Interaction driven subgap spin exciton in the Kondo insulator SmB6.

Using inelastic neutron scattering, we map a 14 meV coherent resonant mode in the topological Kondo insulator SmB6 and describe its relation to the low energy insulating band structure. The resonant intensity is confined to the X and R high symmetry points, repeating outside the first Brillouin zone and dispersing less than 2 meV, with a 5d-like magnetic form factor. We present a slave-boson treatment of the Anderson Hamiltonian with a third neighbor dominated hybridized band structure. This approach produces a spin exciton below the charge gap with features that are consistent with the observed neutron scattering. We find that maxima in the wave vector dependence of the inelastic neutron scattering indicate band inversion.

On the Chemistry and Physical Properties of Flux and Floating Zone Grown SmB6 Single Crystals.

Recent theoretical and experimental findings suggest the long-known but not well understood low temperature resistance plateau of SmB6 may originate from protected surface states arising from a topologically non-trivial bulk band structure having strong Kondo hybridization. Yet others have ascribed this feature to impurities, vacancies, and surface reconstructions. Given the typical methods used to prepare SmB6 single crystals, flux and floating-zone procedures, such ascriptions should not be taken lightly. We demonstrate how compositional variations and/or observable amounts of impurities in SmB6 crystals grown using both procedures affect the physical properties. From X-ray diffraction, neutron diffraction, and X-ray computed tomography experiments we observe that natural isotope containing (SmB6) and doubly isotope enriched ((154)Sm(11)B6) crystals prepared using aluminum flux contain co-crystallized, epitaxial aluminum. Further, a large, nearly stoichiometric crystal of SmB6 was successfully grown using the float-zone technique; upon continuing the zone melting, samarium vacancies were introduced. These samarium vacancies drastically alter the resistance and plateauing magnitude of the low temperature resistance compared to stoichiometric SmB6. These results highlight that impurities and compositional variations, even at low concentrations, must be considered when collecting/analyzing physical property data of SmB6. Finally, a more accurate samarium-154 coherent neutron scattering length, 8.9(1) fm, is reported.

Controlled ovulation in the marmoset monkey (Callithrix jacchus) with human chorionic gonadotropin following prostaglandin-induced luteal regression.

Controlled induction of ovulation in the marmoset monkey was attempted with a single injection of human chorionic gonadotropin (hCG; 50 IU) given on day 7 after prostaglandin-induced luteal regression. Animals given hCG (n = 12) ovulated within a 2-day period (days 9 and 10 after prostaglandin) compared with a 4-day period (days 9 to 12) in the control group (n = 12). The mean interval to ovulation was similar in both groups. There was no difference in the timing of the preovulatory estradiol (E2) peak between groups, although E2 levels on the day of hCG injection were lower than in controls on the day of the onset of the luteinizing hormone surge. All animals given hCG ovulated and 11 of 12 became pregnant. Ten of 11 embryos recovered surgically from six of these animals were normal blastocysts; 5 of the remaining 6 animals carried pregnancies to term. The results are of practical importance for experiments involving follicular and oocyte maturation and the collection and transfer of embryos.

Reversible, long-term inhibition of ovulation with a gonadotropin-releasing hormone antagonist in the marmoset monkey (Callithrix jacchus).

The effects of weekly injections of a gonadotropin-releasing hormone (GnRH) antagonist (GnRHa) ([N-acetyl-DßNal1-D-pCl-Phe2-D-Phe3-D-Arg6-Phe7-Arg8D-Ala10] NH2 GnRH) on pituitary and ovarian function were examined in the marmoset monkey, Callithrix jacchus. In experiment 1, five cyclic females were given weekly injections of vehicle (50% propylene glycol in saline) for 6 weeks followed by GnRHa for 20 weeks, animals receiving either 200 µg GnRHa/injection (n = 2) or 67 µg GnRHa/injection (n = 3) for 10 weeks, after which the treatment was reversed. Bioactive luteinizing hormone (LH) and progesterone (Po) were measured in blood samples (0.2-0.4 ml) collected twice weekly until at least 8 weeks after the last GnRHa injection. GnRHa treatment, timed to begin in the midluteal phase, caused a rapid decline in LH and Po and luteal regression after a single injection (both doses). Po levels were consistently low (<10 ng/ml), and ovulation was inhibited throughout 200 µg treatment in all animals. Short periods of elevated Po (>10 ng/ml) were, however, occasionally seen during 67 µg treatment, indicating incomplete ovarian suppression. Mean LH levels were significantly lower during GnRHa treatment compared with the period of vehicle injection (all animals 200 µg; three animals 67 µg), and there were significant differences in LH levels between GnRHa treatments (200 µg vs. 67 µg) in four animals. Four animals resumed normal ovarian cycles after the end of GnRHa treatment (15/16 days, three animals; 59 days, one animal); the fifth animal died of unknown causes 32 days after the last GnRHa injection. In a second experiment, pituitary responsiveness to exogenous GnRH was tested 1 day after a single injection of vehicle or antagonist (200 or 67 µg). Measurement of bioactive LH indicated that pituitary response to 200 ng native GnRH was significantly suppressed in animals receiving the antagonist, the degree of suppression being dose related. A third experiment examined the effect of four weekly injections of 200 µg GnRHa on follicular size and granulosa cell responsiveness to human follicle-stimulating hormone (hFSH) in vitro. Follicular development beyond 1 mm was inhibited by GnRHa treatment (preovulatory follicles normally 2-4 mm) although granulosa cell responsiveness to FSH during 48 hr of culture was not impaired. These results suggest that the GnRHa-induced suppression of follicular development and ovulation was mediated primarily by an inhibition of pituitary gonadotropin secretion and not by a direct action at the level of the ovary.

Induction of luteal regression in the marmoset monkey (Callithrix jacchus) by a gonadotrophin-releasing hormone antagonist and the effects on subsequent follicular development.

Doses of 100 or 200 micrograms of a novel GnRH antagonist ([N-acetyl-D beta Na11-D-pCl-Phe2-D-Phe3-D-Arg6-Phe7-Arg8-D-Ala10]NH2 GnRH) (4 animals/dose) were administered on Days 10/11 of the luteal phase and induced a marked suppression of circulating bioactive LH and progesterone concentrations within 1 day of treatment (P less than 0.01). Thereafter, progesterone concentrations remained low or undetectable until after the next ovulation. Similar results were obtained when 200 micrograms antagonist were given on Days 5/6 of the luteal phase (N = 4). The interval from injection of antagonist (200 micrograms but not 100 micrograms) to ovulation (based on a rise in progesterone above 10 ng/ml) was significantly longer than that from prostaglandin-induced luteal regression to ovulation in control cycles (N = 4/treatment) (range, 13-15 days after antagonist vs 8-10 days after prostaglandin, P less than 0.01). This delay of 4-5 days was equivalent to the duration for which LH concentrations were significantly suppressed by 200 micrograms antagonist when administered to ovariectomized animals (N = 3). Corpus luteum function during the cycle after GnRH antagonist treatment appeared normal according to the pattern of circulating progesterone. These results show that corpus luteum function and preovulatory follicular development in the marmoset monkey are dependent on pituitary gonadotrophin secretion.