Arthur Gooch : the political, economic, and social influences that led him to the gallows.

Born in 1908, Arthur Gooch came of age in the prosperous 1920s, but something changed for him and for America in 1930. The socioeconomic depravity and increased media coverage of crimes in the Thirties affected those who lived through them, and, as President Franklin Roosevelt tried to reestablish economic, social, and political balance, Gooch experienced the ills that the Depression had to offer the citizens of Oklahoma. With dust storms destroying parts of the landscape and bandits ruling other regions, Gooch, and others like him, battled against poverty, unemployment, and desperation. Facing a lack of opportunities and constant hunger, many, such as Gooch, turned to a life of crime. In this time of crisis, President Roosevelt, United States (U.S.) Attorney General Homer Cummings, and Bureau of Investigation Director J. Edgar Hoover skillfully used the environment of the Depression and the people's fear of nationwide lawlessness to develop a powerful federal police force, resulting in the expansion of the Federal Bureau of Investigation (FBI). One particular unlawful act that influenced the attitudes of the country's citizens was the 1932 kidnapping and death of Charles Lindbergh, Jr., son of the American aviator and hero of the American people. The event horrified the nation and caused congress to pass multiple crime laws, including the Federal Kidnapping Act, popularly known as the Lindbergh Law. Its passage made kidnapping a federal offense. The prosecution and conviction of Bruno Richard Hauptmann, charged with the abduction of the Lindbergh baby, added to the voracity of the government's plans and to Americans' acceptance of federal involvement in state's matters. During this time of burgeoning crime, Arthur Gooch entered the pages of history by abducting two Texas policemen and transporting them into Oklahoma. With this action, Gooch violated the Federal Kidnapping Act and faced a jury and a judge who had the power to sentence him to death. With the amalgamation of the politics of the 1930s, influenced by President Roosevelt and U.S. Attorney General Cummings, and society's view of lawlessness in the aftermath of the Lindbergh baby's kidnapping and the worsening economy prompted the court to conclude that Arthur Gooch was a menace and deserved the ultimate punishment, death. As a result, Gooch became the first person to face the death penalty under the Lindbergh Law. In the wake of the passage of strict crime legislation, Gooch ascended the steps to the gallows, after receiving word that President Roosevelt had refused to grant him clemency. Socioeconomic depravity, restrictive politics, societal demand for reform, and poor personal judgment converged to spell death for Arthur Gooch on June 19, 1936. Consequently, Gooch's five-year-old son, Billy Joe, was left without a father and grew up hiding his true identity; Gooch's extended family struggled to conceal their relationship to him; and his only lasting legacy is one of missed opportunities and crime

Mission to Mars: Connecting Diverse Student Groups with NASA Experts

The Museum of Science and Industry in Chicago has formulated an innovative approach to inspiring the next generation to pursue STEM education. Middle school students in Chicago and at nearby Challenger Learning Centers work in teams to design a mission to Mars. Each mission includes real time access to NASA experts through partnerships with Marshall Space Flight Center, Johnson Space Center, and the Jet Propulsion Laboratory. Interactive videoconferencing connects students at the museum with students at a Challenger Learning Center and with NASA experts. This paper describes the approach, the results from the program s first year, and future opportunities for nationwide expansion

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

Spatial Organization and Molecular Correlation of Tumor-Infiltrating Lymphocytes Using Deep Learning on Pathology Images

Beyond sample curation and basic pathologic characterization, the digitized H&E-stained images of TCGA samples remain underutilized. To highlight this resource, we present mappings of tumorinfiltrating lymphocytes (TILs) based on H&E images from 13 TCGA tumor types. These TIL maps are derived through computational staining using a convolutional neural network trained to classify patches of images. Affinity propagation revealed local spatial structure in TIL patterns and correlation with overall survival. TIL map structural patterns were grouped using standard histopathological parameters. These patterns are enriched in particular T cell subpopulations derived from molecular measures. TIL densities and spatial structure were differentially enriched among tumor types, immune subtypes, and tumor molecular subtypes, implying that spatial infiltrate state could reflect particular tumor cell aberration states. Obtaining spatial lymphocytic patterns linked to the rich genomic characterization of TCGA samples demonstrates one use for the TCGA image archives with insights into the tumor-immune microenvironment

City of Hitchcock Comprehensive Plan 2020-2040

Hitchcock is a small town located in Galveston County (Figure 1.1), nestled up on the Texas Gulf Coast. It lies about 40 miles south-east of Houston. The boundaries of the city encloses an area of land of 60.46 sq. miles, an area of water of 31.64 sq. miles at an elevation just 16 feet above sea level. Hitchcock has more undeveloped land (~90% of total area) than the county combined. Its strategic location gives it a driving force of opportunities in the Houston-Galveston Region.The guiding principles for this planning process were Hitchcock’s vision statement and its corresponding goals, which were crafted by the task force. The goals focus on factors of growth and development including public participation, development considerations, transportation, community facilities, economic development, parks, and housing and social vulnerabilityTexas Target Communitie

Comprehensive Molecular Characterization of Pheochromocytoma and Paraganglioma

SummaryWe report a comprehensive molecular characterization of pheochromocytomas and paragangliomas (PCCs/PGLs), a rare tumor type. Multi-platform integration revealed that PCCs/PGLs are driven by diverse alterations affecting multiple genes and pathways. Pathogenic germline mutations occurred in eight PCC/PGL susceptibility genes. We identified CSDE1 as a somatically mutated driver gene, complementing four known drivers (HRAS, RET, EPAS1, and NF1). We also discovered fusion genes in PCCs/PGLs, involving MAML3, BRAF, NGFR, and NF1. Integrated analysis classified PCCs/PGLs into four molecularly defined groups: a kinase signaling subtype, a pseudohypoxia subtype, a Wnt-altered subtype, driven by MAML3 and CSDE1, and a cortical admixture subtype. Correlates of metastatic PCCs/PGLs included the MAML3 fusion gene. This integrated molecular characterization provides a comprehensive foundation for developing PCC/PGL precision medicine

Comprehensive and Integrated Genomic Characterization of Adult Soft Tissue Sarcomas

Sarcomas are a broad family of mesenchymal malignancies exhibiting remarkable histologic diversity. We describe the multi-platform molecular landscape of 206 adult soft tissue sarcomas representing 6 major types. Along with novel insights into the biology of individual sarcoma types, we report three overarching findings: (1) unlike most epithelial malignancies, these sarcomas (excepting synovial sarcoma) are characterized predominantly by copy-number changes, with low mutational loads and only a few genes (, , ) highly recurrently mutated across sarcoma types; (2) within sarcoma types, genomic and regulomic diversity of driver pathways defines molecular subtypes associated with patient outcome; and (3) the immune microenvironment, inferred from DNA methylation and mRNA profiles, associates with outcome and may inform clinical trials of immune checkpoint inhibitors. Overall, this large-scale analysis reveals previously unappreciated sarcoma-type-specific changes in copy number, methylation, RNA, and protein, providing insights into refining sarcoma therapy and relationships to other cancer types

Comprehensive Pan-Genomic Characterization of Adrenocortical Carcinoma

SummaryWe describe a comprehensive genomic characterization of adrenocortical carcinoma (ACC). Using this dataset, we expand the catalogue of known ACC driver genes to include PRKAR1A, RPL22, TERF2, CCNE1, and NF1. Genome wide DNA copy-number analysis revealed frequent occurrence of massive DNA loss followed by whole-genome doubling (WGD), which was associated with aggressive clinical course, suggesting WGD is a hallmark of disease progression. Corroborating this hypothesis were increased TERT expression, decreased telomere length, and activation of cell-cycle programs. Integrated subtype analysis identified three ACC subtypes with distinct clinical outcome and molecular alterations which could be captured by a 68-CpG probe DNA-methylation signature, proposing a strategy for clinical stratification of patients based on molecular markers