We report the identification and characterization of the major repeats in the centromeric and peri-centromeric heterochromatin of Brassica rapa. The analysis involved the characterization of 88 629 bacterial artificial chromosomes (BAC) end sequences and the complete sequences of two BAC clones. We identified centromere-specific retrotransposons of Brassica (CRB) and various peri-centromere-specific retrotransposons (PCRBr). Three copies of the CRB were identified in one BAC clone as nested insertions within a tandem array of 24 copies of a 176 bp centromeric repeat, CentBr. A complex mosaic structure consisting of nine PCRBr elements and large blocks of 238 bp degenerate tandem repeats (TR238) were found in or near a derivative of 5S-25S rDNA sequences. The chromosomal positions of selected repeats were determined using in situ hybridization. These revealed that CRB is a major component of all centromeres in three diploid Brassica species and their allotetraploid relatives. However, CentBr was not detected in the most distantly related of the diploid species analyzed, B. nigra. PCRBr and TR238 were found to be major components in the pericentromeric heterochromatin blocks of four chromosomes of B. rapa. These repetitive elements were not identified in B. oleracea or B. nigra, indicating that they are A-genome-specific.

Background: The primary objective of this paper is to provide a review of research on argumentation in science education based on publications from 1998 to 2014 in three science education journals. In recent years, the teaching and learning argumentation (i.e. the coordination of evidence and theory to support or refute an explanatory conclusion, model or prediction) has emerged as a significant educational goal. Argumentation is a critically important discourse process in science and it should be taught and learned in the science classroom as part of scientific inquiry and literacy. Argumentation stresses the evidence-based justification of knowledge claims, and it underpins reasoning across STEM domains. Our aim in this study was to investigate how argumentation has been positioned within the publications of three top academic journals: Science Education, International Journal of Science Education, and Journal of Research in Science Teaching. A methodology for content analysis of the journals is described using quantitative and qualitative techniques. Results: One of the contributions of our analysis is the illustration that researchers studying argumentation from a linguistic perspective have been emphasizing related concepts in different ways. While the emphasis has been on discourse and discussion across all journals, the related concepts of talk, conversation, dialogue and negotiation were observed to a lesser extent. Likewise, the fine-level analysis of the key epistemic concepts such as reasoning, evidence and inquiry indicates variation in coverage. Conclusions: The findings can provide evidence-based indicators for where more emphasis needs to be placed in future research on argumentation, and in particular they can provide guidelines for journals in soliciting articles that target underemphasized aspects of argumentation in science education.

Prostaglandin E 2 (PGE 2 ), a product of the cyclooxygenation of arachidonic acid released from membrane phospholipids, plays a critical role in inflammatory neurodegenerative conditions. Despite its classic role as a proinflammatory molecule, exogenous PGE 2 was suggested to have protective roles against neuronal death, although the exact protective mechanisms of PGE 2 are not yet defined. Thus, the aim of this study was to examine the effect of exogenous PGE 2 on inflammatory neurotoxicity. Lipopolysaccharide (LPS) induced neuronal toxicity, which was associated with terminal transferase dUTP nick end labeling (TUNEL)-positive neuronal death with increased caspase-3 activity. In neuron-glial coculture, LPS markedly induced inducible nitric oxide synthase/nitric oxide (iNOS/NO) release from microglial cells, but not from neurons; however, LPS-induced oxidative stress such as reactive oxygen species (ROS), measured with 2,7-dichlorofluorescein diacetate oxidation, was increased in neurons, but not in microglial cells. Exogenous PGE 2 (1 g/ml) rescued the neurons, reducing iNOS/NO release from microglial cells and ROS formation from neurons. PGE 2 has been known to increase intracelluar cyclic adenosine monophosphate (cAMP) levels. In this study, we found that intracellular cAMP elevating agents, forskolin, and cAMP analogue, dbcAMP and 8-Br-cAMP, also prevented LPS-induced neuronal death. Thus, these results indicate that exogenous PGE 2 protects against LPS-induced neuronal apoptotic cell death through the intracellular cAMP system, and is associated with the modulation of NO from microglial cells and ROS production from neurons.

The results of our study suggest that skin barrier function, measured by TEWL and capacitance, and clinical severity show a statistically significant correlation in patients with AD.

The colonization of Staphylococcus aureus is one of the most important aggravating factors of atopic dermatitis (AD). Until now, the importance of S. aureus in AD and a positive correlation between colonization with S. aureus and clinical severity/skin barrier function has been demonstrated. The aim of this study was to determine whether there are certain clones of S. aureus which colonize the skin of AD patients. For this purpose, the genotype of S. aureus isolated from AD patients was examined by newly-developed typing methods. With 36 strains of S. aureus isolated from 35 patients with AD, spa typing, multi-locus sequence typing (MLST), and staphylococcal toxin gene assay by multiplex polymerase chain reaction, were performed. Clinical severity and skin barrier function were evaluated with eczema area and severity index (EASI) and with transepidermal water loss (TEWL). Among 36 strains of S. aureus, 14 sequence types (ST) and 20 spa types were identified, suggesting a very heterogeneous genetic composition of S. aureus and the absence of a prevailing genotype in S. aureus colonized with AD patients. Furthermore, there was no specific genotype of S. aureus which was associated with the clinical severity of AD or skin barrier dysfunction. A toxin gene assay, however, showed the predominance of S. aureus strains carrying sea and/or tsst-1. To the best of our knowledge, this is the first report to show the genetic composition of S. aureus strains isolated from AD patients determined by sequence-based typing methods.

Olanzapine (OLZ) is used to treat bipolar disorder, but its therapeutic mechanism of action is not clear. Arachidonic acid (AA, 20:4n-6) plays a critical role in brain signaling and an upregulated AA metabolic cascade was reported in postmortem brains from bipolar disorder patients. Here we tested whether, similar to the action of the mood stabilizers lithium, carbamazepine and valproate, chronic OLZ treatment would reduce AA turnover in rat brain. We administered OLZ (6 mg/kg/day) or vehicle i.p. to male rats once daily for 21 days. A washout group received 21 days of OLZ followed by vehicle on day 22. Two hours after the last injection, [1-14C]AA (170 µCi/kg) was infused intravenously for 5 min, and timed arterial blood samples were taken. After the rat was euthanized at 5 min, its brain was microwaved, removed and analyzed. Chronic OLZ decreased plasma unesterified AA concentration, AA incorporation rates and AA turnover in brain phospholipids. These effects were absent after washout. Consistent with reduced AA turnover, OLZ decreased brain cyclooxygenase activity and the brain concentration of the proinflammatory AA-derived metabolite, prostaglandin E2. In view of upregulated brain AA metabolic markers in bipolar disorder, the abilities of OLZ and the mood stabilizers to commonly decrease prostaglandin E2 and AA turnover in rat brain phospholipids, albeit by different mechanisms, may be related to their efficacy against the disease.

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