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BACKGROUND: Although the COVID-19 pandemic has increased the prevalence of cases with olfactory loss, other respiratory viruses can also cause this condition. We aimed to compare the prevalence of acute SARS-CoV-2 infection and other respiratory viruses in patients with sudden smell loss, and to assess the impact of SARS-CoV-2 viral load and co-infection on olfactory symptoms. METHODS: Patients with sudden smell loss were recruited in a multicenter prospective cohort study in 15 hospitals in Brazil. Clinical questionnaire, Connecticut Chemosensory Clinical Research Center (CCCRC) olfactory test and nasopharyngeal swab to perform a PCR-based respiratory viral panel were collected at first visit (day 0) and 30 and 60 days after recruitment. RESULTS: 188 of 213 patients presented positive test result for SARS-CoV-2, among which 65 were co-infected with other respiratory viruses (e.g., rhinovirus, enterovirus, and parainfluenza). 25 had negative test results for SARS-CoV-2. Patients in both SARSCoV-2 and non-SARS-CoV-2 groups had objective anosmia (less than 2 points according to the psychophysical olfactory CCCRC) at day 0, with no significant difference between them. Both groups had significant smell scores improvement after 30 and 60 days, with no difference between them. Co-infection with other respiratory viruses, and SARS-CoV-2 viral load did not impact olfactory scores. CONCLUSION: Patients with sudden smell loss associated with SARS-CoV-2 and other respiratory viruses had similar presentation, with most participants initiating with anosmia, and total or near total recovery after 60 days. SARS-CoV-2 viral load and co-infections with other respiratory viruses were not associated with poorer olfactory outcomes.

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A reversed-phase liquid chromatographic separation with pulsed amperometric detection of phenolic acids at a glassy carbon electrode is described. Chromatographic separation was carried out in isocratic conditions using 0.20 mol·L-1 acetic acid (pH 5.0)/water (80 : 20, v/v) as mobile phase under constant working potential mode of 0.80 V. Chromatographic peaks presented high resolution and separation. Calibration curves exhibited excellent correlation coefficients, above 0.995. Linear ranges of the analytes, in mg L-1, were of 0.018-18 (gallic acid), 0.146-19 (vanillic acid), 0.13-17 (caffeic acid), 0.016-16 (ferulic acid), and 0.008-17 (p-coumaric acid), respectively. Limits of detection ranged from 1.6 to 97 µg·L-1 and precision varied in 1.73-3.78% interval. Concentrations of 19 ± 0.51 mg·L-1 and 7.8 ± 2.5 mg·L-1 were found for vanillic and caffeic acids, respectively, in a sugarcane vinasse sample. Gallic, ferulic, and p-coumaric acids were not detected. Recovery results demonstrated that the proposed method is accurate, and it can be used to detect and quantify phenolic acids in sugarcane vinasse without any influence of interferents.

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In this work, we will study how the effective geometry acquired by nematic molecules under thermal vibration contribute to the determination of the Leslie coefficients. To do this, we will divide this work in two sections. In the first section, we present the geometrical fundamentals of the so-called Hess-Baalss (HB) approach [D. Baalss and S. Hess, Phys. Rev. Lett. 57, 86 (1986)] where we show that its basic assumptions can be understood as a geometrical interpretation of de Gennes' passage from the microscopic to the macroscopic order parameter. In the second section, we use an extended version of the HB approach [M. Simões, K. Yamaguti, and A. J. Palangana, Phys. Rev. E 80, 061701 (2009)] to obtain the geometrical contribution to each Leslie coefficient. Our results will be compared with experimental data, and we will show that the Miesowicz's coefficients are connected as long as the ratio α(3)/α(4) between these Leslie coefficients can be considered small.

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This work presents a systematic Raman scattering study and first-principles calculations for the EuB(6) system. Evidence for the presence of an incipient (∼1 × 10(-4) Å) tetragonal symmetry break of its crystalline structure was found. Forbidden Raman modes at ω(fRm(1))∼1170 cm(-1), ω(fRm(2))∼1400 cm(-1), and ω(fRm(3))∼1500  cm(-1) were observed. The tetragonal symmetry of ω(fRm(2)) and ω(fRm(3)) together with spin-polarized first-principles simulations of the structural and magnetic properties fully support such a break of symmetry. Our data and calculations explain the occurrence of ferromagnetism in Eu hexaborides, previously reported.

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Paracoccidioidomycosis is caused by Paracoccidioides brasiliensis, which although not formally considered an intracellular pathogen, can be internalized by epithelial cells in vitro and in vivo. The mechanisms used by P. brasiliensis to adhere to and invade non-professional phagocytes have not been identified. The signal-transduction networks, involving protein tyrosine kinase (PTK) and protein phosphatase activities, can modulate crucial events during fungal infections. In this study, the involvement of PTK has been investigated in P. brasiliensis adherence and invasion in mammalian epithelial cells. A significant inhibition of the fungal invasion occurred after the pre-treatment of the epithelial cells with genistein, a specific tyrosine kinase inhibitor, indicating that the tyrosine kinase pathway is involved in P. brasiliensis internalization. In contrast, when the fungus was treated, a slight (not significant) inhibition of PTK was observed, suggesting that PTK might not be the fungus' transduction signal pathway during the invasion process of epithelial cells. An intense PTK immunofluorescence labeling was observed in the periphery of the P. brasiliensis infected cells, little PTK labeling was found in both uninfected cells and yeast cells, at later infection times (8 and 24 h). Moreover, when the epithelial cells were treated with genistein and infected with P. brasiliensis, no labeling was observed, suggesting the importance of the PTK in the infectious process. These results suggest that PTK pathway participates in the transduction signal during the initial events of the adhesion and invasion processes of P. brasiliensis to mammalian epithelial cells.

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A paracoccidioidomicose apresenta um amplo espectro de manifestações clínicas e Paracoccidioides brasiliensis, seu agente etiológico, pode atingir vários tecidos com ênfase ao pulmão. A migração de fungos patogênicos através da camada de células endoteliais é considerada pré-requisito para a invasão de múltiplos órgãos e sua disseminação. No presente estudo verificou-se a adesão de P. brasiliensis às células endoteliais in vitro e se esta adesão poderia representar um mecanismo para a disseminação do fungo. Para tanto, além da técnica convencional de microscopia ótica, uma outra metodologia foi desenvolvida, emblocando os cordões umbilicais em parafina, no intuito de detectar o fungo presente no material (in vivo). Experimento de migração de P. brasiliensis através da monocamada de células endoteliais também foi realizado, e nos poços sem células, a migração de células leveduriformes foi maior em menor período de tempo. Os fungos conseguiram passar através da monocamada, quando comparados com o controle sem as células, mas com redução em torno de 30%. Isso mostra que a monocamada foi parcialmente impediente para o fungo, mas que este foi capaz de migrar através dessas células. Em nossos experimentos com estas células, houve grande dificuldade de se encontrar P. brasiliensis aderido ao tapete celular nos períodos de tempo padronizados. Sugere-se com esses resultados que o fungo atravessa as células endoteliais de uma maneira muito rápida, que não pode ser detectada através do cultivo in vitro. Portanto, P. brasiliensis teria capacidade de atravessar rapidamente as células endoteliais e provavelmente alcançar tecidos mais profundos

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Paracoccidioides brasiliensis is a dimorphic fungus known to produce invasive systemic disease in humans. The 43-kDa glycoprotein of P. brasiliensis is the major diagnostic antigen of paracoccidioidomycosis and may act as a virulence factor, since it is a receptor for laminin.Very little is known about early interactions between this fungus and the host cells, so we developed in vitro a model system employing cultured mammalian cells (Vero cells), in order to investigate the factors and virulence mechanisms of P.brasiliensis related to the adhesion and invasion process. We found that there is a permanent interaction after 30 min of contact between the fungus and the cells. The yeasts multiply in the cells for between 5 and 24 h. Different strains of P. brasiliensis were compared, and strain 18 (high virulence) was the most strongly adherent, followed by strain 113 (virulent), 265 (considered of low virulence) and 113M (mutant obtained by ultraviolet radiation, deficient in gp43). P. brasiliensis adhered to the epithelial cells by a narrow tube, while depressions were noticed in the cell surface, suggesting an active cavitation process. An inhibition assay was performed and it was verified that anti-gp43 serum and a pool of sera from individuals with paracoccidioidomycosis were able to inhibit the adhesion of P. brasiliensis to the Vero cells. Glycoprotein 43 (gp43) antiserum abolished 85% of the binding activity of P. brasiliensis. This fungus can also invade the Vero cells, and intraepithelial parasitism could be an escape mechanism in paracoccidioidomycosis.

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Vesicle trafficking between organelles occurs through fusion of donor and specific acceptor membranes. This process is highly regulated and ensures proper direction in sorting and packaging of a number of molecules in eukaryotic cells. Monomeric GTPases of the Rab family play a pivotal role in the control of membrane fusion and vesicle traffic. In this paper, we characterize a Trypanosoma cruzi Rab 11 homologue (TcRab11) that shares at, the amino acid level, 40% similarity with human rab11, Arabdopsis thaliana rab11 and yeast rab11 homologue genes. Western blot analysis, using a polyclonal rabbit antiserum raised against a synthetic peptide derived from the COOH-terminus of predicted the TcRab11 protein, reacted to a 26kDa protein. In immunofluorescence assays, TcRab 11, was shown to be expressed in epimastigote and amastigote forms, but it was absent in trypomastigotes. Interestingly, the TcRab11 product seems to be located at the reservosome complex, a site of active endocytosis and vesicle fusion present only in the epimastigote stage. Therefore, TcRab11 may represent the first molecular marker of this peculiar organelle.

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Most of our knowledge concerning the virulence determinants of pathogenic fungi comes from the infected host, mainly from animal models and more recently from in vitro studies with cell cultures. The fungi usually present intra- and/or extracellular host-parasite interfaces, with the parasitism phenomenon dependent on complementary surface molecules. Among living organisms, this has been characterized as a cohabitation event, where the fungus is able to recognize specific host tissues acting as an attractant, creating stable conditions for its survival. Several fungi pathogenic for humans and animals have evolved special strategies to deliver elements to their cellular targets that may be relevant to their pathogenicity. Most of these pathogens express surface factors that mediate binding to host cells either directly or indirectly, in the latter case binding to host adhesion components such as extracellular matrix (ECM) proteins, which act as 'interlinking' molecules. The entry of the pathogen into the host cell is initiated by fungal adherence to the cell surface, which generates an uptake signal that may induce its cytoplasmic internalization. Once this is accomplished, some fungi are able to alter the host cytoskeletal architecture, as manifested by a rearrangement of microtubule and microfilament proteins, and this can also induce epithelial host cells to become apoptotic. It is possible that fungal pathogens induce modulation of different host cell pathways in order to evade host defences and to foster their own proliferation. For a number of pathogens, the ability to bind ECM glycoproteins, the capability of internalization and the induction of apoptosis are considered important factors in virulence. Furthermore, specific recognition between fungal parasites and their host cell targets may be mediated by the interaction of carbohydrate-binding proteins, e.g., lectins on the surface of one type of cell, probably a parasite, that combine with complementary sugars on the surface of host-cell. These interactions supply precise models to study putative adhesins and receptor-containing molecules in the context of the fungus-host interface. The recognition of the host molecules by fungi such as Aspergillus fumigatus, Paracoccidioides brasiliensis and Histoplasma capsulatum, and their molecular mechanisms of adhesion and invasion, are reviewed in this paper.

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