Epidemiologist Joel Selanikio has used the explosion in mobile phone technology and the World Wide Web to deliver more effective public health services throughout the developing world. Dr. Selanikio and his organization DataDyne.org are making a difference by improving the medical information available to public health programs in under-served areas of the world. VOA’s Natalia Ardanza has a profile for this week’s “Making a Difference” series.
In Africa there is another use for mobile phones. Public Health workers in Kenya are now using mobile phones to gather health information from patients in remote areas and upload it to the internet for instant analysis at distant centers. And it is all happening thanks to Dr. Joel Selanikio. “You can really make a difference using just common modern information technologies,” he said. Dr. Selanikio first noticed the need to better use information technology for health care while working as a disease outbrake investigator for the U.S. Centers for Disease Control and Prevention.
“I began to take the first steps toward using things like pocket computers or PDAs [i.e., personal digital assistants] for doing field work,” Selanikio said. Dr. Selanikio left his position five years ago to co-found DataDyne.org with partner Rosa Donna — as a non-profit organization dedicated to providing sustainable information technologies in poor areas. And with financial support from the United Nations Foundation and the Vodaphone Foundation, Selanikio developed EpiSurveyor — a free, mobile, Web-based and open-source data collection tool that is transforming the way public health is practiced in under-served areas of the world.
EpiSurveyor replaces cumbersome and costly paper-based data collection that can take months, and sometimes years to produce results. “Instead of collecting data today to plan for a campaign next year, changing from that to collecting data today to plan for what we do tomorrow,” Selanikio explained. “That is a pretty radical change.” Public health relies on the rapid collection of accurate data to track disease outbreaks, monitor vaccine supplies and other similar functions.
“The issue of flexibility, we need that,” Data Manager Yusuf Ajack Ibrahim said. Ajack is with Kenya’s Health and Sanitation Ministry and saw EpiSurveyor at work when a polio outbreak in 2006 was quickly contained, saving the lives of perhaps hundreds of children. “If you are to respond to an outbreak, I cannot wait for somebody to come all the way from the United States,” he said.
This year, Joel Selanikio received the prestigious Lemelson-MIT Award for Sustainability in recognition of these innovations. EpiSurveyor is being used by more than 500 organizations in more than 100 countries, and it is being adopted for use in areas such as agriculture and public opinion polling.
© 2009 VOA
Manny Hernandez, founder of tudiabetes.com, has created a wonderful and profound YouTube video about the tensions, and learning curbs between type1 & type 2 diabetes. Please watch, it is extremely worth it..
Type 2 diabetes has been loosely defined as “adult onset” diabetes, but as diabetes becomes more common, cases are being diagnosed in younger people and children. In determining the risk of developing diabetes, environmental factors, such as food intake and exercise, are known to have an important role; most people with type 2 diabetes are either overweight or obese. Inherited factors are also important, but the genes involved remain poorly defined. In rare forms of diabetes, mutations of one gene can result in disease, whereas in type 2 diabetes, many genes are thought to be involved. One difficulty in understanding the genetic role is that genes associated with diabetes might show only a subtle variation in their sequence, and these variations may be extremely common. Hence, it can be very hard to link such common gene variations, known as single nucleotide polymorphisms (SNPs), with increased risk of developing diabetes.
One method of finding these diabetes genes is by whole-genome linkage studies in which associations between parts of the genome and risk of developing diabetes are looked for. Studies so far have identified several candidate genes associated with type 2 diabetes, although many results have been difficult to replicate. The list of genes for which there is good evidence from meta-analyses includes genes encoding for PPARG, calpain 10, Kir 6.2, and insulin receptor substrate-1 (IRS1).
These genes have a variety of effects; PPARG P12A polymorphism is associated with enhanced insulin sensitivity and protects against type 2 diabetes. Two SNPs in the gene encoding for cystein protease calpain 10 (CAPN10) confer increased susceptibility to insulin resistance and type 2 diabetes. Kir 6.2 is involved in glucose-stimulated insulin secretion in pancreatic cells. And carriers of a polymorphism in the IRS1 gene have been shown to have reduced islet insulin content in pancreatic islets.
In this issue of PLoS Medicine, Valeriya Lyssenko and colleagues from Lund University sought to consolidate previous work by studying the predictive value of these variants for type 2 diabetes side by side in the largest study of its kind to date. They investigated the effect of these gene variants in 2,293 nondiabetic people aged 18–70 years old in western Finland—the Botnia study—over a median of six, range 2–12, years. In addition, they also studied the uncoupling protein 2 gene (UCP2)—a polymorphism in the promoter of this gene (UCP2 −866G>A) (rs659366) has been associated in some, but not all, studies with increased risk of type 2 diabetes and impaired insulin secretion.
The study took place from 1990 to 2002, and enrolled patients from five health centers in western Finland who were asked to have health checks every two to three years. Six percent (132) of people developed type 2 diabetes. The key finding was that variants in the PPARG and CAPN10 genes increased future risk for type 2 diabetes, particularly in individuals with other risk factors. In individuals with a high risk of developing diabetes—with a fasting plasma glucose (FPG) of 5.6 millimoles per liter and body mass index (BMI) of 30 kilograms per square meter—the hazard ratio increased to 21.2 for the combination of the PPARG PP and CAPN10 SNP43/44 GG/TT genotypes compared with those with low-risk genotypes with normal FPG and BMI less than 30 kilograms per square meter.
The researchers found that replacing the family history with the PPARG and CAPN10 variants in a predictive model (particularly in combination) gave almost the same strong prediction of subsequent type 2 diabetes. These genotypes also influenced the relationship between BMI and FPG, that is, in carriers of risk genotypes, there was a steeper increase in FPG for any given BMI.
The authors argue that the comparison of all the key gene variants side by side in one large study adds substantially to previous papers that have examined the effect of single gene variants on the risk of conversion to type 2 diabetes in interventional trials.
However, it is important to understand the effect of these variants on the risk of disease in a large, prospective observational study before studying additive or synergistic effects with interactions such as lifestyle changes, they said. One of the problems of other studies has been that results have been different between different subgroups.
Although this study has limited power, as the largest of its kind it suggests that genetic variants in candidate genes can predict future type 2 diabetes, particularly in association with conventional risk factors such as obesity and abnormal glucose tolerance. With accumulating data from prospective studies, it should be possible to define whether there will be a future role for genetic prediction of type 2 diabetes or whether these variants will influence response to prevention or treatment.
As U.S. lawmakers work toward a final agreement on overhauling health care, President Barack Obama says some of the reforms will take effect this year. The president admits, however, that other changes will not be in place for several years. President Obama is working with Democrats in both houses of Congress to merge their two versions of health reform. In the meantime, the president is using his weekly radio and Internet address to assure Americans that once he signs a health overhaul bill, they will see immediate benefits. “We are on the verge of passing health insurance reform that will finally offer Americans the security of knowing they will have quality, affordable health care whether they lose their jobs, change their jobs, move or get sick. The worst practices of the insurance industry will be forever banned,” he said.
Mr. Obama hopes to sign the bill into law by early February. Some consumers and advocates are disappointed that parts of the plan will not take effect until as late as 2014. The president acknowledges that some of the changes will take time to implement, but he says others will start working sooner. “Now, it will take a few years to fully implement these reforms in a responsible way. But what every American should know is that once I sign health insurance reform legislation into law, there are dozens of protections and benefits that will take effect this year,” he said.
Mr. Obama says before year’s end, insurance companies will be prohibited from dropping coverage when a person becomes ill, people with medical conditions will be allowed to buy affordable health insurance, and some small businesses will get government help in covering their employees. “All told, these changes represent the most sweeping reforms and toughest restrictions on insurance companies that this country has ever known,” he said.
The president began his address by talking about the economy. The U.S. unemployment rate remained at 10 percent in December, and 85,000 more Americans lost their jobs last month. Mr. Obama said the road to recovery will be long and sometimes bumpy.
© 2009 VOA