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Biomedical subjects

K Hsu

Publications and source records attributed to K Hsu.

106 records · Page 6Linked to original sources
PubMed1978

Binding of antibodies to acetylcholine receptors in Electrophorus and Torpedo electroplax membranes.

Antisera against purified acetylcholine receptors from the electric tissues of Torpedo californica and of Electrophorus electricus were raised in rabbits. The antisera contain antibodies which bind to both autologous and heterologous receptors in solution as shown by an immunoprecipitation assay. Antibodies in both types of antisera bind specifically to the postjunctional membrane on the innervated surface of the intact electroplax from Electrophorus electric tissue as demonstrated by an indirect immunohistochemical procedure using horseradish peroxidase conjugated to anti-rabbit IgG. Only anti-Electrophorus receptor antisera, however, cause inhibition of the receptor-mediated depolarization of the intact Electrophorus electroplax. The lack of inhibition by anti-Torpedo receptor antibodies, which do bind, suggests that the receptor does not undergo extensive movement during activity. The binding of anti-Torpedo antibodies to receptor-rich vesicles prepared by subcellular fractionation of Torpedo electric tissue was demonstrated by both direct and indirect immunohistochemical methods using ferritin conjugates. These vesicles can be conveniently collected and prepared for electron microscopy on Millipore filters, a procedure requiring only 25 micrograms of membrane protein per filter. In addition, it was possible to visualize the binding of anti-Torpedo receptor antibodies directly, without ferritin. These anti-Torpedo receptor antibodies, however, do not inhibit the binding of acetylcholine or of alpha-neurotoxin to receptor in Torpedo microsacs but do inhibit binding of alpha-neurotoxin to Torpedo receptor in Triton X-100 solution. It is likely that the principal antigenic determinants on receptor are at sites other than the acetylcholine-binding sites and that inhibition of receptor function, when it occurs, may be due to a stabilization by antibody binding of an inactive conformational state.

Acetylcholine↗
PubMed1976

Electrical conductivity in lipid bilayer membranes induced by pentachlorophenol.

Electrical conductivity induced in thin lipid bilayer membranes by pentachlorophenol has been studied. The membranes were formed from phosphatidyl choline, phosphatidyl ethanolamine, or phosphatidyl glycerol and various amounts of cholesterol. The position and the magnitude of the maximum of the conductivity vs. pH curve depend on the type of lipids and cholesterol content. At low pentachlorophenol concentrations and low pH the concentration dependence of conductivity is quadratic and becomes linear at higher pH. Above 10(-5) M of pentachlorophenol the concentration dependence of the membrane conductivity tends to saturate. Presence of pentachlorophenol enhances membrane transport of nonactin-K+ complex. Increase of cholesterol content increases pentachlorophenol induced conductivity in all membranes and shifts the conductivity toward lower pH. For phosphatidyl choline the largest rate of change of membrane conductivity with cholesterol occurs at 1:1 phospholipid to cholesterol molar ratio. Pentachlorophenol is found to be a class II uncoupler and the experimental results are consistent with the hypothesis that the membrane permeable species are dimers formed by combination of neutral and dissociated pentachlorophenol molecules. Several schemes of membrane conduction, including dimer formation in the aqueous phase as well as at the membrane-water interface have been considered. Arguments are given in favor of the formation of dimers within the membrane surface.

Electric Conductivity↗
PubMed1975

Membranous nephropathy: an overview.

Membranous nephropathy (MN) accounts for about 20 percent of cases of the nephrotic syndrome. The importance of renal biopsy in establishing the diagnosis is emphasized. In the great majority of MN patients, no etiologic factor can be discerned. In a significant minority, MN appears to be a manifestation of sarcoidosis, diabetes, lupus, syphilis, malaria, or toxicity from heavy metals or drugs. In some cases the "cause" is neoplasia (including lymphoma) or a viral infection. Massive proteinuria, hypoproteinemia and edema are the principal manifestations of MN, finally resulting in renal failure. Treatment consists chiefly of diet and diuretic drugs. In the more pronounced cases, corticosteroids may have a favorable effect and in very resistant cases, cyclophosphamide is indicated. Judicious use of these modalities if often associated with the diminution or disappearance of the clinical signs of MN.

Adult↗
PubMed1969

Immunologic studies of autoimmune disease in NZB-NZW F1 mice. I. Binding of fluorescein-labeled antinucleoside antibodies in lesions of lupus-like nephritis.

For the past 3 years NZB and NZW mice have been maintained by sister-brother matings from English breeder stock. NZB/NZW F(1) hybrids developed lupus-like nephritis during the 6th to 7th month and few survived beyond the 8th month. Renal tissues of these animals were examined with fluorescein-labeled antinucleoside sera, specific for thymine and cytosine, for the presence of denatured DNA in GCW, and with labeled antibody to mouse IgG for the presence of excess host globulin in the same areas. The following results have been obtained: (a) All 51 hybrids, over 5 months of age, had an excess of mouse globulin in GCW. 40 animals between the ages of 5 and 12 months showed, in the same areas, antigens which bound one or both of the antinucleoside antibodies. (b) Renal tissues of 19 NZB mice, 5-19 months old, and 27 NZW mice, 2-18 months old, were examined. Excess host globulin was seen in GCW of 13 NZB and 20 NZW animals. The tissues of only two old NZB mice, 14 months of age, bound antinucleoside antibody but none of the other animals did. The association of rapidly fatal lupus-like nephritis in NZB/NZW F(1) mice with denatured DNA and mouse globulin in GCW supports the hypothesis involving this antigen-antibody complex in the pathogenesis of the disease.

Animals↗
PubMedDate not supplied

Specific detection and semiquantitation of microorganisms in tissue by nucleic acid hybridization. II. Investigation of synovia from pigs with chronic Erysipelothrix arthritis.

Synovial tissues from animals with chronic Erysipelothrix arthritis were examined by a technique based on RNA-DNA hybridization in an attempt to detect the inducing organism, Erysipelothrix insidiosa (EI). Twelve synovial specimens from 5 animals whose joints lacked culturable EI also lacked EI detectable by this technique. Because the technique is capable of detecting approximately one organism per 50 mammalian cells, it is concluded that no more than this number were present in the involved tissue. Implications of these results for proposed pathogenetic mechanisms in this disorder and in human rheumatoid arthritis are discussed.

Animals↗
PubMedDate not supplied

Intrinsic polymorphonuclear chemotactic defect in a boy with chronic granulomatous disease.

A six year old boy is described who suffured from recurrent and protracted infections of multiple organs by various catalase positive bacteria. A severe episode of osteomyelitis involving several bones was caused by Aspergillus fumigatus. Studies of his PMNs revealed impaired metabolic as well as microbicidal functions characteristic of CGD. Chemiluminescence in response to both opsonized zymosan and sodium fluoride was markedly depressed, while control PMNs showed significant responses. Control leukocytes suspended in patient's serum likewise evoked normal chemiluminescence. Microbicidal activity against staphylococcus aureus 502A was also decreased using patient's PMNs, whereas control PMNs were able to reduce the number of colony forming bacteria by 2 logs in 120 minutes. Viable intracellular bacteria after lysis of extracellular bacteria formed 3 X 10(7) colonies from patient's PMNs and less than 2 X 10(5) colonies from the control. NBT dye reduction studies of the family members suggested an x-linked recessive mode of inheritance. The extraordinary nature of this case lies in the discovery of an associated intrinsic cellular defect of chemotaxis involving his polymorphonuclear leukocytes. Specifically, the Rebuck skin window showed predominantly mononuclear cells from 4 up to 24 hours. In addition, the patient's PMNs failed to migrate in response to cultured filtrates of E. coli as the chemoattractant. This abnormality persisted in the presence of autologous plasma or serum as well as in control plasma or serum. Control PMNs showed normal chemotaxis in the presence of the patient's plasma or serum. The extent to which the rare coexistence of these two phenomena influence the clinical disease is not known and remains to be elucidated.

Aspergillosis↗