3,583 research outputs found

    Sprayable birefringent coating enables strain measurements on large surfaces

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    Birefringent coating for strain measurements on large surfaces contains constituents that can be premixed and sprayed as a single component with conventional paint spray equipment. Elevated temperatures are not required for spraying or curing of the coating material which has long pot life

    Birefringent coatings for nondestructive testing of honeycomb sandwich structures Final engineering report no. 8379, 30 Jun. 1965 - 15 Mar. 1966

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    Epoxy birefringent coatings for nondestructive testing of honeycomb sandwich structure

    Qualitative effects on safety and construction materials of 1300 deg F sodium-potassium spray in air and nitrogen

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    Shielding material evaluation for resistance to sodium potassium fires in air and nitroge

    Targeting the Mitotic Catastrophe Signaling Pathway in Cancer

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    Evaluation of the revised sense of coherence scale in a representative German sample

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    Background and objectives To evaluate the Revised Sense of Coherence (SOC-R) scale in a large representative German sample. Design A nationwide household survey involving a total of 2510 face-to-face interviews. Methods In addition to the SOC-R, childhood trauma and maltreatment (CTM), lifetime traumatic events (Childhood Trauma Questionnaire, CTQ, and the Life Events Checklist for DSM-5, LEC-5), and mental health (Patient Health Questionnaire, PHQ-4) were assessed. Results The final sample consisted of N = 2373 participants (52.3% females; M = 48.24 years). Confirmatory factor analyses confirmed a three-factor structure for the SOC-R (‘manageability’, ‘balance’, ‘reflection’) with acceptable indices (RMSEA .066; 90% CI [.062, .071]). Reliability analyses revealed good internal consistency (α = .87). Construct validity was supported by significant but low correlations with psychopathology. Gender marginally influenced SOC-R (t = 1.99, p = .05). Moderation analyses revealed that SOC-R exerted a protective impact on depression in the context of CTQ (t = 2.29, p < .05) and lifetime traumatic events (t = –2.37, p < .05). Conclusions This study supports the psychometric properties of the SOC-R and emphasizes the importance of considering salutogenic effects to better understand interindividual differences in the effect of adversity

    2-Hydr­oxy-3-nitro-N-phenyl­benzamide

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    The asymmetric unit of the title compound, C13H10N2O4, contains two crystallographically independent mol­ecules. The aromatic rings are oriented at dihedral angles of 24.39 (3) and 7.47 (3)° in the two mol­ecules and intra­molecular N—H⋯O and O—H⋯O hydrogen bonds result in the formation of two planar six-membered rings. In the crystal structure, inter­molecular O—H⋯O and C—H⋯O hydrogen bonds link the mol­ecules into chains, forming R 2 2(10) ring motifs. Weak π–π contacts between the benzene and phenyl rings [centroid–centroid distance = 3.955 (3) Å] may further stabilize the structure

    Platelet-derived growth factor receptor-β, carrying the activating mutation D849N, accelerates the establishment of B16 melanoma

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    <p>Abstract</p> <p>Background</p> <p>Platelet-derived growth factor (PDGF)-BB and PDGF receptor (PDGFR)-β are mainly expressed in the developing vasculature, where PDGF-BB is produced by endothelial cells and PDGFR-β is expressed by mural cells, including pericytes. PDGF-BB is produced by most types of solid tumors, and PDGF receptor signaling participates in various processes, including autocrine stimulation of tumor cell growth, recruitment of tumor stroma fibroblasts, and stimulation of tumor angiogenesis. Furthermore, PDGF-BB-producing tumors are characterized by increased pericyte abundance and accelerated tumor growth. Thus, there is a growing interest in the development of tumor treatment strategies by blocking PDGF/PDGFR function. We have recently generated a mouse model carrying an activated PDGFR-β by replacing the highly conserved aspartic acid residue (D) 849 in the activating loop with asparagine (N). This allowed us to investigate, in an orthotopic tumor model, the role of increased stromal PDGFR-β signaling in tumor-stroma interactions.</p> <p>Methods</p> <p>B16 melanoma cells lacking PDGFR-β expression and either mock-transfected or engineered to express PDGF-BB, were injected alone or in combination with matrigel into mice carrying the activated PDGFR-β (D849N) and into wild type mice. The tumor growth rate was followed and the vessel status of tumors, i.e. total vessel area/tumor, average vessel surface and pericyte density of vessels, was analyzed after resection.</p> <p>Results</p> <p>Tumors grown in mice carrying an activated PDGFR-β were established earlier than those in wild-type mice. In this early phase, the total vessel area and the average vessel surface were higher in tumors grown in mice carrying the activated PDGFR-β (D849N) compared to wild-type mice, whereas we did not find a significant difference in the number of tumor vessels and the pericyte abundance around tumor vessels between wild type and mutant mice. At later phases of tumor progression, no significant difference in tumor growth rate was observed between wild type mice and mutant mice, although the pericyte coverage was higher around tumor vessels from mutant mice.</p> <p>Conclusion</p> <p>Our findings suggest that the activated PDGFR-β (D849N) in the host animal increased the total vessel area and the average vessel surface even in PDGF-negative tumors, resulting in a shorter lag phase during tumor establishment.</p

    Myc inhibition is effective against glioma and reveals a role for Myc in proficient mitosis.

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    Gliomas are the most common primary tumours affecting the adult central nervous system and respond poorly to standard therapy. Myc is causally implicated in most human tumours and the majority of glioblastomas have elevated Myc levels. Using the Myc dominant negative Omomyc, we previously showed that Myc inhibition is a promising strategy for cancer therapy. Here, we preclinically validate Myc inhibition as a therapeutic strategy in mouse and human glioma, using a mouse model of spontaneous multifocal invasive astrocytoma and its derived neuroprogenitors, human glioblastoma cell lines, and patient-derived tumours both in vitro and in orthotopic xenografts. Across all these experimental models we find that Myc inhibition reduces proliferation, increases apoptosis and remarkably, elicits the formation of multinucleated cells that then arrest or die by mitotic catastrophe, revealing a new role for Myc in the proficient division of glioma cells

    Children reading to dogs: a systematic review of the literature

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    Background Despite growing interest in the value of human-animal interactions (HAI) to human mental and physical health the quality of the evidence on which postulated benefits from animals to human psychological health are based is often unclear. To date there exist no systematic reviews on the effects of HAI in educational settings specifically focussing on the perceived benefits to children of reading to dogs. With rising popularity and implementation of these programmes in schools, it is essential that the evidence base exploring the pedagogic value of these initiatives is well documented. Methods Using PRISMA guidelines we systematically investigated the literature reporting the pedagogic effects of reading to dogs. Because research in this area is in the early stages of scientific enquiry we adopted broad inclusion criteria, accepting all reports which discussed measurable effects related to the topic that were written in English. Multiple online databases were searched during January-March 2015; grey literature searches were also conducted. The search results which met the inclusion criteria were evaluated, and discussed, in relation to the Oxford Centre for Evidence Based Medicine levels of evidence; 27 papers were classified as Level 5, 13 as Level 4, 7 as Level 2c and 1 as Level 2b. Conclusion The evidence suggests that reading to a dog may have a beneficial effect on a number of behavioural processes which contribute to a positive effect on the environment in which reading is practiced, leading to improved reading performance. However, the evidence base on which these inferences are made is of low quality. There is a clear need for the use of higher quality research methodologies and the inclusion of appropriate controls in order to draw causal inferences on whether or how reading to dogs may benefit children’s reading practices. The mechanisms for any effect remain a matter of conjectur

    EGFR/HER2 inhibitor AEE788 increases ER-mediated transcription in HER2/ER-positive breast cancer cells but functions synergistically with endocrine therapy

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    BACKGROUND: Cross-talk between receptor tyrosine kinases and the oestrogen receptor (ER) is implicated in resistance to endocrine therapy. We investigated whether AEE788 (a combined inhibitor of EGFR, HER2 and VEGFR) plus tamoxifen or letrozole enhanced the individual anti-tumour effects of these agents. METHODS: Breast cancer cell lines modelling endocrine-resistant and -sensitive disease were engineered to express aromatase (A) and examined using proliferation, western blotting and ER-alpha transcription assays. RESULTS: AEE788 enhanced the anti-proliferative effect of tamoxifen and letrozole in ER+ cell lines (MCF-7 2A, ZR75.1 A3 and BT474 A3). This associated with an elevated G1 arrest and nuclear accumulation of p27. It is noteworthy that AEE788 alone or in combination with endocrine therapy increased the expression of progesterone receptor (PGR) and TFF1 in BT474 A3 cells. This may indicate a mechanism of resistance to AEE788 in ER+/HER2(+) breast cancers. In a ZR75.1 A3 xenograft, AEE788 alone or in combination with tamoxifen provided no further benefit compared with letrozole. However, letrozole plus AEE788 produced a significantly greater inhibition of tumour growth compared with letrozole alone. CONCLUSION: These data suggest that AEE788 plus letrozole in breast cancer overexpressing HER2 may provide superior anti-tumour activity, compared with single agents. British Journal of Cancer (2010) 102, 1235-1243. doi: 10.1038/sj.bjc.6605641 www.bjcancer.com (C) 2010 Cancer Research U
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