Gitelman syndrome disclosed by calcium pyrophosphate deposition disease: Early diagnosis by ultrasonographic study

Gitelman's syndrome is a rare autosomal-recessive tubular disorder characterized by hypomagnesemia and hypocalciuria associated to hypokalemia. The clinical spectrum is wide and usually characterized by chronic fatigue, cramps, muscle weakness and paresthesiae. We describe a case of a 43 year-old male patient with early onset of knee arthritis and no other symptoms. Ultrasound revealed diffuse and confluent hyperechoic deposits in cartilage, fibrocartilage of the menisci and synovium and calcium pyrophosphate crystals were observed in the synovial fluid of the knee. The concomitant presence of hypomagnesemia, hypocalciuria and hypokalemia made clear the diagnosis of Gitelman's syndrome associated with chondrocalcinosis

The VLA-COSMOS Survey: V. 324 MHz continuum observations

We present 90 cm VLA imaging of the COSMOS field, comprising a circular area of 3.14 square degrees at 8.0"x6.0" angular resolution with an average rms of 0.5 mJy/beam. The extracted catalog contains 182 sources (down to 5.5sigma), 30 of which are multi-component sources. Using Monte Carlo artificial source simulations we derive the completeness of the catalog, and we show that our 90 cm source counts agree very well with those from previous studies. Using X-ray, NUV-NIR and radio COSMOS data to investigate the population mix of our 90 cm radio sample, we find that our sample is dominated by active galactic nuclei (AGN). The average 90-20 cm spectral index (S_nu~nu**alpha, where S_nu is the flux density at frequency nu, and alpha the spectral index) of our 90 cm selected sources is -0.70, with an interquartile range of -0.90 to -0.53. Only a few ultra-steep-spectrum sources are present in our sample, consistent with results in the literature for similar fields. Our data do not show clear steepening of the spectral index with redshift. Nevertheless, our sample suggests that sources with spectral indices steeper than -1 all lie at z>1, in agreement with the idea that ultra-steep-spectrum radio sources may trace intermediate-redshift galaxies (z>1).Comment: 10 pages, 12 figures, accepted for publication in MNRA

Inaugurating a Dutch Napoleon? Conservative criticism of the 1815 constitution of the United Kingdom of The Netherlands

International audienc

Sex-specific behavioral and neurogenic responses to cocaine in mice lacking and blocking dopamine D1 or dopamine D2 receptors

Adult neurogenesis in rodents is modulated by dopaminergic signaling and inhibited by cocaine. However, the sex-specific role of dopamine D1 and D2 receptors (D1R, D2R) in the deleterious effect of cocaine on adult neurogenesis has not been described yet. Here, we explored sex differences in (a) cell proliferation (5′-bromo-2′-deoxyuridine [BrdU]), (b) neural precursor (nestin), (c) neuronal phenotype (BrdU/β3-tubulin), and (d) neuronal maturity (NeuN) in the subventricular zone (SVZ) of the lateral ventricles and striatum of mice with genetic deletion (D1, D2) or pharmacological blockage (SCH23390: 0.1 mg/kg/day/5 days; Raclopride: 0.3 mg/kg/day/5 days) of D1R and D2R, and treated (10 mg/kg/day/5 days) and then challenged (5 mg/kg, 48 hr later) with cocaine. Results indicated that hyperactivity responses to cocaine were absent in D1 mice and reduced in SCH23390-treated mice. Activity responses to cocaine were reduced in D2 males, but absent in D2 females and increased in Raclopride-treated females. D1R deletion blocked the deleterious effect of cocaine on SVZ cell proliferation in males. Cocaine-exposed D1 males also had reduced neuronal phenotype of SVZ newborn cells and increased striatal neuronal maturity. D2 mice had lower proliferative and neural precursor responses. Cocaine in D2 females or coadministered with Raclopride in wild-type females improved SVZ cell proliferation, an effect that positively correlated with plasma brain-derived neurotrophic factor (BDNF) concentrations. In conclusion, the sex-specific D1R and D2R signaling on SVZ cell proliferation, neural progenitor and neuronal maturity is differentially perturbed by cocaine, and BDNF may be required to link D2R to neuroplasticity in cocaine addiction in females.Consejería de Salud, Junta de Andalucía, Grant/Award Number: C1-0049-2019; Instituto de Salud Carlos III, Grant/Award Numbers: CP19/00068, CPII17/00024, CPII19/00022, CPII19/00031, PI19/01577, PI19/00886, PI17/02026, RD16/0017/0001; Ministerio de Sanidad, Servicios Sociales e Igualdad, Grant/Award Numbers: PND2017/043, PND2018/033, PND2018/044, PND2019/04

Multiple roles of GluN2D-containing NMDA receptors in short-term potentiation and long-term potentiation in mouse hippocampal slices

The GluN2 subunits of N-methyl-d-aspartate receptors (NMDARs) are key drivers of synaptic plasticity in the brain, where the particular GluN2 composition endows the NMDAR complex with distinct pharmacological and physiological properties. Compared to GluN2A and GluN2B subunits, far less is known about the role of the GluN2D subunit in synaptic plasticity. In this study, we have used a GluN2C/2D selective competitive antagonist, UBP145, in combination with a GluN2D global knockout (GluN2D KO) mouse line to study the contribution of GluN2D-containing NMDARs to short-term potentiation (STP) and long-term potentiation (LTP) in the CA1 region of mouse hippocampal slices. We made several distinct observations: First, GluN2D KO mice have higher levels of LTP compared to wild-type (WT) mice, an effect that was occluded by blockade of GABA receptor-mediated inhibition or by using a strong LTP induction protocol. Second, UBP145 partially inhibited LTP in WT but not GluN2D KO mice. Third, UBP145 inhibited a component of STP, termed STP2, in WT but not GluN2D KO mice. Taken together, these findings suggest an involvement for GluN2D-containing NMDARs in both STP and LTP in mouse hippocampus

Fluorogenic cell surface glycan labelling with fluorescence molecular rotor dyes and nucleic acid stains

We show that covalent labelling of sialic acids on live cell surfaces or mucin increases the fluorescence of the fluorescence molecular rotors (FMRs) CCVJ, Cy3 and thioazole orange, enabling wash-free imaging of cell surfaces. Dual labelling with an FMR and an environmentally insensitive dye allows detection of changes that occur, for example, when cross-linking is altered.Deutsche Forschungsgemeinschaft 10.13039/501100001659Peer Reviewe

Fluorogenic cell surface glycan labelling with fluorescence molecular rotor dyes and nucleic acid stains

We show that covalent labelling of sialic acids on live cell surfaces or mucin increases the fluorescence of the fluorescence molecular rotors (FMRs) CCVJ, Cy3 and thioazole orange, enabling wash-free imaging of cell surfaces. Dual labelling with an FMR and an environmentally insensitive dye allows detection of changes that occur, for example, when cross-linking is altered