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Biomedical subjects

S M Wolff

Publications and source records attributed to S M Wolff.

At least 127 records · Page 7Linked to original sources
PubMed1975

Comparison of agents producing a neutrophilic leukocytosis in man. Hydrocortisone, prednisone, endotoxin, and etiocholanolone.

To study the potential application of glucocorticosteroid administration for the measurement of the bone marrow neutrophil reserve response, blood neutrophil count changes were measured in normal subjects after the administration of intravenous hydrocortisone (25, 50, 100, 200, and 400 mg) and oral prednisone (5, 10, 20, 40, and 80 mg). The upper three doses of both steroids increased the blood neutrophil count by approximately 4,000 cells/mm3. The neutrophilia occurring after hydrocortisone (200 mg) and/or prednisone (40 mg) was compared with that observed after endotoxin (0.8 ng/kg) and etiocholanolone (0.1 mg/kg) in 14 normal subjects, 7 patients with Wegener's granulomatosis on cyclophosphamide therapy and 10 patients with chronic idiopathic neutropenia. The normal responses (mean increase of blood neutrophils/mm3 above base line +/- 1 SEM) were: hydrocortisone 4,220 +/- 320, prednisone 4,610 +/- 360, endotoxin 6,060 +/- 880, and etiocholanolone 3,780 +/- 440. In the patient studies, etiocholanolone gave the smallest mean responses, but, in general, the results were similar for all agents. These data indicate that these glucocorticosteroids can be used as equivalent agents to endotoxin and etiocholanolone for measuring the neutrophil reserve response.

Adult↗
PubMed1975

The hypereosinophilic syndrome: analysis of fourteen cases with review of the literature.

Several closely related disease entities make up the idiopathic hypereosinophilic syndrome (HES). The syndrome is manifest by persistent and prolonged eosinophilia with organ damage. A group of 14 patients had hematologic, cardiac, and neurologic abnormalities attributable to this disease. Patient survival and response to chemotherapy was significantly better in this group than in previously reported patients. The etiology of HES remains unknown, as does the mechanism of tissue damage.

Adolescent↗
PubMed1975

Defective mononuclear leukocyte chemotaxis in the Chediak-Higashi syndrome of humans, mink, and cattle.

Chemotaxis of mononuclear leukocytes from humans, mink, and cattle was evaluated in vitro using a morphologic Boyden chamber technique and a new 51-Cr-labeled mononuclear radioassay with a double micropore filter system. Significantly decreased mononuclear leukocyte chemotactic response were noted when human, mink, or cattle Chediak-Higashi cells were tested using autologous serum or endotoxin-activated autolotous serum. A similar Chediak-Higashi mononuclear leukocyte defect was noted in humans when kallikrein or dialyzable transfer factor were used as the chemotactic stimulus. Studies using smaller pore filters in the chemotactic chamber exaggerated the chemotactic defect. Serum from Chediak-Higashi subjects had normal chemotactic activity. Additional studies on the spontaneous (random) locomotion of Chediak-Higashi mononuclear leukocytes revealed normal results when a capillary tube assay system was used, but abnormal results were obtained when a Boyden chamber micropore filter assay was used, demonstrating fundamental differences in these two assays of random locomotion. It is clear from these studies that defective mononuclear leukocyte chemotaxis is another feature of the imparied host defenses in the Chediak-Higashi syndrome that may contribute to the marked susceptibility to pyogenic infections so characteristic of this dease.

Animals↗
PubMed1975

Leucocyte chemotaxis: physiological considerations and abnormalities.

Expression of the inflammatory process is dependent on mobilisation of leucocytes, which require leucocyte chemotaxis. Recent technological advances have enabled extensive in vitro biological characterisation of the chemotatic stimuli (factors) and the cellular events of migration. The chemotatic stimuli include products of complement activation, fibrinolytic and kinin generating systems, collagen products as well as products of bacterial growth and products released from virus-infected tissues. Chemotatic factors are also released as a result of lymphocyte activation and phagocytosis by neutrophils. Other neutrophils products released during phagocytosis activate the complement system. A complex mechanism for limiting production or activity of chemotactic factors has been identified. These antichemotatic agents include serum and cell-derived chemotactic factor inactivators as well as specific inhibitors of leucocyte migration and complement inactivators released from neutrophils during the phagocytic process. The mechanism by which cells respond to chemotatic factors is poorly understood by cell adherence to the substratum, cell deformability, random migration, and directed migration are required. These processes are complex and require modifications of the leucocyte surface, calcium and magnesium, activation of esterases, function of contractile elements and assembly of a cytoskeleton, which is probably modulated by cyclic nucleotide metabolism.

Animals↗
PubMed1975

Lysosomal enzymes in normal and Chediak-Higashi blood leukocytes.

A method of blood granylocyte concentration and isolation of granules from both normal and neutropenic Chediak-Higashi syndrome (CHS) patients is described. the intracellular distribution of activity for several hydrolases in CHS granulocytes differs from normal; significantly more activity is present in the cytoplasmic fraction and correspondingly less is granule-associated. Isolated CHS granules are not more sensitive to the labilizing agents vitamin A, progesterone, or etiocholanolone. Specific activities of myeloperoxidase and ss-glucuronidase in CHS granulocytes are lower than normal while alkaline phosphatase is elevated. Other lysosomal enzyme activities are normal. Lysosomal enzyme distribution and content are similar in CHS and normal mononuclear cells. The possible significance of these findings is discussed.

Acid Phosphatase↗
PubMed1974

Demonstration and characterization of two distinct human leukocytic pyrogens.

Human monocytes and neutrophils were separated from buffy coats of blood obtained from normal donors. Following incubation with heat-killed staphylococci, monocyte preparations contained 20 times more pyrogenic activity in the supernatant media than did supernates from an equal number of neutrophils. During purification of these pyrogens it was discovered that these cell preparations each produced a distinct and different pyrogen. The pyrogen obtained from neutrophils had a mol wt of 15,000 following Sephadex G-75 gel filtration, an isoelectric point of 6.9, and could be precipitated and recovered from 50% ethanol at -10 degrees C. In contrast, the pyrogen derived from monocyte preparations had a mol wt of 38,000, an isoelectric point of 5.1, and was destroyed in cold ethanol. Both molecules were unaffected by viral neuraminidase but biologically destroyed at 80 degrees C for 20 min and with trypsin at pH 8.0. The febrile peak produced by partially purified neutrophil pyrogen occurred at 40 min while that from monocytes was at 60 min. In addition, monocyte pyrogen produced more sustained fevers for the same peak elevation as neutrophil pyrogen. These studies demonstrate for the first time two chemically and biologically distinctive pyrogens derived from circulating human white blood cells and have important implications for our understanding of the pathogenesis of fever in man.

Animals↗
PubMed1974

Infection and immunoglobulin concentrations in Chediak-Higashi mice.

The Chediak-Higashi syndrome (CHS) has been reported in man, cattle, mink, and mice. CHS humans and cattle have an increased incidence of pyogenic infections, whereas CHS mink are more susceptible to Aleutian disease. Age- and sex-matched groups of CHS mice (mutant strain) and C57 Bl/6N (parent strain) were challenged with Candida albicans, Escherichia coli, Klebsiella pneumoniae, and Staphylococcus aureus intravenously and Streptococcus pneumoniae intraperitoneally. A significant increase (P < 0.001) in mortality rate for the CHS mice was demonstrated with all five challenge organisms. Heterozygous mice challenged with C. albicans had a mortality rate essentially the same as C57 Bl/6N mice. The serum immunoglobulin concentrations of CHS mice were found to be the same or greater than the control or heterozygous mice. CHS mice have an increased susceptibility to pyogenic infections, which is not due to immunoglobulin deficiency. These mice may provide a useful laboratory model for the study of increased susceptibility to infection.

Candida albicans↗
PubMed1974

Renal biopsy pathology in Wegener's granulomatosis.

Eighteen renal biopsies from 10 patients with active generalized Wegener's granulomatosis (GWG), with GWG in remission on therapy, and with active localized Wegener's granulomatosis (LWG) have been examined by light and electron microscopy. In all 9 patients with active GWG, light microscopy revealed focal and segmental glomerulonephritis. Electron microscopy revealed subepithelial basement membrane densities resembling immune complex deposits in two biopsies from patients with active GWG. In biopsies from patients on cytotoxic therapy, there was no active inflammatory process, but focal glomercular obsolescence and segmental tuft sclerosis provided evidence of prior focal and segmental glomercular disease. Discrete zones of basement membrane crimping and increased mesangial material along the capillary wall were observed in some patients with apparent LWG, as well as proven GWG, possibly representing foci of previous glomerular injury. The appearance of dense deposits on the epithelial side of the basement membrane suggests that immune complex deposition in the glomeruli may be at least partially responsible for the renal injury in Wegener's granulomatosis.

Antigen-Antibody Complex↗