Spinal canal remodeling in burst fractures of the thoracolumbar spine: a computerized tomographic comparison between operative and nonoperative treatment.

Operative and nonoperative treatment methods of burst fractures were compared regarding canal remodeling. The entire series consisted of 18 patients, with seven in the operative treatment group and 11 in the nonoperative treatment group. All fractures were studied with computed tomography (CT) at the postoperative (operative treatment group) or postinjury (nonoperative treatment group) and the latest follow-up. All patients were followed up for > or = 18 months. There was no statistical difference between postoperative and postinjury canal areas (p = 0.0859). However, a significant difference was found between the rates of remodeling (p = 0.0059). Although spinal canal remodeling occurred in both groups, the resorption of retropulsed fragments was less favorable in nonoperative treatment group.

Degradation of luteinizing hormone-releasing hormone (LHRH) and an LHRH agonist by the rat testis.

Degradation of LHRH and [D-Ser(tBu)6,des-Gly-NH10(2)]LHRH ethylamide (LHRH-A), during incubation with high-speed supernatants of rat testes, as assessed by reversed-phase (RP)-HPLC fractionation of the iodinated peptides and by radioimmunoassays for LHRH or LHRH-A, was principally due to a neutral 43 000 Da peptidase with apparent Km values at 25 degrees C of 0.15 microM for LHRH and 1.19 microM for LHRH-A. The peptidase was inhibited by sulphydryl reagents, TLCK, 1,10-phenanthroline, EDTA, bacitracin, other LHRH analogues, oxytocin, [Lys8]vasopressin and somatostatin. It was predomantly located in seminiferous tubule supernatants (98% of recovered activity), with much lower levels in interstitial fluid (2%), interstitial tissue or testicular particulate fractions (less than 0.8%). Extracts of cultured immature Sertoli cells produced LHRH- and LHRH-A-degradation profiles, as assessed by RP-HPLC, that were identical to those produced by testicular supernatants. Similar levels of peptidase activity/mg protein were observed in immature and adult rat testes. These studies indicate that the principal LHRH-peptidase in the rat testis is produced by cells of the seminiferous epithelium, chiefly the Sertoli cell, and may play an important role in regulating the activity of LHRH and other peptide hormones in the testis.

The effects of carbon disulfide on the reproductive system of the male rat.

Two experimental protocols were employed to determine the effects of carbon disulfide (CS2) on the reproductive system of the male rat. In the first experiment, adult Long Evans hooded rats were exposed to 0, 350 or 600 ppm CS2 vapor for 10 weeks (5 h/day, 5 days/week). CS2 exposure caused no change in reproductive organ weights nor in plasma gonadotropin levels. However, animals exposed to 600 ppm CS2 had slightly lower epididymal sperm counts and significantly reduced plasma testosterone levels. In order to determine if monitoring hormone levels and sperm status in the same male over time might increase the sensitivity of detecting a toxic reaction, the second protocol was employed. Male rats were exposed to 0 or 600 ppm CS2. After 0, 1, 4, 7 and 10 weeks of exposure, males were observed for mating behavior, and ejaculated sperm count and plasma hormone levels were determined. Animals exposed to 600 ppm CS2 had significantly shorter times to mount and to ejaculate and decreased ejaculated sperm counts. Plasma gonadotropin levels were similar in both groups while plasma testosterone levels were marginally depressed in CS2-exposed animals in the early weeks. These data indicate that CS2 is a toxin of the male reproductive system resulting in abnormal coital behavior and decreased sperm counts. The second experimental protocol proves to be a sensitive method for assessing adverse effects in the male reproductive system.