An ABS control logic based on wheel force measurement

The paper presents an anti-lock braking system (ABS) control logic based on the measurement of the longitudinal forces at the hub bearings. The availability of force information allows to design a logic that does not rely on the estimation of the tyre-road friction coefficient, since it continuously tries to exploit the maximum longitudinal tyre force. The logic is designed by means of computer simulation and then tested on a specific hardware in the loop test bench: the experimental results confirm that measured wheel force can lead to a significant improvement of the ABS performances in terms of stopping distance also in the presence of road with variable friction coefficien

Potential for Phototrophy in Venus' Clouds

We show that solar irradiances calculated across Venus clouds support the potential for Earth-like phototrophy and that treatment of Venus aerosols containing neutralized sulfuric acid favor a habitable zone. The phototrophic potential of Venus atmosphere was assessed by calculating irradiances (200-2000 nm, 15 deg solar zenith angle, local noon) using a radiative transfer model that accounted for absorption and scattering by the major and minor atmospheric constituents. Comparisons to Earths surface (46 W m-2, 280-400 nm) suggest that Venus middle and lower clouds receive 87% less normalized UV flux (6-7 W m-2) across 200-400 nm, yet similar normalized photon flux densities (4400-6200 micromol m2 s-1) across 350-1200 nm. Further, Venus signature phototrophic windows and subwindows overlap with the absorption profiles of several photosynthetic pigments, especially bacteriochlorophyll b from intact cells and phycocyanin. Therefore, Venus light, with limited UV flux in the middle and lower clouds, is likely quite favorable for phototrophy. We additionally present interpretations to refractive index and radio occultation measures for Venus aerosols that suggest the presence of lower sulfuric abundances and/or neutralized forms of sulfuric acid, such as ammonium bisulfate. Under these considerations, the aerosols in Venus middle clouds could harbor water activities (0.6) and buffered acidities (Hammett acidity factor, H0 -0.1 to -1.5) that lie within the limits of acidic cultivation (H0 -0.4) and are tantalizingly close to the limits of oxygenic photosynthesis (H0 0.1). Together, these photophysical and chemical considerations support a potential for phototrophy in Venus clouds

Meis1a suppresses differentiation by G-CSF and promotes proliferation by SCF: Potential mechanisms of cooperativity with Hoxa9 in myeloid leukemia

Hoxa9 and Meis1a are homeodomain transcription factors that heterodimerize on DNA and are down-regulated during normal myeloid differentiation. Hoxa9 and Meis1a cooperate to induce acute myeloid leukemia (AML) in mice, and are coexpressed in human AML. Despite their cooperativity in leukemogenesis, we demonstrated previously that retroviral expression of Hoxa9 alone—in the absence of coexpressed retroviral Meis1 or of expression of endogenous Meis genes—blocks neutrophil and macrophage differentiation of primary myeloid progenitors cultured in granulocyte–macrophage colony-stimulating factor (GM-CSF). Expression of Meis1 alone did not immortalize any factor-dependent marrow progenitor. Because HoxA9-immortalized progenitors still execute granulocytic differentiation in response to granulocyte CSF (G-CSF) and monocyte differentiation in response to macrophage CSF (M-CSF), we tested the possibility that Meis1a cooperates with Hoxa9 by blocking viable differentiation pathways unaffected by Hoxa9 alone. Here we report that Meis1a suppresses G-CSF-induced granulocytic differentiation of Hoxa9-immortalized progenitors, permitting indefinite self-renewal in G-CSF. Meis1a also reprograms Hoxa9-immortalized progenitors to proliferate, rather than die, in response to stem cell factor (SCF) alone. We propose that Meis1a and Hoxa9 are part of a molecular switch that regulates progenitor abundance by suppressing differentiation and maintaining self-renewal in response to different subsets of cytokines during myelopoiesis. The independent differentiation pathways targeted by Hoxa9 and Meis1a prompt a “cooperative differentiation arrest” hypothesis for a subset of leukemia, in which cooperating transcription factor oncoproteins block complementary subsets of differentiation pathways, establishing a more complete differentiation block in vivo

Meis1a suppresses differentiation by G-CSF and promotes proliferation by SCF: Potential mechanisms of cooperativity with Hoxa9 in myeloid leukemia

Hoxa9 and Meis1a are homeodomain transcription factors that heterodimerize on DNA and are down-regulated during normal myeloid differentiation. Hoxa9 and Meis1a cooperate to induce acute myeloid leukemia (AML) in mice, and are coexpressed in human AML. Despite their cooperativity in leukemogenesis, we demonstrated previously that retroviral expression of Hoxa9 alone—in the absence of coexpressed retroviral Meis1 or of expression of endogenous Meis genes—blocks neutrophil and macrophage differentiation of primary myeloid progenitors cultured in granulocyte–macrophage colony-stimulating factor (GM-CSF). Expression of Meis1 alone did not immortalize any factor-dependent marrow progenitor. Because HoxA9-immortalized progenitors still execute granulocytic differentiation in response to granulocyte CSF (G-CSF) and monocyte differentiation in response to macrophage CSF (M-CSF), we tested the possibility that Meis1a cooperates with Hoxa9 by blocking viable differentiation pathways unaffected by Hoxa9 alone. Here we report that Meis1a suppresses G-CSF-induced granulocytic differentiation of Hoxa9-immortalized progenitors, permitting indefinite self-renewal in G-CSF. Meis1a also reprograms Hoxa9-immortalized progenitors to proliferate, rather than die, in response to stem cell factor (SCF) alone. We propose that Meis1a and Hoxa9 are part of a molecular switch that regulates progenitor abundance by suppressing differentiation and maintaining self-renewal in response to different subsets of cytokines during myelopoiesis. The independent differentiation pathways targeted by Hoxa9 and Meis1a prompt a “cooperative differentiation arrest” hypothesis for a subset of leukemia, in which cooperating transcription factor oncoproteins block complementary subsets of differentiation pathways, establishing a more complete differentiation block in vivo

An environment-dependent transcriptional network specifies human microglia identity

Microglia play essential roles in central nervous system (CNS) homeostasis and influence diverse aspects of neuronal function. However, the transcriptional mechanisms that specify human microglia phenotypes are largely unknown. We examined the transcriptomes and epigenetic landscapes of human microglia isolated from surgically resected brain tissue ex vivo and after transition to an in vitro environment. Transfer to a tissue culture environment resulted in rapid and extensive down-regulation of microglia-specific genes that were induced in primitive mouse macrophages after migration into the fetal brain. Substantial subsets of these genes exhibited altered expression in neurodegenerative and behavioral diseases and were associated with noncoding risk variants. These findings reveal an environment-dependent transcriptional network specifying microglia-specific programs of gene expression and facilitate efforts to understand the roles of microglia in human brain diseases

An environment-dependent transcriptional network specifies human microglia identity

Microglia play essential roles in central nervous system (CNS) homeostasis and influence diverse aspects of neuronal function. However, the transcriptional mechanisms that specify human microglia phenotypes are largely unknown. We examined the transcriptomes and epigenetic landscapes of human microglia isolated from surgically resected brain tissue ex vivo and after transition to an in vitro environment. Transfer to a tissue culture environment resulted in rapid and extensive down-regulation of microglia-specific genes that were induced in primitive mouse macrophages after migration into the fetal brain. Substantial subsets of these genes exhibited altered expression in neurodegenerative and behavioral diseases and were associated with noncoding risk variants. These findings reveal an environment-dependent transcriptional network specifying microglia-specific programs of gene expression and facilitate efforts to understand the roles of microglia in human brain diseases

Proceso de construcción identitaria del pedagogo universitario en México The process of identity contruction by university pedagogues in Mexico

En este artículo presento algunos resultados de la investigación El pedagogo y su identidad profesional: el caso de los egresados de la carrera de Pedagogía de la Universidad Nacional Autónoma de México (Unam) y de la Universidad Veracruzana (UV)¹. Ella tuvo como objetivo dar cuenta de los procesos de constitución identitaria de los pedagogos egresados de estas universidades en las décadas de 1950, 1970 y 1990, según los planes de estudio por los que se formaram, y, concomitantemente, destacar los rasgos que han definido su identidad. La pregunta central que ha conducido todo el trabajo fue: ¿Cuáles son los rasgos que han ido constituyendo la identidad de los pedagogos de la Unam y de la UV, y, en función de esto, de qué identidad de pedagogo hablamos? Luego de entrevistar a 12 pedagogos (seis por institución, dos por generación), analizar sus testimonios y documentos tales como planes de estudio, publicaciones, etcétera, y poniéndolos a jugar con el referente teórico y las preguntas de investigación, puedo decir que la identidad del pedagogo se ha constituido como una identidad histórica, relacional e híbrida: es un tipo de profesional que cumple funciones diversas pero todas ellas vinculadas a algún ámbito de la educación en general (formal, no formal e informal) y las encara de manera distinta a la de otras profesiones que también se ocupan de la educación.<br>In this article, a few results of a research called 'The pedagogue and his/her professional identity: the case of Pedagogy graduates from the Universidad Nacional Autónoma de Mexico (UNAM) and Universidad Veracruzana (UV)' are presented. The study had two aims: a) to identify the processes of identity construction among pedagogues graduated from these universities in the decades of 1950, 1970 and 1990, according to their undergraduate study programs; and, b) to point out the characteristics which defined their identities. The central question of the investigation was: which were the characteristics that constituted UNAM's and UV's pedagogue identity, and of which pedagogue identity are we talking about? After having interviewed 12 pedagogues (six per institution and two per generation) and analyzed their statements and documents (such as their study programs, papers published etc.), it is possible to say, in the light of the theoretic framework and considering the research's questions, that the pedagogue identity encompasses a historical, relational and hybrid identity: the pedagogue is a professional who performs several functions, all of them linked to a sector of education (formal, non-formal and informal), considering them, however, in a very distinct manner in relationship to other education-related professions

Neutralization of Oxidized Phospholipids Ameliorates Non-alcoholic Steatohepatitis

Oxidized phospholipids (OxPLs), which arise due to oxidative stress, are proinflammatory and proatherogenic, but their roles in non-alcoholic steatohepatitis (NASH) are unknown. Here, we show that OxPLs accumulate in human and mouse NASH. Using a transgenic mouse that expresses a functional single-chain variable fragment of E06, a natural antibody that neutralizes OxPLs, we demonstrate the causal role of OxPLs in NASH. Targeting OxPLs in hyperlipidemic Ldlr-/- mice improved multiple aspects of NASH, including steatosis, inflammation, fibrosis, hepatocyte death, and progression to hepatocellular carcinoma. Mechanistically, we found that OxPLs promote ROS accumulation to induce mitochondrial dysfunction in hepatocytes. Neutralizing OxPLs in AMLN-diet-fed Ldlr-/- mice reduced oxidative stress, improved hepatic and adipose-tissue mitochondrial function, and fatty-acid oxidation. These results suggest targeting OxPLs may be an effective therapeutic strategy for NASH