The Emergence of Cooperative Playing Routines: Optimality and Learning

We investigate the emergence of (optimal and suboptimal) behavioural routines in the context of a cooperative game. In particular we construct a search model of the gradient descent type for the optimization of 'static' and 'dynamic' playing routines. That optimality study sets the basis for the analysis of the dynamics and modelling of routine learning. In the last part of the paper we propose a learning heuristics for the development of routinized behaviour on the basis of a simple network model of the subject player

Mössbauer Study Of Hydrogenated Amorphous Germanium-tin Thin-film Alloys

This work reports on the structure of defects around Sn atoms in amorphous germanium-tin alloys deposited by the rf sputtering of compound targets. The influence of atomic hydrogen on the structure of such defects is reported for the first time. The samples were analyzed by Rutherford backscattering spectrometry and conversion electron Mössbauer spectroscopy. The main conclusion of this research is that, besides the known substitutional position of Sn atoms in the a-Ge network, a new Sn bonding configuration appears, which may be at the origin of the degradation of the optoelectronic properties of the alloy found experimentally. This new configuration is an octahedrally coordinated Sn atom resulting from the trapping of Ge vacancies by Sn atoms, the energetically favored final site being the tin atom in the center of the Ge relaxed divacancy.6652083209

Cell Senescence, Multiple Organelle Dysfunction and Atherosclerosis

Our research is supported by national funds through FCT- Fundação para a Ciência e Tecnologia and by PROGRAMAS DE ATIVIDADES CONJUNTAS (PAC) grant numbers PTDC/MED-PAT/29395/2017 and N◦3/SAICT/2015. ARAM is supported by the CEECIND/01006/2017, funded by FCT.Atherosclerosis is an age-related disorder associated with long-term exposure to cardiovascular risk factors. The asymptomatic progression of atherosclerotic plaques leads to major cardiovascular diseases (CVD), including acute myocardial infarctions or cerebral ischemic strokes in some cases. Senescence, a biological process associated with progressive structural and functional deterioration of cells, tissues and organs, is intricately linked to age-related diseases. Cell senescence involves coordinated modifications in cellular compartments and has been demonstrated to contribute to different stages of atheroma development. Senescence-based therapeutic strategies are currently being pursued to treat and prevent CVD in humans in the near-future. In addition, distinct experimental settings allowed researchers to unravel potential approaches to regulate anti-apoptotic pathways, facilitate excessive senescent cell clearance and eventually reverse atherogenesis to improve cardiovascular function. However, a deeper knowledge is required to fully understand cellular senescence, to clarify senescence and atherogenesis intertwining, allowing researchers to establish more effective treatments and to reduce the cardiovascular disorders' burden. Here, we present an objective review of the key senescence-related alterations of the major intracellular organelles and analyze the role of relevant cell types for senescence and atherogenesis. In this context, we provide an updated analysis of therapeutic approaches, including clinically relevant experiments using senolytic drugs to counteract atherosclerosis.publishersversionpublishe

Lysosome (Dys)function in Atherosclerosis—A Big Weight on the Shoulders of a Small Organelle

Funding: This research was supported by the research project PTDC/MEDPAT/29395/2017, financed by national funds through the Fundação para a Ciência e Tecnologia (FCT) and by PROGRAMAS DE ATIVIDADES CONJUNTAS (PAC), Reference: No. 03/SAICT/2015. AM was supported by the CEECIND/01006/2017, funded by FCT. This manuscript was supported by the LYSOCIL project, which has received funding from the European Union’s Horizon 2020 Research and Innovation Programme under grant agreement no. 811087.Atherosclerosis is a progressive insidious chronic disease that underlies most of the cardiovascular pathologies, including myocardial infarction and ischemic stroke. The malfunctioning of the lysosomal compartment has a central role in the etiology and pathogenesis of atherosclerosis. Lysosomes are the degradative organelles of mammalian cells and process endogenous and exogenous substrates in a very efficient manner. Dysfunction of these organelles and consequent inefficient degradation of modified low-density lipoproteins (LDL) and apoptotic cells in atherosclerotic lesions have, therefore, numerous deleterious consequences for cellular homeostasis and disease progression. Lysosome dysfunction has been mostly studied in the context of the inherited lysosomal storage disorders (LSDs). However, over the last years it has become increasingly evident that the consequences of this phenomenon are more far-reaching, also influencing the progression of multiple acquired human pathologies, such as neurodegenerative diseases, cancer, and cardiovascular diseases (CVDs). During the formation of atherosclerotic plaques, the lysosomal compartment of the various cells constituting the arterial wall is under severe stress, due to the tremendous amounts of lipoproteins being processed by these cells. The uncontrolled uptake of modified lipoproteins by arterial phagocytic cells, namely macrophages and vascular smooth muscle cells (VSMCs), is the initial step that triggers the pathogenic cascade culminating in the formation of atheroma. These cells become pathogenic “foam cells,” which are characterized by dysfunctional lipid-laden lysosomes. Here, we summarize the current knowledge regarding the origin and impact of the malfunctioning of the lysosomal compartment in plaque cells. We further analyze how the field of LSD research may contribute with some insights to the study of CVDs, particularly how therapeutic approaches that target the lysosomes in LSDs could be applied to hamper atherosclerosis progression and associated mortality.publishersversionpublishe

Acousto-optic modulation in a microstructured plastic optical fibre Bragg grating

The present work addresses the control of the mPOF Bragg grating spectrum properties through acousto-optic modulation. For the first time, the interaction of a flexural acoustic wave, generated by longitudinal excitation of different frequencies, with the Bragg grating will be presented. Also it will be demonstrated the quasi linear relationship between PZT load and maximum reflected power/ 3dB bandwidth of the reflected spectrum

Exciton G Factor Of Type-ii Inp Gaas Single Quantum Dots

We investigated the magneto-optical properties of type-II InP GaAs quantum dots using single-dot spectroscopy. The emission energy from individual dots presents a quadratic diamagnetic shift and a linear Zeeman splitting as a function of magnetic fields up to 10 T, as previously observed for type-I systems. We analyzed the in-plane localization of the carriers using the diamagnetic shift results. The values for the exciton g factor obtained for a large number of a InP GaAs dots are mainly constant, independent of the emission energy, and therefore, of the quantum dot dimensions. The result is attributed to the weak confinement of the holes in type-II InP GaAs quantum dots. © 2006 The American Physical Society.733Toda, Y., Shinomori, S., Suzuki, K., Arakawa, Y., (1998) Appl. Phys. Lett., 73, p. 517. , APPLAB 0003-6951 10.1063/1.121919Bayer, M., Kuther, A., Schäfer, F., Reithmaier, J.P., Forchel, A., (1999) Phys. Rev. B, 60, p. 8481. , PRBMDO. 0163-1829. 10.1103/PhysRevB.60.R8481Sugisaki, M., Ren, H.-W., Nishi, K., Sugou, S., Okuno, T., Masumoto, Y., (1998) Physica B, 256-258, p. 169. , PHYBE3 0921-4526Kotlyar, R., Reinecke, T.L., Bayer, M., Forchel, A., (2001) Phys. Rev. B, 63, p. 085310. , PRBMDO 0163-1829 10.1103/PhysRevB.63.085310Ribeiro, E., Govorov, A.O., Carvalho Jr., W., Medeiros-Ribeiro, G., (2004) Phys. Rev. Lett., 92, p. 126402. , PRLTAO 0031-9007 10.1103/PhysRevLett.92.126402Janssens, K.L., Partoens, B., Peeters, F.M., (2002) Phys. Rev. B, 66, p. 075314. , PRBMDO 0163-1829 10.1103/PhysRevB.66.075314Kalameitsev, A.B., Kovalev, V.M., Govorov, A.O., (1989) JETP Lett., 68, p. 669. , JTPLA2 0021-3640 10.1134/1.567926Sugisaki, M., Ren, H.W., Nair, S.V., Nishi, K., Masumoto, Y., (2002) Phys. Rev. B, 66, p. 235309. , PRBMDO 0163-1829 10.1103/PhysRevB.66.235309Godoy, M.P.F., Nakaema, M.K.K., Iikawa, F., Carvalho Jr., W., Ribeiro, E., Gobby, A.L., (2004) Rev. Sci. Instrum., 75, p. 1947. , RSINAK 0034-6748 10.1063/1.1753090Walck, S.N., Reinecke, T.L., (1998) Phys. Rev. B, 57, p. 9088. , PRBMDO 0163-1829 10.1103/PhysRevB.57.9088Laheld, U.E.H., Pedersen, F.B., Hemmer, P.C., (1993) Phys. Rev. B, 48, p. 4659. , PRBMDO 0163-1829 10.1103/PhysRevB.48.4659Bastard, G., Mendez, E.E., Chang, L.L., Esaki, L., (1982) Phys. Rev. B, 26, p. 1974. , PRBMDO 0163-1829 10.1103/PhysRevB.26.1974Nakaoka, T., Saito, T., Tatebayashi, J., Arakawa, Y., (2004) Phys. Rev. B, 70, p. 235337. , PRBMDO 0163-1829 10.1103/PhysRevB.70.235337Yugova, I.A., Ya. Gerlovin, I., Davydov, V.G., Ignatiev, I.V., Kozin, I.E., Ren, H.W., Sugisaki, M., Masumoto, Y., (2002) Phys. Rev. B, 66, p. 235309. , PRBMDO 0163-1829 10.1103/PhysRevB.66.235309Willmann, F., Suga, S., Dreybrodt, W., Cho, K., (1974) Solid State Commun., 14, p. 783. , SSCOA4 0038-1098Landi, S.M., Tribuzy, C.V.B., Souza, P.L., Butendeich, R., Bittencourt, A.C., Marques, G.E., (2003) Phys. Rev. B, 67, p. 085304. , PRBMDO 0163-1829 10.1103/PhysRevB.67.08530

Gcase and limp2 abnormalities in the liver of niemann pick type c mice

Funding Information: This work was supported by the NWO-Building Blocks of Life: GlcCer grant to J.M.F.G.A: BBOL-2007247202. Publisher Copyright: © 2021 by the authors. Licensee MDPI, Basel, Switzerland.The lysosomal storage disease Niemann–Pick type C (NPC) is caused by impaired cholesterol efflux from lysosomes, which is accompanied by secondary lysosomal accumulation of sph-ingomyelin and glucosylceramide (GlcCer). Similar to Gaucher disease (GD), patients deficient in glucocerebrosidase (GCase) degrading GlcCer, NPC patients show an elevated glucosylsphingosine and glucosylated cholesterol. In livers of mice lacking the lysosomal cholesterol efflux transporter NPC1, we investigated the expression of established biomarkers of lipid-laden macrophages of GD patients, their GCase status, and content on the cytosol facing glucosylceramidase GBA2 and lysoso-mal integral membrane protein type B (LIMP2), a transporter of newly formed GCase to lysosomes. Livers of 80-week-old Npc1−/− mice showed a partially reduced GCase protein and enzymatic activity. In contrast, GBA2 levels tended to be reciprocally increased with the GCase deficiency. In Npc1−/− liver, increased expression of lysosomal enzymes (cathepsin D, acid ceramidase) was observed as well as increased markers of lipid-stressed macrophages (GPNMB and galectin-3). Im-munohistochemistry showed that the latter markers are expressed by lipid laden Kupffer cells. Earlier reported increase of LIMP2 in Npc1−/− liver was confirmed. Unexpectedly, immunohistochemistry showed that LIMP2 is particularly overexpressed in the hepatocytes of the Npc1−/− liver. LIMP2 in these hepatocytes seems not to only localize to (endo)lysosomes. The recent recognition that LIMP2 harbors a cholesterol channel prompts the speculation that LIMP2 in Npc1−/− hepatocytes might mediate export of cholesterol into the bile and thus protects the hepatocytes.publishersversionpublishe

potential for soil health improvement anwd plant growth promotion

Funding text: This work was supported by funds from Camões, Instituto da Cooperação e da Língua and Fundação para a Ciência e a Tecnologia through the research unit UIDB/00239/2020 (CEF), the PhD grant SFRH/BD/113951/2015 (Ivete Sandra Maquia), and the contribution to the International Rice Research Institute.(1) Aims: Assessing bacterial diversity and plant-growth-promoting functions in the rhizosphere of the native African trees Colophospermum mopane and Combretum apiculatum in three landscapes of the Limpopo National Park (Mozambique), subjected to two fire regimes. (2) Methods: Bacterial communities were identified through Illumina Miseq sequencing of the 16S rRNA gene amplicons, followed by culture dependent methods to isolate plant growth-promoting bacteria (PGPB). Plant growth-promoting traits of the cultivable bacterial fraction were further analyzed. To screen for the presence of nitrogen-fixing bacteria, the promiscuous tropical legume Vigna unguiculata was used as a trap host. The taxonomy of all purified isolates was genetically verified by 16S rRNA gene Sanger sequencing. (3) Results: Bacterial community results indicated that fire did not drive major changes in bacterial abundance. However, culture-dependent methods allowed the differentiation of bacterial communities between the sampled sites, which were particularly enriched in Proteobacteria with a wide range of plant-beneficial traits, such as plant protection, plant nutrition, and plant growth. Bradyrhizobium was the most frequent symbiotic bacteria trapped in cowpea nodules coexisting with other endophytic bacteria. (4) Conclusion: Although the global analysis did not show significant differences between landscapes or sites with different fire regimes, probably due to the fast recovery of bacterial communities, the isolation of PGPB suggests that the rhizosphere bacteria are driven by the plant species, soil type, and fire regime, and are potentially associated with a wide range of agricultural, environmental, and industrial applications. Thus, the rhizosphere of African savannah ecosystems seems to be an untapped source of bacterial species and strains that should be further exploited for bio-based solutions.publishersversionpublishe