Prostate cancer presenting as facial paralysis.
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Biomedical subjects
Publications and source records attributed to B Gruber.
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The present study investigated the effects of the use of the left and right hands on haptic identification of letters which were presented in either a normal (0 degrees rotation), downward (90 degrees clockwise rotation), upside down (180 degrees rotation), or facing upward (270 degrees rotation) position. Each of the 80 right-handed subjects was given five series of randomly ordered presentations of sets of 8 letters of the alphabet. The subjects were asked to feel and then name each letter correctly as quickly but as accurately as possible. Times showed no effect of hand, but significant effects were found for different sets of letters, degree of rotation and a significant decrease in identification time was observed across the five series. Interactions occurred between hand and rotation as well as set and rotation. Errors showed a significant interaction of hand with degree of rotation; the right was superior at 0 degrees but the left was superior at 90 degrees. The results were discussed in terms of hypotheses of hemisphere function, mental rotation, and stimulus familiarity.
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An unusual fungal infection of the neck caused by Phialophora verrucosa (chromoblastomycosis) is presented. The patient acquired this fungus by cutting his chin on a wooden floor. Surgical and medical therapy of this unusual disease is discussed.
As a result of prolonged hospitalizations and the frequent administration of sclerosing antibiotics and/or chemotherapeutic agents, vascular access frequently becomes difficult in patients with advanced head and neck carcinoma. Eighty-six totally implantable venous access devices were placed in 83 patients with advanced head and neck cancer to facilitate the administration of continuous intravenous infusion chemotherapy. Complications relating to surgical placement or usage of the device occurred in 29 of 86 ports (34%), leading to the removal of eight devices (9%). The implantation of two devices required revision. There were no serious sequelae from any of the complications. The port facilitated the administration of home chemotherapy in 11 patients. Because of our favorable experience, we now routinely recommend placement of these devices to all patients with advanced head and neck cancer at our institution.
Human lung mast cells have been reported recently to contain small amounts of the elastolytic protease present in the neutrophil and implicated in the pathogenesis of alveolar wall destruction in emphysema. Since mast cells are numerous within alveolar walls, release of inflammatory mediators (and possibly elastase) by cigarette smoking could contribute to alveolar injury in this disease. We therefore examined bronchoalveolar lavage (BAL) fluid for the mast cell granule constituents histamine and tryptase. The results, while not conclusive, supported the possibility that cigarette smoking increases secretion of histamine releasing activity by alveolar macrophages with subsequent degranulation of local mast cells. Mast cell discharge of inflammatory mediators (including neutrophil chemotactic factors and perhaps the elastolytic protease) could then participate in the destruction of alveolar walls.
IgE rheumatoid factor activity was found to be significantly elevated (P less than 0.01) using an ELISA assay when paired synovial fluid and sera from 13 patients with active RA were compared to ten control samples. Synovial fluid IgE RF activity was higher than predicted by diffusion alone in 7/11 (64%) of the RA synovial fluids studied when coefficients of diffusion were determined. The specificity of IgE RF activity as measured by the ELISA was confirmed using immunoaffinity chromatography. Mast cells, obtained by enzymatic dispersion of rheumatoid synovial tissue, were sensitized with sera containing either IgE antibodies directed against ragweed or IgE with RF activity. Histamine was released upon challenge with anti-IgE antibodies (33.2% +/- 11), ragweed antigen E (34.6% +/- 11), or aggregated gamma globulin (47.6% +/- 17.9). No histamine release was observed if antigen challenge occurred in the absence of appropriate sensitization, with C3 anaphylatoxin, or after immunoadsorption of IgE from sera containing IgE RF activity.
For determination of the mutagenicity of herbicides and insecticides in working and environmental relevant concentrations we examined 26 pure substances of the chemical groups of polychlorinated alicyclic hydrocarbons, phenoxy fatty acids and and triazines with the Salmonella-microsome-test (S. typhimurium strains TA 97, TA 98, TA 100 and TA 102 with and without metabolic activation with Aroclor 1254 induced rat liver microsome fraction). Only one substance--Chlorthiamide--showed mutagenicity in concentrations of 0.001 microgram/plate. In all the other substances examined we found numbers of revertants near the spontaneous mutagenic rates. However a human carcinogenic potential can't be excluded, because several toxicological studies with mammalians showed a carcinogenic activity of organohalogenic insecticides without mutagenic activity in biological short term tests.
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To determine if tetracyclines can inhibit human synovial collagenase from rheumatoid tissue, paired synovial tissue (or synovial fluid) was collected from 7 patients before and after oral administration of minocycline (100 mg BID) for 10 days. With each patient serving as his own control, the postminocycline collagenase activities fell an average of 67% from pretreatment values. Qualitative SDS-PAGE revealed decreased loss of alpha collagen components and reduced formation of alpha A digestion fragments. Addition of minocycline or a chemically modified tetracycline to synovial culture media in vitro profoundly inhibited collagenase activity. Further study of this action of tetracyclines could serve as a probe of the role of collagenase in rheumatoid arthritis and lead to development of agents capable of modifying the tissue destructive actions of collagenase.
Microscopic analysis of synovial specimens from 35 patients with rheumatoid arthritis (RA) and 7 patients with osteoarthritis revealed mast cell hyperplasia in perivascular regions, in fibrous interstitial areas, and clustered around the periphery of lymphoid aggregates. Metachromatic staining, immunofluorescence studies, and ultrastructural analysis revealed a single population of connective tissue-type mast cells with surface IgE receptors. Total extractable histamine of synovial tissue was 4.15 +/- 2.30 micrograms/gm (n = 8) for RA synovium and 0.53 +/- 0.23 microgram/gm (n = 7) for OA synovium. Mast cell secretion was assessed and specific release of histamine from RA synovial mast cells was observed following stimulation with anti-IgE (32.3%), compound 48/80 (40.1%), calcium ionophore A23187 (25.2%), and a partially purified lymphokine with histamine-releasing activity (23.9%).
Right maxillary sinus mucormycosis developed in a 45-year-old patient with hairy cell leukemia and pancytopenia. The patient recovered with surgical debridement, amphotericin therapy, and institution of alpha-2 interferon as therapy for his hairy cell leukemia. This may be the first case of the use of alpha-2-interferon therapy in a patient with documented systemic fungal infection and hairy cell leukemia and a rare example of recovery from this infection in a hematologic malignancy.
Congenital complete heart block is closely associated with the presence of anti-Ro (SS-A) autoantibodies. Quantitative solid-phase assays for Ro (SS-A) autoantigen and autoantibody have established the presence of Ro (SS-A) in cardiac tissues and have been used to evaluate an informative pedigree. The propositus we describe here had complete congenital heart block and showed anti-Ro (SS-A) binding of 13-fold less than his normal HLA-identical twin sister. Both had identical titers of antinuclear antibody. These data support the hypothesis that anti-Ro (SS-A) may be directly involved in the pathogenesis of congenital complete heart block.
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An enzyme-linked immunosorbent assay has been developed for the quantitation of activated Hageman factor-C1 inactivator (HF-C1 INH) complexes. Addition of increasing quantities of either of the major forms of activated Hageman factor (HFa or HFf) to normal plasma or to Hageman factor-deficient plasma leads to a dose-dependent increase in activated HF-C1 INH complexes. As little as 0.5 micrograms/mL of activated HF added to plasma can be detected, corresponding to activation of approximately 2% of plasma HF. The sensitivity of the assay is increased at least tenfold when complexes are formed in HF-deficient plasma, indicating competition between unactivated HF and activated HF-C1 INH complexes for binding to the antibody. Specificity is demonstrated in that addition of activated HF to hereditary angioedema plasma yields less than 1% of the activated HF-C1 INH complex formation obtained with normal plasma. Kaolin activation of HF-deficient plasma yields no detectable complex formation. Kaolin activation of prekallikrein-deficient plasma demonstrates a time-dependent increase in formation of activated HF-C1 INH complex consistent with the ability of HF in this plasma to autoactivate as the time of incubation with the surface is increased. Kaolin treatment of high-molecular weight (HMW) kininogen-deficient plasma yields an even more profound abnormality in the rate of formation of activated HF-C1 INH complexes reflecting the complex role of HMW kininogen in the initiation of contact activation. Although addition of corn inhibitor to plasma prevents activated HF-C1 INH complex formation, it does not inhibit activated HF sufficiently fast to prevent prekallikrein activation.
The extracellular distribution of 3H-diethylstilbestrol (3H-DES) in mouse skeletal muscle was assessed following intraperitoneal injection. Total muscle extracellular space was measured with 14C-inulin, and the vascular space with 125I-albumin. A significant difference in the distribution of native 3H-DES and its metabolites in muscle and blood was found. This could only be explained if these compounds distributed with the albumin space and not the inulin space.
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