Conditional control of quantum beats in a cavity QED system

We probe a ground-state superposition that produces a quantum beat in the intensity correlation of a two-mode cavity QED system. We mix drive with scattered light from an atomic beam traversing the cavity, and effectively measure the interference between the drive and the light from the atom. When a photon escapes the cavity, and upon detection, it triggers our feedback which modulates the drive at the same beat frequency but opposite phase for a given time window. This results in a partial interruption of the beat oscillation in the correlation function, that then returns to oscillate.Comment: 9 pages, 5 figures, XVII Reuni\'on Iberoamericana de \'Optica, X Encuentro de \'Optica, L\'aseres y Aplicaciones (RIAO-OPTILAS-2010

Relapse of Neuromyelitis Optica Spectrum Disorder Associated with Intravenous Lidocaine

Lidocaine unmasks silent symptoms and eases neuropathic pain in multiple sclerosis patients; however, the effects of lidocaine in neuromyelitis optica have never been reported. We describe the case of a 59-year-old Japanese woman with neuromyelitis optica spectrum disorder who developed optic neuritis 1 day after intravenous lidocaine injection for treating allodynia. Her symptom seemed to result from a relapse of neuromyelitis optica induced by lidocaine administration, and not because of the transient effects of intravenous lidocaine administration. The possibility that lidocaine administration results in relapse of neuromyelitis optica due to its immunomodulating effects cannot be ruled out

New GTC spectroscopic data and a statistical study to better constrain the redshift of the BL Lac RGB J2243 + 203

We present new spectroscopic data of the BL Lac RGB 2243 + 203, and its surroundings, obtained with the OSIRIS Multi Object Spectrograph (MOS) mounted in the Gran Telescopio Canarias (GTC). The spectra of neither the BL Lac nor its host galaxy show any spectral feature, thus hindering direct determination of its redshift. The spectroscopic redshift distribution of objects in the MOS field of view shows four galaxies with redshift between 0.5258 and 0.5288. We make use of a statistical analysis to test the possibility that the targeted BL Lac may be a member of that group. By using the spectroscopic redshifts obtained with our GTC observations, we found that this probability is between 86 and 93 per cent.Fil: Rosa González, D. Instituto Nacional de Astrofísica, Optica y Electrónica; MéxicoFil: Muriel, Hernan. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Astronomía Teórica y Experimental. Universidad Nacional de Córdoba. Observatorio Astronómico de Córdoba. Instituto de Astronomía Teórica y Experimental; ArgentinaFil: Mayya, Y. D.. Instituto Nacional de Astrofísica, Optica y Electrónica; MéxicoFil: Aretxaga, I.. Instituto Nacional de Astrofísica, Optica y Electrónica; MéxicoFil: Becerra González, J.. Instituto de Astrofisica de Canarias; EspañaFil: Carramiñana, Alberto. Instituto Nacional de Astrofísica, Optica y Electrónica; MéxicoFil: Méndez-Abreu, J.. Instituto Nacional de Astrofísica, Optica y Electrónica; MéxicoFil: Vega, O. Instituto Nacional de Astrofísica, Optica y Electrónica; MéxicoFil: Terlevich, E-. Instituto Nacional de Astrofísica, Optica y Electrónica; MéxicoFil: Coutiño de León, S.. Instituto Nacional de Astrofísica, Optica y Electrónica; MéxicoFil: Furniss, A.. Instituto Nacional de Astrofísica, Optica y Electrónica; MéxicoFil: Longinotti, A. L.. Instituto Nacional de Astrofísica, Optica y Electrónica; MéxicoFil: Terlevich, R. J.. Instituto Nacional de Astrofísica, Optica y Electrónica; MéxicoFil: Pichel, Ana Carolina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Ciudad Universitaria. Instituto de Astronomía y Física del Espacio. - Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Instituto de Astronomía y Física del Espacio; ArgentinaFil: Rovero, Adrian Carlos. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Ciudad Universitaria. Instituto de Astronomía y Física del Espacio. - Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Instituto de Astronomía y Física del Espacio; ArgentinaFil: Donzelli, Carlos Jose. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Astronomía Teórica y Experimental. Universidad Nacional de Córdoba. Observatorio Astronómico de Córdoba. Instituto de Astronomía Teórica y Experimental; Argentin

Pathophysiologisch-serologische, bildgebende und klinische Charakteristika der Neuromyelitis Optica

Hintergrund: Neuromyelitis optica-Spektrum-Erkrankungen (NMOSD) stellen eine Gruppe neuroinflammatorischer Erkrankungen dar, die mit dem klinischen Auftreten von Myelitiden und/oder Optikusneuritiden (ON) einhergeht. Aufgrund zahlreicher überlappender klinischer und paraklinischer Eigenschaften beim Nachweis verschiedener Antikörper, vor allem auch in Abgrenzung zur Multiplen Sklerose (MS), besteht weiterhin der Bedarf nach neuen Biomarkern. Methodik: In zwei Studien wurden NMOSD-Patienten mit positivem Nachweis für Aquaporin-4-Antikörper (AQP-4-Ak) mittels 7 Tesla (T) Magnetresonanztomografie (MRT) hinsichtlich der I) periventrikulären Venendichte (PVA) in T2*-gewichteten Aufnahmen und II) der Phasenverschiebung in suszeptibilitätsgewichteten Sequenzen untersucht. Als Vergleich dienten die Ergebnisse von Patienten mit MS und gesunden Kontrollen (HC). In einer dritten Arbeit (III) erfolgte eine retrospektive Auswertung visueller Parameter im Vergleich von AQP-4-Ak-positiven Patienten und Patienten mit Antikörpern gegen das Myelin-Oligodendrozyten-Glykoprotein (MOG) mittels Optischer Kohärenztomografie (OCT), Visuell Evozierter Potenziale (VEP) und der Fernvisus-Messung. Ergebnisse: Bildmorphologisch zeigte sich in den 7T-T2* gewichteten Aufnahmen bei Patienten mit AQP-4-Ak-positiver NMOSD eine normal große PVA (AQP-4-Ak: PVA = 133 mm2; MS: PVA = 117 mm2; HC: PVA =144 mm2) und überwiegend fehlende paramagnetische Phasenverschiebungen (107 von 112 Läsionen, 96%) in den SWI-Sequenzen. Hinsichtlich des Vergleichs von MOG-Ak- gegenüber von AQP4-Ak-positiven Patienten fiel eine größere absolute Schubrate (Mittelwert, Spannweite, MOG-Ak: 4.5, 1 - 13; APQ4-Ak: 2, 1 -4; p = 0.012), bei insgesamt ähnlichem Verlust der im OCT gemessenen peripapillären retinalen Nervenfaserschicht (pRNFL) der AQP-4-Ak-positiven NMOSD im Vergleich zu den MOG-Ak-positiven Patienten auf (Mittelwert Standardabweichung, MOG-Ak: 59 ± 23 µm, AQP-4-Ak: 59 ± 21 µm). Jedoch waren die Werte der pRNFL nach dem Erstereignis einer ON bei den Patienten mit AQP-4-Ak deutlich stärker reduziert, als bei den MOG-Ak-positiven Patienten (AQP-4-Ak: pRNFL-Verlust = 32.8 μm (p<0.001); MOG-Ak: pRNFL-Verlust = 12.8 μm (p=0.001)). Schlussfolgerung: Mit Hilfe von modernen diagnostischen Verfahren, wie dem Ultrahochfeld-MRT und dem OCT wird die bessere Charakterisierung von phänotypisch ähnlichen neuroinflammatorischen Krankheitsentitäten ermöglicht. Die hierfür zugrundeliegenden unterschiedlichen Pathomechanismen sind bisher nicht vollständig verstanden und bedürfen weiterer Untersuchungen.Introduction: Different neuroinflammatory entities define the group of Neuromyelitis optica spectrum disorders (NMOSD) and are usually associated with the presentation of myelitis and/or optic neuritis. Although various antibodies were verified, there is still the challenge of overlapping clinical and paraclinical phenotypes which ask for further new diagnostic parameters. Methods: By using 7 Tesla (T) magnetic resonance imaging (MRI) patients with aquaporin-4-antibodies (AQP-4-ab) were investigated concerning a) the periventricular venous area (PVA) at T2*-weighted images and b) the phase changes within brain lesions at susceptibility-weighted (SWI)-images. The findings were compared to patients with Multiple Sclerosis (MS) and healthy controls (HC). Further patients with AQP-4-ab and antibodies against myelin oligodendrocyte glycoprotein (MOG-ab) were faced by using retrospective data of retinal optical coherence tomography (OCT), visual acuity and visual evoked potentials (VEP). Results: Patients with AQP-4-ab presented equal results like HC concerning the PVA (AQP-4-ab: PVA = 133 mm2; MS: PVA = 117 mm2; HC: PVA =144 mm2) and predominantly missing phase changes in brain lesions at SWI-images (107 of 112 lesions, 96%). Both, AQP-4-ab- and MOGab-positive patients, presented a loss in peripapillary nerve fiber layer (pRNFL) thickness at the same extend (mean ± standard deviation, MOG-ab: 59 ± 23 ±m, AQP4-ab: 59 ± 21 ±m), while the number of episodes of optic neuritis (ON) was lower in AQP4-ab-positive patients (mean, range, MOG-ab: 4.5, 1 - 13; APQ4-ab: 2, 1 -4; p = 0.012). However, the loss of pRNFL thickness after the first episode of ON was greater in patients with AQP-4-ab (AQP-4-ab: pRNFL-loss = 32.8 µm (p<0.001); MOG-ab pRNFL-loss = 12.8 µm (p=0.001). Conclusion: With the help of novel diagnostic tools, like the ultrahighfield-MRI and OCT, it is possible to distinguish between neuroinflammatory entities with similar phenotypes. For a better understanding of the underlying pathomechanisms further investigations are still needed

Marked central nervous system pathology in CD59 knockout rats following passive transfer of Neuromyelitis optica immunoglobulin G.

Neuromyelitis optica spectrum disorders (herein called NMO) is an inflammatory demyelinating disease of the central nervous system in which pathogenesis involves complement-dependent cytotoxicity (CDC) produced by immunoglobulin G autoantibodies targeting aquaporin-4 (AQP4-IgG) on astrocytes. We reported evidence previously, using CD59-/- mice, that the membrane-associated complement inhibitor CD59 modulates CDC in NMO (Zhang and Verkman, J. Autoimmun. 53:67-77, 2014). Motivated by the observation that rats, unlike mice, have human-like complement activity, here we generated CD59-/- rats to investigate the role of CD59 in NMO and to create NMO pathology by passive transfer of AQP4-IgG under conditions in which minimal pathology is produced in normal rats. CD59-/- rats generated by CRISPR/Cas9 technology showed no overt phenotype at baseline except for mild hemolysis. CDC assays in astrocyte cultures and cerebellar slices from CD59-/- rats showed much greater sensitivity to AQP4-IgG and complement than those from CD59+/+ rats. Intracerebral administration of AQP4-IgG in CD59-/- rats produced marked NMO pathology, with astrocytopathy, inflammation, deposition of activated complement, and demyelination, whereas identically treated CD59+/+ rats showed minimal pathology. A single, intracisternal injection of AQP4-IgG in CD59-/- rats produced hindlimb paralysis by 3 days, with inflammation and deposition of activated complement in spinal cord, optic nerves and brain periventricular and surface matter, with most marked astrocyte injury in cervical spinal cord. These results implicate an important role of CD59 in modulating NMO pathology in rats and demonstrate amplification of AQP4-IgG-induced NMO disease with CD59 knockout

The Gut Microbiome in Neuromyelitis Optica.

Neuromyelitis optica (NMO) is a rare, disabling, sometimes fatal central nervous system inflammatory demyelinating disease that is associated with antibodies ("NMO IgG") that target the water channel protein aquaporin-4 (AQP4) expressed on astrocytes. There is considerable interest in identifying environmental triggers that may elicit production of NMO IgG by AQP4-reactive B cells. Although NMO is considered principally a humoral autoimmune disease, antibodies of NMO IgG are IgG1, a T-cell-dependent immunoglobulin subclass, indicating that AQP4-reactive T cells have a pivotal role in NMO pathogenesis. When AQP4-specific proliferative T cells were first identified in patients with NMO it was discovered that T cells recognizing the dominant AQP4 T-cell epitope exhibited a T helper 17 (Th17) phenotype and displayed cross-reactivity to a homologous peptide sequence within a protein of Clostridium perfringens, a commensal bacterium found in human gut flora. The initial analysis of gut microbiota in NMO demonstrated that, in comparison to healthy controls (HC) and patients with multiple sclerosis, the microbiome of NMO is distinct. Remarkably, C. perfringens was the second most significantly enriched taxon in NMO, and among bacteria identified at the species level, C. perfringens was the one most highly associated with NMO. Those discoveries, along with evidence that certain Clostridia in the gut can regulate the balance between regulatory T cells and Th17 cells, indicate that gut microbiota, and possibly C. perfringens itself, could participate in NMO pathogenesis. Collectively, the evidence linking microbiota to humoral and cellular immunity in NMO underscores the importance for further investigating this relationship