Chaos and Synchronized Chaos in an Earthquake Model

We show that chaos is present in the symmetric two-block Burridge-Knopoff model for earthquakes. This is in contrast with previous numerical studies, but in agreement with experimental results. In this system, we have found a rich dynamical behavior with an unusual route to chaos. In the three-block system, we see the appearance of synchronized chaos, showing that this concept can have potential applications in the field of seismology.Comment: To appear in Physical Review Letters (13 pages, 6 figures

Impact of the background region of interest in the relative renal function

Renal scintigraphy with 99mTc-dimercaptosuccinic acid (99mTc-DMSA) is performed with the aim of detect cortical abnormalities related to urinary tract infection and accurately quantify relative renal function (RRF). For this quantitative assessment Nuclear Medicine Technologist should draw regions of interest (ROI) around each kidney (KROI) and peri-renal background (BKG) ROI, although, controversy still exists about BKG-ROI. The aim of this work was to evaluate the effect of the normalization procedure, number and location of BKG-ROI on the RRF in 99mTc-DMSA scintigraphy

Neuronal deletion of GSK3beta increases microtubule speed in the growth cone and enhances axon regeneration via CRMP-2 and independently of MAP1B and CLASP2

BACKGROUND: In the adult central nervous system, axonal regeneration is abortive. Regulators of microtubule dynamics have emerged as attractive targets to promote axonal growth following injury as microtubule organization is pivotal for growth cone formation. In this study, we used conditioned neurons with high regenerative capacity to further dissect cytoskeletal mechanisms that might be involved in the gain of intrinsic axon growth capacity. RESULTS: Following a phospho-site broad signaling pathway screen, we found that in conditioned neurons with high regenerative capacity, decreased glycogen synthase kinase 3β (GSK3β) activity and increased microtubule growth speed in the growth cone were present. To investigate the importance of GSK3β regulation during axonal regeneration in vivo, we used three genetic mouse models with high, intermediate or no GSK3β activity in neurons. Following spinal cord injury, reduced GSK3β levels or complete neuronal deletion of GSK3β led to increased growth cone microtubule growth speed and promoted axon regeneration. While several microtubule-interacting proteins are GSK3β substrates, phospho-mimetic collapsin response mediator protein 2 (T/D-CRMP-2) was sufficient to decrease microtubule growth speed and neurite outgrowth of conditioned neurons and of GSK3β-depleted neurons, prevailing over the effect of decreased levels of phosphorylated microtubule-associated protein 1B (MAP1B) and through a mechanism unrelated to decreased levels of phosphorylated cytoplasmic linker associated protein 2 (CLASP2). In addition, phospho-resistant T/A-CRMP-2 counteracted the inhibitory myelin effect on neurite growth, further supporting the GSK3β-CRMP-2 relevance during axon regeneration. CONCLUSIONS: Our work shows that increased microtubule growth speed in the growth cone is present in conditions of increased axonal growth, and is achieved following inactivation of the GSK3β-CRMP-2 pathway, enhancing axon regeneration through the glial scar. In this context, our results support that a precise control of microtubule dynamics, specifically in the growth cone, is required to optimize axon regrowth

Moduladores CFTR no tratamento da fibrose quística

Trabalho Final do Curso de Mestrado Integrado em Medicina, Faculdade de Medicina, Universidade de Lisboa, 2016A Fibrose Quística é a doença autossómica recessiva mais prevalente na Europa e é causada por uma mutação na proteína CFTR (Cystic Fibrosis Transmembrane Conductance Regulator - regulador da condutância transmembranar da Fibrose Quística), que codifica um canal de cloro. Já foram descritas mais de 1900 mutações causadoras desta doença, motivo pelo qual é uma boa candidata a medicina personalizada. Existem duas abordagens para corrigir o defeito básico: a correção do defeito genético, sem resultados até à data, e a correção do defeito molecular, que tem mostrado resultados promissores com dois fármacos já aprovados - ivacaftor para mutações classe III e uma mutação classe IV e ivacaftor+lumafactor para a mutação mais frequente, F508del, da classe II. Outras moléculas encontram-se ainda em estudo, como o caso do ataluren e do VX-661, no âmbito de mutações classe I e II, respetivamente. Tendo em conta a exigência e complexidade das terapêuticas anteriormente existentes para esta doença, as alternativas revistas neste artigo representam um futuro promissor no âmbito da Fibrose Quística.Cystic fibrosis is the most prevalent autosomal recessive disease in Europe. It’s caused by a mutation in the CFTR (cystic fibrosis transmembrane conductance regulator) protein that codifies a chloride channel. More than 1900 mutations causing this disease have been identified, which is why it is a good candidate for personalized medicine. There are two approaches for correcting the basic defect: correction of the genetic defect, with no results so far, and the correction of the molecular defect, with promising results with two substances approved to date – ivacaftor, for class III mutations and one class IV mutation and ivacaftor+lumacaftor for the most common mutation, F508del, a class II mutation. Other molecules are being studied, for example, ataluren and VX-661, aiming at correcting class I and II mutations, respectively. Regarding the fact that the existing treatments are complex and a burden for the patient, the alternative drugs reviewed in this article represent a promising future in the Cystic Fibrosis field

General (legislative) elections in Japan

Polis. - ISSN 0872-8208. - S. 2, n. 4 (Julho-Dezembro 2021). - p. 235-238