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RISS 인기검색어
- 검색키워드
- 저자 : Jason Barr (검색결과 3 건)
- 무료
- 기관 내 무료
- 유료
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The Economics of Skyscraper Construction in Manhattan: Past, Present, and Future
Barr, Jason Council on Tall Building and Urban Habitat Korea 2016 International journal of high-rise buildings Vol.5 No.2
This paper discusses the economics of skyscraper construction in Manhattan since 1990. First the paper reviews the economic theory of skyscraper height. Next it documents the frequency and heights of skyscraper construction in the last 25 years. Then the paper reviews the relative movements of office rents, condominium prices, and construction costs. Statistical results suggest that the resurgence of Manhattan's skyscraper construction is being driving by the rise in the average price of apartments, and is not being driven by rising office rents or falling construction costs. Statistical evidence shows that the height premium has not been rising over the last decade. Developers have been purchasing air rights (and bidding up the prices) in order to satisfy the demand for supertall buildings. In the next five to ten years, Manhattan is likely to see over thirty 200-meter or taller buildings, as compared to only four since 2010.
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A "Radical Departure"? How the Home Insurance Building Won the "First Skyscraper" Debate
Jason Barr Council on Tall Building and Urban Habitat Korea 2024 International journal of high-rise buildings Vol.13 No.1
Today, most architectural and engineering historians no longer consider the Home Insurance Building to be the first skyscraper. Despite this, the popular belief remains that William Le Baron Jenny invented the first skyscraper when he designed the Home Insurance Building in 1884. This paper recounts the history of how Jenney won the public debate starting in 1896, despite his building being only a small evolutionary step forward. In that year, a series of letters in The Engineering Record allowed Jenney and his colleagues to engage in a public relations campaign to recast the debate about the first skyscraper to place the Home Insurance Building as the pivotal structure in skyscraper history.
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Novel allele-dependent role for APOE in controlling the rate of synapse pruning by astrocytes
Chung, Won-Suk,Verghese, Philip B.,Chakraborty, Chandrani,Joung, Julia,Hyman, Bradley T.,Ulrich, Jason D.,Holtzman, David M.,Barres, Ben A. National Academy of Sciences 2016 PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF Vol.113 No.36
<P>The strongest genetic risk factor influencing susceptibility to lateonset Alzheimer's disease (AD) is apolipoprotein E (APOE) genotype. APOE has three common isoforms in humans, E2, E3, and E4. The presence of two copies of the E4 allele increases risk by similar to 12-fold whereas E2 allele is associated with an similar to twofold decreased risk for AD. These data put APOE central to AD pathophysiology, but it is not yet clear how APOE alleles modify AD risk. Recently we found that astrocytes, a major central nervous system cell type that produces APOE, are highly phagocytic and participate in normal synapse pruning and turnover. Here, we report a novel role for APOE in controlling the phagocytic capacity of astrocytes that is highly dependent on APOE isoform. APOE2 enhances the rate of phagocytosis of synapses by astrocytes, whereas APO4 decreases it. We also found that the amount of C1q protein accumulation in hippocampus, which may represent the accumulation of senescent synapses with enhanced vulnerability to complement-mediated degeneration, is highly dependent on APOE alleles: C1q accumulation was significantly reduced in APOE2 knock-in (KI) animals and was significantly increased in APOE4 KI animals compared with APOE3 KI animals. These studies reveal a novel allele-dependent role for APOE in regulating the rate of synapse pruning by astrocytes. They also suggest the hypothesis that AD susceptibility of APOE4 may originate in part from defective phagocytic capacity of astrocytes which accelerates the rate of accumulation of C1q-coated senescent synapses, enhancing synaptic vulnerability to classical-complement-cascade mediated neurodegeneration.</P>
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