250 research outputs found
Lambda Alpha Anthropology Honors Society (LAB): Bridging The Gap Between Coursework And Career
Many anthropology majors gain an academic familiarity with the subject through coursework, but lack an understanding of how to utilize their anthropological skills outside of academia in future careers. To remedy this issue, the Lambda Alpha Beta Honor Society (LAB), a student-led anthropology organization at Portland State University, provides opportunities for participation in events that get students involved with our local community, such as non-profit organizations and local cultural institutions. Some of these organizations include the Oregon Museum of Science and Industry (OMSI), Clark Public Utilities, The Ridgefield Wildlife Refuge, Potluck in the Park, and Habitat for Humanity. As an unfunded student group, LAB provides opportunities for students at no cost that simultaneously boost their career while also giving back to the community. We also have spearheaded the first crowdsourcing fundraiser in the anthropology department in cooperation with the PSU Foundation to raise money to update our PSU anthropological research photography exhibit. Furthermore, we helped apply for funding to send PSU graduate students to present their research at the Society for Applied Anthropology Conference (SfAA) in Pittsburgh, PA. This conference provides a major networking opportunity for our students and assures our relationship within the applied anthropology subfield in general. Therefore, LAB provides an example of a student group that bridges the gap between studying anthropology in the classroom and practicing anthropology as a career.
Many anthropology majors gain an academic familiarity with the subject through coursework, but lack an understanding of how to utilize their anthropological skills outside of academia in future careers. To remedy this issue, the Lambda Alpha Beta Honor Society (LAB), a student-led anthropology organization at Portland State University, provides opportunities for participation in events that get students involved with our local community, such as non-profit organizations and local cultural institutions. Some of these organizations include the Oregon Museum of Science and Industry (OMSI), Clark Public Utilities, The Ridgefield Wildlife Refuge, Potluck in the Park, and Habitat for Humanity. As an unfunded student group, LAB provides opportunities for students at no cost that simultaneously boost their career while also giving back to the community. We also have spearheaded the first crowdsourcing fundraiser in the anthropology department in cooperation with the PSU Foundation to raise money to update our PSU anthropological research photography exhibit. Furthermore, we helped apply for funding to send PSU graduate students to present their research at the Society for Applied Anthropology Conference (SfAA) in Pittsburgh, PA. This conference provides a major networking opportunity for our students and assures our relationship within the applied anthropology subfield in general. Therefore, LAB provides an example of a student group that bridges the gap between studying anthropology in the classroom and practicing anthropology as a career
A Weighted Estimate for the Square Function on the Unit Ball in \C^n
We show that the Lusin area integral or the square function on the unit ball
of \C^n, regarded as an operator in weighted space has a linear
bound in terms of the invariant characteristic of the weight. We show a
dimension-free estimate for the ``area-integral'' associated to the weighted
norm of the square function. We prove the equivalence of the classical
and the invariant classes.Comment: 11 pages, to appear in Arkiv for Matemati
Fluid shear stress-induced transcriptional activation of the vascular endothelial growth factor receptor-2 gene requires Sp1-dependent DNA binding
AbstractHemodynamic forces play a fundamental role in the regulation of endothelial cell survival. As signaling via the vascular endothelial growth factor (VEGF) receptor-2 pathway has been previously demonstrated to impact endothelial cell survival, we hypothesized that laminar shear stress may facilitate survival in part by inducing VEGF receptor-2 expression. This study shows a time- and dose-dependent upregulation of endothelial VEGF receptor-2 expression by fluid shear stress in microvascular and large-vessel derived endothelial cells. A functional analysis of the 5′-regulatory region of the VEGF receptor-2 promoter localized the shear stress-response element to a sequence between bp −60 and −37 that encompasses two adjacent consensus Sp1 transcription factor binding sites. Constitutive and shear stress-inducible Sp1-dependent complexes are bound to this element, indicating that fluid shear stress-induced transcriptional activation of the VEGF receptor-2 gene requires Sp1-dependent DNA binding. Together, these results suggest that biomechanical stimulation may lead to endothelial cell survival by upregulating VEGF receptor-2 expression
Synthesis, characterisation and in-vitro cytotoxicity of mixed ligand Pt(II) oxadiazoline complexes with hexamethylenetetramine and 7-nitro-1,3,5-triazaadamantane.
Trans-platinum(II) oxadiazoline complexes with 7-nitro-1,3,5-triazaadamantane (NO2-TAA) or hexamethylenetetramine (hmta) ligands have been synthesised from trans-[PtCl2(PhCN)2] via cycloaddition of nitrones to one of the coordinated nitriles, followed by exchange of the other nitrile by NO2-TAA or hmta. Stoichiometric control allows for the selective synthesis of mono- and dinuclear complexes where 7-NO2TAA and hmta act as mono- and bidentate ligands, respectively. Precursors and the target complexes trans-[PtCl2(hmta)(oxadiazoline)], trans-[PtCl2(NO2-TAA)(oxadiazoline)] and trans-[{PtCl2(oxadiazoline)}2(hmta)] were characterised by elemental analysis, IR and multinuclear (1H, 13C, 195Pt) NMR spectroscopy. DFT (B3LYP/6-31G*/LANL08) and AIM calculations suggest a stronger bonding of hmta with the [PtCl2(oxadiazoline)] fragment, in agreement with the experimentally observed reactivity in the ligand exchange (hmta > 7-NO2TAA). Replacement of the nitrile by hmta is predicted more exothermic than that with 7-NO2-TAA, although the activation barriers are similar. Protonation of the non-coordinated N atoms is anticipated to weaken the Pt-N bond and lower the activation barrier for ligand exchange. This effect might help activate these compounds in a slightly acidic environment such as some tumour tissues. Ten of the new compounds were tested for their in vitro cytotoxicity in the human cancer cell lines HeLa and A549. Some of the mononuclear complexes are more potent than cisplatin, and their activity is still high in A549 where cisplatin shows little effect. The dinuclear complexes are inactive, presumably due to their lipophilicity and reduced solubility in water
Development of SNP and microsatellite markers for goldsinny wrasse (Ctenolabrus rupestris) from ddRAD sequencing data
Wrasse (Labridae) species have been used as parasite cleaners in Atlantic salmon farming since the 1980s. However, their use has recently escalated, with millions now being introduced into salmon cages each year. Most fish are of wild origin, their exploitation potentially impacting native populations. Genetic information is urgently required to inform management decisions. We identified 174 microsatellite and 149 SNP markers from ddRAD sequence data. From these, 17 and 48 microsatellite and SNP markers, respectively, were validated by genotyping 150 goldsinny wrasse collected from five locations along the Norwegian and Swedish coasts. Two to 30 alleles were identified at the microsatellite loci, while gene diversity (He) ranged 0.101–0.907. All SNP loci were biallelic, with averagedHeper locus ranging between 0.063 and 0.495
Integrative clinical transcriptome analysis reveals TMPRSS2-ERG dependency of prognostic biomarkers in prostate adenocarcinoma
In prostate adenocarcinoma (PCa), distinction between indolent and aggressive disease is challenging. Around 50% of PCa are
characterized by TMPRSS2-ERG (T2E)-fusion oncoproteins defining two molecular subtypes (T2E-positive/negative). However,
current prognostic tests do not differ between both molecular subtypes, which might affect outcome prediction. To investigate
gene-signatures associated with metastasis in T2E-positive and T2E-negative PCa independently, we integrated tumor
transcriptomes and clinicopathological data of two cohorts (total n = 783), and analyzed metastasis-associated gene-
signatures regarding the T2E-status. Here, we show that the prognostic value of biomarkers in PCa critically depends on the T2E-status. Using gene-set enrichment analyses, we uncovered that metastatic T2E-positive and T2E-negative PCa arecharacterized by distinct gene-signatures. In addition, by testing genes shared by several functional gene-signatures for theirassociation with event-free survival in a validation cohort (n=272), we identifiedfive genes (ASPN,BGN,COL1A1,RRM2andTYMS)—three of which are included in commercially available prognostic tests—whose high expression was significantlyassociated with worse outcome exclusively in T2E-negative PCa. Among these genes,RRM2andTYMSwere validated byimmunohistochemistry in another validation cohort (n=135), and several of them proved to add prognostic information tocurrent clinicopathological predictors, such as Gleason score, exclusively for T2E-negative patients. No prognostic biomarkerswere identified exclusively for T2E-positive tumors. Collectively, our study discovers that the T2E-status, which ispersenot astrong prognostic biomarker, crucially determines the prognostic value of other biomarkers. Our data suggest that themolecular subtype needs to be considered when applying prognostic biomarkers for outcome prediction in PCa.
What’s new?
Genetic rearrangements involving androgen-regulated transmembrane protease serine 2 and genes from the ETS transcription
factor family (T2E), most commonly ERG and ETV1, occur in half of prostate cancers but are currently not considered in risk
predictions. The authors integrate clinical and transcriptomic data from multiple studies and show that the prognostic value of
biomarkers critically depends on the T2E-status. They identify five biomarkers that predict negative outcome exclusively in
T2E-negative prostate cancers, which has implications for outcome prediction based on the molecular subtype.Deutsche Forschungsgemeinschaft 391665916Deutsche Krebshilfe 70112257Dr Leopold and Carmen Ellinger FoundationDr Rolf M. Schwiete FoundationFriedrich-Baur FoundationGert and Susanna Mayer FoundationKind-Philipp FoundationMatthias-Lackas FoundationMehr LEBEN fur Krebskranke Kinder-Bettina-Brau-StiftungWilhelm Sander-Stiftung 2016.167.
Ibrutinib does not impact CCR7-mediated homeostatic migration in T-cells from chronic lymphocytic leukemia patients
Bruton’s tyrosine kinase inhibitor ibrutinib has significantly changed treatment landscape in chronic lymphocytic leukemia (CLL). Growing evidence supports ibrutinib to work beyond the effect on tumor cells by means of, for example, restoring functionality of the T-cell compartment and increasing circulating T-cell numbers. Recent evidence suggests T-cell enhanced expansion, rather than increased egress from secondary lymphoid organs (SLO), as a root cause for ibrutinib-induced lymphocytosis. However, whether the latter physiological change is also a consequence of a forced retention in blood remains undisclosed. Since CCR7 is the main chemokine receptor taking over the homing of T-cells from peripheral compartments to lymph nodes and other SLO, we aimed to investigate the impact of ibrutinib on CCR7 functionality in T-cells. To this end, we documented receptor expression in T-cells from a large cohort of ibrutinib-treated CLL patients, and performed different in vivo and in vitro migration models. Overall, our data confirm that CCR7 expression or receptor-mediated migration in CLL T-cells is not affected by ibrutinib. Furthermore, it does not modulate CCR7-driven homing nor nodal interstitial migration. Together, our results support that ibrutinib-induced CLL T-cell accumulation in the blood stream is not derived from an impairment of CCR7-driven recirculation between the SLO and bloodstream, and therefore T-cell expansion is the most plausible causeA.M.-J. was partially financed by Alfonso MartÃn Escudero Foundation. The other authors received no grants for this wor
Genetic deletion of hepatic NCOR1 protects from atherosclerosis by promoting alternative bile acid-metabolism and sterol excretion
BACKGROUND
The nuclear receptor corepressor 1 (NCOR1) plays an important role in the regulation of gene expression in immunometabolic conditions by connecting chromatin-modifying enzymes, coregulators and transcription factors. NCOR1 has been shown to be involved in cardiometabolic diseases. Recently, we demonstrated that the deletion of macrophage NCOR1 aggravates atherosclerosis by promoting CD36-triggered foam cell formation via PPARG derepression.
PURPOSE
Since NCOR1 modulates the function of several key regulators involved in hepatic lipid and bile acid metabolism, we hypothesized that its deletion in hepatocytes alters lipid metabolism and atherogenesis.
METHODS
To test this hypothesis, we generated hepatocyte-specific Ncor1 knockout mice on a Ldlr-/- background. Besides assessing the progression of the disease in thoracoabdominal aortae en face, we analyzed hepatic cholesterol and bile acid metabolism at expression and functional levels.
RESULTS
Our data demonstrate that liver-specific Ncor1 knockout mice on an atherosclerosis-prone background develop less atherosclerotic lesions than controls. Interestingly, under chow diet, plasma cholesterol levels of liver-specific Ncor1 knockout mice were slightly higher compared to control, but strongly reduced compared to control mice after feeding them an atherogenic diet for 12 weeks. Moreover, the hepatic cholesterol content was decreased in liver-specific Ncor1 knockout compared to control mice. Our mechanistic data revealed that NCOR1 reprograms the synthesis of bile acids towards the alternative pathway, which in turn reduce bile hydrophobicity and enhances fecal cholesterol excretion.
CONCLUSIONS
Our data suggest that hepatic Ncor1 deletion in mice decreases atherosclerosis development by reprograming bile acid metabolism and enhancing fecal cholesterol excretion
Pollen and UV-B radiation strongly affect the inflammasome response in human primary keratinocytes
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