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Biomedical subjects

M M Miller

Publications and source records attributed to M M Miller.

At least 163 records · Page 9Linked to original sources
PubMed1978

Allergic contact dermatitis to 1,4-bis(isopropylamino)anthraquinone. Caused by a felt-tip marker pen.

Adult allergic contact dermatitis to the black ink of a felt-tip marker pen occurred in two adult subjects. In both subjects the cutaneous reaction did not require photoactivation. Patch testing with the ingredients in the black ink demonstrated cutaneous sensitivity to the black dye. Further patch testing with the components of the black dye revealed cutaneous sensitivity in both subjects to the blue component, 1,4-bis(isopropylamino)anthraquinone, commonly known as Colour Index Solvent Blue 36.

Adult↗
PubMed1977

Trimellitic anhydride-induced airway syndromes: clinical and immunologic studies.

This report describes a spectrum of respiratory symptoms in workers exposed to trimellitic anhydride (TMA), a biologically reactive chemical used in the plastics industry. Fourteen workers who had worked on a unit which synthesized TMA were evaluated by clinical and immunologic methods. Respiratory syndromes induced by TMA inhalation included asthma and rhinitis of the immediate type, late onset asthma with systemic symptoms, and airway irritation. TMA was shown to couple rapidly to human serum albumin, forming an immunoreactive hapten-protein complex. The workers' immunologic reactivity to this complex could be quantitated and correlated with the three respiratory syndromes. The asthma-rhinitis syndrome was mediated by IgE antibody specific for the TMA hapten. The syndrome of late onset asthma with systemic symptomes was accompanied by elevated levels of TMA-specific IgG antibody. Rheumatoid factor in high titer was found in one worker with IgE-mediated asthma and in two workers with asthma of late onset. Lymphocyte reactivity of TMA-HSA was demonstrated in three workers representative of the three clinical syndromes. Leukocyte histamine release was demonstrated to TMA-HSA in one worker with high levels of IgE antibody specific for TMA-HSA who had severe symptoms of acute rhinitis and asthma.

Adult↗
PubMed1977

Methacholine and physostigmine airway reactivity in asthmatic and nonasthmatic subjects.

Inhalation challenges using methacholine and physostigmine were performed in 3 human asthmatic and 3 nonallergic normal subjects. Plethysmographic measurements of specific airways conductance (Gaw/Vtg) were used to monitor the response. The dose required to produce a 17% fall in Gaw/Vtg was significantly lower in asthmatic subjects than in normal subjects for both physostigmine (p less than 0.0125) and methacholine (p less than 0.05). Moreover, in all subjects the relative airway sensitivity to methacholine correlated with the relative airway sensitivity to physostigmine. Both methacholine and physostigmine are cholinergic agents. Whereas methacholine acts directly at the end organ cholinergic receptor, physostigmine acts by increasing release and decreasing destruction of endogenous acetycholine at the vagal distal innervation. This suggests that the cholinergic airway hyperreactivity characteristic of asthma is a manifestation of end organ hypersensitivity.

Acetylcholine↗
PubMed1977

Differential airway reactivity to carbachol and physostigmine sulfate in rhesus monkeys with and without reagin-mediated respiratory responses.

Bronchial airway reactivity to carbachol (CAR) and physostigmine (PHY) was individually measured in three rhesus monkeys with and three rhesus monkeys without reagin-mediated respiratory responses (RR). The three monkeys with reagin-mediated RR demonstrated bronchial hyperreactivity to CAR (p less than 0.25) but not PHY when compared with the three control monkeys. No correlation between airway reactivity to CAR and PHY was noted in all six monkeys. We conclude that monkeys with reagin-mediated RR possess airway hyperreactivity to the exogenously administered acetylcholine analogue CAR, but not to the endogenous acetylcholine which is released in vivo by PHY.

Aerosols↗
PubMed1976

Chronic hypersensitivity lung disease with recurrent episodes of hypersensitivity pneumonitis due to a contaminated central humidifer.

A child with a 4-year history of acute and chronic respiratory symptoms of unknown aetiology was investigated for hypersensitivity pneumonitis. Lung disease due to inhalation of material from a contaminated central humidifier was suggested by the clinical history, the presence of precipitating antibodies in the serum against the humidifier water, a pulmonary response to challenge with the humidifier water, and marked improvement after removal of the humidifier. No fungi were cultured from the humidifier nor were antibodies against a number of fungal antigens identified by radioimmunoassay inhibition techniques. Antigenic material was found in the humidifier water and the household water prior to its reaching the humidifier. This antigenic material was not found in laboratory tap water supplied from the same general source (Lake Michigan) but from a different pumping station. Three of the child's siblings gave histories suggestive of a single concurrent episode of acute hypersensitivity pneumonitis and one sibling had a history suggestive of chronic hypersensitivity lung disease. No association could be found between HLA-haplotypy and disease in the patient and the siblings.

Alveolitis, Extrinsic Allergic↗
PubMed1976

Comparative toxicological studies of amphotericin B methyl ester and amphotericin B in mice, rats, and dogs.

In acute and subacute toxicological studies, amphotericin B methyl ester was shown to be much less toxic than the parent antibiotic. As a single intravenous dose in mice, the methyl ester was approximately 20 times less toxic than amphotericin B. Also, the acute toxicity of the methyl ester in mice was not enhanced by the presence of chemically induced hepatic or renal damage or by the concurrent administration of amphotericin B or flucytosine. In a 1-month intraperitoneal study in rats, the methyl ester was about one-fourth as nephrotoxic as amphotericin B. In a 1-month intravenous study in dogs, the methyl ester was about one-eighth as nephrotoxic and one-fourth to one-half as hepatotoxic as the parent compound. In addition, the methyl ester, unlike amphotericin B, produced minimal renal effects, which did not increase in severity with increasing dosage. Based on the results of these studies, it is concluded that amphotericin B methyl ester has the potential for an improved therapeutic ratio in the treatment of systemic mycoses.

Amphotericin B↗
PubMed1976

A comparison of immunologic asthma to two types of cholinergic respiratory responses in the rhesus monkey.

Rhesus monkeys were used to characterize the respiratory response (RR) to aerosolized physostigmine (Phy) and compare the response to the acute, reagin-mediated RR and the carbachol response. In the latter two responses, there are characteristic increases in frequency of respiration (f), pulmonary resistance (PR), and decreases in peak expiratory flow rate (PEFR), tidal volume (TV), and dynamic compliance (C). In contrast, a Phy RR characteristically shows no change in TV and f. The Phy RR is inhibited by atropine and lidocaine. The carbachol RR is inhibited by atropine but not lidocaine. The Phy RR mimics a vagally induced RR more closely than carbachol because it is inhibited by pharmacologic and physiologic vagal blockade produced by atropine and lidocaine, respectively, whereas the carbachol RR is blocked by atropine but not lidocaine. The carbachol block by atropine is primarily not a block of vagal action, but a general pharmacologic block of cholinergic action. The reagin-mediated RR is not inhibited by pharmacologic or physiologic vagal blockade. We conclude that a Phy-induced vagomimetic RR differs from a reagin-mediated, immediate-type RR. Although a minor portion, at most, of a reagin-mediated, immediate-type RR may be mediated via the vagus nerve, the major portion of a reagin-mediated RR occurs independent of the influences of the parasympathetic innervation of the lung.

Acetylcholine↗
PubMed1975

Scanning electron microscopy of epithelia prepared by blunt dissection.

Simple dissection techniques of samples to be examined in the scanning electron microscope allow one to visualize easily the three-dimensional shape of epithelial cells in situ. Such preparations reveal a complex system of ridges and folds on the lateral surface of the cells whose intricacy can best be appreciated with SEM. In many epithelia there is a smooth apical band which corresponds to the region occupied by the junctional complex previously identified with conventional EM techniques. The secretion of chylomicra that result from a fatty meal can be observed. It is possible to study the distribution of concanavalin A binding sites on the lateral surfaces of the cells utilizing hemocyanin as a marker. In the case of the proximal tubule epithelium, the apical cell surface has many more binding sites than the lateral cell surface and there is a sharp demarcation at the level of the apical band. After blunt dissection the relationship of the basal surface of the cells with the basement lamina and the basement membrane can be appreciated as well. Possible physiological meaning of the morphological features observed is briefly discussed.

Animals↗
PubMed1972

Light-induced Changes in the Ultrastructure of Pea Chloroplasts in Vivo: Relationship to Development and Photosynthesis.

Light-induced structural changes of chloroplasts and their lamellae were studied in leaves of Pisum sativum L., cv. Blue Bantam, using electron microscopy. Upon illumination of 14-day-old plants with 2000 lux, the chloroplasts decreased in thickness by about 23% with an accompanying increase in electron scattering by the stroma. Concomitantly, the average thickness of granal lamellae (thylakoids) decreased from 195 +/- 4 angstroms in the dark to 152 +/- 4 angstroms in the light, and this change was half-saturated at only 50 lux. Lamellar flattening at 50 lux and its reversal in the dark both had half-times of a minute or less. The thickness of a partition (a pair of apposed lamellar membranes) was 140 +/- 9 angstroms in both the light and the dark, indicating that the observed light-induced change was in the volume enclosed within the thylakoid. The effect of illumination could be inhibited by various uncouplers of photophosphorylation but not by 3-(3, 4-dichlorophenyl)-1, 1-dimethylurea, suggesting that it depended on ATP (or its precursor). In the presence of 0.5 micromolar nigericin, the thickness of the granal lamellae increased in the light to 213 +/- 3 angstroms; this may reflect an uptake of K(+) into an osmotically responding space within the thylakoids.During development, the capacity of the chloroplasts to flatten upon illumination increased in parallel with the amount of chlorophyll per gram of leaf and the number of lamellae per chloroplast. In contrast, the capacity of the leaves to fix CO(2) lagged nearly 2 days behind the development of chlorophyll. CO(2) fixation developed in parallel with the stacking of the lamellae into grana, supporting the contention that such organization is related to the linkage of photosystem II to photosystem I.

Journal Article↗
PubMed1972

Neutralization of Staphylococcus aureus exfoliatin by antibody.

Alum-precipitated exfoliatin was found to be an efficient antigen for eliciting high titers of neutralizing antibody in rabbits. Antitoxin thus produced, and transferred passively, was shown to protect neonatal mice against challenge with two to three lethal doses of preformed exfoliatin even when administration was delayed until 15 min before exfoliation began in control animals. The same dose of antitoxin afforded some protection against six to eight lethal doses of exfoliatin provided it was given before or at the time of challenge. Antitoxin, in the doses given, did not protect against infection with an exfoliatin-producing Staphylococcus aureus strain although the onset of exfoliation was delayed.

Animals↗
PubMed1971

Product of Staphylococcus aureus responsible for the scalded-skin syndrome.

Certain Staphylococcus aureus strains of phage group 2 produced a protein distinct from the alpha and delta toxins which was capable of causing generalized exfoliation in neonatal mice and presumably is responsible for the scalded-skin syndrome in humans. This protein, named "exfoliatin," was purified and found to have a molecular weight of approximately 24,000. Exfoliatin was acid-labile, rather heat-stabile, and antigenic.

Animals↗