Search PubMed⌕ Search

Biomedical subjects

M A de Almeida

Publications and source records attributed to M A de Almeida.

9 recordsLinked to original sources
PubMed1992

[Peripheral facial paralysis in Petropolis].

The author presents 83 cases of "a frigore" peripheral facial palsy, occurred in the mountain city of Petropolis which has characteristics such as a tropical climate without any traces of a dry season and an average temperature of 50 degrees F to 73.5 degrees F. The author relates them with virus infections which appear within a year period. Fifty six patients belong to his clinic and have a follow up, while other 25 patients proceed from another clinics and from them he only has reports on sex, age, side of palsy and the beginning of illness. He shows that the largest number of cases occurred along the months of May, August, September and October. Season distribution for southern hemisphere is analysed. He also considers etiology, incidence, prevalence, treatment and results on patients studied.

Adolescent↗
PubMed1986

Memory facilitation by histamine.

The immediate posttraining intracerebroventricular administration of histamine (1 or 10, but not 0.1 or 100, ng/rat) facilitated retention test performance of step-down inhibitory avoidance behavior measured 24 hr later, in rats. The effect was antagonized by the simultaneous administration of both promethazine (1000 ng/rat) and cimetidine (1000 ng/rat), but not by either promethazine or cimetidine given alone. The antagonists had no effect of their own on behavior. The findings show that histamine has an extraordinarily powerful effect on memory processes, but do not necessarily suggest that this substance has a physiological role in memory modulation.

Animals↗
PubMed1984

Effect of the intraperitoneal and intracerebroventricular administration of ACTH, epinephrine, or beta-endorphin on retrieval of an inhibitory avoidance task in rats.

Rats were trained in a step-down inhibitory avoidance task using a small start platform (5-cm high, 25 X 7 cm) and a low intensity footshock (0.3 mA, 60 Hz). Retrieval of this task was measured on a test session 24 hr after training. The ip administration of ACTH1-24 (25 ng/rat), epinephrine HCl (625 ng/rat), or human beta-endorphin (125 ng/rat) 5 min prior to testing enhanced retrieval. beta-Endorphin was also effective when given by the icv route at a dose of 25 ng/rat. The icv administration of ACTH (5, 25, or 125 ng/rat) or epinephrine (5, 25, 125, or 625 ng/rat) was ineffective. These findings suggest that memory modulation by beta-endorphin at the time of retrieval may be centrally mediated, whereas the influence of ACTH and epinephrine is probably mediated peripherally.

Adrenocorticotropic Hormone↗
PubMed1983

Memory modulation by post-training intraperitoneal, but not intracerebroventricular, administration of ACTH or epinephrine.

Post-training introparitoneal (ip) administration of ACTH1-24 (25 ng/rat) or epinephrine HCl (625 ng/rat) facilitated retention of a step-down inhibitory avoidance task acquired using a small start platform (5-cm high, 25 X 7 cm) and a low intensity training footshock (0.3 mA, 60 Hz), and caused retrograde amnesia for a similar task acquired using a large platform (5-cm high, 25 X 25 cm) and a high intensity training footshock (0.8 mA, 60 Hz). The post-training intracerebroventricular (icv) administration of 5, 25, or 125 ng/rat of ACTH or of 5, 25, 125, 625, or 1250 ng/rat of epinephrine had no effect on retention of either task. These findings suggest that memory modulation by ACTH and epinephrine is mediated by reflexes initiated at peripheral receptors that affect brain activity during the post-training period.

Adrenocorticotropic Hormone↗
PubMed1983

Effect of chemotherapy on experimental pulmonary schistosomiasis.

Mice with portal hypertension caused by portal vein ligation reproduced the model of severe pulmonary schistosomiasis when infected for 10 weeks with 30 cercariae of Schistosoma mansoni. Curative treatment promoted reversion, without fibrosis, of the periovular granulomatous lesions formed in the alveolar tissue. However, the arterial and arteriolar lesions were defectively repaired, with segmental vascular fibrosis, narrowing, and angiomatoid changes remaining for up to 120 days after treatment. There was also evidence that eggs are destroyed more rapidly and more completely in the lungs than in the liver.

Animals↗
PubMedDate not supplied

Adverse reactions to acetaminophen, ASA, and NSAIDs in children: what alternatives?

ASA and NSAIDs are responsible for a large number of adverse reactions. The association of adverse reactions to acetaminophen and to ASA is uncommon, especially in children, and raises the problem of finding alternative treatments. We present a case report of a 7-year-old boy with combined adverse reaction to acetaminophen and ASA/NSAIDs. The child, who had no history of atopy, first displayed the condition at age 6, when he suffered two episodes of urticaria and angioedema, 2 hours after administration of 500 mg of acetaminophen, following two earlier doses of 500 mg (total 1500 mg). At age 7 he suffered a third episode 3 hours after administration of 180 mg of ASA. The patient submitted to oral challenges with acetaminophen (positive at a cumulative dose of 2,040 mg), ASA (positive at a cumulative dose of 204 mg) and nimesulide (negative at a cumulative dose of 119 mg). In conclusion, nimesulide (an NSAID not available in the United States) may be regarded as an alternative treatment in such patients, but more research is needed in pediatric age groups.

Acetaminophen↗
PubMedDate not supplied

Intracerebroventricular histamine, but not 48/80, causes posttraining memory facilitation in the rat.

The immediate posttraining intracerebroventricular injection of histamine (1 or 10 ng/rat) facilitated memory both of a stepdown inhibitory avoidance task, and of the habituation of rearing responses to an open field. As previously shown for the avoidance task, the combination of cimetidine (1,000 ng/rat) plus prometazine (1,000 ng/rat), but not each drug on its own, blocked the effect of histamine in the habituation task. The effect of histamine was not shared by the intracerebroventricular administration of the mast cell histamine releaser, 48/80 (0.1 to 100 micrograms/rat). The present findings indicate that the memory facilitatory action of histamine might be general across tasks, and that 48/80-releasable, presumably mast cell, endogenous histamine is probably not involved in memory regulation.

Animals↗