Study of crystallization behavior of poly(phenylene sulfide)

Poly(phenylene sulfide) (PPS) is an engineering thermoplastic polymer that presents high temperature resistance (glass transition temperature around 85 ºC and melting point at 285 ºC). These properties combined with its mechanical properties and its high chemical resistance allows its use in technological applications such as molding resins and as matrix for structural thermoplastic composites. During the manufacture of thermoplastic composites, the polymer is exposed to repeated melting, quenching and crystallization processes. The properties of semicrystalline polymers, such as PPS, depend on its crystallization behavior. This work deals with the PPS crystallization kinetics under different thermal cycles. This study was performed under isothermal conditions in a differential scanning calorimetry (DSC), coupled to Perkin Elmer crystallization software referred to as Pyris Kinetics - Crystallization. The results were correlated with microscopic analyses carried out in a polarized light microscope, equipped with a controlled heating and cooling accessory. In this case, the experimental conditions were the same adopted for the DSC analyses. From the results, parameters could be established to be used in the composite manufacture

Mycobacterium tuberculosis Strains of the Modern Sublineage of the Beijing Family Are More Likely To Display Increased Virulence than Strains of the Ancient Sublineage

Made available in DSpace on 2015-05-04T17:07:30Z (GMT). No. of bitstreams: 2 license.txt: 1914 bytes, checksum: 7d48279ffeed55da8dfe2f8e81f3b81f (MD5) lia_gomesetal_IOC_2014.pdf: 2345129 bytes, checksum: 1b32aaff28a0f9a34cdb2bdae8526c41 (MD5) Previous issue date: 2014Universidade Estadual do Norte Fluminense.Laboratório de Morfologia Animal e Patologia. Laboratório de Biologia do Reconhecimento. Campos, RJ, Brasil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Biologia Molecular Aplicada a Micobactérias. Rio de Janeiro, RJ, Brasil.Universidade de São Paulo. Instituto de Ciências Biomédicas. Departamento de Imunologia. São Paulo, SP, BrasilUniversidade Estadual do Norte Fluminense.Laboratório de Morfologia Animal e Patologia. Laboratório de Biologia do Reconhecimento. Campos, RJ, Brasil.Universidade Estadual do Norte Fluminense.Laboratório de Morfologia Animal e Patologia. Laboratório de Biologia do Reconhecimento. Campos, RJ, Brasil.Universidade Estadual do Norte Fluminense.Laboratório de Morfologia Animal e Patologia. Laboratório de Biologia do Reconhecimento. Campos, RJ, Brasil.Universidade Estadual do Norte Fluminense.Laboratório de Morfologia Animal e Patologia. Laboratório de Biologia do Reconhecimento. Campos, RJ, Brasil.Universidade Estadual do Norte Fluminense.Laboratório de Morfologia Animal e Patologia. Laboratório de Biologia do Reconhecimento. Campos, RJ, Brasil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Biologia Molecular Aplicada a Micobactérias. Rio de Janeiro, RJ, Brasil.St. Petersburg Pasteur Institute. Laboratory of Molecular Microbiology. St. Petersburg. Russian Federation.Universidade Estadual do Norte Fluminense.Laboratório de Morfologia Animal e Patologia. Laboratório de Biologia do Reconhecimento. Campos, RJ, Brasil.Strains of the Beijing genotype family of Mycobacterium tuberculosis are a cause of particular concern because of their increasing dissemination in the world and their association with drug resistance. Phylogenetically, this family includes distinct ancient and modern sublineages. The modern strains, contrary to the ancestral counterparts, demonstrated increasing prevalence in many world regions that suggest an enhanced bacterial pathogenicity. We therefore evaluated virulence of modern versus ancient Beijing strains with similar epidemiological and genotype characteristics. For this, we selected six strains that had very similar 24-locus mycobacterial interspersed repetitive-unit–variable-number tandem-repeat (MIRU-VNTR) typing profiles and belonged to the region of difference 181 (RD181) subgroup but differed using markers (mutT2 and mutT4 genes and NTF locus) that discriminate between modern and ancient Beijing sublineages. The strains were isolated from native patients in Brazil and Mozambique, countries with a low prevalence of Beijing strains. The virulence levels of these strains were determined in models of pulmonary infection in mice and in vitro macrophage infection and compared with that of a strain from Russia, part of the epidemic and hypervirulent Beijing clone B0/W148, and of the laboratory strain H37Rv. The results showed that two of the three modern Beijing strains were highly pathogenic, exhibiting levels of virulence comparable with that of the epidemic Russian strain. In contrast, all isolates of the ancient sublineage displayed intermediate or low virulence. The data obtained demonstrate that the strains of the modern Beijing sublineage are more likely to exhibit highly virulent phenotypes than ancient strains and suggest that genetic alterations characteristic of the modern Beijing sublineage favor selection of highly virulent bacteria

Correction: Hypervirulent Mycobacterium tuberculosis strain triggers necrotic lung pathology associated with enhanced recruitment of neutrophils in resistant C57BL/6 mice.

[This corrects the article DOI: 10.1371/journal.pone.0173715.]

Hypervirulent <i>Mycobacterium tuberculosis</i> strain triggers necrotic lung pathology associated with enhanced recruitment of neutrophils in resistant C57BL/6 mice

<div><p>Tuberculosis (TB) is a chronic infectious disease caused by <i>Mycobacterium tuberculosis</i> (Mtb) that in most cases induces irreversible necrosis of lung tissue as a result of excessive inflammatory reactions. The murine model of TB in resistant C57BL/6 mice infected with reference Mtb strains is widely used in TB studies; however, these mice do not show a necrotic pathology, which restricts their use in studies of irreversible tissue damage. Recently, we demonstrated that necrotic lung lesions could be induced in the C57BL/6 mice by highly virulent Mtb strains belonging to the modern Beijing sublineage. However, the pathogenic mechanisms leading to necrosis in this model were not elucidated. In this study, we investigated the dynamics of lung lesions in mice infected with highly virulent Beijing Mtb strain M299, compared with those infected with laboratory Mtb strain H37Rv. The data demonstrate that necrotic lung lesions in mice infected by the strain M299 were associated with enhanced recruitment of myeloid cells, especially neutrophils, and increased levels of proinflammatory cytokines, consistent with exacerbated inflammation. High levels of IFN-γ production contributed to the control of bacterial growth. Further progression to chronic disease was associated with a reduction in the levels of inflammatory mediators in the lungs, the accumulation of foamy macrophages and partial healing of the necrotic tissue by fibrosis. At a late stage of disease, degradation of foamy cells resulted in the liberation of accumulated lipids and persisting bacilli and further activation of inflammation, which promoted lung consolidation. Overall, our studies show that C57BL/6 mice infected with highly virulent Mtb strain may serve as a TB model reproducing an exacerbated inflammatory response in a resistant host to hypervirulent mycobacteria, leading to irreversible necrotic lung lesions.</p></div

Kinetics of myeloid cell recruitment into the lungs of mice infected with strains M299 and H37Rv.

<p><b>A</b>. Total numbers of cells recovered from the lungs over a follow-up period of 60 days after inoculation with bacilli or sterile PBS (control, day 0). Proportions of viable and dead cells were determined by trypan-blue staining. <b>B</b>. Myeloid cell populations were identified by flow cytometry. Total numbers of CD11b⁺ myeloid cells per lung and individual myeloid cell subpopulations, including neutrophils (CD11b⁺Ly6G⁺Ly6C⁺cells), immature neutrophil precursors (CD11b⁺Ly6G^lowLy6C^dim), inflammatory monocytes and macrophages (CD11b⁺Ly6C^hiCD11c^-Ly6G^- cells), monocyte-derived dendritic cells (CD11b⁺CD11c⁺Ly6C^hiLy6G^-) and dendritic cells (CD11b⁺CD11c⁺Ly6C^-Ly6G^-), were calculated. Values shown are the mean numbers of cells per lung ± SD, n = 8–9 lungs at each time point, pooled data from three independent experiments. Mean values of groups infected by strain M299 that were significantly different from the respective mean value of groups infected by H37Rv strain are indicated by asterisks * (p < 0.05). Significant differences between groups infected by each strain are indicated by lines and octothorpes #, (p < 0.05).</p

Lung histopathology at the early chronic stage of infection by highly virulent Mtb strain M299.

<p>Pathological alterations to lung tissue were observed on day 120 after infection by microscopic analysis of lung sections stained by hematoxylin-eosin (<b>A</b> and <b>B</b>), Masson´s trichrome (<b>C</b>) and Ziehl-Neelsen (<b>D</b>). Panel <b>A</b> demonstrates a necrotic lesion (black star) partially healed by fibrosis and surrounded by a rim of lymphocytes and lipid-laden foamy macrophages in the external region. Secondary granulomatous lesions are marked by white stars. Panel <b>B</b> demonstrates a higher-magnification image of two compact perivascular lymphocyte granulomas, surrounded by foamy macrophages. <b>C</b>. Masson’s staining revealed the presence of profuse collagen (in light-blue) in the central area of the necrotic lesion. Note cellular debris in the bronchiole and the absence of a bronchiolar epithelium (black arrow). <b>D</b>. Single AFB, exhibiting weak staining (black arrow heads), could be seen in necrotic areas partially healed by fibrosis and in foamy macrophages within alveoli. Bars represent 500 μm- in the panel <b>A</b>, 200 μm- in the panels <b>B</b> and <b>C</b>; and 100 μm- in the panel <b>D</b>.</p

Kinetics of bacterial growth in the lungs and morbidity of C57BL/6 mice inoculated with Mtb strains.

<p>Mice were infected i.t. with 100 CFU of the hypervirulent strain M299 and laboratory strain H37Rv. <b>A.</b> Bacterial burdens in the lungs were quantified by CFU counting on days 0, 5, 21, 28, 120 and 150 after infection. Data from three experiments (n = 3 for each group and each experiment) are expressed logarithmically as the mean log₁₀ CFU standard deviation (SD) (error bars). Mean values that were significantly different from the respective mean value of the group infected by strain H37Rv are indicated by asterisks *, p < 0.05. <b>B</b>. Kinetics of post-infection changes in mouse body weight. Weight loss was used as an indicator of morbidity. Data are presented as the percentage of peak body weight of each mice (n = 20, pooled data from two independent experiments). Statistical differences are indicated by asterisks *, p < 0.05.</p

Kinetics of lung histopathology during the acute stage of infection in C57BL/6 mice inoculated with strain M299.

<p>Mice were intratracheally infected with ~100 CFU. Pathologic alterations of lung tissue were determined on day 15 p.i. (<b>A</b>), day 21 p.i. (<b>B, C</b>) and day 28 p.i. (<b>D- I</b>) by microscopy of lung sections stained with hematoxylin-eosin (<b>A- F</b>) and Ziehl-Neelsen (<b>G- I</b>). Panel <b>A</b> shows interstitial granulomatous infiltrates on day 15 p.i. Panels <b>B</b> and <b>C</b> show the development of alveolitis through infiltration of alveoli (black arrows) with inflammatory cells, predominantly by neutrophils (enclosed in black circles). Panels <b>D</b> and <b>G</b> show coalescing foci of tuberculous pneumonia leading to the formation of tubercules with extensive areas of central caseous necrosis (black stars). The peripheral zone of the necrotic lesion is amplified in <b>E</b> and <b>H</b>, demonstrating areas of alveolitis (black arrows) with thickened alveolar walls and intra-alveolar cellular exudates composed predominantly of neutrophil debris (<b>E</b>) and numerous AFB (<b>H</b>). The caseous core is amplified in <b>F</b> and <b>I</b>. Note the thrombosed septal capillaries (black arrow heads) and obstruction of small airways with cellular debris (white arrow) in the peripheral rim of the necrotic zone (<b>F</b>). Numerous extracellular AFB and clumps of bacteria can be seen in the necrotic area (<b>I</b>). Data are representative of four independent experiments. Bars represent 500 μm—in the panels D and G, 200 μm—in B, E and H, 100 μm—in A, F and I and 20 μm—in C.</p

Treinamento aeróbio em natação melhora a resposta de parâmetros metabólicos de ratos durante teste de esforço Aerobic swimming training improves metabolic parameters response during exertion test in rats

Foram investigados os efeitos do treinamento aeróbio em natação com baixa intensidade sobre as respostas do lactato e da glicose sanguíneos de ratos durante teste de esforço. Ratos Wistar adultos foram distribuídos aleatoriamente em dois grupos: sedentário (n = 6) e treinado (n = 6). Todos receberam água e ração ad libitum e foram mantidos em ambiente com temperatura de 22 ± 2ºC e ciclo claro/escuro de 12 horas. O grupo treinado foi submetido a um programa de natação contínua sem sobrecarga, 30 min/dia, cinco dias/semana, por seis semanas. Três dias após a última sessão de treino, as concentrações sanguíneas de lactato e glicose foram medidas em três momentos durante dois testes de esforço de 20 minutos (repouso, 10 min e 20 min), sendo um sem carga e outro com carga (5% do peso corporal), separados por dois dias. Observou-se correlação inversa entre lactato e glicose durante o exercício (&#961; = - 0,74; P < 0,001). A concentração de lactato elevou-se do repouso para 10 min (P < 0,05) e estabilizou-se entre 10 e 20 min, em ambos os grupos nos dois testes. No teste com carga, o lactato estabilizou-se em níveis mais elevados frente aos níveis sem carga (P < 0,05), nos dois grupos. Os animais treinados exibiram níveis de lactato mais baixos do que os sedentários (P < 0,05) nos dois testes. A glicose sanguínea decaiu do repouso até 20 min nos sedentários, no teste com carga (P < 0,05). Nos treinados, a glicose sanguínea estabilizou-se em ambos os testes (P > 0,05). Conclui-se que o treinamento aeróbio em natação aplicado foi capaz de alterar as respostas do lactato e glicose sanguíneos de ratos durante os testes de esforço.<br>The effects of low intensity aerobic swimming training on blood lactate and glucose responses in rats were investigated during exertion test. Twelve adult male Wistar rats were randomly divided into two groups: sedentary (n= 6) and trained (n= 6). All animals received water and food ad libitum and were kept in a room with temperature of 22 ± 2ºC and dark/light cycle of 12 hours. Animals from trained group were submitted to a swimming training protocol of 30 min/day, 5 days/week, for 6 weeks. Sedentary animals did not exercise. Three days after the last training session all animals were submitted to two 20-minute swimming tests with 48 hour-interval, being one unloaded and the other with a load of 5 % of body weight. Blood lactate and glucose were measured at rest, 10 min and 20 min of exercise. Negative correlation between blood lactate and glucose levels was observed during the exertion tests (&#961; = - 0.74, P<0.001). Blood lactate concentration increased from rest to 10 min of exercise and stabilized from 10 to 20 min of exercise in both exercised and sedentary animals (P<0.05) during the unloaded exertion test. Blood lactate stabilized at higher levels when compared to those in the unloaded test in both groups (P<0.05) during the loaded exertion test. Trained rats presented lower levels of blood lactate than sedentary animals in both exercise tests (P<0.05). Blood glucose declined from rest to 10 min of exercise in sedentary rats during the loaded test (P<0.05). However, in trained animals blood glucose stabilized in both exercise tests (P>0.05). It was concluded that aerobic swimming training changed blood lactate and glucose response in rats during exertion test