Transverse myelitis associated with larva migrans: finding of larva in cerebrospinal fluid.
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Biomedical subjects
Publications and source records attributed to C Wang.
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New alleles of murine factor B (Bf) protein were demonstrated. When ethylenediaminetetraacetic acid (EDTA)-plasmas from inbred and wild mice were analyzed by isoelectrofocusing (IEF) and immunofixation, murine Bf proteins were visualized as distinct protein bands in all mice tested. Four variants of murine Bf could be demonstrated in a large number of tested mice: Bf 1 (isoelectrofocusing point (P.I.) range of 5.8-6.1) exemplified by B10 and B10.BR, Bf 2 (P.I. range of 5.8-6.0) exemplified by B10.MOL (OHM), Bf 3 (P.I. range of 5.6-5.9) exemplified by B10.MOL (TEN2) and Mus musculus (Mus m.) subspecies Chc, Bf 4 (P.I. range of 6.0-6.3) exemplified by Mus m. subspecies Shh. The genetic linkage between S locus and Bf locus was studied with two backcross progenies--[B10.BR X (B10.BR X Mus m. subspecies Chc)F1] and [B10.BR X (B10.BR X Mus m. subspecies Shh)F1]. Totally, 256 backcross progenies were typed for Bf type and for Ss type (plasma level of the fourth complement protein regulated by S locus). The results indicated that murine Bf was controlled by a single codominant locus located close to the H-2 complex because no mouse showing recombination between Bf locus and S locus was found.
Sitosterol and cholesterol metabolism were studied in a patient with coexisting phytosterolemia and cholestanolemia, and in a control subject, both on similar diets containing about 170 mg cholesterol and 135 mg phytosterols per day. The turnover of 22,23-3H-sitosterol and 4-14C-cholesterol, given intravenously, were followed for up to 372 days. The specific activity-time curves for both sterols were resolved into two exponentials and fitted into a two-pool model. The half-lives of both exponential curves for sitosterol, in the patient, were abnormally long. Equilibration of the tracer between the two pools, in the patient, occurred at about 30 days as compared to 10-15 days in the control subject. The daily turnover of sitosterol in the patient was estimated to be 10 times greater than that in the control subject. The patient's total body exchangeable pool of sitosterol was 9.6 g or about 80 times the amount found in the control. The patient's plasma phytosterol levels fell by 25% when he went on a diet containing only 10 mg phytosterols per day. During this period the specific activity of his plasma sitosterol with respect to an equilibrated dose of 3H-labeled tracer remained constant; this was compatible with the absence of endogenous synthesis. Cholesterol turnover in the patient showed prolonged half-lives for both exponential curves and reduced fractional daily loss from the fast-exchanging pool. The patient's xanthoma sterols underwent 16% and 55% exchange with plasma sitosterol and cholesterol, respectively, on day 60, indicating the presence of a third exchangeable pool.
Forty-six subfertile men with idiopathic oligospermia were randomly assigned to 6 months of treatment with a placebo, clomiphene citrate (25 or 50 mg/day), mesterolone (100 mg/day), or pentoxifylline (1200 mg/day) or 4 months of testosterone enanthate treatment (100 or 250 mg on alternate weeks). Treatment with the placebo, mesterolone, pentoxifylline, and testosterone rebound therapy did not result in a significant increase in the mean sperm concentration or pregnancy in the partners. Clomiphene citrate at both dosages significantly increased the mean sperm concentration without improving sperm motility or morphology during the 6-month treatment period. Pregnancy rates of 36.4% and 22.2% were observed in partners of men receiving clomiphene citrate 25 mg/day and 50 mg/day, respectively. This study also illustrates the difficulties in identifying suitable patients for and assessing the efficacy of different treatment regimens.
Imipenem-cilastatin was compared, in two multicentre clinical trials, with cefazolin or cephalothin, in their efficacy, safety, and tolerance. Safety and tolerance for imipenem-cilastatin was similar to that of these two cephalosporins. There were more transient liver function test changes in the imipenem-cilastatin group, but the frequency was similar to that for beta-lactams in general. There were similar numbers of cases of transient neutropenia in each group. Clinical side effects were few for the treatment groups and all drugs were well tolerated.
We studied the effect of ranitidine on gonadal function in 20 male subjects with chronic duodenal ulcer. Eleven were treated with ranitidine 150 mg twice daily for 3 months and 150 mg at night for 9 months, nine with placebo for 3 months. Similar to placebo, treatment with ranitidine did not influence basal serum concentrations of testosterone (T), luteinizing hormone (LH), follicle stimulating hormone (FSH) and prolactin (PRL). No significant changes were found in sperm concentration, motility or morphology. Ranitidine does not affect gonadal function in man.
The anterior chambers of 27 rabbit eyes were perfused at constant pressure with room temperature (25 degrees C) or cooled (11 degrees C) balanced salt solution at constant flow rates of 4.8 ml/min or 8.5 ml/min. Intraocular temperature changes in the anterior chamber, anterior vitreous, mid vitreous, and posterior vitreous and on the retina surface were monitored with an intraocular thermocouple probe. Perfusion of the anterior chamber of the pigmented rabbit eye with cooled fluid significantly reduced the temperature of the anterior chamber and anterior vitreous and even that of the retina. Both an increase in the rate of perfusion and a lowering of the perfusion temperature enhanced the cooling effect. The observed decrease in temperatures returned to approximately normal 4 minutes following the cessation of perfusion.
We studied the effects of LHRH and a potent agonist on plasminogen activator production by granulosa cells obtained from immature rats. Both LHRH and the agonist produced a dose-related increase in plasminogen activator production. Concomitant addition of LHRH or its agonist together with FSH to the granulosa cell cultures enhanced the stimulatory effects of FSH on plasminogen activator production. These in vitro findings suggest that LHRH exerts a direct stimulatory effect on plasminogen activator secretion by rat granulosa cells which may explain the acute stimulating effects of LHRH and its agonist on ovulation in hypophysectomized rats.
The role of FSH in the regulation of plasminogen activator production was studied in granulosa cells obtained from 23- to 25-day-old female rats. Cells cultured without FSH secreted a negligible amount of plasminogen activator. Purified ovine, rat, and human FSH produced dose-dependent increases in plasminogen activator production. This FSH effect was mimicked by analogs of cAMP, prostaglandin E2, and choleratoxin. Purified ovine LH and ovine PRL had no effect on plasminogen activator production by these immature granulosa cells. However, when these granulosa cells were treated in vitro or in vivo with FSH and then exposed to LH or PRL, the cells responded to LH in a dose-dependent manner with increased plasminogen activator production. These cells remained unresponsive to PRL. Similarly to FSH, in vitro pretreatment of the cells with choleratoxin or analogs of cAMP also induced responsiveness to LH with increased plasminogen activator production. This responsiveness to both FSH and LH with increased plasminogen activator production was also observed in granulosa cells obtained from rat preovulatory follicles. These studies demonstrate that: 1) FSH but not LH regulates plasminogen activator production by immature granulosa cells from preantral follicles; 2) Pretreatment of the undifferentiated granulosa cells with FSH, choleratoxin, or cAMP induced granulosa cell responsiveness to LH with increased plasminogen activator production; and 3) Granulosa cells obtained from preovulatory follicles respond to both FSH and LH with increased plasminogen activator secretion. These results suggest that with the LH surge at ovulation, plasminogen activator production in follicles is increased and may be important in follicular rupture.
The present review summarizes our studies on the hormonal control of the differentiation of granulosa cells in vitro. Studies on the hormonal regulation of granulosa cell oestrogen and progestagen biosynthesis by various regulatory agents facilitate our understanding of the control processes involved in follicular maturation and luteinization in vivo. This multiple hormonal control mechanism also provides an interesting model for future studies on the diverse mode of hormone action.
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In vitro studies showed that organophosphate insecticides have different IC50 values (i.e., concentration of inhibitor required to inhibit 50% enzyme activity) for acetylcholinesterases (AChE's) from different species. Since previous reports indicated that the binding of active cholinesterase inhibitors to non-critical binding proteins is an important mechanism of detoxification of organophosphate insecticides in vivo, we investigated the role of non-critical binding proteins in synaptosomal membrane preparations from monkey, rat and chicken brain tissues as a possible explanation of the differences in the IC50's. The amount of non-critical binding proteins as well as critical binding sites, AChE, were determined by 3H-DFP binding in vitro. The affinity constants (Ka) and phosphorylation constants (Kp) of DFP for AChE's from these preparations were also determined by kinetic studies. In IC50 studies, monkey brain AChE was 1.5X and 3.2X more sensitive to DFP inhibition than chicken and rat brain AChE. The observed differences in IC50's cannot be explained on the basis of differences in the amount of non-critical binding proteins, since only small amount of non-critical binding proteins were found in these preparations. However, in the kinetic studies, monkey brain AChE had 3.7X and 2.1X higher affinity than chicken and rat brain AChE, respectively; and chicken brain AChE had about 2.7X faster rate of phosphorylation than the other two. It is therefore concluded that non-critical binding proteins are relatively unimportant in terms of affecting IC50's. The differences observed in IC50's are primarily due to different affinity and/or rate of phosphorylation of AChE active sites by DFP.
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The role of cyclic AMP in the induction of enzymes involved in estrogen and progestin biosynthesis in undifferentiated granulosa cells was investigated. When granulosa cells from immature hypophysectomized, DES-treated rats were cultured for 2 days in serum-free medium with aromatase substrate (10(-7) M androstenedione) together with graded doses of FSH, prostaglandin E2 (PGE2), cholera toxin (CT), or dibutyryl cyclic AMP (Bu2cAmP), there was a dose-related increase in estrogen (E) production. The induction of E production by saturating doses of FSH, PGE2, CT, and Bu2cAmP required a lag phase of approximately 24 h, after which the E response increased sharply to maximum levels at day 3, and then declined gradually to day 5. Treatment for 24 h ((day 0-1) with FSH, together with 1 microgram/ml of either actinomycin D or cycloheximide, completely abolished the stimulatory action of FSH on E production. When the inhibitors were removed, the FSH-induced increases in E returned to near normal levels after a 24-h lag period. Similar effects of the inhibitors upon E production by CT, PGE2 and Bu2cAMP were observed. As with E, the production of progesterone and 20 alpha-dihydroprogesterone was markedly stimulated by FSH, PGE2, CT and Bu2cAmP, and the results of the time course, dose response, and inhibitor experiments were similar to those for E production. These results indicate that FSH induces the de novo synthesis of enzymes required for both estrogen and progestin biosynthesis by undifferentiated granulosa cells and suggest that this action is mediated by cyclic AMP.
1 To study the effect of cimetidine on gonadal function in man, eleven male subjects with chronic duodenal ulcer were given cimetidine orally at a dosage of 1000 mg per day 3 months and 400 mg nocte for the subsequent 3 months. 2 Testosterone levels were found to be elevated during therapy when compared to pre- and post-treatment periods. Serum LH remained unchanged but FSH was increased during therapy. In five out of eleven subjects serum PRL levels were increased. Mean sperm count was lower during cimetidine therapy when compared with that after drug withdrawal. The motility and morphology of the spermatozoa were not affected.