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Biomedical subjects

A Myers

Publications and source records attributed to A Myers.

At least 73 records · Page 4Linked to original sources
PubMed1989

Glossodynia as an oral manifestation of sex hormone alterations.

Oral inflammation occurs during puberty, pregnancy, menses, and therapy with hormones (especially oral contraceptive agents), and other medications such as phenytoin. Alterations of the oral environment result from fluctuations of plasma and salivary sex steroids. The ratio of the sex steroids to one another, and their absolute concentration, determine the amount of prostanoid and peroxidase production and salivary flow. These relationships are complex and are not readily predictable; however, they are reproducible in both humans and animals. The sex steroids exert profound effects on the function of many nonsexual organs; particularly the skin, bone, liver, salivary glands, and oral tissues. We reviewed the currently available information concerning sex steroid action on salivary glands and oral epithelium. In light of the dramatic drop in sex steroid levels at menopause, the purely psychogenic nature of glossodynia or burning mouth (stomatopyrosis), first manifested at menopause, requires further consideration and study.

Glossalgia↗
PubMed1988

Diagnostic yield of the autopsy in a university hospital and a community hospital.

To determine the extent to which autopsies yield unexpected findings that are relevant to the patient's death and whether cases with a high yield of such findings can be identified selectively, we studied a total of 233 autopsies at a university hospital and at a community hospital. The rates at which autopsies detected major unexpected findings whose premortem diagnosis would probably have improved survival were 11 percent at the university hospital and 12 percent at the community hospital. Major unexpected findings whose premortem diagnosis would not have prolonged survival were found in another 12 and 21 percent of cases, respectively. Pulmonary embolism and fungal infections in immuno-compromised hosts were the most common major unexpected findings. Neither we nor the patients' physicians were able to identify from the clinical data the autopsies likely to have high yields. Furthermore, the physicians' estimates of an autopsy's expected yield were similar for patients evaluated by autopsy and for matched patients who were not. We conclude that the autopsy continues to yield clinically relevant findings at a high level and that it is not currently possible to predict which cases will have high yields. Autopsies are vital to ensure the quality of medical care, and autopsy rates must be increased substantially if this role is to be fully realized.

Adolescent↗
PubMed1987

The drug approval process and the information it provides.

By law, the commissioner of the Food and Drug Administration (FDA) is responsible for determining whether a new drug is safe and efficacious before it is approved for marketing in the U.S. and for monitoring its use after approval. This paper provides a brief overview of the approval process, in terms of responsibilities of the sponsor in submitting an application for review to the FDA and FDA's responsibilities and organizational procedures for reviewing and approving those applications. A brief history on the legislation regarding the FDA's responsibility in the drug approval area is discussed along with recent regulations, legislation, and FDA initiatives aimed at improving the drug approval process. Specific information that can be released to the public upon request is also discussed. This paper is limited to the regulation of drugs; somewhat different regulations govern the review and regulation of biological products and abbreviated new drug applications.

Chemistry, Pharmaceutical↗
PubMed1986

Sex differences in mouse platelet aggregation.

The role of platelets in the sex difference observed in mouse thrombosis models was evaluated by examining platelet diminution in vivo after thrombotic challenge, and aggregation of mouse platelets in PRP. A fall in platelet count was observed in both sexes after i.v. injection of either arachidonic acid or the thromboxane agonist, U46619. Platelet diminution induced by high dose arachidonate (50 mg/kg) was significantly greater in males compared to female mice. Responses to U46619 were similar in both sexes. In PRP, male platelets exhibited a greater response than female platelets to both ADP (15 uM) and arachidonate (0.3 mM), but not to U46619 (4.6 and 6.9 uM). These results suggest that the gender difference in arachidonate-induced sudden death, in which males are more susceptible than females, is related to a sex difference in mouse platelet function.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1986

High-level, heat-regulated synthesis of proteins in eukaryotic cells.

Plasmids have been constructed in which promoters of 70-kDa heat-shock protein genes (hsp70) of human and Drosophila origin were linked to three different eukaryotic genes encoding human growth hormone (hGH), chicken lysozyme (cL) and a human influenza haemagglutinin (HA). Following transfection into widely divergent eukaryotic cells, the hybrid genes direct the transient, heat-regulated synthesis of the three proteins. hGH and cL are secreted into the medium. A human hsp70-hGH construct was used to establish stable mouse fibroblast lines that are capable of producing and secreting hGH at high levels following heat induction: hGH is secreted at a 500-1200-fold higher rate by heat-treated than by untreated cells.

Animals↗
PubMed1984

A new immunologic test for CNS cysticercosis.

A new radioimmunoassay for cerebral cysticercosis was studied in 70 patients. The assay showed nearly 100% sensitivity for ventricular cysts or meningitis, 86% sensitivity for multiple parenchymal cysts, and a false-positive rate of 7%. Both serum and CSF antibody levels were useful diagnostically, and the contribution of both improved accuracy. In some patients, there was endogenous CNS production of IgG against the cysticercus antigen, which leads to elevated CSF levels and normal serum levels. Patients with high CSF total IgG levels may show false-positive CSF antibody elevation with normal serum levels.

Antibodies↗
PubMed1983

Glucocorticoid protection against PAF-acether toxicity in mice.

Intravenous platelet activating factor (PAF-acether, 10 to 25 micrograms/kg body weight) produced dose-dependent mortality in both male and female mice. Pretreatment with indomethacin (50 mg/kg), verapamil (40 mg/kg) or nifedipine (4 mg/kg) failed to inhibit the lethal effect of 20 micrograms/kg PAF-acether. This suggests that neither arachidonate cyclo-oxygenase products nor availability of extracellular Ca2+ mediate the toxic action. In contrast, pretreatment with 100 mg/kg cortisone acetate (s.c.) daily for four days exerted a highly protective effect, i.e. 100% and 93% survival in males and females, compared to 13% and 7% respectively, in untreated animals. PAF-acether-induced death may be a useful model for the in vivo evaluation of pharmacological agents in anaphylactic shock.

Animals↗
PubMed1983

Thromboxane agonism and antagonism in a mouse sudden death model.

The effects of the stable thromboxane agonist, U46619, and sodium arachidonate were tested by i.v. injection into male and female mice. U46619 produced dose-dependent mortality in both sexes equally, in contrast to the gender-differentiated effects of arachidonic acid. The thromboxane receptor antagonist, SQ 26,536, protected in a dose-dependent manner against both arachidonate and U46619. The thromboxane antagonist was more effective against arachidonate toxicity in male than in female mice, but was equiactive against U46619 in both sexes. Neither the thromboxane synthetase inhibitor, OKY-1581, nor the cyclooxygenase inhibitor, indomethacin, protected against U46619-induced sudden death. However, cortisone acetate increased survival of mice challenged with U46619. The results support the hypothesis that thromboxane A2 mediates arachidonate-induced sudden death. The effects of arachidonate can be mimicked by the thromboxane agonist and are attenuated by the thromboxane antagonist. The gender difference in arachidonate toxicity is apparently not due to differences in sensitivity to thromboxane A2, as the thromboxane agonist was equally toxic in males and females. The greater protective effect of the thromboxane antagonist against arachidonate toxicity in males suggests that thromboxane A2 is a more important mediator of arachidonate-induced sudden death in males compared to female mice.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1982

Sexual differentiation of arachidonate toxicity in mice.

Mature male and female mice 50 days of age were challenged with i.v. sodium arachidonate at doses of 12.5, 25, 50 and 100 mg/kg. A dose-dependent response in terms of mortality was observed. Males were significantly more susceptible to arachidonate-induced mortality than females at the 25 and 50 mg/kg doses (P less than .05). The 100 mg/kg dose produced 100% mortality in both sexes. When mice aged 23, 29, 35 and 50 days were challenged with 50 mg/kg of arachidonate, no gender difference was observed until mice were 35 days of age, at which time the male mortality was 80%, compared to 57% for female mice (P less than .05). Mice gonadectomized at 23 days and intact mice 23 days of age were treated with s.c. estradiol, testosterone or vehicle for 7 days before arachidonate challenge. Among these groups, the gonadectomized females and intact males were significantly protected by estradiol when compared to the appropriate controls (P less than .05). In contrast, testosterone pretreatment had no significant effect on mortality. These results demonstrate that the development of the gender difference in arachidonate-induced mortality in mice is dependent upon the presence of gonadal hormones in the immature stages.

Adrenal Glands↗
PubMed1981

Acute protection against arachidonate toxicity by hydrocortisone and dexamethasone in mice.

1. Pharmacologic doses of hydrocortisone sodium succinate (100 mg/kg) has a rapid protective action against arachidonate-induced mortality in mice when administered intravenously 5 to 60 min before intravenous infusion of arachidonate. 2. Intravenous dexamethasone sodium phosphate (4 mg/kg) has a similar protective effect. 3. The time course of the development of the protective effect of intravenous glucocorticoids suggests that DNA transcription and protein synthesis are not involved in the mechanism of this action. 4. Longer pretreatment with glucocorticoids are required to reduce mortality when subcutaneous or intraperitoneal routes of administration of the steroids used.

Animals↗
PubMed1981

IgD levels in white and Metis communities in Saskatchewan.

Levels of serum IgD have been measured in white and Metis (Cree Indian) communities in Saskatchewan. IgD levels in the Metis were, on average, 10 times as high as those in the white population. In both groups IgD levels rose rapidly to reach, by the age of two years, levels which did not differ significantly from those found in the adult. From the age of two to three years, levels in the populations remained relatively constant with time, although levels in any of individual may rise or fall over a three-year period by factors ranging from 10 to 20.

Adolescent↗