11,943 research outputs found
Portrait of Louis Nowra, author, 1981, 2 [picture] /
Title devised by cataloguer from inscription.; Part of the collection: Portraits of Louis Nowra, author, 1981.; Inscriptions: "Louis Nowra 5/2/81, H de Berg"--In ink on verso of print.; Condition: Soiled, scratched.; Also available in an electronic version via the Internet at: http://nla.gov.au/nla.pic-vn4728375
Portrait of Louis Nowra, author, 1981, 1 [picture] /
Title devised by cataloguer from inscription.; Part of the collection: Portraits of Louis Nowra, author, 1981.; Inscriptions: "Louis Nowra 5/2/81, H de Berg"--In ink on verso of print.; Condition: Soiled, scratched.; Also available in an electronic version via the Internet at: http://nla.gov.au/nla.pic-vn4728368
Portrait of Louis Nowra, author, 1981, 3 [picture] /
Title devised by cataloguer from inscription.; Part of the collection: Portraits of Louis Nowra, author, 1981.; Inscriptions: "Louis Nowra 5/2/81, H de Berg"--In ink on verso of print.; Condition: Soiled, scratched.; Also available in an electronic version via the Internet at: http://nla.gov.au/nla.pic-vn4728377
Clair Montine Cox Brunck scrapbook
This collection contains a scrapbook compiled by Clair Montine Cox Brunck from 1942 to 1946 during her time as a student in Little Rock, Arkansas. The scrapbook contains photographs, newspaper clippings, programs, and pamphlets primarily concerning Little Rock, Arkansas, and St. Louis, Missouri
Portrait of Louis Nowra, author, in front of a tree, 1981 [picture] /
Title devised by cataloguer from inscription.; Part of the collection: Portraits of Louis Nowra, author, 1981.; Inscriptions: "Louis Nowra 5/2/81, H de Berg"--In ink on verso of print.; Condition: Soiled, scratched.; Also available in an electronic version via the Internet at: http://nla.gov.au/nla.pic-vn4728421
Portrait of Louis Nowra, author, leaning on a railing, 1981 [picture] /
Title devised by cataloguer from inscription.; Part of the collection: Portraits of Louis Nowra, author, 1981.; Inscriptions: "Louis Nowra 5/2/81, H de Berg"--In ink on verso of print.; Condition: Soiled, scratched.; Also available in an electronic version via the Internet at: http://nla.gov.au/nla.pic-vn4728382
Personal Papers (MS 80-0002)
Letter from Harris L. Kempner to Louis L. Cox discussing Louis being in Cleveland and thanking him for offering his services
Personal Papers (MS 80-0002)
Letter from Harris L. Kempner to Louis L. Cox congratulating him on his lieutenancy and asking about his condition
Hormesis for Fine Particulate Matter (PM 2.5)
The hypothesis of hormesis – that substances that harm health at high exposures can reduce risks below background at low exposures, e.g., if they activate defenses without overwhelming them – becomes important for practical policy making if it holds for regulated substances. Recently, the U.S. EPA concluded that reductions in ambient concentrations of fine particulate matter (PM2.5) in air caused trillions of dollars worth of human health benefits for a compliance cost of only about $65 billion per year. This conclusion depends on an unverified assumption of a positive, causal, straight-line relation between PM2.5 concentrations and mortality risks. We review empirical data on PM2.5 and mortality risks (and their precursors, inflammatory responses) and conclude that the PM2.5 concentration-response relation may be J-shaped, rather than linear. This possibility implies that the 1990 Clean Air Act Amendment may well have produced no (or negative) human health benefits, rather than the trillions of dollars worth of reduced mortalities ascribed to it by EPA; and that attempts to achieve further risk-reduction benefits by further reducing PM2.5 concentrations may be counterproductive. This creates a very high value for scientific information that better reveals the true shape of the PM2.5 concentration-response function at and below current ambient levels
Dose-Response Thresholds for Progressive Diseases
Many diseases, including cancers, heart diseases, and lung diseases, can usefully be viewed as arising from disruption of feedback control systems that normally maintain homeostasis of tissues and cell populations. Excessive exposure can destabilize feedback control loops, leading to sustained elevation of variables to saturated levels and clinical consequences such as chronic unresolved inflammation, destruction of tissue (as in emphysema), proliferation of cell populations (as in lung cancer), and increases in reactive oxygen species and protease levels (as in coronary heart diseases and chronic obstructive lung disease). We propose a framework for understanding how exposure can destabilize normally homeostatic feedback control systems and create sustained imbalances and elevated levels of disease-related variables, by creating a new, locally stable, alternative equilibrium for the dynamic system, in addition to its normal (homeostatic) equilibrium. The resulting model, which we call alternative-equilibria (AE) theory, implies the existence of an exposure threshold below which transition to the alternative equilibrium (potential disease) state will not occur. Once this threshold is exceeded, progression to the alternative equilibrium continues spontaneously, even without further exposure. These predictions may help to explain patterns observed in experimental and epidemiological data for diseases such as COPD, silicosis, and inflammation-mediated lung cancer
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