Improving Pediatric Provider Preparedness for Postpartum Depression Screening

Background: Postpartum depression (PPD) is one of the most common complications of childbirth, affecting approximately 10-20% of mothers within the child’s first year of life with negative impact on both mother and child. . Pediatric primary care providers have frequent contact over the infant’s first year of life. The American Academy of Pediatrics (AAP) recommends screening mothers for PPD at the 1, 2, 4, and 6-month well-baby visits, yet due to barriers, pediatric providers are not consistently screening for PPD. Barriers include lack of preparedness and knowledge of resources and inadequate time. Aims of Service Change: To improve pediatric provider preparedness to screen for PPD at a large multi-site pediatric group practice in Southern California and lead to increased screening, detection, and treatment of PPD. Details of Innovation: The core intervention was provider education regarding recommendations for postpartum depression screening. Provider education also included provider responsibility in identifying PPD, community resources, and an overview of PPD diagnostic criteria. This project assessed provider preparedness using a pre-post education online anonymous survey. Outcome: Implementation of provider education increased self-reported preparedness to screen for PPD at well-baby visits with an increase of average score in all categories. Knowledge of resources and provider confidence had the most substantial increases. Discussion: Implementing provider education regarding screening for PPD at well-baby visits is a simple and cost-effective intervention. This leads to improved provider preparedness, potential increased identification of PPD in mothers, and improved overall outcomes for mothers and babies

Finding new signaling pathways that govern biofilm formation by P. aeruginosa

Pseudomonas aeruginosa is an opportunistic pathogen that is often associated with severe forms of many infections, including bronchiectasis and infections in the gut. Mortality is increased in patients who become infected with P. aeruginosa. P. aeruginosa poses a special treatment challenge due to its propensity to form biofilms, in which cells are surrounded by a self-produced extracellular matrix of proteins, DNA, and polysaccharides. Biofilms can help bacteria evade the host immune response, and the matrix represents a barrier that protects bacteria against antibiotic therapy. Because biofilms are difficult to treat once established in an infection, new strategies to prevent biofilm formation are critical to combat these infections. However, effective prevention depends on a fuller understanding of the signaling pathways that control biofilm formation. To identify new control points in the pathways governing biofilm formation by P. aeruginosa, we use transposon mutagenesis in conjunction with a visual assay for colony morphology, in which colony wrinkling indicates biofilm formation. Using these screens, we have been able to identify many promising candidates. For example, we have identified mutations in the genes fdnG and PA14_42090 as having smoother colony morphology, suggesting that these genes are involved in biofilm formation. Conversely, we have found that mutations in the purU2 and trxB1 genes show increased colony wrinkling, suggesting that these genes normally suppress biofilm formation. We will continue characterizing these genes by deleting them from the genome to confirm their roles in biofilm production and then testing how their absence or presence affects other known biofilm signaling molecules such as cyclic-di-GMP. Our detailed characterization of these candidate genes will provide fundamental knowledge that can then be used to devise future treatments to prevent biofilm formation in patients infected with P. aeruginosa

Identification of new signaling components that govern biofilm formation by P. aeruginosa

Pseudomonas aeruginosa is an opportunistic pathogen that is often associated with severe forms of many infections, including bronchiectasis and infections in the gut. Mortality is increased in patients who become infected with P. aeruginosa. P. aeruginosa poses a special treatment challenge due to its propensity to form biofilms, in which cells are surrounded by a self-produced extracellular matrix of proteins, DNA, and polysaccharides. Biofilms can help bacteria evade the host immune response, and the matrix represents a barrier that protects bacteria against antibiotic therapy. Because biofilms are difficult to treat once established in an infection, new strategies to prevent biofilm formation are critical to combat these infections. However, effective prevention depends on a fuller understanding of the signaling pathways that control biofilm formation. To identify new control points in the pathways governing biofilm formation by P. aeruginosa, we use transposon mutagenesis in conjunction with a visual assay for colony morphology, in which colony wrinkling indicates biofilm formation. Using these screens, we have been able to identify many promising candidates. For example, we have identified mutations in the genes fdnG and PA14_42090 as having smoother colony morphology, suggesting that these genes are involved in biofilm formation. Conversely, we have found that mutations in the purU2 and trxB1 genes show increased colony wrinkling, suggesting that these genes normally suppress biofilm formation. We will continue characterizing these genes by deleting them from the genome to confirm their roles in biofilm production and then testing how their absence or presence affects other known biofilm signaling molecules such as cyclic-di-GMP. Our detailed characterization of these candidate genes will provide fundamental knowledge that can then be used to devise future treatments to prevent biofilm formation in patients infected with P. aeruginosa.Lew Wentz FoundationMicrobiology and Molecular Genetic

TRY plant trait database – enhanced coverage and open access

Plant traits - the morphological, anatomical, physiological, biochemical and phenological characteristics of plants - determine how plants respond to environmental factors, affect other trophic levels, and influence ecosystem properties and their benefits and detriments to people. Plant trait data thus represent the basis for a vast area of research spanning from evolutionary biology, community and functional ecology, to biodiversity conservation, ecosystem and landscape management, restoration, biogeography and earth system modelling. Since its foundation in 2007, the TRY database of plant traits has grown continuously. It now provides unprecedented data coverage under an open access data policy and is the main plant trait database used by the research community worldwide. Increasingly, the TRY database also supports new frontiers of trait‐based plant research, including the identification of data gaps and the subsequent mobilization or measurement of new data. To support this development, in this article we evaluate the extent of the trait data compiled in TRY and analyse emerging patterns of data coverage and representativeness. Best species coverage is achieved for categorical traits - almost complete coverage for ‘plant growth form’. However, most traits relevant for ecology and vegetation modelling are characterized by continuous intraspecific variation and trait–environmental relationships. These traits have to be measured on individual plants in their respective environment. Despite unprecedented data coverage, we observe a humbling lack of completeness and representativeness of these continuous traits in many aspects. We, therefore, conclude that reducing data gaps and biases in the TRY database remains a key challenge and requires a coordinated approach to data mobilization and trait measurements. This can only be achieved in collaboration with other initiatives

Medicaid policy data for evaluating eligibility and programmatic changes

Abstract Objectives Medicaid and the Children’s Health Insurance Program (CHIP) provide health insurance coverage to more than 90 million Americans as of early 2023. There is substantial variation in eligibility criteria, application procedures, premiums, and other programmatic characteristics across states and over time. Analyzing changes in Medicaid policies is important for state and federal agencies and other stakeholders, but such analysis requires data on historical programmatic characteristics that are often not available in a form ready for quantitative analysis. Our objective is to fill this gap by synthesizing existing qualitative policy data to create a new data resource that facilitates Medicaid policy research. Data description Our source data were the 50-state surveys of Medicaid and CHIP eligibility, enrollment, and cost-sharing policies, and budgets conducted near annually by KFF since 2000, which we coded through 2020. These reports are a rich source of point-in-time information but not operationalized for quantitative analysis. Through a review of the measures captured in the KFF surveys, we developed five Medicaid policy domains with 122 measures in total, each coded by state-quarter—1) eligibility (28 measures), 2) enrollment and renewal processes (39 measures), 3) premiums (16 measures), 4) cost-sharing (26 measures), and 5) managed care (13 measures)

Screening Sexually Active Adolescents for Chlamydia trachomatis : What About the Boys?

Objectives. We sought to determine the effectiveness of a systems-based intervention designed to increase Chlamydia trachomatis (CT) screening among adolescent boys. Methods. An intervention aimed at increasing CT screening among adolescent girls was extended to adolescent boys (14–18 years). Ten pediatric clinics in a health maintenance organization with an ethnically diverse population were randomized. Experimental clinics participated in a clinical practice improvement intervention; control clinics received traditional information on screening. Results. The intervention significantly increased CT screening at the experimental sites from 0% (baseline) to 60% (18-month posttest); control sites evidenced a change only from 0% to 5%. The overall prevalence of CT was 4%. Conclusions. Although routine CT screening is currently recommended only for young sexually active women, the present results show that screening interventions can be successful in the case of adolescent boys, among whom CT is a moderate problem

Two patients with chronic mucocutaneous candidiasis caused by TRAF3IP2 deficiency

Background: TRAF3 interacting protein 2 (TRAF3IP2) (Act1) is an adapter protein that interacts with IL-17R via its similar expression to fibroblast growth factor genes and IL-17R domain and coordinates 2 separate proinflammatory pathways following IL-17 cytokine stimulation. Objective: We sought to elucidate the immunologic consequences of TRAF3IP2 homozygous mutations to improve treatments for immunodeficiency patients with chronic mucocutaneous candidiasis. Methods: We describe 2 patients presenting with chronic mucocutaneous candidiasis who harbor biallelic nonsense mutations in TRAF3IP2. The cellular and molecular features of this genetic defect were assessed using in vitro cytokine assays and protein analysis. Results: We show that the homozygous mutation causes complete loss of protein expression. We also show that the absence of TRAF3IP2 was associated with a defective response to combined IL-2/IL-25 (IL-17E) stimulation. Conclusions: Failure to initiate normal signaling downstream of IL-17R engagement likely contributes to the patients & rsquo; recurrent fungal infections. These findings add to our molecular understanding of genetic defects affecting this critical pathway of antifungal immunity. (J Allergy Clin Immunol 2021;148:256-61.

Breadth of HIV-induced IFN-γ T-cell recognition.

<p>The peptides sets evaluated were dictated by availability from the NIH AIDS reagent programme; clades A, B, C and D Gag peptides were obtainable while only clade B was available for Nef, Tat, Rev, Vif, Vpr, Pol and Vpu proteins. <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0004188#pone-0004188-g003" target="_blank">Figure 3</a> compares the proportion of participants (%) inducing HIV-specific IFN-γ responses using clade B peptides only, <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0004188#pone-0004188-g003" target="_blank">figure 3A</a>; as opposed to multiple clade Gag peptide sets, <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0004188#pone-0004188-g003" target="_blank">figure 3B</a>.</p