Street Earnings Activation Delay

Street earnings are non-GAAP earnings, adjusted for consistency with the analyst majority basis and disseminated by forecast data providers (FDPs). We find that the time it takes an FDP to incorporate street earnings in its products (activation delay, hereafter) reflects variation in the difficulty of constructing street earnings, investor demand for timely street earnings, and FDPs' limited attention and resources. Furthermore, the market reaction to reported earnings is more timely when activation delay is shorter, and price discovery is highly concentrated during the hour after street earnings are activated. Finally, activation delay increases the delay with which street earnings are incorporated in analyst forecasts. We conclude that frictions in information processing prevent market participants from instantaneously constructing and incorporating street earnings in their decisions, and that FDPs play a key role in alleviating these frictions

Cholinergic Interneurons Mediate Fast VGluT3-Dependent Glutamatergic Transmission in the Striatum

The neurotransmitter glutamate is released by excitatory projection neurons throughout the brain. However, non-glutamatergic cells, including cholinergic and monoaminergic neurons, express markers that suggest that they are also capable of vesicular glutamate release. Striatal cholinergic interneurons (CINs) express the Type-3 vesicular glutamate transporter (VGluT3), although whether they form functional glutamatergic synapses is unclear. To examine this possibility, we utilized mice expressing Cre-recombinase under control of the endogenous choline acetyltransferase locus and conditionally expressed light-activated Channelrhodopsin2 in CINs. Optical stimulation evoked action potentials in CINs and produced postsynaptic responses in medium spiny neurons that were blocked by glutamate receptor antagonists. CIN-mediated glutamatergic responses exhibited a large contribution of NMDA-type glutamate receptors, distinguishing them from corticostriatal inputs. CIN-mediated glutamatergic responses were insensitive to antagonists of acetylcholine receptors and were not seen in mice lacking VGluT3. Our results indicate that CINs are capable of mediating fast glutamatergic transmission, suggesting a new role for these cells in regulating striatal activity

Coexpression of vesicular glutamate transporters 1 and 2, glutamic acid decarboxylase and calretinin in rat entorhinal cortex

We studied the distribution and coexpression of vesicular glutamate transporters (VGluT1, VGluT2), glutamic acid decarboxylase (GAD) and calretinin (CR, calcium-binding protein) in rat entorhinal cortex, using immunofluorescence staining and multichannel confocal laser scanning microscopy. Images were computer processed and subjected to automated 3D object recognition, colocalization analysis and 3D reconstruction. Since the VGluTs (in contrast to CR and GAD) occurred in fibers and axon terminals only, we focused our attention on these neuronal processes. An intense, punctate VGluT1-staining occurred everywhere in the entorhinal cortex. Our computer program resolved these punctae as small 3D objects. Also VGluT2 showed a punctate immunostaining pattern, yet with half the number of 3D objects per tissue volume compared with VGluT1, and with statistically significantly larger 3D objects. Both VGluTs were distributed homogeneously across cortical layers, with in MEA VGluT1 slightly more densely distributed than in LEA. The distribution pattern and the size distribution of GAD 3D objects resembled that of VGluT2. CR-immunopositive fibers were abundant in all cortical layers. In double-stained sections we noted ample colocalization of CR and VGluT2, whereas coexpression of CR and VGluT1 was nearly absent. Also in triple-staining experiments (VGluT2, GAD and CR combined) we noted coexpression of VGluT2 and CR and, in addition, frequent coexpression of GAD and CR. Modest colocalization occurred of VGluT2 and GAD, and incidental colocalization of all three markers. We conclude that the CR-containing axon terminals in the entorhinal cortex belong to at least two subpopulations of CR-neurons: a glutamatergic excitatory and a GABAergic inhibitory

Differentiation of human adipose-derived stem cells into neuron/motoneuron-like cells for cell replacement therapy of spinal cord injury

Human adipose-derived stem cells (hADSCs) are increasingly presumed to be a prospective stem cell source for cell replacement therapy in various degenerative and/or traumatic diseases. The potential of trans-differentiating hADSCs into motor neuron cells indisputably provides an alternative way for spinal cord injury (SCI) treatment. In the present study, a stepwise and efficient hADSC trans-differentiation protocol with retinoic acid (RA), sonic hedgehog (SHH), and neurotrophic factors were developed. With this protocol hADSCs could be converted into electrophysiologically active motoneuron-like cells (hADSC-MNs), which expressed both a cohort of pan neuronal markers and motor neuron specific markers. Moreover, after being primed for neuronal differentiation with RA/SHH, hADSCs were transplanted into SCI mouse model and they survived, migrated, and integrated into injured site and led to partial functional recovery of SCI mice. When ablating the transplanted hADSC-MNs harboring HSV-TK-mCherry overexpression system with antivirial Ganciclovir (GCV), functional relapse was detected by motor-evoked potential (MEP) and BMS assays, implying that transplanted hADSC-MNs participated in rebuilding the neural circuits, which was further confirmed by retrograde neuronal tracing system (WGA). GFP-labeled hADSC-MNs were subjected to whole-cell patch-clamp recording in acute spinal cord slice preparation and both action potentials and synaptic activities were recorded, which further confirmed that those pre-conditioned hADSCs indeed became functionally active neurons in vivo. As well, transplanted hADSC-MNs largely prevented the formation of injury-induced cavities and exerted obvious immune-suppression effect as revealed by preventing astrocyte reactivation and favoring the secretion of a spectrum of anti-inflammatory cytokines and chemokines. Our work suggests that hADSCs can be readily transformed into MNs in vitro, and stay viable in spinal cord of the SCI mouse and exert multi-therapeutic effects by rebuilding the broken circuitry and optimizing the microenvironment through immunosuppression

Primary CD30-positive cutaneous T-cell lymphomas and lymphomatoid papulosis frequently express cytotoxic proteins

Alms: To analyse the relationship between expression of cytotoxic proteins. histopathology and the CD30 status in primary cutaneous T-cell disorders, we investigated the expression of TIA-1, granzyme B and perforin in CD30 negative and CD30 positive cutaneous T-cell lymphomas (CTCL) and lymphomatoid papulosis (LP). Methods and results: We studied 26 cases of CTCL and 12 cases of LP for the expression of TIA-1, granzyme B and perforin which are granule-associated proteins of cytotoxic lymphocytes involved in the mechanism of apoptosis. We showed that most cases (10/13) of CD30 negative pleomorphic lymphomas expressed cytotoxic proteins only in scattered, apparently reactive lymphocytes, the exception being one CD8+ CTCL and two gamma delta subcutaneous 'panniculitis-like' T-cell lymphomas. We also showed that at least one cytotoxic protein was expressed in a proportion of neoplastic cells in 77% (10/13) of CD30+ T-cell lymphomas (3/4 pleomorphic and 7/9 anaplastic) and in a proportion of atypical cells in 75% (9/12) of LP. Conclusions: Our findings show a strong correlation between the CD30 phenotype and the expression of cytotoxic proteins in primary CTCL. In addition, these results provide further evidence for an overlap between lymphomatoid papulosis and cutaneous CD30+ pleomorphic and anaplastic lymphomas. These entities, which belong to the spectrum of CD30 positive cutaneous T-cell lymphoproliferations, appear to be derived from cytotoxic cells

Catalogue de la bibliothèque théatrale de M. Léon Sapin : dont la vente aura lieu ... Rue des bons-enfants 28, salle n⁰ 1 (Maison Silvestre) /

Printer's device on covers and title pages; headpieces; tailpieces.Dates of sales: Pt. 1: Feb. 22-24, 1877; pt. 2: Feb. 25-Mar. 1, 1878; [pt. 3]: Mar. 11, 1878.Colophon: Paris. Imp. de Ch. Noblet, 13, rue Cujas.Part 1: [4], iv, 79, [1] p.; pt. 2: [2], v, [1], 143, [1] p.; pt. 3: [4], ii, 43, [1] p.Parts 1-3 bound in one volume.Part 3 imprint: Paris : Etienne Charavay : Antonin Voisin ; Londres : Frédéric Naylor.Part 3 title: Catalogue des lettres autographes et des documents historiques composant la collection théâtrale de M. Léon Sapin, dont la vente aura lieu ... salle n⁰ 1 (Maison Silvestre), par le ministre de Me. Boulland ... assisté de M. Etienne Charavay ... et de M. A. Voisin, libraire ...1. ptie. Architecture théâtrale. Histoire des théâtres. Almanachs. Législation. Art du comédien. Documents manuscrits. Autographes -- 2. ptie. Opéra. Opéra-comique. Littérature musicale. Danse et ballets. Facéties et satires. Théâtre burlesque. Biographies. Chansonniers. Estampes et dessins. Bibliographie. Documents manuscrits -- [3. ptie.] Catalogue des autographes Sapin.NUC pre-1956Mode of access: Internet