Two-Photon Doppler cooling of alkaline-earth-metal and ytterbium atoms

A new possibility of laser cooling of alkaline-earth-metal and Ytterbium atoms using a two-photon transition is analyzed. We consider a $^{1}S_{0}$ - $^{1}S_{0}$ transition, with excitation in near resonance with the $^{1}P_{1}$ level. This greatly increases the two-photon transition rate, allowing an effective transfer of momentum. The experimental implementation of this technique is discussed and we show that for Calcium, for example, two-photon cooling can be used to achieve a Doppler limit of 123 microKelvin. The efficiency of this cooling scheme and the main loss mechanisms are analyzed.Comment: 7 pages, 5 figure

Temperature limits in laser cooling of free atoms with three-level cascade transitions

FAPESP - FUNDAÇÃO DE AMPARO À PESQUISA DO ESTADO DE SÃO PAULOFACEPE - FUNDAÇÃO DE AMPARO À CIÊNCIA E TECNOLOGIA DO ESTADO DE PERNAMBUCOCNPQ - CONSELHO NACIONAL DE DESENVOLVIMENTO CIENTÍFICO E TECNOLÓGICOWe employ semiclassical theoretical analysis to study laser cooling of free atoms using three-level cascade transitions, where the upper transition is much weaker than the lower one. This represents an alternate cooling scheme, particularly useful for group II atoms. We find that temperatures below the Doppler limits associated with each of these transitions are expected. The lowest temperatures arise from a remarkable increase in damping and reduced diffusion compared to two-level cooling. They are reached at the two-photon resonance, where there is a crossing between the narrow and the partially dark dressed states, and can be estimated simply by the usual Doppler limit considering the decay rate of the optical coherence between these states.We employ semiclassical theoretical analysis to study laser cooling of free atoms using three-level cascade transitions, where the upper transition is much weaker than the lower one. This represents an alternate cooling scheme, particularly useful for group II atoms. We find that temperatures below the Doppler limits associated with each of these transitions are expected. The lowest temperatures arise from a remarkable increase in damping and reduced diffusion compared to two-level cooling. They are reached at the two-photon resonance, where there is a crossing between the narrow and the partially dark dressed states, and can be estimated simply by the usual Doppler limit considering the decay rate of the optical coherence between these states.87615FAPESP - FUNDAÇÃO DE AMPARO À PESQUISA DO ESTADO DE SÃO PAULOFACEPE - FUNDAÇÃO DE AMPARO À CIÊNCIA E TECNOLOGIA DO ESTADO DE PERNAMBUCOCNPQ - CONSELHO NACIONAL DE DESENVOLVIMENTO CIENTÍFICO E TECNOLÓGICOFAPESP - FUNDAÇÃO DE AMPARO À PESQUISA DO ESTADO DE SÃO PAULOFACEPE - FUNDAÇÃO DE AMPARO À CIÊNCIA E TECNOLOGIA DO ESTADO DE PERNAMBUCOCNPQ - CONSELHO NACIONAL DE DESENVOLVIMENTO CIENTÍFICO E TECNOLÓGICOSem informaçãoSem informaçãoSem informaçãoThis work has been supported by FAPESP, FACEPE, CNPq, and CEPOF

Secreted frizzled related protein is a target of PaxB and plays a role in aquiferous system development in the freshwater sponge, Ephydatia muelleri.

Canonical and non-canonical Wnt signaling, as well as the Pax/Six gene network, are involved in patterning the freshwater sponge aquiferous system. Using computational approaches to identify transcription factor binding motifs in a freshwater sponge genome, we located putative PaxB binding sites near a Secreted Frizzled Related Protein (SFRP) gene in Ephydatia muelleri. EmSFRP is expressed throughout development, but with highest levels in juvenile sponges. In situ hybridization and antibody staining show EmSFRP expression throughout the pinacoderm and choanoderm in a subpopulation of amoeboid cells that may be differentiating archeocytes. Knockdown of EmSFRP leads to ectopic oscula formation during development, suggesting that EmSFRP acts as an antagonist of Wnt signaling in E. muelleri. Our findings support a hypothesis that regulation of the Wnt pathway by the Pax/Six network as well as the role of Wnt signaling in body plan morphogenesis was established before sponges diverged from the rest of the metazoans

Clinical variability of neuroacanthocytosis syndromes : A series of six patients with long follow-up

Objective To provide clinical clues to differential diagnosis in patients with chorea and other movement disorders with blood acanthocytes. Methods We present a long-term video accompanied follow-up of six Caucasian patients with neuroacanthocytosis from several centers, three diagnosed with chorea-acanthocytosis (ChAc): 34-y.o.(no.1), 36-y.o.(no.2), 43-y.o.(no.3), two diagnosed with McLeod Syndrome (MLS): 52-y.o.(no.4), 61-y.o.(no.5) and one 63-y.o.(no.6), a brother of no.5, with clinical suspicion of MLS. Additionally we report pathological findings of the mother of two brothers with MLS reported in our series with acanthocytes on peripheral blood smear Results The patients had an unremarkable family history and were asymptomatic until adulthood. Patients no. 1,2,4,5,6 developed generalized chorea and patient no. 3 had predominant bradykinesia. Patients no. 1,2,3 had phonic and motor tics, additionally patients no. 1 and 2 exhibited peculiar oromandibular dystonia with tongue thrusting. In patients no. 2 and 3 dystonic supination of feet was observed, patient no. 3 subsequently developed bilateral foot drop. Patients no. 2 and 4 had signs of muscle atrophy. Tendon reflexes were decreased or absent and electroneurography demonstrated sensorimotor neuropathy in patients no. 1,2,3,4,5, except no. 6. Generalized seizures were seen in patients no. 2,3,5,6 and myoclonic jerks in patient no. 1. Cognitive deterioration was reported in patients no. 1,2,3,5,6. Serum creatine kinase levels were elevated in all six patients. Conclusion We highlight the variability of clinical presentation of neuroacanthocytosis syndromes and the long time from the onset to diagnosis with the need to screen the blood smears in uncertain cases, however, as in one of our cases acanthocytes may even be not found. Based on our observations and data from the literature we propose several red flags that should raise the suspicion of an NA syndrome in a patient with a movement disorder: severe orofacial dyskinesia with tongue and lip-biting (typical of ChAc), feeding dystonia, psychiatric and cognitive disturbances, seizures, peripheral neuropathy, elevation of creatine kinase, elevation of transaminases, hepatosplenomegaly, cardiomyopathy and arrhythmias, and an X-linked pattern of inheritance (McLeod Syndrome, MLS)

Leucine-rich repeat kinase-2 (LRRK2) R1441G knockin mice are more susceptible to rotenone toxicity

This journal suppl. entitled: Supplement: Abstracts of the Eighteenth International Congress of Parkinson's Disease and Movement Disorders / Poster PresentationOBJECTIVE: To assess the susceptibility of LRRK2 R1441G knockin mice against (1) striatal dopamine (DA) uptake deficit, (2) locomotor inactivity and, (3) dopaminergic neuronal cell death, as induced by rotenone (mitochondrial complex-I inhibitor). BACKGROUND: LRRK2 mutations are the commonest genetic risk in Parkinson's disease (PD). LRRK2 is linked to synapse functions. However, the pathogenic mechanism of LRRK2 mutation in striatal DA homeostasis and mitochondria dysfunction is unknown. METHODS: Cell viability of primary DA neurons from R1441G knockin mice and their wild-type littermates were compared after rotenone exposure. Total [3H]-DA uptake in isolated striatal synaptosomes incubated with rotenone, and the locomotor activity in open-field test after chronic (20 weeks) oral gavage of rotenone were also assessed. RESULTS: Without rotenone, R1441G mutant mice show no overt phenotype. However, synaptosomes from young (3-month-old) mutant mice exhibited lower DA uptake when incubated with rotenone (100nM), compared with wild-type controls. Number of tyrosine hydroxylase (TH)-positive neurons in mutant culture after rotenone exposure (5nM) was significantly lower. Also, chronic exposure to rotenone (5mg/kg, twice per week orally) for 20 weeks caused significantly lower locomotor activity in mutant mice compared with the wild-type controls. CONCLUSIONS: Similar to R1441C [1], LRRK2 R1441G mutant mice show no overt phenotype. However, R1441G mutant synaptosomes were more vulnerable to rotenone toxicity as shown by lower DA uptake, indicating that R1441G mutation contributes to mitochondrial dysfunction-induced synaptic dysfunction. Re-uptake of extracellular DA requires mitochondrial ATP for synaptic recycling. Uptake deficits associated with LRRK2 mutation may adversely affects striatal neuronal survival and locomotor activity as observed in our mutant mice. This differential susceptibility against rotenone toxicity of the mutant mice suggests that LRRK2 R1441G mutation may be a predisposing genetic factor in synaptic energy deficiency leading to early striatal synaptic dysfunction [2], and later nigrostriatal DA cell death in LRRK2-associated PD.link_to_OA_fulltex