Comparison of forces measured between phosphatidylcholine bilayers.
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Biomedical subjects
Publications and source records attributed to R G Horn.
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A technique using India ink in electron microscopic preparations was used to study bacterial capsules. Capsules were demonstrated on Streptococcus pneumoniae and Staphylococcus aureus (strain M and the Smith diffuse variant) from in vitro cultures. Two types of false capsules were observed on Neisseria gonorrhoeae grown in vitro or obtained from human urethral exudates. No true capsules were definitively identified on gonococci from these sources. The technique described does not require the use of specific anticapsular antibody or specific polysaccharide stains and permits the detection of artifacts that may, by the use of light microscopic methods, be misinterpreted as capsules.
In contrast to information in the literature which indicates that meningococci rapidly lose pili upon cultivation in vitro, we found that piliation of meningococci could be maintained in vitro for 15 or more passages. Pili were present on all eight isolates tested, whether from asymptomatic carriers or from subjects with meningococcal disease. Complete loss of piliation occurred in the same two strains on two of the three media tested. On one medium (Thayer-Martin medium with supplement B), there was partial or complete loss of pili by all strains. The optimal medium for maintaining pili was chocolate agar with 1% IsoVitaleX; 95% or more of the microorganisms of six of the eight strains tested were piliated after 15 passages in vitro, and more than 60% of the microorganisms of the other two strains were piliated. Meningococci passed on this medium generally maintained their initial density of piliation (3 to 34 pili per diplococcus). The ability to predictably cultivate piliated meningococci in vitro and to select piliated and nonpiliated clones of the same strain should allow investigation of the biochemical and immunological properties of meningococcal pili as well as their possible role in the pathogenicity of Neisseria meningitidis.
Because systemic intravenous immunotherapy with Corynebacterium parvum is an effective immunopotentiating and immunotherapeutic agent in animals, clinical studies of this agent have been undertaken. Toxicities in man have been noted, but most are treated symptomatically. Three patients with metastatic melanoma developed oliguria, edema, diffuse bilateral pulmonary infiltrates, azotemia, hypoalbuminemia and hypocomplementemia, while receiving intravenous C. parvum therapy. All had renal biopsies that showed a proliferative glomerulonephritis with subendothelial basement membrane deposits. Immunofluorescence showed glomerular IgG, IgA, IgM, and the C3 component of complement. A fourth patient was found in retrospective chart review of 87 patients registered on two C. parvum-containing protcols. The frequency of the complication in this group was 3/87. Renal failure resolved in all four patients spontaneously after the cessation of C. parvum immunotherapy. Serial evaluation of renal function should be carried out in all patients on systemic adjuvant immunotherapy.
Light, electron, and immunofluorescence microscopy on tissues from 63 domestic cats revealed that glomerulonephritis occurred in almost one third of cats with hematopoietic neoplasms of the type linked with feline leukemia virus (FeLV). Glomerular lesions were of the immune complex type with subepithelial, subendothelial, and mesangial dense deposits and reticular aggregates, similar to the nephropathy associated with systemic lupus erythematosus in humans. Evidence that the glomerular lesions may be viral-induced raises the possibility of similar pathogenetic mechanisms in human disease.
Six patients without overt diabetes mellitus underwent renal biopsy for suspected glomerulonephritis. All were demonstrated to have diabetic glomerulosclerosis and subsequently were found to have abnormal glucose tolerance tests. Electron microscopy was critical in making the correct diagnosis in five of six patients. The reported cases represent 3% of a series of 200 patients who had a renal biopsy to evaluate possible glomerulonephritis. Renal manifestations of diabetes mellitus may antedate glycosuria and other more common presenting symptoms of this disease.
Acute renal insufficiency developed in three patients receiving chemotherapy for tuberculosis. It is proposed that acute diffuse interstitial nephritis related to the drugs was responsible for the renal injury. Recovery of renal function was slow and incomplete. Physicians administering chemotherapy to patients with tuberculosis must be aware of the potential nephrotoxicity of the common treatment regimens.
Lymphomas with histologic features indicating a follicular center cell (FCC) origin were analyzed from 26 patients of a group of 45 consecutive non-Hodgkin's lymphoma patinets whose tumors were studied for B- and T-cell characteristics. They were compared with benign, reactive lymphoid tissue from 14 patients. Cell suspensions from biopsy material, blood, or bone marrow were examined for surface Ig and for rosette formation with sheep erythrocytes (E rosettes). Of the 26 patients with FCC lymphomas, 22 had 40% or more Ig-bearing cells; all patients with FCC lymphoma tissues had 25% or less E rosette-forming cells. Cells from most FCC lymphomas of the cleaved type had surfac IgM; those from several FCC lymphomas had both IgM and IgD. Cells from lymphomas of noncleaved cell type had surface IgG or IgA. Light-chain analysis showed that cells from FCC lymphomas bore a predominant light-chain type, which indicated their monoclonal nature. Neoplastic cells from several FCC lymphomas synthesized the surface Ig which they bore. Reactive tissues usually contained fewer Ig-bearing and more E rosette-forming cells than FCC lymphomas; the Ig-bearing cells, with one exception, had a polyclonal distribution. Correlation of histologic and immunologic observations indicates that most lymphomas identified as FCC in origin by light micorscopic criteria mark as B cells with the use of immunologic techniques and that FCC lymphomas are the most common type of non-Hodgkin's lymphoma.
Tissues from malignant lymphomas with both nodular and diffuse growth patterns, thought by light microscopy to be composed of cells of follicular center cell (FCC) origin, Were examined by electron microscopy; the tumor cells were similar to lymphoid cells found in reactive follicular centers. Tumor cells from neoplasms thought to be composed of cleaved FCC often had more pronounced nuclear folding than did cleaved FCC of reactive follicles, whereas cells in tumors of noncleaved FCC type were indistinguishable from their presumed counterparts in reactive follicles. Large cell noeplasms, previously classified as "histiocytic" lymphomas were composed of cells with ultrastructural characteristics of transformed lymphocytes; they showed neither ultrastructural nor cytochemical features of mononuclear phagocytes. These findings support the concept that a major group of lymphomas arises from lymphocytes of follicular centers.
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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.
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