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Several other cities with low rates of home ownership in 1970 have managed to increase their rates two to four percent over the past 25 years, but the home ownership rate in Cincinnati has been stable over that period at 38 percent.\r\n\r\nThe best explanation for Cincinnati’s low home ownership rate is that the topography of the city encouraged dense development involving multiple-unit structures up until World War II. When the highway programs of the post-war period opened up the suburbs to development, the city was already built-out and could not compete for new single-unit construction that the federal government was subsidizing on a massive scale.\r\n\r\nIn the last 50 years, the Hamilton County suburbs have gained 140,000 owners while the number of owners in the city has decreased by 1,000. 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The city needs to assemble and prepare sites in order to reduce the additional costs associated with building in the city as opposed to the suburbs. City Hall must continue to eliminate barriers to development and provide new services to builders. Cincinnati will not be able to increase the number of middle-class owners without creating new neighborhood areas with the appropriate mix of amenities. At the lower end of the owner-market, the city needs to move aggressively to convert abandoned structures into units people will want to buy and rehabilitate.\r\n\r\nHelp Renters Become Owners\r\nWhile converting renters to owners is an essential component of an overall strategy, the City of Cincinnati must recognize that not everyone can be an owner and target its resources appropriately. The city does not have unlimited funds to change the cost equation of owning a home and will, therefore, have to learn from other cities how to work with lending institutions to increase the flow of dollars under Community Reinvestment Act initiatives. Other cities have had some limited success with programs to convert people renting duplex and condo units into owners. The city needs to increase the availability, extent and quality of education and counseling programs. \r\n\r\nAttract New Households to the City\r\nThe city has to market its neighborhoods, and in some cases, smaller areas within neighborhoods. This will require market research, training programs for Realtors, investments in street furniture, increased services, publications extolling city neighborhoods, and programs comparable to the Living in Cleveland program. The city needs to start working cooperatively with the Cincinnati Public Schools. Specific market niches in which the city can hope to compete very successfully include the empty nesters, the gay and lesbian community, first time buyers, and people interested in downtown living.\r\n\r\nMaintain the Existing Pool of Owners\r\nAbout 75 percent of the time a home owner in Cincinnati sells and buys another home in the Cincinnati area, the home purchased will be in the suburbs. The city must create opportunities for the home seller to move up without moving out of the city.\r\n\r\nIn addition to the above strategies, which involve the central city market, the City of Cincinnati needs to actively promote strategies that will help slow the rate of suburbanization and that will create low income housing opportunities in the suburbs. If suburbanization continues at the current rate, and if the city continues to be the governmental unit with de facto responsibility for low income housing, there is every reason to wonder if there is anything that the city can do to increase its rate of home ownership.\r\n"],"score":0.00049999997},{"system_create_dtsi":"2019-01-23T19:09:20Z","system_modified_dtsi":"2019-05-23T18:40:25Z","has_model_ssim":["Document"],"id":"6t053g883","accessControl_ssim":["957bc231-d4fa-4a59-949b-4624af8c3036"],"hasRelatedMediaFragment_ssim":["6w924d08k"],"hasRelatedImage_ssim":["6w924d08k"],"depositor_ssim":["robertrl@ucmail.uc.edu"],"depositor_tesim":["robertrl@ucmail.uc.edu"],"title_tesim":["EndNote X8 Workbook"],"date_uploaded_dtsi":"2019-01-23T19:09:20Z","date_modified_dtsi":"2019-05-23T18:40:25Z","isPartOf_ssim":["admin_set/default"],"genre_tesim":["Document"],"college_tesim":["Libraries"],"department_tesim":["Research, Teaching \u0026 Services"],"creator_tesim":["Roberts, Randall"],"publisher_tesim":["University of Cincinnati"],"subject_tesim":["EndNote","Citation \u0026 Reference Management"],"description_tesim":["This document is a workshop workbook for EndNote X8, a citation and reference management software product. 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Holokai et al., 2018"],"date_uploaded_dtsi":"2018-12-21T20:49:29Z","date_modified_dtsi":"2018-12-21T21:10:11Z","isPartOf_ssim":["admin_set/default"],"doi_tesim":["doi:10.7945/C2Q120"],"college_tesim":["Medicine"],"department_tesim":["Department of Pharmacology and Systems Physiology"],"required_software_tesim":[""],"note_tesim":[""],"creator_tesim":["Zavros, Yana"],"publisher_tesim":["University of Cincinnati"],"description_tesim":["ABSTRACT\r\nHelicobacter pylori (H. pylori) is the major risk factor for the development of gastric cancer.  Our laboratory has reported that the Sonic Hedgehog (Shh) signaling pathway is an early response to infection that is fundamental to the initiation of H. pylori-induced gastritis.  H. pylori also induces programmed death ligand 1 (PD-L1) expression on gastric epithelial cells, yet the mechanism is unknown.  We hypothesize that H. pylori-induced PD-L1 expression within the gastric epithelium is mediated by the Shh signaling pathway during infection.  To identify the role of Shh signaling as a mediator of H. pylori-induced PD-L1 expression, human gastric organoids generated from either induced pluripotent stem cells (HGOs) or tissue (huFGOs) were microinjected with bacteria and treated with Hedgehog/Gli inhibitor GANT61. Gastric epithelial monolayers generated from the huFGOs were also infected with H. pylori and treated with GANT61 to study the role of Hedgehog signaling as a mediator of induced PD-1 expression. A patient-derived organoid/autologous immune cell co-culture system infected with H. pylori and treated with PD-1 inhibitor (PD-1Inh) was developed to study the protective mechanism of PD-L1 in response to bacterial infection. H. pylori significantly increased PD-L1 expression in organoid cultures 48 hours post-infection when compared to uninfected controls.  The mechanism was cytotoxic associated gene A (CagA) dependent.  This response was blocked by pretreatment with GANT61.  Anti-PD-L1 treatment of H. pylori infected huFGOs, co-cultured with autologous patient cytotoxic T lymphocytes and dendritic cells, induced organoid death.  H. pylori-induced PD-L1 expression is mediated by the Shh signaling pathway within the gastric epithelium. Cells infected with H. pylori that express PD-L1 may be protected from the immune response, creating premalignant lesions progressing to gastric cancer."],"license_tesim":["http://rightsstatements.org/vocab/InC/1.0/"],"date_created_tesim":[""],"thumbnail_path_ss":"/assets/work-ff055336041c3f7d310ad69109eda4a887b16ec501f35afc0a547c4adb97ee72.png","suppressed_bsi":false,"actionable_workflow_roles_ssim":["admin_set/default-default-depositing"],"workflow_state_name_ssim":["deposited"],"member_ids_ssim":["05741s85v"],"file_set_ids_ssim":["05741s85v"],"visibility_ssi":"open","admin_set_tesim":["Default Admin Set"],"sort_title_ssi":"INCREASED PROGRAMMED DEATHLIGAND 1 IS AN EARLY EPITHELIAL CELL RESPONSE TO HELICOBACTER PYLORI INFECTION HOLOKAI ET AL 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