31 research outputs found

    Realization of a high power optical trapping setup free from thermal lensing effects

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    Transmission of high power laser beams through partially absorbing materials modifies the light propagation via a thermally-induced effect known as thermal lensing. This may cause changes in the beam waist position and degrade the beam quality. Here we characterize the effect of thermal lensing associated with the different elements typically employed in an optical trapping setup for cold atoms experiments. We find that the only relevant thermal lens is represented by the TeO2TeO_2 crystal of the acousto-optic modulator exploited to adjust the laser power on the atomic sample. We then devise a simple and totally passive scheme that enables to realize an inexpensive optical trapping apparatus essentially free from thermal lensing effects

    Realization of a Cold Mixture of Fermionic Chromium and Lithium Atoms

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    We report on the production of a novel cold mixture of fermionic 53^{53}Cr and 6^{6}Li atoms delivered by two Zeeman-slowed atomic beams and collected within a magneto-optical trap (MOT). For lithium, we obtain clouds of up to 4 1084 \,10^8 atoms at temperatures of about 500 Ό500\,\muK. A gray optical molasses stage allows us to decrease the gas temperature down to 45(5) Ό45(5)\,\muK. For chromium, we obtain MOTs comprising up to 1.5 1061.5\, 10^6 atoms. The availability of magnetically trappable metastable DD-states, from which PP-state atoms can radiatively decay onto, enables to accumulate into the MOT quadrupole samples of up to 10710^7 53^{53}Cr atoms. After repumping DD-state atoms back into the cooling cycle, a final cooling stage decreases the chromium temperature down to 145(5) Ό145(5)\,\muK. While the presence of a lithium MOT decreases the lifetime of magnetically trapped 53^{53}Cr atoms, we obtain, within a 5 seconds duty cycle, samples of about 4 1064\, 10^6 chromium and 1.5 1081.5\,10^8 lithium atoms. Our work provides a crucial step towards the production of degenerate Cr-Li Fermi mixtures.Comment: 14 pages, 8 figure

    Universality of the three-body Efimov parameter at narrow Feshbach resonances

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    We measure the critical scattering length for the appearance of the first three-body bound state, or Efimov three-body parameter, at seven different Feshbach resonances in ultracold 39K atoms. We study both intermediate and narrow resonances, where the three-body spectrum is expected to be determined by the non-universal coupling of two scattering channels. We observe instead approximately the same universal relation of the three-body parameter with the two-body van der Waals radius already found for broader resonances, which can be modeled with a single channel. This unexpected observation suggests the presence of a new regime for three-body scattering at narrow resonances

    Effects of the coronary artery disease associated LPA and 9p21 loci on risk of aortic valve stenosis

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    Background: Aortic valve stenosis (AVS) and coronary artery disease (CAD) have a significant genetic contribution and commonly co-exist. To compare and contrast genetic determinants of the two diseases, we investigated associations of the LPA and 9p21 loci, i.e. the two strongest CAD risk loci, with risk of AVS. Methods: We genotyped the CAD-associated variants at the LPA (rs10455872) and 9p21 loci (rs1333049) in the GeneCAST (Genetics of Calcific Aortic STenosis) Consortium and conducted a meta-analysis for their association with AVS. Cases and controls were stratified by CAD status. External validation of findings was undertaken in five cohorts including 7880 cases and 851,152 controls. Results: In the meta-analysis including 4651 cases and 8231 controls the CAD-associated allele at the LPA locus was associated with increased risk of AVS (OR 1.37; 95%CI 1.24–1.52, p = 6.9 × 10−10) with a larger effect size in those without CAD (OR 1.53; 95%CI 1.31–1.79) compared to those with CAD (OR 1.27; 95%CI 1.12–1.45). The CAD-associated allele at 9p21 was associated with a trend towards lower risk of AVS (OR 0.93; 95%CI 0.88–0.99, p = 0.014). External validation confirmed the association of the LPA risk allele with risk of AVS (OR 1.37; 95%CI 1.27–1.47), again with a higher effect size in those without CAD. The small protective effect of the 9p21 CAD risk allele could not be replicated (OR 0.98; 95%CI 0.95–1.02). Conclusions: Our study confirms the association of the LPA locus with risk of AVS, with a higher effect in those without concomitant CAD. Overall, 9p21 was not associated with AVS

    Novel SCARB2 mutation in action myoclonus-renal failure syndrome and evaluation of SCARB2 mutations in isolated AMRF features

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    Background: Action myoclonus-renal failure syndrome is a hereditary form of progressive myoclonus epilepsy associated with renal failure. It is considered to be an autosomal-recessive disease related to loss-of-function mutations in SCARB2. We studied a German AMRF family, additionally showing signs of demyelinating polyneuropathy and dilated cardiomyopathy. To test the hypothesis whether isolated appearance of individual AMRF syndrome features could be related to heterozygote SCARB2 mutations, we screened for SCARB2 mutations in unrelated patients showing isolated AMRF features. Methods: In the AMRF family all exons of SCARB2 were analyzed by Sanger sequencing. The mutation screening of unrelated patients with isolated AMRF features affected by either epilepsy (n = 103, progressive myoclonus epilepsy or generalized epilepsy), demyelinating polyneuropathy (n = 103), renal failure (n = 192) or dilated cardiomyopathy (n = 85) was performed as high resolution melting curve analysis of the SCARB2 exons. Results: A novel homozygous 1 bp deletion (c.111delC) in SCARB2 was found by sequencing three affected homozygous siblings of the affected family. A heterozygous sister showed generalized seizures and reduction of nerve conduction velocity in her legs. No mutations were found in the epilepsy, renal failure or dilated cardiomyopathy samples. In the polyneuropathy sample two individuals with demyelinating disease were found to be carriers of a SCARB2 frameshift mutation (c.666delCCTTA). Conclusions: Our findings indicate that demyelinating polyneuropathy and dilated cardiomyopathy are part of the action myoclonus-renal failure syndrome. Moreover, they raise the possibility that in rare cases heterozygous SCARB2 mutations may be associated with PNP features

    High prevalence of NMDA receptor IgA/IgM antibodies in different dementia types

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    OBJECTIVE: To retrospectively determine the frequency of N-Methyl-D-Aspartate (NMDA) receptor (NMDAR) autoantibodies in patients with different forms of dementia. METHODS: Clinical characterization of 660 patients with dementia, neurodegenerative disease without dementia, other neurological disorders and age-matched healthy controls combined with retrospective analysis of serum or cerebrospinal fluid (CSF) for the presence of NMDAR antibodies. Antibody binding to receptor mutants and the effect of immunotherapy were determined in a subgroup of patients. RESULTS: Serum NMDAR antibodies of IgM, IgA, or IgG subtypes were detected in 16.1% of 286 dementia patients (9.5% IgM, 4.9% IgA, and 1.7% IgG) and in 2.8% of 217 cognitively healthy controls (1.9% IgM and 0.9% IgA). Antibodies were rarely found in CSF. The highest prevalence of serum antibodies was detected in patients with “unclassified dementia” followed by progressive supranuclear palsy, corticobasal syndrome, Parkinson’s disease-related dementia, and primary progressive aphasia. Among the unclassified dementia group, 60% of 20 patients had NMDAR antibodies, accompanied by higher frequency of CSF abnormalities, and subacute or fluctuating disease progression. Immunotherapy in selected prospective cases resulted in clinical stabilization, loss of antibodies, and improvement of functional imaging parameters. Epitope mapping showed varied determinants in patients with NMDAR IgA-associated cognitive decline. INTERPRETATION: Serum IgA/IgM NMDAR antibodies occur in a significant number of patients with dementia. Whether these antibodies result from or contribute to the neurodegenerative disorder remains unknown, but our findings reveal a subgroup of patients with high antibody levels who can potentially benefit from immunotherapy
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