Publications by authors named "Sandra M Carvalho"

Article Synopsis
  • - The study focuses on the toxicity of certain -[Re(CO)(N-N)L] complexes, emphasizing how changes to the axial ligand L can significantly impact their effectiveness against microbial and tumoral cells, unlike previous research which mainly examined modifications to the bidentate diimine ligand (N-N).
  • - The high toxicity of the -[Re(CO)(bpy)(Ctz)] complex is linked to the structural presence of the trityl group in clotrimazole, and modifications to the axial ligand maintain high activity levels, suggesting ligand structure is key in inhibiting bacterial cell processes.
  • - Compounds containing PhE groups demonstrated tenfold increased toxicity compared to cisplatin in mammalian cells, with the
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  • The study focuses on how a common skin bacterium, which can cause infections in implants, survives under stress from toxic nitric oxide (NO) produced by the body's immune cells during biofilm formation.
  • Researchers investigated gene expression, metabolism, and biofilm structure in two clinical strains of the bacterium to understand their responses to NO, finding differences in how each strain manages biofilm mass and metabolic processes like lactate and acetate production.
  • The findings reveal that NO impacts biofilm matrix structure and production of adhesion molecules in a strain-specific way, suggesting that the bacteria adapt their metabolic functions to enhance their survival and fitness when exposed to the immune response.
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Bacterial pathogens have sophisticated systems that allow them to survive in hosts in which innate immunity is the frontline of defense. One of the substances produced by infected hosts is nitric oxide (NO) that together with its derived species leads to the so-called nitrosative stress, which has antimicrobial properties. In this review, we summarize the current knowledge on targets and protective systems that bacteria have to survive host-generated nitrosative stress.

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Staphylococcus aureus is a Gram-positive bacterium with capacity to form biofilms, which constitute an important resistance mechanism and virulence factor. Flavohaemoglobin (Hmp) is a major nitric oxide (NO) detoxifier of several bacteria, including S. aureus.

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Pseudomonas putida is a highly attractive production system for industrial needs. However, for its improvement as a biocatalyst at the industrial level, modulation of its gene expression is urgently needed. We report the construction of a plasmid expressing a small RNA-based system with the potential to be used for different purposes.

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Article Synopsis
  • Carbon monoxide-releasing molecules (CORMs), particularly the ruthenium(II) complex CORM-3, have shown promise as antimicrobials but their specific mechanisms of action on bacterial cells are not well understood.
  • Using a metabolomics approach, the study demonstrates that CORM-3 treatment leads to increased levels of glycolytic intermediates and inhibits the synthesis of glutamate and certain enzymes in the tricarboxylic acid (TCA) cycle, regardless of oxygen levels.
  • The toxic effects of CORM-3 can be alleviated by adding compounds like fumarate and glutamate, revealing that its antimicrobial action is linked to disrupting nitrogen and TCA cycles due to intracellular glutamate deficiency.
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Pyrimidine nucleotides play an important role in the biosynthesis of activated nucleotide sugars (NDP-sugars). NDP-sugars are the precursors of structural polysaccharides in bacteria, including capsule, which is a major virulence factor of the human pathogen . In this work, we identified a spontaneous non-reversible mutant of strain D39 that displayed a non-producing capsule phenotype.

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is a worldwide pathogen that colonizes the human nasal cavity and is a major cause of respiratory and cutaneous infections. In the nasal cavity, thrives with high concentrations of nitric oxide (NO) produced by the innate immune effectors and has available for growth slow-metabolizing free hexoses, such as galactose. Here, we have used deep sequencing transcriptomic analysis (RNA-Seq) and H-NMR to uncover how grown on galactose, a major carbon source present in the nasopharynx, survives the deleterious action of NO.

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We demonstrate that Ru(II)(CO)2-protein complexes, formed by the reaction of the hydrolytic decomposition products of [fac-RuCl(κ(2)-H2NCH2CO2)(CO)3] (CORM-3) with histidine residues exposed on the surface of proteins, spontaneously release CO in aqueous solution, cells, and mice. CO release was detected by mass spectrometry (MS) and confocal microscopy using a CO-responsive turn-on fluorescent probe. These findings support our hypothesis that plasma proteins act as CO carriers after in vivo administration of CORM-3.

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Neurological adverse events following administration of the 17DD substrain of yellow fever vaccine (YEL-AND) in the Brazilian population are described and analyzed. Based on information obtained from the National Immunization Program through passive surveillance or intensified passive surveillance, from 2007 to 2012, descriptive analysis, national and regional rates of YFV associated neurotropic, neurological autoimmune disease, and reporting rate ratios with their respective 95% confidence intervals were calculated for first time vaccinees stratified on age and year. Sixty-seven neurological cases were found, with the highest rate of neurological adverse events in the age group from 5 to 9 years (2.

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Pyruvate oxidase is a key function in the metabolism and lifestyle of many lactic acid bacteria and its activity depends on the presence of environmental oxygen. In Streptococcus pneumoniae the protein has been suggested to play a major role in metabolism and has been implicated in virulence, oxidative stress survival and death in stationary phase. Under semi-aerobic conditions, transcriptomic and metabolite profiling analysis of a spxB mutant grown on glucose showed minor changes compared to the wild type, apart from the significant induction of two operons involved in carbohydrate uptake and processing.

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Serious vaccine-associated adverse events are rare. To further minimize their occurrence and to provide adequate care to those affected, careful monitoring of immunization programs and case management is required. Unfounded vaccine safety concerns have the potential of seriously derailing effective immunization activities.

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Article Synopsis
  • Researchers investigated how carbohydrate metabolism affects the virulence of Streptococcus pneumoniae by creating a controlled environment to grow different strains.
  • They found that the encapsulated strain D39 benefited from high levels of uracil and semi-aerobic conditions, whereas the nonencapsulated strain R6 thrived in anaerobic environments without uracil's influence.
  • The study also utilized advanced NMR techniques to analyze sugar metabolism in S. pneumoniae R6, marking the first non-invasive metabolic profiling for this bacterium, which could enhance our understanding of its metabolism regulation.
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  • CcpA is a crucial transcriptional regulator in gram-positive bacteria, particularly linked to the virulence of the human pathogen Streptococcus pneumoniae, influencing gene expression based on nutrient availability.
  • Research on S. pneumoniae D39 and a ccpA mutant showed that CcpA regulates a significant portion of the genome, affecting processes related to virulence and metabolism when growing on different sugars like glucose and galactose.
  • The study also revealed that CcpA's role extends beyond just gene regulation, impacting the bacterium's metabolism and interactions with its host, highlighting the importance of looking at multiple levels of cellular data for a complete understanding of microbial
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Knowledge of the in vivo physiology and metabolism of Streptococcus pneumoniae is limited, even though pneumococci rely on efficient acquisition and metabolism of the host nutrients for growth and survival. Because the nutrient-limited, hypoxic host tissues favor mixed-acid fermentation, we studied the role of the pneumococcal pyruvate formate lyase (PFL), a key enzyme in mixed-acid fermentation, which is activated posttranslationally by PFL-activating enzyme (PFL-AE). Mutations were introduced to two putative pfl genes, SPD0235 and SPD0420, and two putative pflA genes, SPD0229 and SPD1774.

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