001) and 33% had executive function problems by parent proxy-report (vs. 20% of teens with low level of disordered eating behaviours, p=0.056). A greater level of disordered eating behaviours was associated with executive function problems by teen self report on the General Executive Composite (p<0.001), Behavioral Regulation Index (p<0.001), emotional control clinical scale (p<0.001), shift clinical scale (p<0.001) and by parent proxy-report on the task initiation clinical scale (p=0.008).

Assessing executive function and screening for disordered eating behaviours in teens with type 1 diabetes could help identify a subset of teens at high risk for adverse outcomes and need for intervention.

Assessing executive function and screening for disordered eating behaviours in teens with type 1 diabetes could help identify a subset of teens at high risk for adverse outcomes and need for intervention.Macrophages display marked plasticity with functions in both inflammation and tissue repair. Evidence demonstrates that this spectrum of macrophage phenotypes is influenced by their local microenvironment and tissue origin. However, in vitro macrophage experiments often do not or cannot readily use macrophages from the most relevant tissue of origin. This study investigated if the origin of two C57BL/6 mouse macrophage cell lines of alveolar (AMJ2-C11) and peritoneal (IC-21) origin may influence their response to mycobacterial infection. Both cell lines equally controlled the growth of Mycobacterium bovis BCG and Mycobacterium tuberculosis, although the expression of all proinflammatory cytokines and chemokines measured (TNF, IL-6, MCP-1, MIP-1α, MIP-1β, and RANTES) was significantly higher in AMJ2-C11 cells than in IC-21 cells. During M. tuberculosis infection, IL-6, MCP-1, and RANTES expression increased 5-fold, and MIP-1β expression increased 30-fold. Additionally, AMJ2-C11 cells exhibited significantly higher inducible nitric oxide synthase activity than IC-21 cells, indicative of a more polarized M1 response. FPS-ZM1 nmr The expression of multiple surface markers was also assessed by flow cytometry. CD80 and CD86 were significantly upregulated in AMJ2-C11 cells and downregulated in IC-21 cells during M. tuberculosis infection. The results support the notion that the origin of tissue-resident macrophages influences their phenotype and antimicrobial response and demonstrate hereto unrecognized potential for these cell lines in in vitro studies.

This study aimed to explore the association of mucosa-associated lymphoid tissue lymphoma translocation protein 1 (MALT1) with acute ischemic stroke (AIS) risk and also to explore its association with T helper type 1 (Th1) cells, Th17 cells, disease severity, and prognosis in AIS patients.

One hundred twenty first-episode AIS patients and 120 non-AIS patients with high-stroke-risk factors (as controls) were recruited. Besides, in the cluster of differentiation 4-positive (CD4

) T cells, the MALT1gene expression was detected by reverse transcription quantitative polymerase chain reaction; meanwhile, Th1 and Th17 were detected by flow cytometry. Moreover, serum interferon (IFN)-γ and interleukin (IL)-17 were determined by enzyme-linked immunosorbent assay.

MALT1 expression was increased in AIS patients compared with controls and also it could differentiate AIS patients from controls, with an area under curve of 0.905 (95% confidence interval 0.869-0.941). In AIS patients, MALT1 positively correlated with Th1 cells, Th17 cells, IFN-γ, and IL-17. Besides, MALT1 positively correlated with the National Institutes of Health Stroke Scale score. Furthermore, the Kaplan-Meier curve and univariate Cox’s regression analyses showed no correlation of MALT1high expression with recurrence-free survival (RFS) in AIS patients, although after adjustment using multivariant Cox’s regression, high MALT1 expression independently correlated with worse RFS in AIS patients.

MALT1 expression is increased and positively correlates with disease severity, Th1 cells, and Th17 cells, whose high expression severs as an independent risk factor for worse RFS in AIS patients.

MALT1 expression is increased and positively correlates with disease severity, Th1 cells, and Th17 cells, whose high expression severs as an independent risk factor for worse RFS in AIS patients.During the COVID-19 pandemic, schools around the world rapidly transitioned from in-person to remote learning, providing an opportunity to examine the impact of in-person vs remote learning on sleep, circadian timing, and mood. We assessed sleep-wake timing using wrist actigraphy and sleep diaries over 1-2 weeks during in-person learning (n = 28) and remote learning (n = 58, where n = 27 were repeat assessments) in adolescents (age M ± SD = 12.79 ± 0.42 years). Circadian timing was measured under a single condition in each individual using salivary melatonin (Dim Light Melatonin Onset; DLMO). Online surveys assessed mood (PROMIS Pediatric Anxiety and Depressive Symptoms) and sleepiness (Epworth Sleepiness Scale – Child and Adolescent) in each condition. During remote (vs in-person) learning (i) on school days, students went to sleep 26 minutes later and woke 49 minutes later, resulting in 22 minutes longer sleep duration (all P less then .0001); (ii) DLMO time did not differ significantly between conditions, although participants woke at a later circadian phase (43 minutes, P = .03) during remote learning; and (iii) participants reported significantly lower sleepiness (P = .048) and lower anxiety symptoms (P = .006). Depressive symptoms did not differ between conditions. Changes in mood symptoms were not mediated by sleep. Although remote learning continued to have fixed school start times, removing morning commutes likely enabled adolescents to sleep longer, wake later, and to wake at a later circadian phase. These results indicate that remote learning, or later school start times, may extend sleep and improve some subjective symptoms in adolescents.Imbalance in the metabolic pathway linking excitatory and inhibitory neurotransmission has been implicated in multiple psychiatric and neurologic disorders. Recently, we described enantiomer-specific effects of 2-methylglutamate, which is not decarboxylated to the corresponding methyl analogue of gamma-aminobutyric acid (GABA) 4-aminopentanoic acid (4APA). Here, we tested the hypothesis that 4APA also has enantiomer-specific actions in brain. Mouse cerebral synaptosome uptake (nmol/mg protein over 30 min) of (R)-4APA or (S)-4APA was time and temperature dependent; however, the R enantiomer had greater uptake, reduction of endogenous GABA concentration, and release following membrane depolarization than did the S enantiomer. (S)-4APA exhibited some weak agonist (GABAA α4β3δ, GABAA α5β2γ2, and GABAB B1/B2) and antagonist (GABAA α6β2γ2) activity while (R)-4APA showed weak agonist activity only with GABAA α5β2γ2. Both 4APA enantiomers (100 mg/kg IP) were detected in mouse brain 10 min after injection, and by 1 hr had reached concentrations that were stable over 6 hr; both enantiomers were cleared rapidly from mouse serum over 6 hr.