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Death Profiles (death + profile)

Distribution by Scientific Domains

Life Sciences	75%

Selected Abstracts

Life expectancy among people with cerebral palsy in Western Australia

DEVELOPMENTAL MEDICINE & CHILD NEUROLOGY, Issue 8 2001
E Blair PhD
This report describes trends, predictors, and causes of mortality in persons with cerebral palsy (CP)using individuals identified by the Western Australian Cerebral Palsy Register and born between 1958 and 1994. Two thousand and fourteen people were identified (1154 males, 860 females), of whom 225 had died by 1 June 1997. Using date-of-death data, crude and standardized mortality rates were estimated and predictors of mortality sought using survival analysis stratified by decade of birth, description of impairments, and demographic and perinatal variables. For those born after 1967, the cause of death profile was examined over time. Mortality exceeded 1% per annum in the first 5 years and declined to age 15 years after which it remained steady at about 0.35% for the next 20 years. The strongest single predictor was intellectual disability, but all forms of disability contributed to decreased life expectancy. Half of those with IQ/DQ score <20 survived to adulthood, increasing to 76% with IQ/DQ score 20,34, and exceeding 92% for higher scores. Severe motor impairment primarily increased the risk of early mortality. Despite there being 72 persons aged from 25 to 41 years with severe motor impairment in our data set, none had died after the age of 25 years. Infants born after more than 32 weeks'gestation were at significantly higher risk of mortality than very preterm infants, accounted for by their higher rates of intellectual disability. No improvements in survival of persons with CP were seen over the study period despite advances in medical care, improved community awareness, and the increasing proportion of very preterm births among people with CP. This may be the result of improved neonatal care enabling the survival of infants with increasingly severe disabilities. [source]

Hepatotoxicity assay using human hepatocytes trapped in microholes of a microfluidic device

ELECTROPHORESIS, Issue 18 2010
Ju Hun Yeon
Abstract Hepatocytes have been used for in vitro hepatotoxicity assays because of their ability to sustain intact liver-specific functions. Here, we demonstrate a hepatotoxicity assay system using primary human hepatocytes trapped in microholes of a microfluidic device, providing a microscale in vivo liver-like environment. We performed microfluidic hepatotoxicity assays of several drugs, including acetaminophen, verapamil, diclofenac, and benzopyrene, all of which are known to specifically affect hepatic function. The drug sensitivities in hepatocytes and HepG2 cells were measured by calculating the live cell fraction at various drug concentrations. The results indicated that hepatocytes were more sensitive to these drugs than HepG2 cells. The lethal concentration 50 values for all drugs tested were similar to those from the in vitro toxicity data with human hepatocytes obtained from the literature. Furthermore, we developed a mathematical hepatotoxicity model based on the time-dependent cell death profiles measured by our device. This novel assay system enabled us to analyze in vivo -like hepatotoxicity in a microfluidic device by exploiting microstructures to mimic the microenvironment of the liver. [source]

Quantifying Viral Propagation in Vitro: Toward a Method for Characterization of Complex Phenotypes

BIOTECHNOLOGY PROGRESS, Issue 6 2001
Karen A. Duca
For a eukaryotic virus to successfully infect and propagate in cultured cells several events must occur: the virion must identify and bind to its cellular receptor, become internalized, uncoat, synthesize viral proteins, replicate its genome, assemble progeny virions, and exit the host cell. While these events are taking place, intrinsic host defenses activate in order to defeat the virus, e.g., activation of the interferon system, induction of apoptosis, and attempted elicitation of immune responses via chemokine and cytokine production. As a first step in developing an imaging methodology to facilitate direct observation of such complex host/virus dynamics, we have designed an immunofluorescence-based system that extends the traditional plaque assay, permitting simultaneous quantification of the rate of viral spread, as indicated by the presence of a labeled viral protein, and cell death in vitro, as indicated by cell loss. We propose that our propagation and cell death profiles serve as phenotypic read-outs, complementing genetic analysis of viral strains. As our virus/host system we used vesicular stomatitis virus (VSV) propagating in hamster kidney epithelial (BHK-21) and murine astrocytoma (DBT) cell lines. Viral propagation and death profiles were strikingly different in these two cell lines, displaying both very different initial titer and cell age effects. The rate of viral spread and cell death tracked reliably in both cell lines. In BHK-21 cells, the rate of viral propagation, as well as maximal spread, was relatively insensitive to initial titer and was roughly linear over several days. In contrast, viral plaque expansion in DBT cells was contained early in the infections with high titers, while low titer infections spread in a manner similar to the BHK-21 cells. The effect of cell age on infection spread was negligible in BHK-21 cells but not in DBTs. Neither of these effects was clearly observed by plaque assay. [source]