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Biomedical subjects

M Salazar

Publications and source records attributed to M Salazar.

At least 109 records · Page 6Linked to original sources

Proliferative myositis in an infant: report of a case with electron microscopic observations.

Proliferative myositis presented in a 7-month-old female infant as a poorly circumscribed mass growing rapidly within the interscapular skeletal muscle. Muscle fascicles and individual fibers were dissected by an inflammatory infiltrate of lymphocytes, plasma cells, and histiocytes immersed in a basophilic intercellular substance. Numerous ganglionlike giant cells were present and had ultrastructural features suggestive of histiocytic origin. The possible relation to other rapidly growing lesions that appear in soft tissues is discussed. This probably represents the first reported case of proliferative myositis in a pediatric patient.

Female↗

[Evaluation of the bronchial provocation test with histamine in asthmatic children].

Histamine inhalation challenge was performed in 32 asthmatic children aged 6 through 13, 20 control children aged 8 through 14, and 16 control adults aged 24 through 37 years. Histamine concentration producing a 20% fall in baseline FEV1 (PC20FEV1) was obtained. No control adult had a value below 8 mg/ml unlike 7 (35%) control children, all of them with values between 4 and 8 mg/ml. Asthmatics only on intermittent bronchodilators had higher PC20FEV1 values than those requiring daily medications. A value of 2 mg/ml was roughly the limit between these two subpopulations of asthmatic children. Test showed a high reproducibility in a two hour interval. Histamine inhalation challenge is useful in diagnosis of asthma and in assessment of its, severity. A PC20FEV1 value of less than 8 mg/ml may not be always reliable in indicating bronchial hyperreactivity, depending on the method used and-or the population studied.

Adolescent↗

(3H) spiroperidol binding decreases in brains of rats infected with Venezuelan equine encephalomyelitis virus.

After i.p. inoculation with the Guajira strain of Venezuelan equine encephalomyelitis virus a significant decrease in the density of (3H) spiroperidol binding sites in the striatum, midbrain and frontal cortex was observed. No changes in the affinity of the receptors could be demonstrated. This finding is compatible with neuronal degeneration caused by the viral infection.

Animals↗

Effect of Venezuelan equine encephalomyelitis virus infection on brain choline acetyltransferase and acetylcholinesterase activities.

Mice and rats infected with the Venezuelan equine encephalomyelitis virus showed a significant decrease in the choline acetyltransferase activity of caudate nucleus, hypothalamus, midbrain, hippocampus and frontal cortex. Acetylcholinesterase activity was not affected in any of the same brain regions analyzed. In surviving rats no alterations were observed in the activities of choline acetyltransferase, tyrosine hydroxylase, and glutamate decarboxylase 3 months after the infection.

Acetylcholinesterase↗

[Haemophilus influenzae meningitis. Review of 21 cases].

Twenty-one cases of "Haemophilus influenzae" meningitis occurred over a seven year period. An ampicillin-resistant strain was isolated in three (14,2%), but the percentage of ampicillin-resistant strains rose to 33% over the last two years, in meningitis and to 38% in all patients whose blood or CSF grew "Haemophilus influenzae". One case (4,7%) had severe neurologic damage, and 3 (14%) had minor damage. The estimated duration of symptoms prior to proper treatment correlated with duration of fever conscience depression, and hospital stay. Both of the patients with symptoms prior to treatment lasting over 72 hours had sequellae. Chloramphenicol should be included in the therapy of every patient suspected of having severe "Haemophilus influenzae" infection in our region.

Ampicillin↗

Tyrosine hydroxylase activity in Venezuelan equine encephalomyelitis virus infection.

In rats inoculated with the Venezuelan equine encephalomyelitis (VEE) virus, a significant decrease was found in the tyrosine hydroxylase activity of neostriatum, midbrain, and hypothalamus during the acute phase of the infection. In animals that survived the acute infection, we observed no changes in the enzymatic activity in the same regions studied. Our findings suggest a vulnerability of the dopaminergic and noradrenergic pathways to the infection produced by VEE virus.

Animals↗

Binding of 14C-imipramine by pigmented and non-pigmented tissues.

When pigmented and non-pigmented rabbit irides were incubated with various concentrations of 14C-imipramine at equilibrium (120 min), the accumulation of the drug by the pigmented iris was 1.5 times as great as that by the non-pigmented iris. The accumulated drug is lost from both types of irides in a complex fashion. However, even after 120 min of washing, the differences in accumulation remain nearly constant. When accumulation of the drug in the non-pigmented iris was analyzed by discontinuous sucrose density gradient, it was observed that the drug was bound mainly by the low density sucrose fractions where the synaptosomes separate. On the contrary, in the pigmented iris approximately 70% of the drug was found in the melanin-containing fraction. The homogenate from the substantia nigra accumulated 1.5 times more than that from the human brain cortex. The affinity of the drug for bovine iris melanin granules and the synthetic L-dopa melanin was 9.9 X 10(5) M-1 and 3.8 X 10(3) M-1, respectively. On the rabbit iris sphincter muscles, imipramine was evaluated for antimuscarinic effects. The apparent dissociation constants, KB values, for the antagonist in the non-pigmented and pigmented iris were 1.7 X 10(-7) M and 3.8 X 10(-6) M, respectively. The low antimuscarinic activity in the pigmented iris is attributed to the loss of the drug to the pigment. On this basis, relevancy of the drug binding by pigmented tissues to the effects of this tricyclic drug is discussed.

Animals↗

Iris pigmentation and atropine mydriasis.

The experiments were designed to study the well-known pigment-dependent mydriatic effect of atropine in the eye. In vitro, relative to the accumulation of 3H-atropine by the nonpigmented rabbit iris, the pigmented iris accumulated high amounts of the drug. A nonpigmented tissue, stomch fundus strip, obtained from either albino or nonalbino animals, accumulated relatively low amounts of 3H-atropine. On repeated washings, the accumulated drug from the nonpigmented tissues was rapidly lost, T 1/2 of 14 minutes, while that accumulated by the pigmented iris was retained much longer. Although in vitro aqueous humor from serum-atropinesterase positive rabbits rapidly degraded atropine, extracts from irides of the same type of rabbit gave a single peak radioactivity, with Rf identical to the authentic atropine sulfate. The accumulation of 3H-atropine by pigmented human iris or pigment epithelium was similar to that observed for the pigmented rabbit iris. pA2 values of atropine from nonpigmented iris and from fundus strips varied between 8.58 and 8.88 with slope values close to 1. The pA2 value of atropine in pigmented iris was 8.82; at higher concentrations, atropine was less effective compared to the nonpigmented iris. In the pigmented iris, the lesser effectiveness of the drug at high concentration could be explained on the basis of accumulation of the drug by the pigment cell and its constituents. Thus, the free concentration of the drug in the vicinity of the muscarinic receptor will fall. The lesser concentration will give weaker muscarinic blockade in the pigmented iris. On repeated washing, the atropine blockade of the nonpigmented iris could be easily washed out while that in the pigmented iris was retained. In vivo, the relative T 1/2 for the duration of atropine mydriasis in rabbits were: albino atropinesterase-positive, 3.8 hours; nonalbino atropinesterase-positive, 12.4 hours; albino atropinesterase-negative is greater than or equal to 96 hours. Only the latter T 1/2 for the duration of atropine mydriasis is quite clear. The small magnitude of the mydriatic effect in humans is explained by the loss of free drug to the pigment cells and their constituents. The longer duration of mydriatic effect in the heavily pigmented eye is explained on the basis of slow release of the accumulated drug onto the muscarinic receptor.

Animals↗

An explanation for the long duration of mydriatic effect of atropine in eye.

The mydriatic effect of topically applied 3H-atropine (2%) was compared in the pigmented rabbits (black fur and dark brown irides) and nonpigmented (albino) atropinesterase-negative rabbits. The duration, t1/2, of the mydriatic effect in the nonpigmented and pigmented rabbit was 43.5 and greater than 96 hours, respectively. At hour 96, the tissue 3H-atropine in the pigmented iris was greater than that in the nonpigmented iris by the factor of eight. The longer duration of mydriatic effect in the pigmented iris is explained by the slow release of the bound drug from the pigment onto the muscarinic receptors.

Administration, Topical↗