Activity

In addition, this dataset provides a resource for use in further functional comparisons across other vegetable oils, and also expands the proteomic resources to non-model species, thus also allowing further comparative inter-species studies. The data presented here are related to the research article of Castro et al. [1].The dataset is about innovation dynamics in the pharmaceutical industry in China. Innovation dynamics is interpreted as knowledge transfer across technologies and through time (velocity). The dataset provides access to 143,916 Jaccard similarity indices. A Jaccard similarity indice is a distance measure between two units. Here, they proxy relatedness across technologies (classes) and through time (velocity). The Jaccard similarity indices are computed based on a Natural Language Processing treatment of 69,923 patents in the pharmaceutical industry in China from 1990 to 2017.The Southern California Bight (SCB) is an upwelling-dominated, open embayment on the U.S. West Coast and receives discharges of anthropogenically-enhanced freshwater, nutrients, carbon, and other materials. These inputs include direct point sources discharged from wastewater treatment (WWT) plants via ocean outfalls and point, non-point, and natural sources discharged via coastal rivers. We assembled a daily time series over 1971-2017 of discharges from large WWT plants ≥ 50 million gallon per day (MGD) and 1997-2017 from small WWT plants and coastal rivers. Constituents include nitrogen, phosphorus, organic carbon, alkalinity, iron, and silica. Data from research studies, several government and non-government agency databases containing discharge monitoring reports, river flow gauges, and other collateral information were compiled to produce this dataset. Predictive models and expert analysis addressed unmonitored sources and data gaps. The time series of terrestrial discharge and fluxes are provided with location of coastal discharge point or tributary. The data are deposited in a repository found in Sutula et al. [1].Epidemiologic studies recognize that trauma and posttraumatic stress are associated with heightened suicidal behavior severity, yet examination of these associations from a genetic perspective is limited. We performed a multivariate gene-by-environment genome-wide interaction study (GEWIS) of suicidality in 123,633 individuals using a covariance matrix based on 26 environments related to traumatic experiences, posttraumatic stress, social support, and socioeconomic status. We discovered five suicidality risk loci, including the male-associated rs2367967 (CWC22), which replicated in an independent cohort. All GEWIS-significant loci exhibited interaction effects where at least 5% of the sample had environmental profiles conferring opposite SNP effects from the majority. We identified PTSD as a primary driving environment for GxE at suicidality risk loci. The male suicidality GEWIS was enriched for three middle-temporal-gyrus inhibitory neuron transcriptomic profiles SCUBE- and PVALB-expressing cells (β = 0.028, p = 3.74 × 10-4), OPRM1-expressing cells (β = 0.030, p = 0.001), and SPAG17-expressing cells (β = 0.029, p = 9.80 × 10-4). Combined with gene-based analyses (CNTN5 p association = 2.38 × 10-9, p interaction = 1.51 × 10-3; PSMD14 p association = 2.04 × 10-7, p interaction = 7.76 × 10-6; HEPACAM p association = 2.43 × 10-6, p interaction = 3.82 × 10-7) including information about brain chromatin interaction profiles (UBE2E3 in male neuron p = 1.07 × 10-5), our GEWIS points to extracellular matrix biology and synaptic plasticity as biological interactors with the effects of potentially modifiable lifetime traumatic experiences on genetic risk for suicidality. Characterization of molecular basis for the effects of traumatic experience and posttraumatic stress on risk of suicidal behaviors may help to identify novel targets for which more effective treatments can be developed for use in high-risk populations.Mild traumatic brain injury (mTBI) is often characterized by deficits in response inhibition, which can contribute to marked social and occupational dysfunction. mTBI often occurs in the context of psychologically traumatic events. This can cause posttraumatic stress disorder (PTSD), which also impedes response inhibition. The overlap or distinction in these inhibitory deficits in mTBI and PTSD is unclear. This study aimed to assess behavioral, neurophysiological, and neuroimaging indices of response inhibition in mTBI by also assessing these parameters in healthy controls (HC) and PTSD participants. Participants with mTBI (without PTSD) (n = 46), PTSD (without mTBI) (n = 41), and HC (n = 40) were assessed during a response inhibition task (the Go/NoGo task) during neuropsychological testing and separate functional magnetic imaging and event-related potentials sessions. read more PTSD symptom severity was assessed with the Clinician-Administered PTSD Scale. Both mTBI and PTSD participants performed more omission errors on the Go/NoGo task and were associated with greater N2 amplitude, greater left inferior parietal activation and reduced connectivity of the left inferior parietal cluster and left angular gyrus compared to HC. There were no differences between mTBI and PTSD on any of these measures. These findings highlight that both mTBI and PTSD contribute to neural dysfunction during response inhibition, and arguably these occur due to distinct mechanisms. In the context of the common comorbidity between these two conditions, strategies to address response inhibition deficits in mTBI may need to consider causative factors underpinning neurological insult of mTBI and psychological effects associated with PTSD.Sex differences in the brain have prompted many researchers to investigate the underlying molecular actors, such as the glucocorticoid receptor (GR). This nuclear receptor controls gene expression, including microRNAs (miRNAs), in non-neuronal cells. Here, we investigated sex-biased effects of GR on hippocampal miRNA expression and neuronal morphology by generating a neuron-specific GR knockout mouse (Emx1-Nr3c1-/-). The levels of 578 mature miRNAs were assessed using NanoString technology and, in contrast to males, female Emx1-Nr3c1-/- mice showed a substantially higher number of differentially expressed miRNAs, confirming a sex-biased effect of GR ablation. Based on bioinformatic analyses we identified several transcription factors potentially involved in miRNA regulation. Functional enrichment analyses of the miRNA-mRNA interactions revealed pathways related to neuronal arborization and both spine morphology and density in both sexes. Two recognized regulators of dendritic morphology, CAMKII-α and GSK-3β, increased their protein levels by GR ablation in female mice hippocampus, without changes in males.