Does the Intensity of Prudential Regulation Affect Banks? Evidence from the 2007-2009 Crises

The main objective of this research is to gather empirical evidence on the effects of more or less stringency and more or less risk sensitivity in regulatory capital requirements on the observed behaviour of European banks during the initial years of the financial crisis. To do so, we use the indices built in Argimón and Ruiz (2010), which capture such characteristics of capital regulation. We test their incidence using changes in yearly data for individual banks for 25 countries of the European Union covering the period 2007-2009. Our results show that more stringency and risk sensitivity in capital regulation resulted in higher capital increases, with limited effect on risk taking. However, for well capitalized banks, higher risk sensitivity resulted in higher capital and higher risk, thus requiring striking the right balance, so as to lead to increased stability

Inflammatory Response of Ischemic Tolerance in Circulating Plasma : Preconditioning-Induced by Transient Ischemic Attack (TIA) Phenomena in Acute Ischemia Patients (AIS)

Ischemic tolerance (IT) refers to a state where cells are resistant to the damaging effects caused by periods of ischemia. In a clinical scenario, the IT phenomenon would be activated by a recent transient ischemic attack (TIA) before an ischemic stroke (IS). The characterization of inflammatory protein expression patterns will contribute to improved understanding of IT. A total of 477 IS patients from nine hospitals, recruited between January 2011 and January 2016, were included in the current study and divided in three groups: 438 (91.9%) patients without previous TIA (group 1), 22 (4.6%) patients who suffered TIA 24 h before IS (group 2), and 17 (3.5%) patients who suffered TIA between 24 h and 7 days prior to IS (group 3). An inflammatory biomarker panel (IL-6, NT-proBNP, hsCRP, hs-Troponin, NSE, and S-100b) on plasma and a cytokine antibody array was performed to achieve the preconditioning signature potentially induced by TIA phenomena. Primary outcome was modified rankin scale (mRs) score at 90 days. Recent previous TIA was associated with better clinical outcome at 90 days (median mRS of group 1: 2.0 [1.0-4.0]; group 2: 2.0 [0.0-3.0]; group 3: 1.0 [0-2.5]; p = 0.086) and smaller brain lesion (group 1: 3.7 [0.7-18.3]; group 2: 0.8 [0.3-8.9]; group 3: 0.6 [0.1-5.5] mL; p = 0.006). All inflammation biomarkers were down regulated in the groups of recent TIA prior to IS compared to those who did not suffer a TIA events. Moreover, a cytokine antibody array revealed 30 differentially expressed proteins between the three groups. Among them, HRG1-alpha (Fold change 74.4 between group 1 and 2; 74.2 between group 1 and 3) and MAC-1 (Fold change 0.05 between group 1 and 2; 0.06 between group 1 and 3) expression levels would better stratify patients with TIA 7 days before IS. These two proteins showed an earlier inflammation profile that was not detectable by the biomarker panel. Inflammatory pathways were activated by transient ischemic attack, however the period of time between this event and a further ischemic stroke could be determined by a protein signature that would contribute to define the role of ischemic tolerance induced by TIA

Behavioral characterization of a mouse model overexpressing DSCR1/ RCAN1

DSCR1/ RCAN1 is a chromosome 21 gene found to be overexpressed in the brains of Down syndrome (DS) and postulated as a good candidate to contribute to mental disability. However, even though Rcan1 knockout mice have pronounced spatial learning and memory deficits, the possible deleterious effects of its overexpression in DS are not well understood. We have generated a transgenic mouse model overexpressing DSCR1/RCAN1 in the brain and analyzed the effect of RCAN1 overexpression on cognitive function. TgRCAN1 mice present a marked disruption of the learning process in a visuo-spatial learning task. However, no significant differences were observed in the performance of the memory phase of the test (removal session) nor in a step-down passive avoidance task, thus suggesting that once learning has been established, the animals are able to consolidate the information in the longer term

Fostering Sustainable Innovation through Creative Destruction Theory

The current information age is modelled on the advancement of innovative mindset of creative thinkers, championed through means associated with transformative technologies embodied on events like, high speed internet and payment system, thereby making it possible for transactions to be dealt with almost instantaneously. Such developments are essentially vital, given its prospect for championing growth rate and dynamism in the world economy and also, the need to ensure living conditions are adequately satisfied, particularly in the direction of the Sustainable Development Goals (SDG) earmarked for full implementation in the year 2030. The concept of innovation is widely used in all walks of life - the effort of Schumpeter’s paradoxical term, “creative destruction” became highly prominent in the 1950s, which many economists in recent time have endeavoured to linked with free market economics (Cozzi and Galli, 2019; Benigno and Fornaro, 2018). Creative destruction as proposed by Schumpeter, and also explained by Alm and Cox (Online) is essentially facts about capitalism, which is thought to be a shorthand description of free market’s messy way of delivering progress

Lipidomic signature of stroke recurrence after transient ischemic attack

Abstract While TIA patients have transient symptoms, they should not be underestimated, as they could have an underlying pathology that may lead to a subsequent stroke: stroke recurrence (SR). Previously, it has been described the involvement of lipids in different vascular diseases. The aim of the current study was to perform a lipidomic analysis to identify differences in the lipidomic profile between patients with SR and patients without. Untargeted lipidomic analysis was performed in plasma samples of 460 consecutive TIA patients recruited < 24 h after the onset of symptoms. 37 (8%) patients suffered SR at 90 days. Lipidomic profiling disclosed 7 lipid species differentially expressed between groups: 5 triacylglycerides (TG), 1 diacylglyceride (DG), and 1 alkenyl-PE (plasmalogen) [specifically, TG(56:1), TG(63:0), TG(58:2), TG(50:5), TG(53:7, DG(38:5)) and PE(P-18:0/18:2)]. 6 of these 7 lipid species belonged to the glycerolipid family and a plasmalogen, pointing to bioenergetics pathways, as well as oxidative stress response. In this context, it was proposed the PE(P-18:0/18:2) as potential biomarker of SR condition. The observed changes in lipid patterns suggest pathophysiological mechanisms associated with lipid droplets metabolism and antioxidant protection that is translated to plasma level as consequence of a more intensive or high-risk ischemic condition related to SR

Prevalence of intestinal helminths, anemia, and malnutrition in Paucartambo, Peru

Objective. To evaluate the prevalence of soil-transmitted helminth infections, anemia, and malnutrition among children in the Paucartambo province of Cusco region, Peru, in light of demographic, socio-economic, and epidemiologic contextual factors. Methods. Children from three to twelve years old from six communities in Huancarani district in the highlands of Peru were evaluated for helminth infections, anemia, and nutritional status. Data collected included demographic variables, socioeconomic status, exposures, complete blood counts, and direct and sedimentation stool tests. Results. Of 240 children analyzed, 113 (47%) were infected with one or more parasites. Giardia (27.5%) and Fasciola (9.6%) were the most commonly identified organisms. Eosinophilia was encountered in 21% of the children. Anemia (48.8%) was associated with age (3-4 vs 5-12 years old; odds ratio (OR): 5.86; 95% confidence interval (CI): 2.81-12.21). Underweight (10%) was associated with male sex (OR: 5.97; CI: 1.12-31.72), higher eosinophil count (OR: 4.67; CI: 1.31-16.68) and education of the mother (OR: 0.6; CI: 0.4-0.9). Stunting (31.3%) was associated with education of the mother (OR: 0.83; CI: 0.72-0.95); wasting (2.7%) was associated with higher eosinophil count (OR: 2.75; CI: 1.04-7.25). Conclusions. Anemia and malnutrition remain significant problems in the Peruvian highlands. These findings suggest that demographic factors, socio-economic status, and possibly parasitic infections intertwine to cause these health problems

The EMBO Journal / Hypothalamic CNTF volume transmission shapes cortical noradrenergic excitability upon acute stress

Stressinduced cortical alertness is maintained by a heightened excitability of noradrenergic neurons innervating, notably, the prefrontal cortex. However, neither the signaling axis linking hypothalamic activation to delayed and lasting noradrenergic excitability nor the molecular cascade gating noradrenaline synthesis is defined. Here, we show that hypothalamic corticotropinreleasing hormonereleasing neurons innervate ependymal cells of the 3rd ventricle to induce ciliary neurotrophic factor (CNTF) release for transport through the brain's aqueductal system. CNTF binding to its cognate receptors on norepinephrinergic neurons in the locus coeruleus then initiates sequential phosphorylation of extracellular signalregulated kinase 1 and tyrosine hydroxylase with the Ca2+sensor secretagogin ensuring activity dependence in both rodent and human brains. Both CNTF and secretagogin ablation occlude stressinduced cortical norepinephrine synthesis, ensuing neuronal excitation and behavioral stereotypes. Cumulatively, we identify a multimodal pathway that is ratelimited by CNTF volume transmission and poised to directly convert hypothalamic activation into longlasting cortical excitability following acute stress. Synopsis A multimodal signaling pathway initiated by CRH neurons using aqueductal CNTF volume transmission explains how acute stress is communicated from the hypothalamus to the cerebral cortex. Hypothalamic CRH output gates cortical norepinephrine (NE) signaling upon stress. CRH neurons induce ciliary neurotrophic factor (CNTF) release from ventricular ependyma. CNTF primes NE neurons by volume transmission. CNTF signaling recruits secretagogin to activate tyrosine hydroxylase for NE production. CNTF infusion or driving secretagogin+ NE neuron excitability accentuates stressinduced freezing.(VLID)340657