Adam J. Krause
Mar 20, 2019; 39:2291-2300
BehavioralSystemsCognitive

Benjamin E. Reese
Mar 2, 2005; 25:2167-2175
BehavioralSystemsCognitive

Nancy Kanwisher
Jun 1, 1997; 17:4302-4311
Articles

Tatiana Stepanova
Apr 1, 2003; 23:2655-2664
Cellular

Jasper Akerboom
Oct 3, 2012; 32:13819-13840
Cellular

Fiona Doetsch
Jul 1, 1997; 17:5046-5061
Articles

Randy L. Buckner
Feb 11, 2009; 29:1860-1873
Neurobiology of Disease

Matteo Carandini
Nov 1, 1997; 17:8621-8644
Articles

M Steriade
Aug 1, 1993; 13:3252-3265
Articles

A Bragin
Jan 1, 1995; 15:47-60
Articles

Nancy Kanwisher
Jun 1, 1997; 17:4302-4311
Articles

Italian translation of the BIS Press Release on the presentation of the Annual Report (25 June 2017)

Italian translation of the BIS press release about the BIS Quarterly Review, September 2017

Italian translation of the BIS press release about the BIS Quarterly Review, December 2017

Italian translation of the BIS press release about the BIS Quarterly Review, March 2018

Italian translation of the BIS Quarterly Review, March 2018

Italian translation of Annual Economic Report 2018 of the BIS, June 2018 - Le autorità possono fare in modo che l'attuale ripresa economica si mantenga oltre il breve termine avviando riforme strutturali, ridando margine di manovra alle politiche monetarie e di bilancio per affrontare eventuali future minacce, e incoraggiando la pronta attuazione delle riforme regolamentari, scrive la Banca dei Regolamenti Internazionali (BRI) nella sua Relazione economica annuale.

Italian translation of the BIS press release about the BIS Quarterly Review, September 2018

Italian translation of the BIS Quarterly Review, March 2019

Italian version of BIS Press Release - Big tech in finance: opportunities and risks, 23 June 2019

Italian translation of the BIS press release on the presentation of the Annual Economic Report 2019, 30 June 2019.

French version of Press release about Pablo Hernández de Cos appointed as Chairman of Basel Committee on Banking Supervision

Spanish translation of the BIS press release about the BIS Quarterly Review, March 2018

Spanish translation of the BIS Quarterly Review, March 2018

Spanish translation of "Basel III: Finalising post-crisis reforms", December 2017.

Spanish translation of the Press Release on the pre-release of two special chapters of the Annual Economic Report of the BIS, 17 June 2018. Trust is the missing link in today's cryptocurrencies - Cryptocurrencies' model of generating trust limits their potential to replace conventional money, the Bank for International Settlements (BIS) writes in its Annual Economic Report (AER), a new title launched this year.

Spanish translation of press release - the Basel Committee on Banking Supervision is finalising stress-testing principles, reviews ways to stop regulatory arbitrage behaviour, agrees on annual G-SIB list, discusses leverage ratio, crypto-assets, market risk framework and implementation, 20 September 2018.

Spanish translation of "Pillar 3 disclosure requirements - updated framework", December 2018

Spanish translation of the BIS press release about the BIS Quarterly Review, December 2018

Spanish translation of the BIS press release about the BIS Quarterly Review, March 2019

Spanish translation of the BIS Quarterly Review, March 2019

Spanish version of Press release about Pablo Hernández de Cos appointed as Chairman of Basel Committee on Banking Supervision, 7 March 2019. Pablo Hernández de Cos, nombrado Presidente del Comité de Supervisión Bancaria de Basilea.

Discurso del Dr. Agustín Carstens, Director General del Banco de Pagos Internacionales, en la Celebración del 25 Aniversario de la Autonomía del Banco de México, Ciudad de México, 22 de noviembre de 2019.

Edge conditions and the change they drive are fascinating. Some people use the word "margin" because it's at the margin that things change. A situation exists more or less in equilibrium with the rest of its environment until in one way or another the stresses become so great that change happens. We have lots of metaphors, like "tipping point" and "the straw that broke the camel's back."

Oracle and Zoom just entered a deal that for once is more about technological audacity than about dollars -- a partnership to host Zoom on Oracle Cloud Infrastructure. In just a few months -- basically since the beginning of the novel coronavirus pandemic -- Zoom has seen demand for its service grow from about 10 million daily meeting participants to more than 300 million.

You can reduce the story of CRM to a lot of things, especially its many component parts. Social networking, cloud computing and analytics are mentioned often. We don't need an exhaustive list, but if we stop there I think we miss a lot. To me CRM isn't about the parts, although like most people following the industry, I get a modicum of joy when a vendor adds something new to the toolbox.

Speech by Mr Agustín Carstens, General Manager of the BIS, at the Founding Ceremony, Swiss Centre BIS Innovation Hub, Zurich, 8 October 2019.

Original quotes from interview by Mr Agustin Carstens, General Manager of the BIS, with Exame, conducted by Mr Felipe Serrano on 9 October 2019 and published on 24 October 2019.

Interview with Luiz A Pereira da Silva, Deputy General Manager of the BIS, in Central Banking, conducted by Ms Rachael King and published on 16 February 2020.

The cerebellum influences motor control through Purkinje target neurons, which transmit cerebellar output. Such output is required, for instance, for larval zebrafish to learn conditioned fictive swimming. The output cells, called eurydendroid neurons (ENs) in teleost fish, are inhibited by Purkinje cells and excited by parallel fibers. Here, we investigated the electrophysiological properties of glutamatergic ENs labeled by the transcription factor olig2. Action potential firing and synaptic responses were recorded in current clamp and voltage clamp from olig2⁺ neurons in immobilized larval zebrafish (before sexual differentiation) and were correlated with motor behavior by simultaneous recording of fictive swimming. In the absence of swimming, olig2⁺ ENs had basal firing rates near 8 spikes/s, and EPSCs and IPSCs were evident. Comparing Purkinje firing rates and eurydendroid IPSC rates indicated that 1-3 Purkinje cells converge onto each EN. Optogenetically suppressing Purkinje simple spikes, while preserving complex spikes, suggested that eurydendroid IPSC size depended on presynaptic spike duration rather than amplitude. During swimming, EPSC and IPSC rates increased. Total excitatory and inhibitory currents during sensory-evoked swimming were both more than double those during spontaneous swimming. During both spontaneous and sensory-evoked swimming, the total inhibitory current was more than threefold larger than the excitatory current. Firing rates of ENs nevertheless increased, suggesting that the relative timing of IPSCs and EPSCs may permit excitation to drive additional eurydendroid spikes. The data indicate that olig2⁺ cells are ENs whose activity is modulated with locomotion, suiting them to participate in sensorimotor integration associated with cerebellum-dependent learning.

SIGNIFICANCE STATEMENT The cerebellum contributes to movements through signals generated by cerebellar output neurons, called eurydendroid neurons (ENs) in fish (cerebellar nuclei in mammals). ENs receive sensory and motor signals from excitatory parallel fibers and inhibitory Purkinje cells. Here, we report electrophysiological recordings from ENs of larval zebrafish that directly illustrate how synaptic inhibition and excitation are integrated by cerebellar output neurons in association with motor behavior. The results demonstrate that inhibitory and excitatory drive both increase during fictive swimming, but inhibition greatly exceeds excitation. Firing rates nevertheless increase, providing evidence that synaptic integration promotes cerebellar output during locomotion. The data offer a basis for comparing aspects of cerebellar coding that are conserved and that diverge across vertebrates.

Although the etiology of schizophrenia is still unknown, it is accepted to be a neurodevelopmental disorder that results from the interaction of genetic vulnerabilities and environmental insults. Although schizophrenia's pathophysiology is still unclear, postmortem studies point toward a dysfunction of cortical interneurons as a central element. It has been suggested that alterations in parvalbumin-positive interneurons in schizophrenia are the consequence of a deficient signaling through NMDARs. Animal studies demonstrated that early postnatal ablation of the NMDAR in corticolimbic interneurons induces neurobiochemical, physiological, behavioral, and epidemiological phenotypes related to schizophrenia. Notably, the behavioral abnormalities emerge only after animals complete their maturation during adolescence and are absent if the NMDAR is deleted during adulthood. This suggests that interneuron dysfunction must interact with development to impact on behavior. Here, we assess in vivo how an early NMDAR ablation in corticolimbic interneurons impacts on mPFC and ventral hippocampus functional connectivity before and after adolescence. In juvenile male mice, NMDAR ablation results in several pathophysiological traits, including increased cortical activity and decreased entrainment to local gamma and distal hippocampal theta rhythms. In addition, adult male KO mice showed reduced ventral hippocampus-mPFC-evoked potentials and an augmented low-frequency stimulation LTD of the pathway, suggesting that there is a functional disconnection between both structures in adult KO mice. Our results demonstrate that early genetic abnormalities in interneurons can interact with postnatal development during adolescence, triggering pathophysiological mechanisms related to schizophrenia that exceed those caused by NMDAR interneuron hypofunction alone.

SIGNIFICANCE STATEMENT NMDAR hypofunction in cortical interneurons has been linked to schizophrenia pathophysiology. How a dysfunction of GABAergic cortical interneurons interacts with maturation during adolescence has not been clarified yet. Here, we demonstrate in vivo that early postnatal ablation of the NMDAR in corticolimbic interneurons results in an overactive but desynchronized PFC before adolescence. Final postnatal maturation during this stage outspreads the impact of the genetic manipulation toward a functional disconnection of the ventral hippocampal-prefrontal pathway, probably as a consequence of an exacerbated propensity toward hippocampal-evoked depotentiation plasticity. Our results demonstrate a complex interaction between genetic and developmental factors affecting cortical interneurons and PFC function.

One of the first signs of viral infection is body-wide aches and pain. Although this type of pain usually subsides, at the extreme, viral infections can induce painful neuropathies that can last for decades. Neither of these types of pain sensitization is well understood. A key part of the response to viral infection is production of interferons (IFNs), which then activate their specific receptors (IFNRs) resulting in downstream activation of cellular signaling and a variety of physiological responses. We sought to understand how type I IFNs (IFN-α and IFN-β) might act directly on nociceptors in the dorsal root ganglion (DRG) to cause pain sensitization. We demonstrate that type I IFNRs are expressed in small/medium DRG neurons and that their activation produces neuronal hyper-excitability and mechanical pain in mice. Type I IFNs stimulate JAK/STAT signaling in DRG neurons but this does not apparently result in PKR-eIF2α activation that normally induces an anti-viral response by limiting mRNA translation. Rather, type I IFNs stimulate MNK-mediated eIF4E phosphorylation in DRG neurons to promote pain hypersensitivity. Endogenous release of type I IFNs with the double-stranded RNA mimetic poly(I:C) likewise produces pain hypersensitivity that is blunted in mice lacking MNK-eIF4E signaling. Our findings reveal mechanisms through which type I IFNs cause nociceptor sensitization with implications for understanding how viral infections promote pain and can lead to neuropathies.

SIGNIFICANCE STATEMENT It is increasingly understood that pathogens interact with nociceptors to alert organisms to infection as well as to mount early host defenses. Although specific mechanisms have been discovered for diverse bacterial and fungal pathogens, mechanisms engaged by viruses have remained elusive. Here we show that type I interferons, one of the first mediators produced by viral infection, act directly on nociceptors to produce pain sensitization. Type I interferons act via a specific signaling pathway (MNK-eIF4E signaling), which is known to produce nociceptor sensitization in inflammatory and neuropathic pain conditions. Our work reveals a mechanism through which viral infections cause heightened pain sensitivity

FAO Director-General José Graziano da Silva underlined his firm belief that a hunger-free world is possible "within our lifetimes," during high-level talks in New York. "The Zero Hunger Challenge calls for something new – something bold, but long overdue," he said. It was a "decisive global commitment to end hunger, eliminate childhood stunting, make all food systems sustainable, eradicate rural poverty, [...]