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This work investigates the role of shear and turbulent fluctuations on multi-species biofilm growth. The study is mostly motivated by understanding biofouling on microplastics (MPs) in oceanic environments. By increasing particle stickiness, biofilms promote MP aggregation and sinking; therefore, a thorough understanding of this multi-scale process is crucial to improve predictions of the MPs fate. We conducted a series of laboratory experiments using an oscillating-grid system to promote biofilm growth on small plastic surfaces under homogeneous isotropic turbulence with grid Reynolds numbers between 305 and 2220. Two configurations were analyzed: one where plastic samples move along with the grid (shear-dominated) and another one where the samples are kept fixed downstream the grid, thus experiencing turbulence but no mean flow (shear-free). Biofilm formed in all cases in a time scale of days, then the biomass formed on the plastic pieces was carefully measured and analyzed as a function of the turbulence level. The shear-free results were further interpreted using a parsimonious physical model, coupling the nutrient uptake rate within the biofilm (Monod kinetics) with the turbulent diffusion of the surrounding bulk liquid. Results show that: (i) under shear-dominated conditions, the biofilm mass initially grows with turbulence intensity before decaying, presumably due to shear-induced erosion; (ii) in the shear-free experiments, the mass increases monotonically following an enhanced availability of nutrients, and then saturates due to uptake-limited kinetics. This latter behavior is well reproduced by the physical model. Furthermore, a subset of plastic pieces were analyzed with a scanning electron microscope, revealing that turbulence also affects the microscopic configuration of biofilm clusters, increasing their compactness as the amplitude of turbulent fluctuations increases. These results contribute not only to our fundamental understanding of biofilms under flow, but can also inform global models of MP transport in marine environments.

•This study represents one of the largest series of culture confirmed pneumonia that evaluates the impact of PCV10 in children.•Describes the important decrease of PCV10 serotypes with an increase in PCV13.•This study shows how in the post-vaccine period, PCV13 serotypes (19A, 6A and 3) were associated with greater severity. Pneumococcal conjugate vaccines (PCVs) have decreased pneumonia in children. Colombia introduced mass vaccination with PCV10 in 2012. Cases of pneumococcal pneumonia from 10 hospitals were included. Two periods were compared: pre-PCV10: 2008–2011 and post-PCV10: 2014–2019. The objective was to compare epidemiological and clinical characteristics before and after PCV10 vaccination. A total of 370 cases were included. Serotypes 1 (15, 11.2%) and 14 (33, 24.6%) were the most frequent in the pre-PCV10 period, with only 4 (3%) cases of serotype 19A and 1 case (0.7%) serotype 3. From the pre-PCV10 period to the post-PCV10 period, cases of serotypes 1 (6, 3.1%) and 14 (1, 7.8%) decreased, while cases of serotypes 19A (58, 30.2%), serotype 3 (32, 16.7%) and 6A (7, 3.6%) increased (p < 0.001); complicated pneumonia (CP) increased significantly (13.4% to 31.8%) (p < 0.001); hospitalizations increased from 8 (5.5–15) to 12 (7–22) days (p < 0.001); and the frequency of PICU admission increased from 32.8% to 51.6% (p = 0.001). The use of ampicillin-sulbactam (0.7% to 24%) and ceftriaxone/clindamycin (0.7% to 5.7%) increased in the post-PCV10 period. The duration of empirical antibiotic treatment was 7 (4–11) days in the pre-PCV10 period and increased to 10 (6–17) days (p < 0.001) in the post-PCV10 period. Lethality showed a slight nonsignificant increase (7.5% vs. 9.9%; p = 0.57) in the post-PCV10 period. PCV10 significantly decreased cases of serotypes 1 and 14, with an increase in cases of serotypes 19A, 3 and 6A, which were the predominant serotypes and had greater severity (e.g., admission to the PICU, CP and more resistance, with an increase in the use of broad-spectrum antibiotics and longer hospitalization) and subsequently included in PCV13. Current data support national and regional evidence on the importance of replacing PCV10 with a higher valence that includes 19A, such as PCV13, with the aim of reducing circulation, particularly of this serotype.

Background: The effect of low-frequency functional variation on anti-tumor necrosis factor alpha (TNF) response in Crohn’s disease (CD) patients remains unexplored. The objective of this study was to investigate the impact of functional rare variants in clinical response to anti-TNF therapy in CD. Methods: CD anti-TNF naïve patients starting anti-TNF treatment due to active disease [Crohn’s Disease Activity Index (CDAI > 150)] were included. The whole genome was sequenced using the Illumina Hiseq4000 platform. Clinical response was defined as a CDAI score <150 at week 14 of anti-TNF treatment. Low-frequency variants were annotated and classified according to their damaging potential. The whole genome of CD patients was screened to identify homozygous loss-of-function (LoF) variants. The TNF signaling pathway was tested for overabundance of damaging variants using the SKAT-O method. Functional implication of the associated rare variation was evaluated using cell-type epigenetic enrichment analyses. Results: A total of 41 consecutive CD patients were included; 3250 functional rare variants were identified (2682 damaging and 568 LoF variants). Two homozygous LoF mutations were found in HLA-B and HLA-DRB1 genes associated with lack of response and remission, respectively. Genome-wide LoF variants were enriched in epigenetic marks specific for the gastrointestinal tissue (colon, p = 4.11e–4; duodenum, p = 0.011). The burden of damaging variation in the TNF signaling pathway was associated with response to anti-TNF therapy (p = 0.016); damaging variants were enriched in epigenetic marks from CD8+ (p = 6.01e–4) and CD4+ (p = 0.032) T cells. Conclusions: Functional rare variants are involved in the response to anti-TNF therapy in CD. Cell-type enrichment analysis suggests that the gut mucosa and CD8+ T cells are the main mediators of this response.

To determine the incidence of congenital toxoplasmosis in Colombian newborns from 19 hospital or maternal child health services from seven different cities of five natural geographic regions (Caribbean, Central, Andean, Amazonia and Eastern). We collected 15,333 samples from umbilical cord blood between the period of March 2009 to May 2010 in 19 different hospitals and maternal-child health services from seven different cities. We applied an IgM ELISA assay (Vircell, Spain) to determine the frequency of IgM anti Toxoplasma. The results in blood cord samples were confirmed either by western blot and repeated ELISA IgM assay. In a sub-sample of 1,613 children that were negative by the anti-Toxoplasma IgM assay, the frequency of specific anti-Toxoplasma IgA by the ISAGA assay was determined. All children with positive samples by IgM, IgA, clinical diagnosis or treatment during pregnancy were recalled for confirmatory tests after day 10 of life. 61 positive samples for specific IgM (0.39%) and 9 positives for IgA (0.5%) were found. 143 questionnaires were positive for a clinical diagnosis or treatment for toxoplasmosis during pregnancy. 109 out of the 218 children that had some of the criteria for postnatal confirmatory tests were followed. Congenital toxoplasmosis infection was confirmed in 15 children: 7 were symptomatic, and three of them died before the first month of life (20% of lethality). A significant correlation was found between a high incidence of markers for congenital toxoplasmosis and higher mean annual rainfall for the city. Incidence for congenital toxoplasmosis is significantly different between hospitals or maternal child health services from different cities in Colombia. Mean annual rainfall was correlated with incidence of congenital toxoplasmosis.