Entanglement of Trapped-Ion Qubits Separated by 230 Meters.

We report on an elementary quantum network of two atomic ions separated by 230 m. The ions are trapped in different buildings and connected with 520(2) m of optical fiber. At each network node, the electronic state of an ion is entangled with the polarization state of a single cavity photon; subsequent to interference of the photons at a beam splitter, photon detection heralds entanglement between the two ions. Fidelities of up to (88.0+2.2-4.7)% are achieved with respect to a maximally entangled Bell state, with a success probability of 4×10^{-5}. We analyze the routes to improve these metrics, paving the way for long-distance networks of entangled quantum processors.

Release of gentamicin from bone regenerative materials: an in vitro study.

Antibiotic loading of bone regenerative materials is a promising way to protect augmentation procedures from infection during the resorption phase of bone substitutes. Especially in the early stage of implantation, it should protect the grafted site against microbiological pathogens. The present study reports the release kinetics of gentamicin after loading from two synthetic bone filling materials. The first, BONITmatrix, is a biphasic calcium phosphate silica composite obtained by the sol-gel route consisting of 13% silicon dioxide (w/w) and calcium phosphates (hydroxyapatite/beta-tricalcium phosphate 60/40 w/w). The second, Synthacer, is a sintered hydroxyapatite ceramic. Gentamicin was loaded by dipping and by vacuum coating. Release kinetics of the loaded Gentamicin was investigated by fluorescence polarization immunoassay and by staphylococcus aureus assay. By dipping, loading failed for Synthacer, and it was 12.7 mg gentamicin per gram bone substitute for BONITmatrix. By vacuum coating, loading was 11.3 mg gentamicin per gram bone substitute for Synthacer and 7.4 mg gentamicin per gram bone substitute for BONITmatrix. Distinct release kinetics were measured. For Synthacer, a high initial release was followed by a lower protracted release level up to 28 days. For BONITmatrix release was continuous over the investigated 70-day period. The present data suggest that the porosity properties at the nano- and microscopic levels, or the composition are responsible for antibiotic loading and subsequent release.

Aging and cancerogenesis. IV. Interrelationships among age, immune response, and tumor incidence in several strains of mice.

Immune reactivity of mice with various incidences of spontaneous tumors was measured at different points in their lifespan. Cytotoxic activity of immune sera from 3- and 12-month-old mice was high or moderately high in AKR/J, SJL/J, and A/HeJ mice in which high incidences of spontaneous tumors occur by the 12th month, and in SWR/J and C3HeB/-FeJ mice in which high incidences of spontaneous tumors reportedly occur after 18 months of age. A decrease in primary antibody response accompanied old age in 4 of the 6 strains tested (including randombred Swiss ICR/Ha), but not in AKR/J or A/HeJ mice. These facts, together with previous tests of cellular response in these mice, imply that under these experimental conditions little correspondence exists between humoral and cellular response. Further, host immunity may be only secondarily implicated in neoplastic formation.

Increased incidence of mammary tumors in rats after direct or transplacental exposure to 3-hydroxyxanthine.

Rats were exposed directly or transplacentally to the carcinogenic purine N-oxide 3-hydroxyxanthine (3-OH-X). Among female noninbred Wistar rats given 3-OH-X sc, beginning at suckling or weaning ages, there was a significantly greater proportion of mammary tumor bearers and a higher mean number of mammary tumors per rat than among controls. This effect was seen even at low doses producing no other neoplasms such as hepatic carcinomas or fibrosarcomas and fibromas at the site of injection. Noninbred Sprague-Dawley rats, treated transplacentally with 3-OH-X by ip injection into pregnant females, also also had a significantly greater incidence of mammary tumors than did controls.

Oncogenicity of purine 3-oxide and unsubstituted purine in rats.

Injection s.c. of purine 3-oxide into Wistar rats resulted in the appearance of sarcomas and fibromas at the interscapular site of administration, carcinomas in the liver, and a high incidence of s.c. fibromas in the hip at a distance from the site of injection. A small number of liver tumors but not tumors at the injection site appeared in rats to which the parent compound, purine, was administered. Oxidation of purine 3-oxide by xanthine oxidase was found to occur in two steps to yield the potent oncogen 3-hydroxyxanthine. A similar process may occur in vivo since a protein preparation from rat s.c. tissue has similar oxidizing activity.

Therapy of 7,12-dimethylbenz(a)anthracene-induced rat mammary carcinomas with combinations of 5-fluorouracil and 2 alpha-methyldihydrotestosterone propionate.

This investigation was undertaken to determine whether a combination of a cytotoxic drug with a sex hormone would provide efficacious therapy for mammary carcinomas. Established, 7,12-dimethylbenz(a)anthracene-induced rat mammary carcinomas were treated with 5-fluorouracil (5-FUra) and 2 alpha-methyldihydrotestosterone propionate (MDTP) for 4 weeks. At end of therapy, pooled data showed 21% of the tumors in complete remission (CR) in rats given 5-FUra at 17.5 mg/kg/day and 3% in those given 8 mg/kg/day. Administration of MDTP at 1.25 to 5 mg/kg/day yielded 15 to 48% tumor CR. The combination of 5-FUra at 17.5 mg/kg/day with MDTP at 5, 2.5, and 1.25 mg/kg/day induced, respectively, 96, 91, and 75% CR. Maxima of 100, 100, and 92% CR were obtained in single tests at these respective doses. Therapy with combinations of 5-FUra at 8 mg/day and MDTP at 2.5 and 1.25 mg/kg/day yielded, respectively, 69 and 61% tumor CR. Appearance of new tumors during and after therapy was controlled more effectively by combinations of the two agents. Analysis of percentage of tumor CR showed marked synergism for 5-FUra and MDTP. A second course of combination therapy effectively prolonged duration of CR. Therapy with the cytotoxic drug 5-FUra in combination with the androgen analog MDTP is highly efficacious against induced mammary carcinomas.

Comparative effects of a series of prolactin inhibitors, 17beta-estradiol and 2alpha-methyldihydrotestosterone propionate, on growth of 7,12-dimethylbenz(a)anthracene-induced rat mammary carcinomas.

Eight ergot alkaloids and ergoline derivatives, effective prolactin inhibitors, were tested for activity against DMBA-induced rat mammary carcinomas. Compounds were administered daily, 5 times/week for 4 weeks, and rats were observed for an additional 4 weeks. Groups treated with androgen and estrogen were used as positive controls. Those ergot compounds and ergolines that proved to be highly effective in reducing tumor size or in inducing regression of tumors to nonpalpability were Deprenon (D-6-methyl-8-ergolin-I-ylacetic acid amide) and ergocryptine; effective to an intermediate degree were Dironyl [N-(D-6-methyl-8-isoergolin-I-yl)-N',N'-diethylurea], ergocornine, and Lysenyl [N-(D-6-methyl-8-isoergolenyl)-N',N'-diethyl-urea]; and effective to a minimal degree were Lergotrile (2-chloro-6-methylergoline-8beta-acetonitrile), CB-154, and 6605-VUFB (D-6-methyl-8-cyanomethylergolin-I). Remission of many individual carcinomas was brief, and duration of complete regression (all tumors in the rat were nonpalpable) was less than 10 weeks.