Extracting typed entity mentions from text is a fundamental component to language understanding and reasoning. While there exist substantial labeled text datasets for multiple subsets of biomedical entity types-such as genes and proteins, or chemicals and diseasesit is rare to find large labeled datasets containing labels for all desired entity types together. This paper presents a method for training a single CRF extractor from multiple datasets with disjoint or partially overlapping sets of entity types. Our approach employs marginal likelihood training to insist on labels that are present in the data, while filling in "missing labels". This allows us to leverage all the available data within a single model. In experimental results on the Biocreative V CDR (chemicals/diseases), Biocreative VI ChemProt (chemicals/proteins) and Med-Mentions (19 entity types) datasets, we show that joint training on multiple datasets improves NER F1 over training in isolation, and our methods achieve state-of-the-art results.

The present study is an attempt to replicate with some modification Silverman's earlier studies which examine the effects of subliminal neutral and aggressive stimuli on the thought processes of schizophrenics. The present sample consisted of 24 male patients all diagnosed as schizophrenic with no secondary diagnosis. Utilizing classical experimental procedures, they were seen in counterbalanced order for an experimental and control session. Inkblot responses were obtained following tachistoscopic exposure of four milliseconds to an aggressive and neutral (relatively unaggressive) stimulus. The responses were scored according to the latest version of Holt's Manual for scoring primary process. In addition, a measure of non-verbal pathological behaviour was obtained. The findings did not confirm those of Silverman with respect to an increase in pathological thinking and/or non-verbal pathological behaviour following subliminal aggressive stimulation.

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18 experienced joggers showed altered Mood Adjective Check List responding after jogging 12.5 miles, highlighted by increased pleasantness. Results support a broad-spectrum, unipolar approach to quantification of exercise-induced mood change.

Age‐related vascular endothelial dysfunction is mediated by excess reactive oxygen species (ROS)—mitochondria (mito) being a key source—which can reduce nitric oxide (NO) bioavailability. Cellular senescence, a fundamental mechanism of aging, may exacerbate mito ROS and be a potential therapeutic target to combat age‐related vascular dysfunction. Purpose To determine if treatment with the natural flavonoid fisetin improves endothelial function with aging by suppressing cellular senescence, scavenging excess whole‐cell and mito ROS, and increasing NO bioavailability. Methods & Results Old (27 mo) male C57BL/6 mice were treated with vehicle (V; 10% EtOH, 30% PEG400 and 60% Phosal 50 PG; n = 9) or fisetin (Fis; 50 mg/kg/day in V; n = 10) by oral gavage following a 1 wk on – 2 wk off – 1 wk on dosing paradigm. Endothelial function Endothelial function was assessed by ex vivo carotid artery endothelium‐dependent dilation (EDD) and endothelium‐independent dilation (EID) to increasing doses of acetylcholine and sodium nitroprusside, respectively. EDD was greater in Fis vs V treated mice (Peak EDD [%]: 97 ± 1 vs 84 ± 3, P < .05) and no differences were observed among groups in EID (P = .54). Cellular senescence Fis‐treated mice had lower vascular abundance of p16, an established marker of cellular senescence (Fis, .12 ± .01 vs V, .19 ± .02 chemiluminescence units [CU], P < .05). Next, we administered Fis or V to old (27 mo) p16‐3MR mice (a model that allows for clearance of senescent cells with ganciclovir [GCV]; n = 6/group). Fis‐treated p16‐3MR mice had greater EDD (Peak EDD [%]: Fis, 93 ± 2 vs V, 74 ± 5, P < .05). Ex vivo carotid artery incubations with GCV eliminated group differences in EDD, suggesting that Fis reduced senescent cells to improve EDD. Whole‐cell ROS Electron paramagnetic resonance (EPR) spectroscopy was used to assess whole‐cell vascular (aortic) ROS. Fis‐treated mice had lower whole‐cell ROS (Fis, 4703 ± 455 vs V, 8173 ± 1243 amplitude units [AU], P < .05). Incubation with the ROS scavenger TEMPOL eliminated group differences in EDD, implying that Fis ameliorated ROS‐related suppression of EDD. Mito ROS EPR was used to assess vascular mito ROS. Fis‐treated mice had lower mito ROS (Fis, 2527 ±440 vs V, 6603 ± 1956 AU, P < .05). Further, Fis‐treated mice had lower abundance of vascular p‐p66SHC, a recognized marker of mito oxidative stress (Fis, .029 ± .003 vs V, .049 ± .008 CU, P < .05) and greater abundance of Mn superoxide dismutase, a mito antioxidant enzyme (Fis, .41 ± .1 vs V, .20 ± .02 CU, P < .05). Incubation with the mito‐specific antioxidant, MitoQ, eliminated group differences in EDD, implying that Fis ameliorated mito ROS‐related suppression of EDD. NO Addition of the NO‐synthase inhibitor, L‐NAME, abolished group differences in EDD suggesting Fis improved age‐related EDD impairments by increasing NO bioavailability. Conclusion Fisetin supplementation may be a novel strategy to target excess cellular senescence and thereby reduce mito ROS to improve NO‐mediated endothelial function with ag...