Detecting Discrimination in Small Business Lending

With limited financial sophistication, entrepreneurial consumers approach the financial marketplace more like retail financial consumers than business customers. However, the assumption of both legislators and regulators is that business-borrowers are more financially savvy than consumer-borrowers, and thus do not require as broad-reaching protections. This gap between marketplace policy protections and the lived reality of the vast majority of small business entrepreneurs sets the stage for entrepreneurial consumers to fall through the regulatory cracks and sets the stage for possible exploitation and abuse. This situation is potentially exacerbated for minority entrepreneurs who belong to protected classes that are generally more vulnerable to exploitation in the marketplace including the small business lending marketplace. In this paper, we highlight the current state of this policy gap in the marketplace relative to minority entrepreneurial consumers and present a matched-paired mystery shopping study that demonstrates the critical need for reliable, primary data to inform regulatory agencies as they work to implement available protections to ensure equal access to credit within the small business lending marketplace

Genetic structure of First Nation communities in the Pacific Northwest

This study presents genetic data for nine Native American populations from northern North America. Analyses of genetic variation focus on the Pacific Northwest (PNW). Using mitochondrial, Y chromosomal and autosomal DNA variants, we aim to more closely address the relationships of geography and language with present genetic diversity among the regional PNW Native American populations. Patterns of genetic diversity exhibited by the three genetic systems were consistent with our hypotheses, in that we expected genetic variation to be more strongly explained by geographic proximity than linguistic structure. Our findings were corroborated through a variety on analytic approaches, with the unrooted trees for the three genetic systems consistently separating inland from coastal PNW populations. Furthermore, the AMOVA tests support the trends exhibited by the unrooted trees, with geographic partitioning of PNW populations (FCT = 19.43%, p = 0.010 ± 0.009) accounting for over twice as much of the observed genetic variation compared with linguistic partitioning of the same populations (FCT = 9.15%, p = 0.193 ± 0.013). These findings demonstrate a consensus with previous PNW population studies examining the relationships of genome-wide variation, mitochondrial haplogroup frequencies, and skeletal morphology with geography and language

Detecting T-cell Reactivity to Whole Cell Vaccines

BCR-ABL$^+$ K562 cells hold clinical promise as a component of cancer vaccines, either as bystander cells genetically modified to express immunostimulatory molecules, or as a source of leukemia antigens. To develop a method for detecting T-cell reactivity against K562 cell-derived antigens in patients, we exploited the dendritic cell (DC)-mediated cross-presentation of proteins generated from apoptotic cells. We used UVB irradiation to consistently induce apoptosis of K562 cells, which were then fed to autologous DCs. These DCs were used to both stimulate and detect antigen-specific CD8+ T-cell reactivity. As proof-of-concept, we used cross-presented apoptotic influenza matrix protein-expressing K562 cells to elicit reactivity from matrix protein-reactive T cells. Likewise, we used this assay to detect increased anti-CML antigen T-cell reactivity in CML patients that attained long-lasting clinical remissions following immunotherapy (donor lymphocyte infusion), as well as in 2 of 3 CML patients vaccinated with lethally irradiated K562 cells that were modified to secrete high levels of granulocyte macrophage colony-stimulating factor (GM-CSF). This methodology can be readily adapted to examine the effects of other whole tumor cell-based vaccines, a scenario in which the precise tumor antigens that stimulate immune responses are unknown

Dialysis Initiation in Patients With Chronic Coronary Disease and Advanced Chronic Kidney Disease in ISCHEMIA-CKD

BACKGROUND: In participants with concomitant chronic coronary disease and advanced chronic kidney disease (CKD), the effect of treatment strategies on the timing of dialysis initiation is not well characterized. METHODS AND RESULTS: In ISCHEMIA‐CKD (International Study of Comparative Health Effectiveness With Medical and Invasive Approaches–Chronic Kidney Disease), 777 participants with advanced CKD and moderate or severe ischemia were randomized to either an initial invasive or conservative management strategy. Herein, we compare the proportion of randomized participants with non–dialysis‐requiring CKD at baseline (n=362) who initiated dialysis and compare the time to dialysis initiation between invasive versus conservative management arms. Using multivariable Cox regression analysis, we also sought to identify the effect of invasive versus conservative chronic coronary disease management strategies on dialysis initiation. At a median follow‐up of 23 months (25th–75th interquartile range, 14–32 months), dialysis was initiated in 18.9% of participants (36/190) in the invasive strategy and 16.9% of participants (29/172) in the conservative strategy (P=0.22). The median time to dialysis initiation was 6.0 months (interquartile range, 3.0–16.0 months) in the invasive group and 18.2 months (interquartile range, 12.2–25.0 months) in the conservative group (P=0.004), with no difference in procedural acute kidney injury rates between the groups (7.8% versus 5.4%; P=0.26). Baseline clinical factors associated with earlier dialysis initiation were lower baseline estimated glomerular filtration rate (hazard ratio [HR] associated with 5‐unit decrease, 2.08 [95% CI, 1.72–2.56]; P<0.001), diabetes (HR, 2.30 [95% CI, 1.28–4.13]; P=0.005), hypertension (HR, 7.97 [95% CI, 1.09–58.21]; P=0.041), and Hispanic ethnicity (HR, 2.34 [95% CI, 1.22–4.47]; P=0.010). CONCLUSIONS: In participants with non–dialysis‐requiring CKD in ISCHEMIA‐CKD, randomization to an invasive chronic coronary disease management strategy (relative to a conservative chronic coronary disease management strategy) is associated with an accelerated time to initiation of maintenance dialysis for kidney failure

Characterization, sources and reactivity of volatile organic compounds (VOCs) in Seoul and surrounding regions during KORUS-AQ

The Korea-United States Air Quality Study (KORUS-AQ) took place in spring 2016 to better understand air pollution in Korea. In support of KORUS-AQ, 2554 whole air samples (WAS) were collected aboard the NASA DC-8 research aircraft and analyzed for 82 C₁–C₁₀ volatile organic compounds (VOCs) using multi-column gas chromatography. Together with fast-response measurements from other groups, the air samples were used to characterize the VOC composition in Seoul and surrounding regions, determine which VOCs are major ozone precursors in Seoul, and identify the sources of these reactive VOCs. (1) The WAS VOCs showed distinct signatures depending on their source origins. Air collected over Seoul had abundant ethane, propane, toluene and n-butane while plumes from the Daesan petrochemical complex were rich in ethene, C₂–C₆ alkanes and benzene. Carbonyl sulfide (COS), CFC-113, CFC-114, carbon tetrachloride (CCl₄) and 1,2-dichloroethane were good tracers of air originating from China. CFC-11 was also elevated in air from China but was surprisingly more elevated in air over Seoul. (2) Methanol, isoprene, toluene, xylenes and ethene were strong individual contributors to OH reactivity in Seoul. However methanol contributed less to ozone formation based on photochemical box modeling, which better accounts for radical chemistry. (3) Positive Matrix Factorization (PMF) and other techniques indicated a mix of VOC source influences in Seoul, including solvents, traffic, biogenic, and long-range transport. The solvent and traffic sources were roughly equal using PMF, and the solvents source was stronger in the KORUS-AQ emission inventory. Based on PMF, ethene and propene were primarily associated with traffic, and toluene, ethylbenzene and xylenes with solvents, especially non-paint solvents for toluene and paint solvents for ethylbenzene and xylenes. This suggests that VOC control strategies in Seoul could continue to target vehicle exhaust and paint solvents, with additional regulations to limit the VOC content in a variety of non-paint solvents

Characterization, sources and reactivity of volatile organic compounds (VOCs) in Seoul and surrounding regions during KORUS-AQ

The Korea-United States Air Quality Study (KORUS-AQ) took place in spring 2016 to better understand air pollution in Korea. In support of KORUS-AQ, 2554 whole air samples (WAS) were collected aboard the NASA DC-8 research aircraft and analyzed for 82 C₁–C₁₀ volatile organic compounds (VOCs) using multi-column gas chromatography. Together with fast-response measurements from other groups, the air samples were used to characterize the VOC composition in Seoul and surrounding regions, determine which VOCs are major ozone precursors in Seoul, and identify the sources of these reactive VOCs. (1) The WAS VOCs showed distinct signatures depending on their source origins. Air collected over Seoul had abundant ethane, propane, toluene and n-butane while plumes from the Daesan petrochemical complex were rich in ethene, C₂–C₆ alkanes and benzene. Carbonyl sulfide (COS), CFC-113, CFC-114, carbon tetrachloride (CCl₄) and 1,2-dichloroethane were good tracers of air originating from China. CFC-11 was also elevated in air from China but was surprisingly more elevated in air over Seoul. (2) Methanol, isoprene, toluene, xylenes and ethene were strong individual contributors to OH reactivity in Seoul. However methanol contributed less to ozone formation based on photochemical box modeling, which better accounts for radical chemistry. (3) Positive Matrix Factorization (PMF) and other techniques indicated a mix of VOC source influences in Seoul, including solvents, traffic, biogenic, and long-range transport. The solvent and traffic sources were roughly equal using PMF, and the solvents source was stronger in the KORUS-AQ emission inventory. Based on PMF, ethene and propene were primarily associated with traffic, and toluene, ethylbenzene and xylenes with solvents, especially non-paint solvents for toluene and paint solvents for ethylbenzene and xylenes. This suggests that VOC control strategies in Seoul could continue to target vehicle exhaust and paint solvents, with additional regulations to limit the VOC content in a variety of non-paint solvents

Pan-Cancer Analysis of lncRNA Regulation Supports Their Targeting of Cancer Genes in Each Tumor Context

Long noncoding RNAs (lncRNAs) are commonly dys-regulated in tumors, but only a handful are known toplay pathophysiological roles in cancer. We inferredlncRNAs that dysregulate cancer pathways, onco-genes, and tumor suppressors (cancer genes) bymodeling their effects on the activity of transcriptionfactors, RNA-binding proteins, and microRNAs in5,185 TCGA tumors and 1,019 ENCODE assays.Our predictions included hundreds of candidateonco- and tumor-suppressor lncRNAs (cancerlncRNAs) whose somatic alterations account for thedysregulation of dozens of cancer genes and path-ways in each of 14 tumor contexts. To demonstrateproof of concept, we showed that perturbations tar-geting OIP5-AS1 (an inferred tumor suppressor) andTUG1 and WT1-AS (inferred onco-lncRNAs) dysre-gulated cancer genes and altered proliferation ofbreast and gynecologic cancer cells. Our analysis in-dicates that, although most lncRNAs are dysregu-lated in a tumor-specific manner, some, includingOIP5-AS1, TUG1, NEAT1, MEG3, and TSIX, synergis-tically dysregulate cancer pathways in multiple tumorcontexts

Pan-cancer Alterations of the MYC Oncogene and Its Proximal Network across the Cancer Genome Atlas

Although theMYConcogene has been implicated incancer, a systematic assessment of alterations ofMYC, related transcription factors, and co-regulatoryproteins, forming the proximal MYC network (PMN),across human cancers is lacking. Using computa-tional approaches, we define genomic and proteo-mic features associated with MYC and the PMNacross the 33 cancers of The Cancer Genome Atlas.Pan-cancer, 28% of all samples had at least one ofthe MYC paralogs amplified. In contrast, the MYCantagonists MGA and MNT were the most frequentlymutated or deleted members, proposing a roleas tumor suppressors.MYCalterations were mutu-ally exclusive withPIK3CA,PTEN,APC,orBRAFalterations, suggesting that MYC is a distinct onco-genic driver. Expression analysis revealed MYC-associated pathways in tumor subtypes, such asimmune response and growth factor signaling; chro-matin, translation, and DNA replication/repair wereconserved pan-cancer. This analysis reveals insightsinto MYC biology and is a reference for biomarkersand therapeutics for cancers with alterations ofMYC or the PMN

Genomic, Pathway Network, and Immunologic Features Distinguishing Squamous Carcinomas

This integrated, multiplatform PanCancer Atlas study co-mapped and identified distinguishing molecular features of squamous cell carcinomas (SCCs) from five sites associated with smokin