Impact of Trauma on Brain Morphology & Maladaptive School Behaviors

Wendi Trummert, DrOT, OTR/L, the collaborating clinician for this project, works with students in a self-contained program. Wendi wanted to know how childhood trauma affects brain structure and morphology and how it is linked to behaviors seen in children affected by trauma. A synthesis of all articles looking at the brain reveals differences in both structure and function in the brains of individuals exposed to childhood trauma versus those not exposed (e.g. Daniels, Lamke, Gaebler, Walter, & Scheel, 2013; McGowan et al., 2009; Saleh et al., 2017). A synthesis of articles looking at maladaptive behaviors finds that those often seen in children affected by trauma, including aggression, emotional dysregulation, decreased executive functioning, and hyporeactivity may be linked to these brain changes and may explain why traditional behavioral approaches are often ineffective with this population (e.g. Briggs-Gowan et al., 2010; Lemmey et al., 2001; Shields & Cicchetti, 1998). It is recommended this information be disseminated to educators and others who work with children exposed to trauma to increase understanding and promote appropriate supports. A toolkit including a presentation, pamphlet, and conversational sound bytes were created for the clinician to increase knowledge and combat bias about problem behaviors in children affected by trauma amongst educators and coworkers. Insiders’ perspectives were included to generate empathy, help guide the best type of support for additional student services, and reduce occurrences of inappropriate interventions for maladaptive behaviors. Options and resources to effectively address maladaptive behaviors should be provided to educators after they are presented with this information

Feeding and metabolic consequences of scheduled consumption of large, binge-type meals of high fat diet in the Sprague–Dawley rat

Peer reviewedPublisher PD

Neurones à kisspeptine et oestrogènes. Etude chez le poisson zèbre et le loup de mer. Kisspeptin neurones and their relationships with estrogens. Study in two fish species the zebrafish and the sea bass.

Supported by EU Project LIFECYCLE (FP7-222719-1) to OK and SZ, NEMO project to OK and ACOM/2010/086-GV. SE was supported by a JAE-Predoc (CSIC, Spain).Peer Reviewe

Biological activity of Ipomoea pauciflora Martens and Galeotti (Convolvulaceae) extracts and fractions on larvae of Spodoptera frugiperda J. E. Smith (Lepidoptera: Noctuidae)

Hexane, chloroform and methanol extracts of different parts of Ipomoea pauciflora were tested for their effects on the survival and development of Fall Armyworm (Spodoptera frugiperda), a Lepidoptera pest. For seven days, neonatal larvae (grown at 27 ± 2°C with a 16: 8 (L: D) h photoperiod) were exposed to different concentrations of crude I. pauciflora extracts (ranging from 0 to 4 mg/ml) that were incorporated into an artificial diet. Surviving larvae were weighed at days 6, 9 and 13 and were maintained until moths emerged. Eleven of the 18 crude extracts showed more than 30% larval mortality. The highest mortality was produced by hexane and chloroform extracts of seeds at 4 mg/ml(96.9 and 93.8%, respectively), with LC50 values of 1.85 mg/ml and 0.54 mg/ml, respectively. Fractions of both seed extracts were isolated by gravity column chromatography over silica gel and analyzed for their active compounds. Eight fractions of the hexane extract and six fractions of the chloroform extract from I. pauciflora seeds, exhibited larvicidal effects at 1 mg/ml (mortality from 33.3 to 88.9% and from 47.2 to 77%, respectively). Changes in larval weight were observed as compared with the control group. Phytochemical analysis through GC-MS and H1 NMR revealed the presence of fatty acids and aldehydes in the active fractions. These results indicate that the bioactive extracts from the seed of I. pauciflora can induce lethal toxicity in S. frugiperda larvae or affect the weight of the surviving larvae

A comparison of transgenic rodent mutation and in vivo comet assay responses for 91 chemicals.

A database of 91 chemicals with published data from both transgenic rodent mutation (TGR) and rodent comet assays has been compiled. The objective was to compare the sensitivity of the two assays for detecting genotoxicity. Critical aspects of study design and results were tabulated for each dataset. There were fewer datasets from rats than mice, particularly for the TGR assay, and therefore, results from both species were combined for further analysis. TGR and comet responses were compared in liver and bone marrow (the most commonly studied tissues), and in stomach and colon evaluated either separately or in combination with other GI tract segments. Overall positive, negative, or equivocal test results were assessed for each chemical across the tissues examined in the TGR and comet assays using two approaches: 1) overall calls based on weight of evidence (WoE) and expert judgement, and 2) curation of the data based on a priori acceptability criteria prior to deriving final tissue specific calls. Since the database contains a high prevalence of positive results, overall agreement between the assays was determined using statistics adjusted for prevalence (using AC1 and PABAK). These coefficients showed fair or moderate to good agreement for liver and the GI tract (predominantly stomach and colon data) using WoE, reduced agreement for stomach and colon evaluated separately using data curation, and poor or no agreement for bone marrow using both the WoE and data curation approaches. Confidence in these results is higher for liver than for the other tissues, for which there were less data. Our analysis finds that comet and TGR generally identify the same compounds (mainly potent mutagens) as genotoxic in liver, stomach and colon, but not in bone marrow. However, the current database content precluded drawing assay concordance conclusions for weak mutagens and non-DNA reactive chemicals

SLC45A2 protein stability and regulation of melanosome pH determine melanocyte pigmentation.

SLC45A2 encodes a putative transporter expressed primarily in pigment cells. SLC45A2 mutations cause oculocutaneous albinism type 4 (OCA4) and polymorphisms are associated with pigmentation variation, but the localization, function, and regulation of SLC45A2 and its variants remain unknown. We show that SLC45A2 localizes to a cohort of mature melanosomes that only partially overlaps with the cohort expressing the chloride channel OCA2. SLC45A2 expressed ectopically in HeLa cells localizes to lysosomes and raises lysosomal pH, suggesting that in melanocytes SLC45A2 expression, like OCA2 expression, results in the deacidification of maturing melanosomes to support melanin synthesis. Interestingly, OCA2 overexpression compensates for loss of SLC45A2 expression in pigmentation. Analyses of SLC45A2- and OCA2-deficient mouse melanocytes show that SLC45A2 likely functions later during melanosome maturation than OCA2. Moreover, the light skin-associated SLC45A2 allelic F374 variant restores only moderate pigmentation to SLC45A2-deficient melanocytes due to rapid proteasome-dependent degradation resulting in lower protein expression levels in melanosomes than the dark skin-associated allelic L374 variant. Our data suggest that SLC45A2 maintains melanosome neutralization that is initially orchestrated by transient OCA2 activity to support melanization at late stages of melanosome maturation, and that a common allelic variant imparts reduced activity due to protein instability

The decoupling between genetic structure and metabolic phenotypes in Escherichia coli leads to continuous phenotypic diversity

To assess the extent of intra-species diversity and the links between phylogeny, lifestyle (habitat and pathogenicity) and phenotype, we assayed the growth yield on 95 carbon sources of 168 Escherichia strains. We also correlated the growth capacities of 14 E. coli strains with the presence/absence of enzyme-coding genes. Globally, we found that the genetic distance, based on multilocus sequence typing data, was a weak indicator of the metabolic phenotypic distance. Besides, lifestyle and phylogroup had almost no impact on the growth yield of non-Shigella E. coli strains. In these strains, the presence/absence of the metabolic pathways, which was linked to the phylogeny, explained most of the growth capacities. However, few discrepancies blurred the link between metabolic phenotypic distance and metabolic pathway distance. This study shows that a prokaryotic species structured into well-defined genetic and lifestyle groups can yet exhibit continuous phenotypic diversity, possibly caused by gene regulatory effects

Alternative reproductive adaptation predicts asymmetric responses to climate change in lizards

Anthropogenic climate change ranks among the major global-scale threats to modern biodiversity. Extinction risks are known to increase via the interactions between rapid climatic alterations and environmentally-sensitive species traits that fail to adapt to those changes. Accumulating evidence reveals the influence of ecophysiological, ecological and phenological factors as drivers underlying demographic collapses that lead to population extinctions. However, the extent to which life-history traits influence population responses to climate change remains largely unexplored. The emerging ‘cul-de-sac hypothesis’ predicts that reptilian viviparity (‘live-bearing’ reproduction), a ‘key innovation’ facilitating historical invasions of cold climates, increases extinction risks under progressively warming climates compared to oviparous reproduction – as warming advances polewards/mountainwards, historically cold-climates shrink, leading viviparous species to face demographic collapses. We present the first large-scale test of this prediction based on multiple lizard radiations and on future projections of climate-based ecological niche models. Viviparous species were found to experience stronger elevational range shifts (and potentially increased extinctions) in coming decades, compared to oviparous lizards. Therefore, our analyses support the hypothesis’s fundamental prediction that elevational shifts are more severe in viviparous species, and highlight the role that life-history adaptations play in the responses of biodiversity to ongoing climate change