Translating neuroscience research to practice through grassroots professional learning communities.

The fields of Educational Neuroscience and Mind, Brain, and Education explore how neuroscience and psychology research can be applied to education practice. Prior work in these fields helped to distill and convey various learning strategies to educators, but bidirectional communication between researchers and educators is still very limited. Given the current challenges facing students and educators, such as the student mental health crisis [[1-4] and educator burnout [5-7], there is a great need for more inclusive research translation efforts.

Reversal of CYLD phosphorylation as a novel therapeutic approach for adult T-cell leukemia/lymphoma (ATLL).

Adult T-cell leukemia/lymphoma (ATLL) is a malignancy of mature T cells associated with chronic infection by human T-cell lymphotropic virus type-1 (HTLV-1). ATLL patients with aggressive subtypes have dismal outcomes. We demonstrate that ATLL cells co-opt an early checkpoint within the tumor necrosis factor receptor 1 (TNFR1) pathway, resulting in survival advantage.

CYLD Proteolysis Protects Macrophages from TNF-Mediated Auto-necroptosis Induced by LPS and Licensed by Type I IFN.

Tumor necrosis factor (TNF) induces necroptosis, a RIPK3/MLKL-dependent form of inflammatory cell death. In response to infection by Gram-negative bacteria, multiple receptors on macrophages, including TLR4, TNF, and type I IFN receptors, are concurrently activated, but it is unclear how they crosstalk to regulate necroptosis. We report that TLR4 activates CASPASE-8 to cleave and remove the deubiquitinase cylindromatosis (CYLD) in a TRIF- and RIPK1-dependent manner to disable necroptosis in macrophages.

Cloaked in ubiquitin, a killer hides in plain sight: the molecular regulation of RIPK1.

In the past decade, studies have shown how instrumental programmed cell death (PCD) can be in innate and adaptive immune responses. PCD can be a means to maintain homeostasis, prevent or promote microbial pathogenesis, and drive autoimmune disease and inflammation. The molecular machinery regulating these cell death programs has been examined in detail, although there is still much to be explored.

Effect of valacyclovir on viral shedding in immunocompetent patients with recurrent herpes simplex virus 2 genital herpes: a US-based randomized, double-blind, placebo-controlled clinical trial.

Objective: To determine the efficacy of daily suppressive therapy with a 1-g dose of valacyclovir in reducing total (clinical and subclinical) herpes simplex virus 2 (HSV-2) shedding compared with placebo in Immunocompetent patients diagnosed as having recurrent HSV-2 genital herpes.

Patients And Methods: From June 18, 2004, to December 17, 2004, patients from 27 US sites with a history of 6 or more genital herpes recurrences per year were randomized in a 3:1 ratio to receive 1 g/d of valacyclovir or placebo. During the double-blind suppressive therapy, patients were provided with the study drug (500-mg valacyclovir caplets or matching placebo) and Instructed to take 2 caplets once daily without regard to meals for 60 days.

Herpes virus type 2 infection and genital symptoms in primary care patients.

Objective: We aimed to identify whether genital symptoms were associated with unrecognized herpes simplex virus type 2 (HSV-2) infection in a primary care population.

Study Design: Five thousand four hundred fifty-two individuals aged 18 to 59 seeking general care at 36 suburban medical offices in 6 U.S.

Seroprevalence of herpes simplex virus-2 in suburban primary care offices in the United States.

Objective: The objective of this study was to estimate herpes simplex virus-2 (HSV-2) seroprevalence from a weighted sample of adults attending relatively affluent, suburban primary care physician (PCP) offices.

Goal: Many PCPs in relatively affluent areas do not believe national estimates of HSV-2 seroprevalence are representative of their patient populations. This study aimed to measure HSV-2 seroprevalence in these patient populations.