Abstract
Introduction: The Geographic Management of Cancer Health Disparities Program (GMaP) is a national NCI program with the goal of increasing cancer health disparities (CHD) research. GMaP ...Region 1 North (R1N) is one of seven GMaP Regional “hubs” based at NCI-designated cancer centers (CCs) across the country, covering the states of DE, KY, ME, MD, NH, VA, VT, WV, and the District of Columbia. The National Outreach Network (NON) is a national NCI program with the goal of conducting cancer education and outreach in underserved communities to reduce CHD. NON Community Health Educators (CHEs) are based at 38 NCI-designated CCs across the country. Six NCI-designated CCs with NON CHEs fall within the GMaP R1N coverage area.
Methods: GMaP R1N staff and NON CHEs within the R1N coverage area met bimonthly to collaborate on the Screen to Save (S2S): NCI Colorectal Cancer (CRC) Outreach and Screening Initiative. The goal of S2S was to educate underserved communities on CRC and CRC screening. NON CHEs conducted the projects in diverse urban and rural communities within their CC catchment areas. Participants attended a CRC education event that provided an inflatable colon or a PowerPoint presentation and completed demographic and pre-/post-event surveys to gauge their knowledge of CRC screening. Surveys were submitted to NCI Center to Reduce Cancer Health Disparities program staff for review and data entry. Raw data files were returned to NON CHEs and shared with GMaP R1N staff for analysis. R1N staff provided research expertise to compare results between urban and rural S2S participants.
Results: There were a total of 328 participants in S2S (n=200 urban; n=128 rural) in the GMaP R1N/NON coverage area. The median age of urban participants was 59.5 vs. 49.0 for rural participants. 95% of urban participants and 96.1% of rural participants reported having health insurance (public or private). 92.9% of urban and 88.1% of rural participants attained at least a high school diploma or GED. 76.5% of urban and 41.4% of rural participants reported ever being screened for CRC by any method. The percent increase between pre- and post-test scores for the educational intervention was 15% for urban vs. 13.3% for rural participants, with an overall percent increase in knowledge of 14.2%.
Conclusions: The urban and rural participants were similar in educational and health insurance attainment levels. Urban residents reported much higher rates of previous CRC screening than rural residents, but this is likely due to the fact that more rural participants were younger than the recommended CRC initial screening age at the time (age 50). The S2S educational intervention was effective in increasing knowledge of CRC screening among both rural and urban participants, with similar increase between the two groups. Overall, this project demonstrated that two different yet complementary programs, GMaP and NON, can work together by utilizing program strengths to successfully implement an educational intervention conducted across a wide and diverse geographic area.
Citation Format: Mark Cromo, Rhonda Boozer-Yeary, Melinda L. Rogers, Katelyn Schifano, Jenna Schiffelbein, Katherine L. Jones, Marcela Blinka, Julia F. Houston, Betsy Grossman, Lindsay Hauser, James Zabora, Mark B. Dignan, Tracy Onega. Integrating research and outreach to increase CRC screening knowledge in underserved communities: The Geographic Management of Cancer Health Disparities Program and National Outreach Network Screen to Save partnership abstract. In: Proceedings of the Eleventh AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2018 Nov 2-5; New Orleans, LA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2020;29(6 Suppl):Abstract nr A015.
Ladder and web polymorphic forms of cocrystals of tetramethylpyrazinedioxide (TMPDO) and tetracyanoethylene (TCNE) are obtained by rapid or slow crystallization, respectively. In the ...thermodynamically less stable, purple (TMPDO)2− TCNE crystals the donor and acceptor building blocks are linked through N+O−°C(alkene) interactions to form one‐dimensional ladders (see picture below).
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In order to investigate the antiproliferative and anti-invasive effects of tumor necrosis factor (TNF)-alpha on human glioblastoma cells, an in vitro three-dimensional (anchorage-independent) assay ...was performed using Matrigel, a mixture of extracellular matrix proteins. Four glioblastoma-derived cell lines, including one cloned line, were cultured in Matrigel with or without TNF-alpha. In the Matrigel containing TNF-alpha, three of the four cell lines, including the cloned line, showed significant growth inhibition in a dose-dependent manner. Dramatic three-dimensional morphological differences were observed between TNF-treated and untreated glioblastoma cells cultured in Matrigel. Untreated cells formed large and highly branched colonies throughout the gel. In contrast, the majority of TNF-treated cells demonstrated truncated branching processes and, at a high TNF-alpha dose, an increasing number of cells remained in relatively small spherical aggregates, their cell processes being significantly reduced. Quantitative invasion assay using a micro-Boyden chamber system confirmed that TNF-treated cells lost invasiveness in a dose-dependent manner. These results suggest that TNF-alpha exerts not only antiproliferative but also anti-invasive effects on human glioblastoma cells in vitro. It is believed that this is the first report showing the anti-invasive effect of TNF-alpha on tumor cells.
As part of continuing studies to investigate the possible regulatory effects of cytokines on malignant astrocytes, we investigated the effects of interleukin-4 (IL-4) alone and in combination with ...tumor necrosis factor-alpha (TNF alpha) and/or interferon-gamma (IFN gamma) on the cell growth and major histocompatibility complex (MHC) antigen expression of a cloned human glioblastoma cell line (9C). The 9C cells were treated with IL-4 alone or in combination with TNF alpha and/or IFN gamma and were examined for proliferation by crystal violet assay and for Class II MHC antigen by flow cytometry. Results indicated that IL-4 alone did not affect 9C proliferation. In combination with TNF alpha or IFN gamma, however, IL-4 significantly and dose-dependently inhibited cell growth. As previous reports have shown, TNF alpha combined with IFN gamma exerted an additive growth suppressive effect on glioblastoma cells, probably by enhancing TNF receptor expression. This additive effect of TNF alpha and IFN gamma was further enhanced by IL-4. In contrast, IL-4 did not modulate expression of Class II MHC antigen on 9C cells, even in combination with IFN gamma, which predictably enhanced this antigen. These results suggest that IL-4 is capable of modulating glioblastoma growth only in the presence of other cytokines, such as TNF alpha and/or IFN gamma. Further, the effect of IL-4 on glioblastoma proliferation is selective and independent of the mechanisms involved in regulating MHC antigen expression.
The authors describe the clinical behavior of eight patients with cerebral astrocytomas, in whom computerized tomography (CT) or magnetic resonance (MR) imaging of the brain was characterized by ...diffuse bilateral cerebral hemisphere tissue density abnormalities and minimal focal mass effect. Five patients were newly diagnosed, and three others had been treated for focal low-grade astrocytoma. Histological diagnoses included anaplastic astrocytoma (three patients), low-grade astrocytoma (three patients), glioblastoma (one patient), and gliosis with later development of glioblastoma (one patient). In five patients, brain tumor was not suspected from the neuroimaging studies, the findings of which were mistaken for radiation leukoencephalopathy, vasogenic edema, or multiple sclerosis. Serial CT scans or MR images undertaken over intervals of 3 to 184 weeks showed progression of abnormal tissue densities in seven patients and multifocal contrast-enhancing masses developed on CT scan in two patients. An autopsy in each of four patients showed diffuse cerebral infiltration by astrocytoma. It is concluded that neuroimaging studies in some patients with diffusely infiltrating cerebral astrocytoma are atypical for neoplasm and can be mistaken for other diseases, especially those that predominantly affect cerebral hemisphere white matter.
Fire is a powerful ecological and evolutionary force that regulates organismal traits, population sizes, species interactions, community composition, carbon and nutrient cycling and ecosystem ...function. It also presents a rapidly growing societal challenge, due to both increasingly destructive wildfires and fire exclusion in fire‐dependent ecosystems. As an ecological process, fire integrates complex feedbacks among biological, social and geophysical processes, requiring coordination across several fields and scales of study.
Here, we describe the diversity of ways in which fire operates as a fundamental ecological and evolutionary process on Earth. We explore research priorities in six categories of fire ecology: (a) characteristics of fire regimes, (b) changing fire regimes, (c) fire effects on above‐ground ecology, (d) fire effects on below‐ground ecology, (e) fire behaviour and (f) fire ecology modelling.
We identify three emergent themes: the need to study fire across temporal scales, to assess the mechanisms underlying a variety of ecological feedbacks involving fire and to improve representation of fire in a range of modelling contexts.
Synthesis: As fire regimes and our relationships with fire continue to change, prioritizing these research areas will facilitate understanding of the ecological causes and consequences of future fires and rethinking fire management alternatives.
We describe the diversity of ways in which fire operates as a fundamental ecological and evolutionary process on Earth. We explore research priorities in six categories of fire ecology. We identify three needs: to study fire across temporal scales, to assess the mechanisms underlying a variety of ecological feedbacks involving fire and to improve representation of fire in modeling contexts.
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Monocyte-mediated tumoricidal activity, tumor necrosis factor alpha (TNF alpha) secretion and gene expression were examined in astrocytoma patients, patients with other types of brain tumors (primary ...or metastatic), and normal individuals. The spontaneous monocyte-mediated tumoricidal activity of either patient group against an astrocytoma cell line was significantly greater than normal. There was no difference between patient groups. When monocytes were stimulated with lipopolysaccharide in vitro, tumoricidal activity increased in all patient groups. Patient monocyte activity tested shortly (48 h) after surgery was not different from that before surgery. Both spontaneous and stimulated monocyte cytocidal activities were tumor-cell-restricted: melanoma and astrocytoma cells were equally susceptible but non-neoplastic glial cells were not affected. Examination of monocyte TNF alpha secretion and mRNA expression indicated that patient activity was comparable to or greater than normal. These results demonstrate that, despite steroid therapy, circulating monocytes in astrocytoma and other brain tumor patients retain intact functional activity.
Angelman syndrome (AS), a genetic disorder occurring in approximately one in every 15,000 births, is characterized by severe mental retardation, seizures, difficulty speaking and ataxia. The gene ...responsible for AS was discovered to be UBE3A and encodes for E6-AP, an ubiquitin ligase. A unique feature of this gene is that it undergoes maternal imprinting in a neuron-specific manner. In the majority of AS cases, there is a mutation or deletion in the maternally inherited UBE3A gene, although other cases are the result of uniparental disomy or mismethylation of the maternal gene. While most human disorders characterized by severe mental retardation involve abnormalities in brain structure, no gross anatomical changes are associated with AS. However, we have determined that abnormal calcium/calmodulin-dependent protein kinase II (CaMKII) regulation is seen in the maternal UBE3A deletion AS mouse model and is responsible for the major phenotypes. Specifically, there is an increased αCaMKII phosphorylation at the autophosphorylation sites Thr(286) and Thr(305/306), resulting in an overall decrease in CaMKII activity. CaMKII is not produced until after birth, indicating that the deficits associated with AS are not the result of developmental abnormalities. The present studies are focused on exploring the potential to rescue the learning and memory deficits in the adult AS mouse model through the use of an adeno-associated virus (AAV) vector to increase neuronal UBE3A expression. These studies show that increasing the levels of E6-AP in the brain using an exogenous vector can improve the cognitive deficits associated with AS. Specifically, the associative learning deficit was ameliorated in the treated AS mice compared to the control AS mice, indicating that therapeutic intervention may be possible in older AS patients.
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DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
Leitern bzw. Netze liegen in den beiden polymorphen Formen der durch unterschiedlich rasches Kristallwachstum erhaltenen Kristalle von (TMPDO)2TCNE vor. In kinetisch bevorzugten, purpurfarbenen ...Kristallen sind die Donor‐ und Acceptorbausteine über N+O− … C(Alken)‐Wechselwirkungen zu Leitern organisiert (siehe unten).
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