Université libre de Bruxelles

About: Université libre de Bruxelles is a education organization based out in Brussels, Belgium. It is known for research contribution in the topics: Population & Breast cancer. The organization has 24974 authors who have published 56969 publications receiving 2084303 citations. The organization is also known as: ULB.

Does corruption grease or sand the wheels of growth

Abstract: This paper assesses the relationship between the impact of corruption on growth and investment and the quality of governance in a sample of 63 to 71 countries between 1970 and 1998. Like previous studies, we find a negative effect of corruption on both growth and investment. Unlike previous studies, we find that corruption has a negative impact on growth independently from its impact on investment. These impacts are, however, different depending on the quality of governance. They tend to worsen when indicators of the quality of governance deteriorate. This supports the “sand the wheels” view on corruption and contradicts the “grease the wheels” view, which postulates that corruption may help compensate bad governance.

Observation of a Localized Flat-Band State in a Photonic Lieb Lattice

Abstract: We demonstrate the first experimental realization of a dispersionless state, in a photonic Lieb lattice formed by an array of optical waveguides. This engineered lattice supports three energy bands, including a perfectly flat middle band with an infinite effective mass. We analyze, both experimentally and theoretically, the evolution of well-prepared flat-band states, and show their remarkable robustness, even in the presence of disorder. The realization of flat-band states in photonic lattices opens an exciting door towards quantum simulation of flat-band models in a highly controllable environment.

Inhibition of the glucose transporter SGLT2 with dapagliflozin in pancreatic alpha cells triggers glucagon secretion

Abstract: Type 2 diabetes (T2D) is characterized by chronic hyperglycemia resulting from a deficiency in insulin signaling, because of insulin resistance and/or defects in insulin secretion; it is also associated with increases in glucagon and endogenous glucose production (EGP). Gliflozins, including dapagliflozin, are a new class of approved oral antidiabetic agents that specifically inhibit sodium-glucose co-transporter 2 (SGLT2) function in the kidney, thus preventing renal glucose reabsorption and increasing glycosuria in diabetic individuals while reducing hyperglycemia. However, gliflozin treatment in subjects with T2D increases both plasma glucagon and EGP by unknown mechanisms. In spite of the rise in EGP, T2D patients treated with gliflozin have lower blood glucose levels than those receiving placebo, possibly because of increased glycosuria; however, the resulting increase in plasma glucagon levels represents a possible concerning side effect, especially in a patient population already affected by hyperglucagonemia. Here we demonstrate that SGLT2 is expressed in glucagon-secreting alpha cells of the pancreatic islets. We further found that expression of SLC5A2 (which encodes SGLT2) was lower and glucagon (GCG) gene expression was higher in islets from T2D individuals and in normal islets exposed to chronic hyperglycemia than in islets from non-diabetics. Moreover, hepatocyte nuclear factor 4-α (HNF4A) is specifically expressed in human alpha cells, in which it controls SLC5A2 expression, and its expression is downregulated by hyperglycemia. In addition, inhibition of either SLC5A2 via siRNA-induced gene silencing or SGLT2 via dapagliflozin treatment in human islets triggered glucagon secretion through KATP channel activation. Finally, we found that dapagliflozin treatment further promotes glucagon secretion and hepatic gluconeogenesis in healthy mice, thereby limiting the decrease of plasma glucose induced by fasting. Collectively, these results identify a heretofore unknown role of SGLT2 and designate dapagliflozin an alpha cell secretagogue.

Can sequence learning be implicit? New evidence with the process dissociation procedure

Abstract: Can we learn without awareness? Although this issue has been extensively explored through studies of implicit learning, there is currently no agreement about the extent to which knowledge can be acquired and projected onto performance in an unconscious way. The controversy, like that surrounding implicit memory, seems to be at least in part attributable to unquestioned acceptance of the unrealistic assumption that tasks are process-pure—that is, that a given task exclusively involves either implicit or explicit knowledge. Methods such as the process dissociation procedure (PDP, Jacoby, 1991) have been developed to overcome the conceptual limitations of the process purity assumption but have seldom been used in the context of implicit learning research. In this paper, we show how the PDP can be applied to a free generation task so as to disentangle explicit and implicit sequence learning. Our results indicate that subjects who are denied preparation to the next stimulus nevertheless exhibit knowledge of the sequence through their reaction time performance despite remaining unable (1) to project this knowledge in a recognition task and (2) to refrain from expressing their knowledge when specifically instructed to do so. These findings provide strong evidence that sequence learning can be unconscious.

Possible Future Issues in the Treatment of Glioblastomas: Special Emphasis on Cell Migration and the Resistance of Migrating Glioblastoma Cells to Apoptosis

Abstract: PURPOSE: The present review aims to emphasize that malignant gliomas are characterized by the diffuse invasion of distant brain tissue by a myriad of single migrating cells that exhibit decreased levels of apoptosis (programmed cell death type I), thus a resistance to cytotoxic insult. METHODS: The present review surveys the molecular mechanisms of migration in malignant gliomas and potential issues arising from treatments, in addition to relationships between glioma cell migration and resistance to apoptosis in terms of the molecular signaling pathways. RESULTS: Clinical and experimental data demonstrate that glioma cell migration is a complex combination of multiple molecular processes, including the alteration of tumor cell adhesion to a modified extracellular matrix, the secretion of proteases by the cells, and modifications to the actin cytoskeleton. Intracellular signaling pathways involved in the acquisition of resistance to apoptosis by migrating glioma cells concern PI3K, Akt, mTOR, NF-kappaB, and autophagy (programmed cell death type II). CONCLUSION: A number of signaling pathways can be constitutively activated in migrating glioma cells, thus rendering these cells resistant to cytotoxic insults. However, these pathways are not all constitutively activated at the same time in any one glioma. Particular inhibitors should therefore only be chosen if the target is present in the tumor tissue, but this is only possible if individual patients are submitted to the molecular profiling of their tumors before undergoing any treatment to combat their migratory glioma cells. Specific antimigratory compounds should be added to conventional radio- and/or chemotherapy.