The One Million Death Study in India and More
Monumental measurement of mortality
The world’s largest prospective study on mortality, in which a staff of a thousand are monitoring 14 million people in 2.4 million representative households, is currently underway in India. As described in the open access journal PLoS Medicine, the study will ascertain the causes of one million deaths expected to occur among these people in the period between 1998 and 2014. Three quarters of the 9.5 million annual deaths in India occur in the home, and most of them do not have a certified cause. Reliable mortality measurements for the Indian population are urgently needed, particularly in light of the rising adult mortality from HIV/AIDS and non-communicable diseases like heart disease and cancer. The routine collection of mortality data, covering variations in age, sex, socioeconomic status and region, is critical to the success of public health programs.
To tackle the daunting task, over a dozen prominent Indian and global institutions - led by Prabhat Jha of St. Michael’s Hospital and the University of Toronto - have formed a novel partnership with the Indian government. India’s Sample Registration System (SRS) works by sending two independent surveyors to monitor selected households in rural and urban areas across India. To better document the causes of death within the SRS framework, the study has trained 800 full-time government staff to use a simple and validated method called verbal autopsy. Family or close associates of the deceased discuss the details of his or her death in structured one-on-one interviews. To ensure the robustness of the method, a random 10% of the fieldwork is repeated by an independent audit team. About 300,000 deaths from 1998-2003 are expected to be recorded in the first phase of the study, and 700,000 from the second phase between 2004 and 2014. Around 850,000 of these will be coded by two independent physicians, with a third arbitrating in the case of disagreement, to record causes of death. The study to date has already demonstrated that causes of death can be measured reliably in young and middle age, when most avoidable deaths occur.
The results of this large-scale effort will improve the understanding of various health risk factors such as tobacco and alcohol use, indoor air pollution, fertility preferences for male children, immunization, and migration. But Jha and colleagues have even bigger ambitions: they are testing the feasibility of collecting physical measurements, such as blood pressure and obesity, and blood samples from adults in the survey to measure other risk factors. The study could substantially improve our understanding of genetic and environmental factors that influence an individual’s risk for a variety of conditions, including infectious diseases common to developing countries and chronic diseases common worldwide.
Citation: Jha P, Gajalakshmi V, Gupta PC, Kumar R, Mony P, et al. (2006) Prospective study of 1 million deaths in India: Rationale, design, and validation results. PLoS Med 3(2): e18.
PLEASE ADD THE LINK TO THE PUBLISHED ARTICLE IN ONLINE VERSIONS OF YOUR REPORT: http://dx.doi.org/10.1371/journal.pmed.0030018
PRESS-ONLY PREVIEW OF THE ARTICLE: http://www.plos.org/press/plme-03-02-jha.pdf
PRESS-ONLY PREVIEW OF THE SYNOPSIS: http://www.plos.org/press/plme-03-02-jha-syn.pdf
Dr. Prabhat Jha
University of Toronto
Centre for Global Health Research, St Michaels Hospital
70 Richmond Street
Toronto, ON Canada M5C1N8
St. Michaels Hospital
Tel: + 1 416.864.5047
or page via Locating +1 416-864-5431
New method holds promise for better understanding of prion diseases
Prions cause neurodegenerative diseases in humans and animals like cows, sheep, or deer. In most cases, humans or animals get sick sporadically, when, for unknown reasons, normal proteins in the brain called PrPc change to harmful prions (called PrPSc). The PrPSc proteins then cause severe degeneration of the brain that kills the victims within a matter of months. There are no cures or therapies for prion diseases. The most common human prion disease is sporadic Creutzfeld-Jacob Disease, or sCJD. Scientists still understand little about why and how in some cases normal proteins change to prions and destroy the brain. All patients die, most of them within a few months, but there are differences between individual cases. The hope is that understanding the differences between individual cases might eventually provide some insight into the causes of the disease and suggest ways to treat it. To catalogue and examine those differences, it is important to come up with standard assays that allow meaningful comparisons. Markus Glatzel (Hamburg University) and colleagues have developed such an assay. Applying it to 50 postmortem samples from patients with sCJD reveals substantial differences in molecular pathology, suggesting that this approach could indeed help to understand this mysterious and devastating disease.
Citation: Schoch G, Seeger H, Bogousslavsky J, Tolnay M, Janzer RC, et al. (2006) Analysis of prion strains by PrPSc profiling in sporadic Creutzfeldt–Jakob disease. PLoS Med 3(2): e14.
PLEASE ADD THE LINK TO THE PUBLISHED ARTICLE IN ONLINE VERSIONS OF YOUR REPORT: http://dx.doi.org/10.1371/journal.pmed.0030014
PRESS-ONLY PREVIEW OF THE ARTICLE: http://www.plos.org/press/plme-03-02-glatzel.pdf
PRESS-ONLY PREVIEW OF THE SYNOPSIS: http://www.plos.org/press/plme-03-02-glatzel-syn.pdf
Institute of Neuropathology
Hamburg, Germany 20246
+0049 40 42803 2218
+0049 40 42803 4929 (fax)
How do islet cells die during early stages of diabetes?
Type 1 diabetes (also called autoimmune diabetes or juvenile diabetes) is an autoimmune disease. For unknown reasons, at some point in childhood or adolescence, the body’s own immune system starts attacking and destroying the insulin-producing islet cells in the pancreas. Once the majority of islet cells are destroyed, patients can no longer produce insulin to regulate their blood sugar and depend on strict diets and insulin injections. Scientists are trying to understand the early events during the development of the disease. John Corbett and colleagues (St. Louis University) have found that the early in the disease the islet cells die by a process called necrosis. Moreover, their study suggests some of the key factors involved. These are important results that will inform future studies toward the goal of understanding autoimmune diabetes well enough to prevent or stop its development.
Citation: Steer SA, Scarim AL, Chambers KT, Corbett JA (2005) Interleukin-1 stimulates b-cell necrosis and release of the immunological adjuvant HMGB1. PLoS Med 3(2): e17.
PLEASE ADD THE LINK TO THE PUBLISHED ARTICLE IN ONLINE VERSIONS OF YOUR REPORT: http://dx.doi.org/10.1371/journal.pmed.0030017
PRESS-ONLY PREVIEW OF THE ARTICLE: http://www.plos.org/press/plme-03-02-corbett.pdf
PRESS-ONLY PREVIEW OF THE SYNOPSIS: http://www.plos.org/press/plme-03-02-corbett-syn.pdf
John A Corbett
Saint Louis University School of Medicine
1402 South Grand Boulevard
Saint Louis, MO USA 63104
A new player in human atherosclerosis
Karen Badellino and colleagues (University of Pennsylvania) had previously found a link between a molecule called endothelial lipase (EL) and atherosclerosis in mice. In mice, EL seems to decrease the levels of HDL-C, the “good cholesterol”, and make the mice more prone to atherosclerosis. Overall, mice with lower levels of EL seemed to be better off. The question was whether EL levels influenced cholesterol levels and atherosclerosis in humans as well. Human studies until now had searched for a connection between different variants of the EL gene and atherosclerosis, but had not yielded clear answers. In a study of over 800 patients, Badellino and colleagues now found a link between high EL concentrations in the blood, low levels of HDL-C, and early stages of atherosclerosis. This suggests that EL concentrations influence the development of atherosclerosis in humans as well and might be useful to predict an individual’s risk.
Citation: Badellino KO, Wolfe ML, Reilly MP, Rader DJ (2006) Endothelial lipase concentrations are increased in metabolic syndrome and associated with coronary atherosclerosis. PLoS Med 3(2): e22.
PLEASE ADD THE LINK TO THE PUBLISHED ARTICLE IN ONLINE VERSIONS OF YOUR REPORT: http://dx.doi.org/10.1371/journal.pmed.0030022
PRESS-ONLY PREVIEW OF THE ARTICLE: http://www.plos.org/press/plme-03-02-badellino.pdf
PRESS-ONLY PREVIEW OF THE SYNOPSIS: http://www.plos.org/press/plme-03-02-badellino-syn.pdf
Dr. Karen Badellino
University of Pennsylvania
Institute for Experimental Medicine and Therapeutics
Room 646 BRB II/III
421 Curie Blvd
Philadelphia, PA USA 19104
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