138 research outputs found

    O Atlântico enfermo e os agentes da saúde no período do tráfico ilegal

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    Resenha de:BARCIA, Manuel. The Yellow Demon of Fever: Fighting Disease in the Nineteenth-Century Transatlantic Slave Trade. New Heaven: Yale University Press, 2020. 269p

    Louis Figuier en Brasil: algunas consideraciones acerca de los vulgarizadores de las ciencias en el último cuarto del siglo XIX

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    This article aims to address aspects of the history of the divulgation of sciences in Brazil in the nineteenth century, through the analysis of the circulation of some translations into Portuguese of the works of French popularizer of science, Louis Figuier. His works, which were translated to different languages, received editions in Brazil and Portugal since late 1860. During this period, a model of popularization of science for non-specialists - working class, women and youth - with emphasis on applied science was gaining terrain. However, this model was also marked by limitations and discontinuities that reflect social issues in the passage to the twentieth century. This paper attempts to highlight the role of translators and editors, understood as mediators of science, whose projects of social reform was primarily focused in popular instruction.Este artículo pretende abordar aspectos de la historia de la divulgación científica en Brasil en el siglo XIX, a través del análisis de la circulación de algunas traducciones para el portugués de las obras del vulgarizador de la ciencia francés, Louis Figuier. Sus obras, que fueron traducidas para diversas lenguas, recibieron ediciones en Brasil y en Portugal a partir de fines de la década de 1860. En este período, ganaba terreno un modelo de divulgación de las ciencias que se alineaba con la idea de ampliación de conocimientos científicos, con énfasis en las ciencias aplicadas para no especialistas - clase trabajadora, mujeres y jovenes. Sin embargo, ese modelo fue marcado igualmente por limitaciones y discontinuidades que reflejan cuestiones sociales de fondo, en el pasaje al siglo XX. Este trabajo pretende, destacar el papel de los traductores y editores, entendidos como mediadores de las ciencias, que tenían en vista proyectos cuyo principal enfoque era la educación

    Identification and Characterization of a Novel Polysaccharide Deacetylase C (PdaC) from Bacillus subtilis

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    Cell wall metabolism and cell wall modification are very important processes that bacteria use to adjust to various environmental conditions. One of the main modifications is deacetylation of peptidoglycan. The polysaccharide deacetylase homologue, Bacillus subtilis YjeA (renamed PdaC), was characterized and found to be a unique deacetylase. The pdaC deletion mutant was sensitive to lysozyme treatment, indicating that PdaC acts as a deacetylase. The purified recombinant and truncated PdaC from Escherichia coli deacetylated B. subtilis peptidoglycan and its polymer, (-GlcNAc-MurNAc[-L-Ala-D-Glu]-)(n). Surprisingly, RP-HPLC and ESI-MS/MS analyses showed that the enzyme deacetylates N-acetylmuramic acid (MurNAc) not GlcNAc from the polymer. Contrary to Streptococcus pneumoniae PgdA, which shows high amino acid sequence similarity with PdaC and is a zinc-dependent GlcNAc deacetylase toward peptidoglycan, there was less dependence on zinc ion for deacetylation of peptidoglycan by PdaC than other metal ions (Mn2+, Mg2+, Ca2+). The kinetic values of the activity toward B. subtilis peptidoglycan were K-m = 4.8 mM and k(cat) = 0.32 s(-1). PdaC also deacetylated N-acetylglucosamine (GlcNAc) oligomers with a K-m = 12.3 mM and k(cat) = 0.24 s(-1) toward GlcNAc(4). Therefore, PdaC has GlcNAc deacetylase activity toward GlcNAc oligomers and MurNAc deacetylase activity toward B. subtilis peptidoglycan.ArticleJOURNAL OF BIOLOGICAL CHEMISTRY. 287(13):9765-9776 (2012)journal articl

    Long-term monitoring of the short period SU UMa-type dwarf nova, V844 Herculis

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    We report on time-resolved CCD photometry of four outbursts of a short-period SU UMa-type dwarf nova, V844 Herculis. We successfully determined the mean superhump periods to be 0.05584(64) days, and 0.055883(3) for the 2002 May superoutburst, and the 2006 April-May superoutburst, respectively. During the 2002 October observations, we confirmed that the outburst is a normal outburst, which is the first recorded normal outburst in V844 Her. We also examined superhump period changes during 2002 May and 2006 April-May superoutbursts, both of which showed increasing superhump period over the course of the plateau stage. In order to examine the long-term behavior of V844 Her, we analyzed archival data over the past ten years since the discovery of this binary. Although photometry is not satisfactory in some superoutbursts, we found that V844 Her showed no precursors and rebrightenings. Based on the long-term light curve, we further confirmed V844 Her has shown almost no normal outbursts despite the fact that the supercycle of the system is estimated to be about 300 days. In order to explain the long-term light curves of V844 Her, evaporation in the accretion disk may play a role in the avoidance of several normal outbursts, which does not contradict with the relatively large X-ray luminosity of V844 Her.Comment: 10 pages, 11 figures, accepted for PAS

    Porencephaly in a Cynomolgus Monkey (Macaca Fascicularis)

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    Porencephaly was observed in a female cynomolgus monkey (Macaca fascicularis) aged 5 years and 7 months. The cerebral hemisphere exhibited diffuse brownish excavation with partial defects of the full thickness of the hemispheric wall, and it constituted open channels between the lateral ventricular system and arachnoid space. In addition, the bilateral occipital lobe was slightly atrophied. Histopathologically, fibrous gliosis was spread out around the excavation area and its periphery. In the roof tissue over the cavity, small round cells were arranged in the laminae. They seemed to be neural or glial precursor cells because they were positive for Musashi 1 and negative for NeuN and GFAP. In the area of fibrous gliosis, hemosiderin or lipofuscin were deposited in the macrophages, and activated astroglias were observed extensively around the excavation area

    Two Regulators of Vibrio parahaemolyticus Play Important Roles in Enterotoxicity by Controlling the Expression of Genes in the Vp-PAI Region

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    Vibrio parahaemolyticus is an important pathogen causing food-borne disease worldwide. An 80-kb pathogenicity island (Vp-PAI), which contains two tdh (thermostable direct hemolysin) genes and a set of genes for the type III secretion system (T3SS2), is closely related to the pathogenicity of this bacterium. However, the regulatory mechanisms of Vp-PAI's gene expression are poorly understood. Here we report that two novel ToxR-like transcriptional regulatory proteins (VtrA and VtrB) regulate the expression of the genes encoded within the Vp-PAI region, including those for TDH and T3SS2-related proteins. Expression of vtrB was under control of the VtrA, as vector-expressed vtrB was able to recover a functional protein secretory capacity for T3SS2, independent of VtrA. Moreover, these regulatory proteins were essential for T3SS2-dependent biological activities, such as in vitro cytotoxicity and in vivo enterotoxicity. Enterotoxic activities of vtrA and/or vtrB deletion strains derived from the wild-type strain were almost absent, showing fluid accumulation similar to non-infected control. Whole genome transcriptional profiling of vtrA or vtrB deletion strains revealed that the expression levels of over 60 genes were downregulated significantly in these deletion mutant strains and that such genes were almost exclusively located in the Vp-PAI region. These results strongly suggest that VtrA and VtrB are master regulators for virulence gene expression in the Vp-PAI and play critical roles in the pathogenicity of this bacterium

    Spectral evolution of GRB 060904A observed with Swift and Suzaku -- Possibility of Inefficient Electron Acceleration

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    We observed an X-ray afterglow of GRB 060904A with the Swift and Suzaku satellites. We found rapid spectral softening during both the prompt tail phase and the decline phase of an X-ray flare in the BAT and XRT data. The observed spectra were fit by power-law photon indices which rapidly changed from Γ=1.510.03+0.04\Gamma = 1.51^{+0.04}_{-0.03} to Γ=5.300.59+0.69\Gamma = 5.30^{+0.69}_{-0.59} within a few hundred seconds in the prompt tail. This is one of the steepest X-ray spectra ever observed, making it quite difficult to explain by simple electron acceleration and synchrotron radiation. Then, we applied an alternative spectral fitting using a broken power-law with exponential cutoff (BPEC) model. It is valid to consider the situation that the cutoff energy is equivalent to the synchrotron frequency of the maximum energy electrons in their energy distribution. Since the spectral cutoff appears in the soft X-ray band, we conclude the electron acceleration has been inefficient in the internal shocks of GRB 060904A. These cutoff spectra suddenly disappeared at the transition time from the prompt tail phase to the shallow decay one. After that, typical afterglow spectra with the photon indices of 2.0 are continuously and preciously monitored by both XRT and Suzaku/XIS up to 1 day since the burst trigger time. We could successfully trace the temporal history of two characteristic break energies (peak energy and cutoff energy) and they show the time dependence of t3t4\propto t^{-3} \sim t^{-4} while the following afterglow spectra are quite stable. This fact indicates that the emitting material of prompt tail is due to completely different dynamics from the shallow decay component. Therefore we conclude the emission sites of two distinct phenomena obviously differ from each other.Comment: 19 pages, 9 figures, accepted for publication in PASJ (Suzaku 2nd Special Issue

    Bile Acid-Induced Virulence Gene Expression of Vibrio parahaemolyticus Reveals a Novel Therapeutic Potential for Bile Acid Sequestrants

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    Vibrio parahaemolyticus, a bacterial pathogen, causes human gastroenteritis. A type III secretion system (T3SS2) encoded in pathogenicity island (Vp-PAI) is the main contributor to enterotoxicity and expression of Vp-PAI encoded genes is regulated by two transcriptional regulators, VtrA and VtrB. However, a host-derived inducer for the Vp-PAI genes has not been identified. Here, we demonstrate that bile induces production of T3SS2-related proteins under osmotic conditions equivalent to those in the intestinal lumen. We also show that bile induces vtrA-mediated vtrB transcription. Transcriptome analysis of bile-responsive genes revealed that bile strongly induces expression of Vp-PAI genes in a vtrA-dependent manner. The inducing activity of bile was diminished by treatment with bile acid sequestrant cholestyramine. Finally, we demonstrate an in vivo protective effect of cholestyramine on enterotoxicity and show that similar protection is observed in infection with a different type of V. parahaemolyticus or with non-O1/non-O139 V. cholerae strains of vibrios carrying the same kind of T3SS. In summary, these results provide an insight into how bacteria, through the ingenious action of Vp-PAI genes, can take advantage of an otherwise hostile host environment. The results also reveal a new therapeutic potential for widely used bile acid sequestrants in enteric bacterial infections

    PPAR beta/delta activation of CD300a controls intestinal immunity

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    Macrophages are important for maintaining intestinal immune homeostasis. Here, we show that PPAR beta/delta (peroxisome proliferator-activated receptor beta/delta) directly regulates CD300a in macrophages that express the immunoreceptor tyrosine based-inhibitory motif (ITIM)-containing receptor. In mice lacking CD300a, high-fat diet (HFD) causes chronic intestinal inflammation with low numbers of intestinal lymph capillaries and dramatically expanded mesenteric lymph nodes. As a result, these mice exhibit triglyceride malabsorption and reduced body weight gain on HFD. Peritoneal macrophages from Cd300a(-/-) mice on HFD are classically M1 activated. Activation of toll-like receptor 4 (TLR4)/MyD88 signaling by lipopolysaccharide (LPS) results in prolonged IL-6 secretion in Cd300a(-/-) macrophages. Bone marrow transplantation confirmed that the phenotype originates from CD300a deficiency in leucocytes. These results identify CD300a-mediated inhibitory signaling in macrophages as a critical regulator of intestinal immune homeostasis
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