Mortality transition

Ferrie, Joseph P., and Werner Troesken. 2004. Death and the City Chicago s Mortality Transition. Unpublished paper. Northwestern University and the University of Pittsburgh. 

Haines, Michael R. 2001. The Urban Mortality Transition in the United States, 1800-1940. Historical Paper no. 134, National Bureau of Economic Research. Haines, Michael R., Lee A. Craig, and Thomas Weiss. 2003. The Short and the Dead Nutrition, Mortality, and the Antebellum Puzzle in the United States. Journal of Economic History 63 382-413. 

Figure 26.1 Immortalization of human cells Cells enter replicative senescence at mortality stage 1 (Ml Hayflick limit) after about 60 population doublings (PD). The protein p 16 accumulates in senescent cells. The simian virus 40 (SV40) large T antigen as well as the human papilloma virus (HPV) type 16-E6 and E7 proteins sequester the retinoblastoma protein (Rb) and/or p53 constitutively releases the transcription factor E2F. E2F induces expression proteins required for progression through Gl/S transition, thus the cells escape cell cycle arrest. At mortality stage 2 (M2), transformed cells must overcome senescence and crisis before they are immortalized. This is likely to involve the activation of telomerase either by the introduction of hTERT cDNA or by a genetic change that activates telomerase.

Fig. 3. Lethal temperature thresholds for aquatic species. Patterns are general for all species, but exact temperatures are species-specific, (a) Tolerance polygon of upper and lower lethal (50%) temperatures for one-week exposures of an example species (juvenile sockeye salmon) which has been held at the acclimation temperature, with more restrictive thresholds indicated as dashed lines (b) time-dependent mortality (50%) of an example species (juvenile chinook salmon) at temperatures above the one-week lethal threshold after holding at different acclimation temperatures. The dashed line ABC indicates transition to less than 50% mortality at lower temperatures and coincides with the upper lethal threshold of this species tolerance polygon. Reproduced by...

You cannot. I am a prisoner here, just as she is a prisoner there, in her time, her life. We are each locked to our respective mortal coils, Doctor, and physical transit through time would destroy us utterly. Think of it as a curse. But in actual fact, it is an imposition of prison regulations. Much, much more effective than bars. ... 

Acute coronary syndromes (ACS) are a major cause of morbidity and mortality. They are characterized by intracoronary thrombus formation at the site of atherosclerotic plaques. Coronary thrombosis is the underlying mechanism in the transition from stable angina to the unstable angina (UA) syndrome, characterized by embolization of the developed thrombus and atherosclerotic plaque rupture. 

In the late 1960s, testifying before Congress, U.S. Surgeon General William T. Stewart claimed victory in the war against infectious diseases. Stewart, along with other members of the medical and scientific communities, believed that there had been a transition in which infectious disease had waned and chronic disease had become the dominant cause of morbidity and mortality in the modern age (Fauci, 2001). 

Severe sepsis and septic shock are common and are associated with a mortality rate which is still around the 50% mark. There are an estimated 751,000 cases of sepsis or septic shock in the United States each year, and they are responsible for as many deaths as acute myocardial infarction [63]. The transition from a systemic inflammatory response syndrome, typical of the initial onset of a septic shock, to severe sepsis, multi-organ failure, and irreversible shock, involves a multitude of pathogenic changes. 

Certain substances have been reported to potentiate the toxicity of paraquat. These include transition metal ions such as copper (Kohen and Chevion 1985) and ethanol (Kuo and Nanikawa 1990). Blood paraquat levels showed significant elevation in rabbits, and the mortality rates increased when the animals were orally administered paraquat combined with ethanol in amounts of 2.0 and 3.8 g/kg. Continuous breathing of high oxygen concentrations 12-24 hours after administration of paraquat caused severe and extensive pulmonary lesions and interstitial fibrosis (Selman et al. 1985). On the other hand, a reverse sequence of treatment— inhalation of high oxygen concentrations followed by paraquat administration—caused no mortality and pulmonary lesions. 

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