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Magnetars are a subclass of neutron stars whose intense soft-gamma-ray bursts and quiescent X-ray emission are believed to be powered by the decay of a strong internal magnetic field. We reanalyze neutrino emission in such stars in the plausibly relevant regime in which the Landau band spacing $\Delta E$of both protons and electrons is much larger than kT(where kis the Boltzmann constant and Tis the temperature), but still much smaller than the Fermi energies. Focusing on the direct Urca process, we find that the emissivity oscillates as a function of density or magnetic field, peaking when the Fermi level of the protons or electrons lies about ~$3 kT$above the bottom of any of their Landau bands. The oscillation amplitude is comparable to the average emissivity when $\Delta E$is roughly the geometric mean of kTand the Fermi energy (excluding mass), i.e., at fields much weaker than required to confine all particles to the lowest Landau band. Since the density and magnetic field strength vary continuously inside the neutron star, there will be alternating surfaces of high and low emissivity. Globally, these oscillations tend to average out, making it unclear whether there will be any observable effects.

ABSTRACTLeptospirosis is a global zoonotic disease caused by different Leptospiraspecies, such as Leptospira interrogans, that colonize the renal tubules of wild and domestic animals. Thus far, attempts to develop effective leptospirosis vaccines, both for humans and animals, have failed to induce immune responses capable of conferring protection and simultaneously preventing renal colonization. In this study, we evaluated the protective immunity induced by subunit vaccines containing seven different recombinant Leptospira interrogansouter membrane proteins, including the carboxy-terminal portion of the immunoglobulinlike protein A (LigAC) and six novel antigens, combined with aluminum hydroxide (alum) or Salmonellaflagellin (FliC) as adjuvants. Hamsters vaccinated with the different formulations elicited high antigen-specific antibody titers. Immunization with LigAC, either with alum or flagellin, conferred protective immunity but did not prevent renal colonization. Similarly, animals immunized with LigACor LigACcoadministered with six leptospiral proteins with alum adjuvant conferred protection but did not reduce renal colonization. In contrast, immunizing animals with the pool of seven antigens in combination with flagellin conferred protection and significantly reduced renal colonization by the pathogen. The present study emphasizes the relevance of antigen composition and added adjuvant in the efficacy of antileptospirosis subunit vaccines and shows the complex relationship between immune responses and renal colonization by the pathogen.

Olecranisation of the patella was described and first used by Grammont (1984) to maintain reduction of the knee joint after posterior cruciate repair and reconstruction. Since 1985 we used this technique in 18 acute posterior ruptures and knee dislocations which did not undergo surgery. Knee laxity is assessed under general anaesthesia with radiographic control. A 4 or 5 mm. Steinmann pin is introduced medially at the top of the patella and drilled vertically through the bone to continue behind the patella tendon. After reduction of the posterior drawer, the pin is passed into the anterior part of the tibia. Full mobility between 0° and 90° is maintained. Physiotherapy started immediately and early weight bearing is allowed with a posterior splint. Olecranisation prevents posterior subluxation of the tibia and gives an anterior tibial subluxation force which is minor in flexion but major in extension. We followed up our patients for 1 to 8 years. The latest testing with radiographs demonstrate posterior drawer but all patients report good results. Early physiotherapy avoids stiffness, amyotrophy, and reflex sympathetic dystrophy. Olecranisation appears to give similar results more quickly and with fewer complications than P. C. L. surgery.

Friedreich ataxia and ataxia with selective vitamin E deficiency (AVED) share very similar clinical phenotypes. We have mapped the AVED locus to proximal 8q with only three large consanguinous Tunisian families, representing to our knowledge the first use of homozygosity mapping for primary linkage analysis. Subsequently, three additional families showed linkage with the same markers. A maximum lod score of 17.9 was obtained at θ = 0 for the haplotype D8S260–D8S510, consisting of the two closest markers. With only 6 families, the AVED locus is therefore mapped precisely as illustrated by the lod–1 confidence interval of 2.4 cM on either side of D8S260–D8S510. Isolation of a yeast artificial chromosome contig >800 kilobases (kb) showed that D8S260 and D8S510 are less than 400 kb apart.

We have developed a panel of whole-genome radiation hybrids by fusing irradiated diploid human fibroblasts with recipient hamster cells. This panel of 168 cell lines has been typed with microsatellite markers of known genetic location. Of 711 AFM genetic markers 404 were selected to construct a robust framework map that spans all the autosomes and the X chromosome. To demonstrate the utility of the panel, 374 expressed sequence tags (ESTs) previously assigned to chromosomes 1, 2, 14 and 16 were localized on this map. All of these ESTs could be positioned by pairwise linkage to one of the framework markers with a LOD score of greater than 8. The whole genome radiation hybrid panel described here has been used as the starting material for the Genebridge4 panel that is being made widely available for genome mapping projects.

In Pseudomonas aeruginosa, resistance to imipenem is mainly related to a lack of protein OprD and resistance to fluoroquinolones is mainly related to alterations in DNA gyrase. However, strains cross resistant to fluoroquinolones and imipenem have been selected in vitro and in vivo with fluoroquinolones. We investigated the mechanisms of resistance to fluoroquinolones in 30 clinical strains of P. aeruginosa resistant to ciprofloxacin (mean MIC, >8 micrograms/ml), 20 of which were also resistant to imipenem (mean MIC, >16 micrograms/ml). By immunoblotting, OprD levels were markedly decreased in all of the imipenem-resistant strains. Plasmids carrying the wild-type gyrA gene (pPAW207) or gyrB gene (pPBW801) of Escherichia coli were introduced into each strain by transformation. MICs of imipenem did not change after transformation, whereas those of ciprofloxacin and sparfloxacin dramatically decreased (25- to 70-fold) for all of the strains. For 28 of them (8 susceptible and 20 resistant to imipenem), complementation was obtained with pPAW207 but not with pPBW801. After complementation, the geometric mean MICs of ciprofloxacin and sparfloxacin (MICs of 0.3 microgram/ml and 0.5 microgram/ml, respectively) were as low as those for wild-type strains. Complementation was obtained only with pPBW801 for one strain and with pPAW207 and pPBW801 for one strain highly resistant to fluoroquinolones. These results demonstrate that in clinical practice, gyrA mutations are the major mechanism of resistance to fluoroquinolones even in the strains of P. aeruginosa resistant to imipenem and lacking OprD, concomitant resistance to these drugs being the result of the addition of at least two independent mechanisms.

Eighty-nine clinical isolates resistant (n=61) or susceptible (n=28) to imipenem and exhibiting the main patterns of susceptibility to other ß-lactam agents (wild type pattern, penicillinase pattern, constitutive cephalosporinase pattern) were studied in order to investigate (i) the mechanism of resistance involved and (ii) whether resistance to carbapenems affects the level of resistance to other ß-lactam agents and, conversely, if resistance to other ß-lactam agents affects the level of resistance to carbapenems. For this purpose, the presence of OprD protein in the cell wall was detected by Western blot and ß-lactamase activity by spectrophotometric assay and isoelectric focusing. OprD expression was not detectable in the imipenem-resistant (MIC=16 µg/ml) strains. It was decreased in half the strains for which MICs of imipenem were 2 to 8 µg/ml and was close to a normal level in the most susceptible strains (MIC =1 µg/ml), thus demonstrating a direct correlation between the level of susceptibility to imipenem and the level of OprD expression. No imipenemase activity was detected in imipenem-resistant strains. Synergy between imipenem or meropenem and BRL42715 was observed for all of the strains, demonstrating the role of cephalosporinase in carbapenem resistance. Within each pattern of susceptibility, the mean MICs of ß-lactam agents other than carbapenems were similar, whether the strains were susceptible or resistant to imipenem. Conversely, the mean MICs of imipenem or meropenem for either the imipenem-resistant or the imipenem-susceptible strains were similar, regardless of the susceptibility of these strains to the other ß-lactam agents. Thus, when several mechanisms of resistance to ß-lactam agents are present in the same strain ofPseudomonas aeruginosa, there is no additive effect between these mechanisms.

La rupture antéro-supérieure (AS) de coiffe est définie par l’association d’une rupture des tendons supra-épineux et sous-scapulaire. Notre hypothèse est que les résultats des ruptures AS sont influencés par la taille de la rupture et l’infiltration graisseuse préopératoire du sous-scapulaire.