PubMed Health⌕ Search

Biomedical subjects

F R Nelson

Publications and source records attributed to F R Nelson.

9 recordsLinked to original sources
PubMed1989

Orthopedic history and examination in the etiology of overuse injuries.

Overuse injuries, and stress fractures in particular, afflict many runners and military recruits. This investigation sought to identify pretraining factors which may predispose to overuse injuries. Orthopedic and running history questionnaires and an orthopedic examination were administered to 505 trainees entering an intensive military training school. A novel method for evaluating ankle dorsiflexion was developed, and alignment measures, in units of centimeters rather than degrees, were obtained. Over 10% of the trainees were removed from the school for overuse-related injuries, and over half of these were tibial stress fractures. The incidence of clinically diagnosed stress fractures was 6.3%. No single orthopedic history question or combination of questions could discriminate between trainees who did or did not subsequently incur overuse injuries. Results from the running history indicated that those running 25 or more miles.wk-1 (mpw) had a significantly (P less than 0.027) lower incidence of stress fractures (3.0%) than those running 4 or fewer mpw over the previous year (11.5%). The orthopedic examination did not identify any predisposing alignment characteristics, perhaps due to the low incidence of overuse injuries. Population means are presented for future use in comparative studies.

Adolescent↗
PubMed1986

Anti-estrogenic action of chlordecone in rat pituitary gonadotrophs in vitro.

Estradiol-17 beta (E2) enhances the response of rat pituitary gonadotrophs to gonadotrophin-releasing hormone (GnRH) in vitro. This effect of E2 on rat gonadotrophs in vitro was applied as a model to study the estrogenic or anti-estrogenic activity of chlordecone in gonadotrophs. Rat pituitary cell cultures were treated with E2 (10(-10) M), chlordecone (10(-7) to 10(-5) M), or both before a 6-hr challenge of D-Lys6-GnRH (GnRH-A). Secretion of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) during the 6-hr of GnRH-A treatment was measured. Pretreatment of cells with E2 for 2 days increased the GnRH-A-stimulated LH and FSH secretion approximately twofold. This effect of E2 was antagonized by the coexistence of chlordecone in a dose-dependent manner. The effect of E2 (10(-10) M) could be totally abolished by 10(-6) M chlordecone. Further, chlordecone alone had little or no effect on basal secretion of LH and FSH, but it significantly suppressed the response of gonadotrophs to GnRH-A. [Mirex, a compound with a similar chemical structure to chlordecone, did not suppress GnRH-A-stimulated secretion of LH or FSH under any condition tested.] The present study demonstrated that chlordecone had two specific effects on rat pituitary gonadotrophs: (1) to antagonize the effects of estrogen, and (2) to reduce the response of gonadotrophs to GnRH-A. Thus, chlordecone is not estrogenic in rat pituitary cells in vitro.

Animals↗
PubMed1978

Pathologic changes induced in respiratory tract mucosa by polycyclic hydrocarbons of differing carcinogenic activity.

Seven aromatic polycyclic hydrocarbons (PCHs) were investigated for their toxic effects on respiratory mucosa: benzo(e)pyrene (BeP), pyrene, anthracene, benz(a)anthracene(BaA), dibenz(a,c)anthracene(DBacA), benzo (a)pyrene (BaP), and dimethylbenz(a)anthracene (DMBA). The compounds were chosen because they comprise a spectrum of PCHs ranging from noncarcinogens, to initiators, to weak and strong carcinogens. All of them except DMBA are environmentally relevant chemicals. The chemicals were tested over an 8-week period. Heterotopic tracheal transplants were continously exposed and the histopathologic effects induced by the various PCHs were periodically assessed semiquantitatively. All PCHs exhibited varying degrees of toxicity for respiratory epithelium and submucosa. BeP clearly showed the least toxicity followed by pyrene and anthracene. BaA and DBacA caused marked epithelial and submucosal changes. In addition to epithelial hyperplasia, undifferentiated epithelium and squamous metaplasia developed. Marked mononuclear infiltration occurred in the subepithelial connective tissue. With BaP the epithelial and submucosal changes were similar but were much stronger. DMBA was the most toxic substance, causing epithelial necrosis followed by generalized keratinizing squamous metaplasia; the subepithelial changes consisted of an early acellular exudate and, later (at 8 weeks), marked condensation and hyalinization of the lamina propria. The toxic response pattern of the tracheal mucosa to carcinogenic agents was characterized by the chronicity of epithelial and connective tissue damage, as opposed to the short-lived hyperplastic and inflammatory response elicited by the noncarcinogens and weak initiators.

9,10-Dimethyl-1,2-benzanthracene↗
PubMedDate not supplied

Disposition of acrivastine in the male beagle dog.

Three male beagle dogs were given 10 mg/kg iv and oral doses of [14C]acrivastine, a novel nonsedating antihistaminic agent, in a nonrandomized crossover experiment. Urine and feces were collected for 72 hr after dosing. After iv dosing, a mean of 34% was recovered in the urine, and 63% was recovered in the feces. After po dosing, a mean of 29% of the radiocarbon was recovered in the urine, and 63% was recovered in the feces (dose adjusted for 14% lost in vomitus). Acrivastine and three major metabolites were detected in the excreta. The metabolites were identified as a side-chain-reduced analog of acrivastine (metabolite 3, 270C81), a gamma-aminobutyric acid analog of 270C81 (metabolite 2), and a benzoic acid analog of 270C81 (metabolite 1). After iv dosing, 34% of the dose was excreted as parent drug, 21% as metabolite 3, 15% as metabolite 2, and 6% as metabolite 1, while after po dosing, 35% of the dose was excreted as parent drug, 18% as metabolite 3, 11% as metabolite 2, and 7% as metabolite 1. Pharmacokinetic analysis of acrivastine plasma concentration-time curves after both routes of administration indicated a mean total body clearance of 17.3 ml/min/kg, a Vss of 0.93 liter/kg, a terminal half-life of 0.7 hr, and an oral bioavailability of 40%. The apparent plasma half-life of the metabolite, 270C81, was 1.5 hr. Analysis of AUC values indicated that greater amounts of 270C81 than acrivastine circulated in plasma after both iv and po dosing, and that first-pass metabolism of acrivastine to 270C81 occurred. The results indicated that acrivastine was extensively metabolized in the dog to 270C81 and suggested that 270C81 itself underwent further metabolism to metabolites 1 and 2.

Animals↗