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At least 19 recordsLinked to original sources
PubMed1975

Structure and synthesis of a lipid-containing bacteriophage. Chemical modifications of bacteriophage PM2 and the resulting alterations in acyl-chain motion in the PM2 membrane.

The nucleocapsid proteins of bacteriophage PM2 and the inner lamella of the lipid bilayer, containing most of the phosphatidlethanolamine residues, were selectively cross-linked in the presence of 0.1-0.5% glutaraldehyde, 5 mM dimethylsuberimidate, or 0.05% toluene 2,4-diisocyanate. The biological activity (p.f.u.) of PM2 modified by these reagents decreased 10(6)-fold in all cases. The spike and coat proteins were selectively cross-linked in the presence of 7.5 mM N,N'-p-phenylenedimaleimide. The biological activity of virus modified by this reagen was unaffected. The electron paramagnetic resonance spectra of fatty acid spin labels incorporated into native and chemically modified viral membranes were qualitatively similar but show quantitative differences. Fixation with glutaraldehyde increased the rigidity of the membrane while Triton X-100 induced a more flexible structure. There was no change in the electron paramagnetic resonance spectrum of virus treated with N,N'-p-phenylenedimaleimide, however.

Bacteriophages↗
PubMedDate not supplied

Pathology produced by isocyanates: methods of immunological investigation.

A group of 182 workers exposed to diisocyanates (varnishers, carpenters, producers of polyurethane resins and expanded plastic) were examined to study the immunogenic capacity of these substances. The skin tests, particularly the intradermal tests, revealed reactions of the immediate, accelerated and/or delayed types due to the presence of IgE and IgG, in addition to responses of the cellular type. This was confirmed by passive transfer in guinea-pigs and man and immunohaematological tests such as passive haemagglutination and lymphocyte transformation. In 4 cases it was possible to demonstrate thermoresistant, homocytotropic immunoglobulins, that were not dependent on complement and behaved like reagins (i.e. short-term anaphylactic IgG). Exposure tests were performed on 45 cases; the results are analyzed and compared with those of the skin tests. It is concluded that both these groups of tests are of value in investigating the aetiopathogenesis of the pathology of the isocyanates: the skin tests for initial screening, and then the exposure tests for resolving doubtful diagnoses. Cross-reactions were also demonstrated between toluene-diisocyanate and methylene-diisocyanate. Two phases could be considered in the pathogenesis; in the first phase, signs of inflammation appeared at the primary sites of contact with the irritant, then the ability of the diisocyanates to form a conjugate with organic proteins results in the production of a complete antigen and consequent sensitization of the exposed person. The appearance of symptoms naturally depends on subsequent exposure and the immunogenic capacity of the patient: the response is mainly of the reagin type in atopic patients and of type 3 in non-atopic patients.

Animals↗
PubMed1978

A method using toluene-2,4-diisocyanate and glutaraldehyde to stabilize and conjugate antigens to erythrocytes for use in passive hemagglutination tests.

Erythrocytes were stabilized and activated for conjugation by simultaneous treatment with toluene-2,4-diisocyanate and glutaraldehyde. Following conjugation with an antigen, these cells were suitable for use in passive hemagglutination tests and could be stored in either hypo- or hyper-tonic solutions at 4 degrees C for at least 3 months without hemolysis or loss of agglutinating properties. Furthermore, these cells can be lyophilized and reconstituted with minimal loss of conjugation ability or of agglutination titer.

Aldehydes↗
PubMed1976

Toluene diisocyanate (TDI) pulmonary disease: immunologic and inhalation challenge studies.

Clinical and serologic effects of TDI exposure were studied in 112 occupationally exposed plant workers. Sera were obtained before and after commencement of TDI production. All subjects were skin-tested with common inhalant allergens and a TDI-HSA conjugate. Total eosinophil counts, immunoglobulin quantitations, and specific antibody assays by PCA, P-K, and radioimmunoassay were performed. Clinically "sensitive" individuals were tested by provocative inhalation challenge with from 0.005 ppm to the threshold limit value of 0.02 ppm TDI. No TDI-induced immunologic changes were noted with the exception of 3 individuals who demonstrated small positive wheal-and-erythema reactions to TDI-HSA but not to HSA alone. Inhalation challenge with TDI vapor produced airways obstruction, as measured by FEF (25-75). These responses were of the immediate, delayed, and dual type, and were provoked in some cases with levels as low as 0.005 ppm TDI.

Airway Obstruction↗
PubMed1977

The in vitro effect of toluene diisocyanate on lymphocyte cyclic adenosine monophosphate production by isoproterenol, prostaglandin, and histamine: a possible mode of action.

Toluene diisocyanate (TDI) significantly inhibits the rise in intracellular cyclic 3',5'-adenosine monophosphate (cAMP) that follows in vitro incubation of human lymphocytes with 6.7 x 10(-3) M isoproterenol and 1 x 10(-6) M prostagladin E1 (p less than 0.05). TDI has no significant effect on th production of lymphocyte cAMP following incubation with histamine (1 x 10(-3) M). The inhibitory action of TDI is greatest at a concentration of 3.3 x 10(-4) M and diminishes as the TDI concentration is increased or decreased. TDI also caused four- to fivefold stimulation of lymphocyte cAMP, an effect that is maximal at 1 x 10(-3) M, a concentration which has no significant inhibitory effect on stimulation of cAMP by isoproterenol or prostagladin E1. Conversely, 3.3 x 10(-4) M TDI, which inhibits cAMP production by isoproterenol and prostaglandin, has little stimulatory effect itself on cAMP production. This evidence suggests that TDI might induce obstructive airways disease through pharmacologic mechanisms and that TDI may be acting as a partial agonist.

Asthma↗
PubMed1977

Toluene diisocyanate pulmonary disease: immunopharmacologic and mecholyl challenge studies.

Selected workers exhibiting clinical "sensitivity" to toluene diiosocyanate (TDI) (wheezing, cough, and dyspnea upon entering a TDI-containing area) were studied for : (1) in vitro TDI-induced leukocyte histamine release; (2) determination of cyclic 3',5' adenosine monophosphate (cAMP) levels of lymphocytes exposed to TDI; (3) effect of TDI on the isoproterenol-induced increase of lymphocyte cAMP levels: and (4) acetyl-beta-methylcholine (mecholyl) inhalation challenge. TDI did not induce histamine release from leukocytes of "sensitive" or "nonsensitive" individuals, nor were lymphocyte cAMP levels affected by in vitro TDI exposure, TDI did, however, diminish in vitro stimulation of cAMP by isoproterenol. This effect, seen with cells of "sensitive" and "nonsensitive" individuals, appeared to be dose-dependent; there were no significant differences between the two groups. When challenged with mecholyl, 7 of 10 "sensitive" but only 1 of 10 "nonsensitive" individuals showed a greater than 20% decrease in FEV1. These results suggest that TDI-induced obstructive airways disorders may be associated with altered beta-adrenergic function.

Administration, Intranasal↗
PubMed1979

Inhalation challenge and pharmacologic studies of toluene diisocyanate (TDI)-sensitive workers.

Workers with "sensitivity" to toluene diisocyanate (TDI) studied in depth in an attempt to determine mechanisms of bronchial hyperreactivity. Tests included provocative inhalation challenge (PIC) with TDI and methacholine challenge. Blood samples obtained prior to and at various times after PIC were used to measure complement and split products of complement and plasma histamine levels and to determine dose-response slopes of lymphocyte cyclic adenosine monophosphate (cAMP) following stimulation with agonists. TDI-reactive individuals were all reactive to methacholine and responded to PIC with TDI by immediate, delayed, or dual bronchospastic reactions. No change in plasma histamine, total complement levels, or split products of complement were measurable. TDI reactors gave decreased lymphocyte cAMP dose response slopes to stimulation with isoproterenol, prostaglandin E1, and TDI, which suggests that impairment of adrenergic receptors may play an important role in TDI reactivity.

Aerosols↗