMed1983

Mechanisms of proteinuria in diabetic nephropathy. II. A study of the size-selective glomerular filtration barrier.

We evaluated the size-selective properties of the glomerular barrier in 30 patients in whom diabetic nephropathy was associated with urinary IgG losses. Neutral dextrans of graded size were used to characterize glomerular membrane-pore structure. A fractional IgG clearance (relative to freely permeable inulin) smaller or greater than 0.001 was used to distinguish patients with minor (group 1, N = 14) and major (group 2, N = 16) urinary IgG leakage, respectively. Fractional clearances of dextrans (theta D) of smaller size (radii 20-40 A) were similar, but those of larger dextrans (radii 42-60 A) were elevated in group 2 relative to group 1 patients. When plotted on log-normal probability coordinates, the correlation between theta D and radius in healthy subjects is linear, suggesting that glomerular pores form one population with a normal distribution. In diabetic nephropathy with urinary IgG leakage, however, theta D for large molecules was elevated and departed from linearity, suggesting a bimodal pore size distribution within the glomerular membrane. A pore model of solute transport revealed (1) the upper pore mode was highly permeable to large dextrans equivalent in size to IgG and (2) the fraction of glomerular filtrate permeating the large pores was greater in group 2 than in group 1 patients with diabetic nephropathy, 6% versus 3%, respectively. We conclude that urinary IgG leakage in diabetic nephropathy is determined by the development of a subpopulation of enlarged pores. The magnitude of urinary IgG losses appears to be a function of the membrane area-fraction occupied by the enlarged pores.

Cell Membrane↗
PubMed1982

Identification of eleven human hemoglobin variants by high-performance liquid chromatography: additional data on functional properties and clinical expression.

Eleven abnormal hemoglobins were detected in the course of cord blood screening or in the evaluation of evident hematological problems in individual cases. Identification of the variant in each case was done by high-performance liquid chromatography (HPLC); HPLC provides a rapid, sensitive means for the examination of abnormal hemoglobins. Some of the 11 variants that were identified have been described repeatedly and are included to provide information on the HPLC behavior of tryptic peptides. Others are much rarer. Additional information is provided about the hematological and clinical expression as well as ethnic and geographical distribution of the abnormal hemoglobin.

Chromatography, High Pressure Liquid↗
PubMed1982

The double-blind situation in families of disturbed children.

The interpersonal conditions of the double-blind situation were examined in the interaction of 15 families containing a symptom-bearing child. It was found that the greatest prevalence of conflicting communication occurred between the symptomatic children and their mothers, that the symptomatic children responded to incongruous communication with more avoidance behavior than their siblings, and that extreme interpersonal closeness or distance between mother and symptomatic child was associated with greater occurrence of conflicting communication.

Adolescent↗
PubMed1982

Bactericidal effect of 5-azacytidine on Escherichia coli carrying EcoRII restriction-modification enzymes.

5-Azacytidine was found to be bactericidal to Escherichia coli carrying plasmids specifying EcoRII restriction-modification systems, but not to the same strains lacking these plasmids. Of other base analogs tested, only 5(beta-D-ribofuranosyl)isocytidine had similar, although weaker, effects. Plasmids that had lost the EcoRII restriction-modification system did not confer sensitivity to 5-azacytidine. Mutants defective in the restriction function remained sensitive to the toxic effects of the drug; however, a mutant defective in the modification function lost most of the sensitivity to 5-azacytidine. For the bactericidal effect to be seen, the cells had to be growing; cells in the stationary phase of growth were not killed by the drug. The drug inhibited the methylase enzyme, and an inhibitor of the enzyme could be detected in vitro in extracts of cells that had been treated with 5-azacytidine. This nalidixic acid inhibited its formation. Coumermycin but not nalidixic acid antagonized the bactericidal effect of the drug; however, coumermycin was more effective in preventing the inhibition of the methylase by 5-azacytidine than was nalidixic acid.

Azacitidine↗