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A comparative analysis of Irish history at school in the two parts of Ireland from 1921 to the 1990s is proposed here through an examination of history curricula and textbooks. The main focus is on the 1980s and 1990s, which were pivotal decades, usually described as having brought about a gradual convergence between the Republic of Ireland and Northern Ireland in terms of the treatment of Irish history within a wider context and related conceptions of Irish identity. The article argues that the new perspectives in fact reveal a dual trend, with elements of convergence but also enduring or even consolidated aspects of distinctiveness or divergence, in the treatment of both Irish history and European history: the more open, more transnational approaches of Irish history went hand in hand with a consolidation of state and regional identifications, as well as with a different view of the place of European history.

The paper presents the development and test of a skull phantom, which can be used for the assessment of the radiographic visibility of neurovascular implants. State of the art methods are based on specimens of the human skull. These are highly individual and not suitable for comparison of different radiographic data sets. The development process of the skull phantom is described from data generation to image processing, design and manufacturing using 3D printing. An experimental setup is recommended to generate reproducible data sets for implant visibility assessment with bone mimicking structures of the phantom. The model is evaluated by qualitative comparison with equivalent data sets of the original human skull model. The results show, that contrast characteristics of the phantom and the human skull model are similar. X-ray attenuation of the human bone is higher than the polymeric phantom material. The introduced phantom allows the determination of X-ray attenuation characteristics of different neurovascular implants for medical approval and testing processes.

A common history curriculum was introduced for the first time in Northern Ireland schools in 1991, which attempted to bridge the longstanding gap between Catholic and state schools in this field. This paper outlines the various aspects of the crucial role played by a number of historians from all the major universities in Ireland, North and South, but especially from Queen's University, Belfast, in making this change possible, through the development of new historiographical perspectives on Irish history, but also through their more direct and deliberate drive to popularise these perspectives within Northern Ireland society from the 1960s to the end of the 1980s. This engagement of many historians above and beyond their work as researchers shows that they tried to reconcile their scientific work as academics with a recognition of their social role, thus providing a good illustration of the ambiguous nature of the social function of historians in contemporary democracies. (Contains 52 footnotes.)

A comparative analysis of Irish history at school in the two parts of Ireland from 1921 to the 1990s is proposed here through an examination of history curricula and textbooks. The main focus is on the 1980s and 1990s, which were pivotal decades, usually described as having brought about a gradual convergence between the Republic of Ireland and Northern Ireland in terms of the treatment of Irish history within a wider context and related conceptions of Irish identity. The article argues that the new perspectives in fact reveal a dual trend, with elements of convergence but also enduring or even consolidated aspects of distinctiveness or divergence, in the treatment of both Irish history and European history: the more open, more transnational approaches of Irish history went hand in hand with a consolidation of state and regional identifications, as well as with a different view of the place of European history. [ABSTRACT FROM AUTHOR]

An experiment was conducted to test whether the front pre-spore cells of Dictyostelium discoideum are converted to rear pre-spore cells when transplanted in the rear. Results showed that cells on both sides sorted themselves with those in front shifting posteriorly and those at the rear shifting anteriorly. This behavior results from the innate differences between cells rather than from positional signals.

The two layered heterotrophic bacterial communities can corrupt the three linear alkylbenzenesulfonate (LAS) which are approximately 8 congeners out of the complete mixture of 20 congeners. The conclusion drawn is that the community mineralized the important sulfophenylcarboxylates (SPCs), which are obtained from 8 out of the 20 LAS congeners.

To easily edit the genome of naïve human embryonic stem cells (hESC), we introduced a dual cassette encoding an inducible Cas9 into the AAVS1 site of naïve hESC (iCas9). The iCas9 line retained karyotypic stability, expression of pluripotency markers, differentiation potential, and stability in 5iLA and EPS pluripotency conditions. The iCas9 line induced efficient homology-directed repair (HDR) and non-homologous end joining (NHEJ) based mutations through CRISPR-Cas9 system. We utilized the iCas9 line to study the epigenetic regulator, PRC2 in early human pluripotency. The PRC2 requirement distinguishes between early pluripotency stages, however, what regulates PRC2 activity in these stages is not understood. We show reduced H3K27me3 and pluripotency markers in JARID2 2iL-I-F hESC mutants, indicating JARID2 requirement in maintenance of hESC 2iL-I-F state. These data suggest that JARID2 regulates PRC2 in 2iL-I-F state and the lack of PRC2 function in 5iLA state may be due to lack of sufficient JARID2 protein. [ABSTRACT FROM AUTHOR]

In both mice and humans, pluripotent stem cells (PSCs) exist in at least two distinct states of pluripotency, known as the naïve and primed states. Our understanding of the intrinsic and extrinsic factors that enable PSCs to self-renew and to transition between different pluripotent states is important for understanding early development. In mouse embryonic stem cells (mESCs), Wnt proteins stimulate mESC self-renewal and support the naïve state. In human embryonic stem cells (hESCs), Wnt/β-catenin signaling is active in naïve-state hESCs and is reduced or absent in primed-state hESCs. However, the role of Wnt/β-catenin signaling in naïve hESCs remains largely unknown. Here, we demonstrate that inhibition of the secretion of Wnts or inhibition of the stabilization of β-catenin in naïve hESCs reduces cell proliferation and colony formation. Moreover, we showthat addition of recombinant Wnt3a partially rescues cell proliferation in naïve hESCs caused by inhibition of Wnt secretion. Notably, inhibition of Wnt/β-catenin signaling in naïve hESCs did not cause differentiation. Instead, it induced primed hESC-like proteomic andmetabolic profiles. Thus, our results suggest that naïve hESCs secrete Wnts that activate autocrine or paracrine Wnt/β-catenin signaling to promote efficient self-renewal and inhibit the transition to the primed state. [ABSTRACT FROM AUTHOR]

A TOP ACADEMIC DEAN at the University of Medicine and Dentistry of New Jersey allegedly falsified financial statements so that he could be paid a $15,000 annual bonus, while a [...]

With help from U.S. Rep. Dave Weldon, a Republican from Florida and a supporter of Mr. DeLay, the Florida Institute of Technology, a private university in Melbourne, was awarded a [...]

The article discusses different approaches to social policy with reference to Brazil, South Africa and India. Topics covered include the reassessment of the relationship between targeting and universalism in the global South, an examination of the different types of social incorporation such as social insurance, targeted assistance and universalism and an analysis of the groups that have historically been include in, or excluded from, the social welfare system.

Background: Presently, there is no effective treatment for the lethal muscle wasting disease Duchenne muscular dystrophy (DMD). Here we show that increased sphingosine-1-phoshate (S1P) through direct injection or via the administration of the small molecule 2-acetyl-4(5)-tetrahydroxybutyl imidazole (THI), an S1P lyase inhibitor, has beneficial effects in acutely injured dystrophic muscles of mdx mice. Methods: We treated mdx mice with and without acute injury and characterized the histopathological and functional effects of increasing S1P levels. We also tested exogenous and direct administration of S1P on mdx muscles to examine the molecular pathways under which S1P promotes regeneration in dystrophic muscles. Results: Short-term treatment with THI significantly increased muscle fiber size and extensor digitorum longus (EDL) muscle specific force in acutely injured mdx limb muscles. In addition, the accumulation of fibrosis and fat deposition, hallmarks of DMD pathology and impaired muscle regeneration, were lower in the injured muscles of THI-treated mdx mice. Furthermore, increased muscle force was observed in uninjured EDL muscles with a longerterm treatment of THI. Such regenerative effects were linked to the response of myogenic cells, since intramuscular injection of S1P increased the number of Myf5nlacz/+ positive myogenic cells and newly regenerated myofibers in injured mdx muscles. Intramuscular injection of biotinylated-S1P localized to muscle fibers, including newly regenerated fibers, which also stained positive for S1P receptor 1 (S1PR1). Importantly, plasma membrane and perinuclear localization of phosphorylated S1PR1 was observed in regenerating muscle fibers of mdx muscles. Intramuscular increases of S1P levels, S1PR1 and phosphorylated ribosomal protein S6 (P-rpS6), and elevated EDL muscle specific force, suggest S1P promoted the upregulation of anabolic pathways that mediate skeletal muscle mass and function. Conclusions: These data show that S1P is beneficial for muscle regeneration and functional gain in dystrophic mice, and that THI, or other pharmacological agents that raise S1P levels systemically, may be developed into an effective treatment for improving muscle function and reducing the pathology of DMD. [ABSTRACT FROM AUTHOR]

Duchenne muscular dystrophy is a lethal genetic disease characterized by the loss of muscle integrity and function over time. Using Drosophila, we show that dystrophic muscle phenotypes can be significantly suppressed by a reduction of wunen, a homolog of lipid phosphate phosphatase 3, which in higher animals can dephosphorylate a range of phospholipids. Our suppression analyses include assessing the localization of Projectin protein, a titin homolog, in sarcomeres as well as muscle morphology and functional movement assays. We hypothesize that wunen-based suppression is through the elevation of the bioactive lipid Sphingosine 1- phosphate (S1P), which promotes cell proliferation and differentiation in many tissues, including muscle. We confirm the role of S1P in suppression by genetically altering S1P levels via reduction of S1P lyase (Sply) and by upregulating the serine palmitoyl-CoA transferase catalytic subunit gene lace, the first gene in the de novo sphingolipid biosynthetic pathway and find that these manipulations also reduce muscle degeneration. Furthermore, we show that reduction of spinster (which encodes a major facilitator family transporter, homologs of which in higher animals have been shown to transport S1P) can also suppress dystrophic muscle degeneration. Finally, administration to adult flies of pharmacological agents reported to elevate S1P signaling significantly suppresses dystrophic muscle phenotypes. Our data suggest that localized intracellular S1P elevation promotes the suppression of muscle wasting in flies. [ABSTRACT FROM AUTHOR]

A common history curriculum was introduced for the first time in Northern Ireland schools in 1991, which attempted to bridge the longstanding gap between Catholic and state schools in this field. This paper outlines the various aspects of the crucial role played by a number of historians from all the major universities in Ireland, North and South, but especially from Queen's University, Belfast, in making this change possible, through the development of new historiographical perspectives on Irish history, but also through their more direct and deliberate drive to popularise these perspectives within Northern Ireland society from the 1960s to the end of the 1980s. This engagement of many historians above and beyond their work as researchers shows that they tried to reconcile their scientific work as academics with a recognition of their social role, thus providing a good illustration of the ambiguous nature of the social function of historians in contemporary democracies. [ABSTRACT FROM AUTHOR]

Abstract: Novel immunosuppressive strategies are targeting for an antigen-specific deletion of T cells responsible for organ damage in autoimmunity and allograft rejection. Here, we present a new flow cytometry-based assay that allows the reliable and efficient detection of T cells that were eliminated in an antigen-specific fashion. A stable cell-labelling technique utilizing the two membrane dyes PKH26 and PKH67 has been combined with annexin V and 7-aminoactinomycin (7-AAD) staining to detect apoptotic cells. A differential gating strategy enabled us to determine the viability/apoptosis for each PKH-stained T cell subpopulation independently. The capability to simultaneously analyze apoptosis within T cell mixtures of different antigen specificities establishes this assay as a superior tool for the further development of novel antigen-specific immunosuppressive approaches. [Copyright &y& Elsevier]

The immune attack against malignant tumors require the concerted action of CD8+ cytotoxic T lymphocytes (CTL) as well as CD4+ T helper cells. The contribution of T cell receptor (TCR) αβ+ CD4− CD8− double-negative (DN) T cells to anti-tumor immune responses is widely unknown. In previous studies, we have demonstrated that DN T cells with a broad TCR repertoire are present in humans in the peripheral blood and the lymph nodes of healthy individuals. Here, we characterize a human DN T cell clone (T4H2) recognizing an HLA-A2-restricted melanoma-associated antigenic gp100-peptide isolated from the peripheral blood of a melanoma patient. Antigen recognition by the T4H2 DN clone resulted in specific secretion of IFN-γ and TNF. Although lacking the CD8 molecule the gp100-specifc DN T cell clone was able to confer antigen-specific cytotoxicity against gp100-loaded target cells as well as HLA-A2+ gp100 expressing melanoma cells. The cytotoxic capacity was found to be perforin/granzymeB-dependent. Together, these data indicate that functionally active antigen-specific DN T cells recognizing MHC class I-restricted tumor-associated antigen (TAA) may contribute to anti-tumor immunity in vivo. [ABSTRACT FROM AUTHOR]

It is important to understand the regulation of stem cell division because defects in this process can cause altered tissue homeostasis or cancer. The cyclin-dependent kinase inhibitor Dacapo (Dap), a p21p27 homolog, acts downstream of the microRNA (miRNA) pathway to regulate the cell cycle in Drosophila melanogaster germline stem cells (GSCs). Tissue-extrinsic signals, including insulin, also regulate cell division of GSCs. We report that intrinsic and extrinsic regulators intersect in GSC division control; the Insulin receptor (InR) pathway regulates Dap levels through miRNAs, thereby controlling GSC division. Using GFP-dap 3'UTR sensors in vivo, we show that in GSCs the dap 3'UTR is responsive to Dicer-1, an RNA endonuclease III required for miRNA processing. Furthermore, the dap 3'UTR can be directly targeted by miR-7, miR-278 and miR-309 in luciferase assays. Consistent with this, miR-278 and miR-7 mutant GSCs are partially defective in GSC division and show abnormal cell cycle marker expression, respectively. These data suggest that the GSC cell cycle is regulated via the dap 3'UTR by multiple miRNAs. Furthermore, the GFP-dap 3'UTR sensors respond to InR but not to TGF-β signaling, suggesting that InR signaling utilizes Dap for GSC cell cycle regulation. We further demonstrate that the miRNA-based Dap regulation may act downstream of InR signaling; Dcr-1 and Dap are required for nutrition-dependent cell cycle regulation in GSCs and reduction of dap partially rescues the cell cycle defect of InR-deficient GSCs. These data suggest that miRNA- and Dap-based cell cycle regulation in GSCs can be controlled by InR signaling. [ABSTRACT FROM AUTHOR]

The Dystroglycan-Dystrophin (Dg-Dys) complex has a capacity to transmit information from the extracellular matrix to the cytoskeleton inside the cell. It is proposed that this interaction is under tight regulation; however the signaling/regulatory components of Dg-Dys complex remain elusive. Understanding the regulation of the complex is critical since defects in this complex cause muscular dystrophy in humans. To reveal new regulators of the Dg-Dys complex, we used a model organism Drosophila melanogaster and performed genetic interaction screens to identify modifiers of Dg and Dys mutants in Drosophila wing veins. These mutant screens revealed that the Dg-Dys complex interacts with genes involved in muscle function and components of Notch, TGF-β and EGFR signaling pathways. In addition, components of pathways that are required for cellular and/or axonal migration through cytoskeletal regulation, such as Semaphorin-Plexin, Frazzled-Netrin and Slit-Robo pathways show interactions with Dys and/or Dg. These data suggest that the Dg-Dys complex and the other pathways regulating extracellular information transfer to the cytoskeletal dynamics are more intercalated than previously thought [ABSTRACT FROM AUTHOR]

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The article discusses the impact of the COVID-19 pandemic on international education. Topics covered include an uncertainty created by the crisis about international education's future, the challenges facing international students who have been stranded in far-away foreign campuses, and the role of the research community in helping these students confront the challenges.

Background: The follicle cells of the Drosophila egg chamber provide an excellent model in which to study modulation of the cell cycle. During mid-oogenesis, the follicle cells undergo a variation of the cell cycle, endocycle, in which the cells replicate their DNA, but do not go through mitosis. Previously, we showed that Notch signaling is required for the mitotic-to-endocycle transition, through downregulating String/Cdc25, and Dacapo/p21 and upregulating Fizzy-related/Cdh1. Results: In this paper, we show that Notch signaling is modulated by Shaggy and temporally induced by the ligand Delta, at the mitotic-to- ndocycle transition. In addition, a downstream target of Notch, tramtrack, acts at the mitotic-to-endocycle transition. We also demonstrate that the JNK pathway is required to promote mitosis prior to the transition, independent of the cell cycle components acted on by the Notch pathway. Conclusion: This work reveals new insights into the regulation of Notch-dependent mitotic-toendocycle switch. [ABSTRACT FROM AUTHOR]

We present a rapid flow cytometric and non-radioactive functional assay developed for the determination of the cytotoxic activity of T lymphocytes, natural killer cells, and lymphokine-activated killer cells. In contrast to indirect evaluation of cytotoxicity using radioactive assays, this assay is based on the quantitative and qualitative flow cytometric analysis of cell damage on a single cell level. Target cells are stained with PKH-26, a lipophilic dye that stably integrates into the cell membrane, without disturbing its surface marker expression. It, thus, permits the distinction between target and effector cells. After short term in vitro incubation (1.5–3 h), AnnexinV-FITC (ann-FITC) staining allows to discriminate between apoptotic and non-apoptotic target cells. Data analysis is performed first by gating on PKH-26 positive target cells, followed by the analysis of the ann-FITC positive subpopulation. The percentage of cytotoxicity in the PKH-26 gated cell population is calculated by subtracting unspecific ann-FITC positive target cells, measured in appropriate controls without effector cells. Using in vitro generated antigen-specific cytotoxic T lymphocytes, we demonstrate that this flow cytometric assay is sensitive, correlates well with the standard 51Cr release assay, and is easy to handle. [Copyright &y& Elsevier]

In extracellular tip recordings from long trichoid sensilla of male Manduca sexta moths, we studied dose-response relationships in response to bombykal stimuli of two different durations in the adapted and the non-adapted state. Bombykal-responsive cells could be distinguished from non-bombykal-sensitive cells in each trichoid sensillum because the bombykal-responsive cell always generated the action potentials of larger initial amplitude. The bombykal cell, which was recorded at a defined location within a distal flagellar annulus, can resolve at least four log[sub 10]-units of pheromone concentrations but is apparently unable to encode all stimulus durations tested. Parameters of the amplitudemodulated sensillar potential and the frequencymodulated action potential responses were examined in different states of adaptation. Evidence is presented for the existence of several mechanisms of adaptation, which affect distinct steps of the transduction cascade. After adapting pheromone stimuli, the sensillar potential rises to a lower amplitude and declines faster compared with the non-adapted response. In addition, the frequency of the adapted action potential response is reduced. Only the time of rise of the sensillar potential is differentially affected by adapting pheromone stimuli of different duration. The time of rise does not increase after short, but only after long, adapting stimuli. Both short and long adapting stimuli shift the dose-response curves of the sensillar potential amplitude, as well as the initial slope of its rising phase, to higher stimulus concentrations by approximately one log[sub 10]-unit. The shift in the dose-response curve of the action potential response is larger than for the sensillar potential response, suggesting that an additional adaptation mechanism acts at the level of action potential generation. Furthermore, a faster decline of the sensillar potential after short and long adapting stimuli suggests that the resting potential... [ABSTRACT FROM AUTHOR]

Examines the influence of octopamine and serotonin on the oscillation of the transepithelial potential of moth olfactory sensilla. Enhancement of the male moth sensitivity; Potential activity of unstimulated olfactory receptor neurons.