Yu Logan (knightdash4)
Surveillance of antimicrobial resistance (AMR) in Neisseria gonorrhoeae, supported by molecular typing, ideally through genome sequencing, is imperative. We defined N. gonorrhoeae Sequence Typing for Antimicrobial Resistance (NG-STAR) clonal complexes (CCs) and validated their usefulness in gonococcal AMR surveillance. All NG-STAR alleles and STs available in the public database (https//ngstar.canada.ca/) were analysed using PHYLOViZ 2.0 to define CCs according to the closest founder ST with ≥5 identical alleles and founding ST with the highest number of links. The published 2013 European gonococcal dataset (n = 1054), the 2016 WHO reference strain panel (n = 14) and N. gonorrhoeae isolates with ceftriaxone resistance determinant penA-60.001 (n = 7) from several countries were used for validation. The majority of the isolates (n = 1063) were designated to 71 CCs. The most common CC was CC90 (n = 194), followed by CC63 (n = 166), CC139 (n = 73), CC158 (n = 73) and CC127 (n = 62). CC90 included isolates b(for WGS and conventional Sanger sequencing data); and predict AMR lineages. Phenotypic AMR surveillance, supplemented with WGS, is imperative and NG-STAR CCs can effectively support this.Receptor degradation terminates signaling by activated receptor tyrosine kinases. Degradation of EGFR occurs in lysosomes and requires the switching of RAB5 for RAB7 on late endosomes to enable their fusion with the lysosome, but what controls this critical switching is poorly understood. We show that the tyrosine kinase FER alters PKCδ function by phosphorylating it on Y374, and that phospho-Y374-PKCδ prevents RAB5 release from nascent late endosomes, thereby inhibiting EGFR degradation and promoting the recycling of endosomal EGFR to the cell surface. The rapid association of phospho-Y374-PKCδ with EGFR-containing endosomes is diminished by PTPN14, which dephosphorylates phospho-Y374-PKCδ. In triple-negative breast cancer cells, the FER-dependent phosphorylation of PKCδ enhances EGFR signaling and promotes anchorage-independent cell growth. Importantly, increased Y374-PKCδ phosphorylation correlating with arrested late endosome maturation was identified in ∼25% of triple-negative breast cancer patients, suggesting that dysregulation of this pathway may contribute to their pathology. Research has demonstrated associations between parental depression (PD) and negative psychological outcomes among their children. However, little is known about the pathways through which lifetime parent traumatic events (PTEs) influence their adolescents' internalizing symptoms. Our study examined whether PD mediates the association between PTE and adolescent depressive and anxious symptoms among youth with persistent postconcussive symptoms (PPCS). We used baseline data from a randomized effectiveness trial of collaborative care for treatment of persistent postconcussive symptoms among sports-injured adolescents aged 11-18 years. Parent-adolescent dyads were recruited from pediatric clinics throughout western Washington. Eligible adolescents had three or more PPCS that lasted for at least 1 month but <9 months and spoke English. Of 1,870 potentially eligible adolescents, 1,480 (79%) were excluded for not meeting the inclusion criteria. Of the eligible 390 adolescents, 189 (49%) declined to participate/consent. Participants included 200 parent-adolescent dyads (adolescent Mage = 14.7 years, SD = 1.7). Parent respondents were mostly female (83%) and mothers (81%). Adolescents reported on their depressive (Patient Health Questionnaire-9; PHQ-9) and anxious symptoms (Revised Child Anxiety and Depression Scale-Short Version [anxiety subscale]) and parents reported on their depressive symptoms (M = 3.7, SD = 3.7; PHQ-9). Mediation analyses revealed two (out of four) significant indirect effects of PTE on both adolescent and parent report of depressive symptoms, but not anxiety. This study elucidate
