There’s a reason emergency personnel train for the aftermath of a dirty bomb or an explosion at a nuclear power plant. They’ll be faced with a deluge of urgent tasks, such as identifying who’s been irradiated, who has an injury-induced infection, and who’s suffering from both.
Unfortunately, there isn’t a quick way to screen for people exposed to dangerous levels of radiation. There also isn’t a quick way to distinguish between people suffering from radiation exposure versus an infection due to an injury or chemical exposure.
The most common way to measure exposure is a blood assay that tracks chromosomal changes. Another approach is to watch for the onset of physical symptoms. But these methods can take several days to provide results, which is far too late to identify people who’d benefit from immediate treatment.
A much faster way could be coming. Research conducted by scientists from the U.S. Department of Energy’s Lawrence Berkeley National Laboratory (Berkeley Lab) could lead to a blood test that detects if a person has been exposed to radiation, measures their dose, and separates people suffering from inflammation injuries—all in a matter of hours.
The scientists identified eight DNA-repair genes in human blood whose expression responses change more than twofold soon after blood is exposed to radiation. They also learned how these genes respond when blood is exposed to inflammation stress, which can occur because of an injury or infection. Inflammation can mimic the effects of radiation and lead to false diagnoses.
The result is a panel of biochemical markers that can discriminate between blood samples exposed to radiation, inflammation, or both. The scientists believe these markers could be incorporated into a blood test that quickly triages people involved in radiation-related incidents.
‘In an emergency involving radiation exposure, it’s likely that only a small fraction of all possibly exposed people will be exposed to high doses that require immediate medical attention,’ says Andy Wyrobek of Berkeley Lab’s Life Sciences Division. ‘The goal is to quickly screen for these people so they can get treatment, and avoid overwhelming medical facilities with the larger number of people exposed to low levels of radiation with no immediate medical needs. Our research could lead to a blood test that enables this.’
Wyrobek conducted the research with fellow Berkeley Lab scientists Helen Budworth and Antoine Snijders, as well as several other scientists from Berkeley Lab and other institutions.
Because DNA is one of the major targets of radiation, the Berkeley Lab scientists began their research by focusing on 40 genes that regulate the expression of proteins that carry out DNA-repair tasks. They studied these genes in blood samples taken from healthy people before and after exposing the samples to 2 Gray of X-rays per year, which is about the radiation dose received by radiotherapy patients. They found twelve genes that underwent more than a twofold change in response after exposure. From these, they isolated eight genes that had no overlap between unirradiated and irradiated samples.
The scientists also treated the blood samples with a compound that mimics inflammatory stress. This enabled them to account for gene-expression responses that could be mistaken for signs of radiation exposure, but which are actually caused by injury or infection. In addition, they irradiated a portion of these samples to learn how the genes respond to both inflammation and radiation.
To validate their findings, the scientists analysed a separate dataset of blood samples that had also been irradiated. They found a close match between their own data and the independent dataset in how the eight genes respond after radiation exposure.
They also compared their findings to a large group of bone marrow transplant patients who received total-body radiation. Again, they found a close match between their data and the gene-expression responses of the patients after they received treatment.
More work is needed, but Wyrobek envisions a blood test using their biochemical markers could be administered via a handheld device similar to what diabetes patients use to check their blood sugar. The test could help emergency personnel quickly identify people exposed to high radiation doses who need immediate care, and people exposed to lower doses who only need long-term monitoring. Lawrence Berkeley National Laboratory

In a study, researchers from Monash University tracked the movements of white blood cells, or leukocytes, leading to a new understanding of their behaviour in both healthy and diseased kidneys.
Leukocytes play important protective roles in the body’s immune system, but in some cases they cause damaging inflammation. Glomerulonephritis is an inflammatory disease of the kidney that can lead to the need for transplantation or regular dialysis. More than 20 per cent of end-stage renal failure cases result from glomerulonephritis.
Lead researcher, Associate Professor Michael Hickey of the University’s Centre for Inflammatory Diseases in the Department of Medicine said the team used advanced microscopy techniques to visualise the movements of leukocytes through the kidney.
‘In order to manipulate a system, you must understand it. Now, we have a really clear understanding of the disease process and the molecules involved in the key steps,’ Associate Professor Hickey said.
‘Contrary to conventional medical and scientific opinion, we found that leukocytes are constantly circulating through and patrolling the blood vessels within healthy kidneys. It was previously believed that they only arrived in the kidney during the development of disease. That’s not the case. However, during disease they linger in the kidney during the course of their normal journey, become agitated and cause inflammation and kidney damage.’
End-stage renal failure leads to significant health and personal impacts, including ongoing visits to a dialysis unit several times a week, or a significant wait for a donor.
Renal Physician and co-investigator Professor Richard Kitching said therapies to effectively target glomerulonephritis were needed before end-stage was reached.
‘The treatments we have can be fairly effective, but they are non-specific and they often have unacceptable side effects,’ Professor Kitching said.
‘Currently, we have to suppress the immune system to combat the inflammation and this immunosuppression leaves the body more prone to infections. Additionally, some of the drugs have metabolic side effects, such as weight gain and bone thinning.
‘Now we have a better understanding of how the disease develops, we can identify targets for more specific drugs, with fewer side-effects.’ Monash University

Testing asthmatic children for a specific gene could prevent their condition worsening, according to new research by scientists in Brighton and Dundee.
The arginine-16 genotype of the beta-2 receptor is carried by one in seven sufferers and the research found their condition could be aggravated by the use of the long-term controller medicine, Salmeterol, a long acting beta-receptor stimulant, which is administered through an inhaler.
Testing children for the genotype would identify those who might react poorly to Salmeterol and means their asthma control may improve with the use of alternative medicines.
The research was carried out by – Professor Somnath Mukhopadhyay from the Brighton and Sussex Medical School (BSMS) which is run jointly by Brighton and Sussex universities, and Professor Brian Lipworth and genetics expert Professor Colin Palmer, both from the University of Dundee.
They carried out the first genotyped study comparing additional treatments given to asthmatic children who continue to experience symptoms despite use of their prescribed inhaled steroid preventer.
More than a million UK children have asthma and over 150,000 are affected by this genetic change, making them less likely to respond to Salmeterol. The researchers tested 62 children with the susceptible arginine-16 genotype. They had all missed school or had treatment at hospital or out-of-hours GP surgeries as a result of their asthma, despite being treated with regular inhaled steroids.
While continuing with their usual preventer, the children were randomly assigned to two treatment groups for the period of a year – Montelukast or Salmeterol.
The research found they responded better to an alternative anti-inflammatory medicine, Montelukast. They experienced an improved quality of life, wheezed and coughed much less, and were less likely to experience worsening of their symptoms and needing more ‘reliever’ treatment, compared to the Salmeterol users.
At the start of the research, 36 per cent of these children tested needed to use their relievers every day. But by the end of the year-long study, the number of children needing daily reliever use had halved in the group using Montelukast. In contrast, there was no improvement for the children in the Salmeterol group. This is despite the fact that Salmeterol is currently the preferred drug for children with asthma who are not controlled with inhaled steroids.
The researchers have warned that many children with serious asthma respond poorly to Salmeterol and may be suffering needlessly from asthma, regularly missing out on sports and recording low school attendances during long-term treatment with this medicine. They said their treatment may be made more effective with the help of a simple relatively inexpensive gene test. Brighton and Sussex Medical School

New research reveals a shared genetic susceptibility to epilepsy and migraine. Findings indicate that having a strong family history of seizure disorders increases the chance of having migraine with aura (MA).
Medical evidence has established that migraine and epilepsy often co-occur in patients; this co-occurrence is called ‘comorbidity.’ Previous studies have found that people with epilepsy are substantially more likely than the general population to have migraine headache. However, it is not clear whether that comorbidity results from a shared genetic cause.
‘Epilepsy and migraine are each individually influenced by genetic factors,’ explains lead author Dr. Melodie Winawer from Columbia University Medical Center in New York. ‘Our study is the first to confirm a shared genetic susceptibility to epilepsy and migraine in a large population of patients with common forms of epilepsy.’
For the present study, Dr. Winawer and colleagues analysed data collected from participants in the Epilepsy Phenome/Genome Project (EPGP)—a genetic study of epilepsy patients and families from 27 clinical centres in the U.S., Canada, Argentina, Australia, and New Zealand. The study examined one aspect of EPGP: sibling and parent-child pairs with focal epilepsy or generalised epilepsy of unknown cause. Most people with epilepsy have no family members affected with epilepsy. EPGP was designed to look at those rare families with more than one individual with epilepsy, in order to increase the chance of finding genetic causes of epilepsy.
Analysis of 730 participants with epilepsy from 501 families demonstrated that the prevalence of MA—when additional symptoms, such as blind spots or flashing lights, occur prior to the headache pain— was substantially increased when there were several individuals in the family with seizure disorders. EPGP study participants with epilepsy who had three or more additional close relatives with a seizure disorder were more than twice as likely to experience MA than patients from families with fewer individuals with seizures. In other words, the stronger the genetic effect on epilepsy in the family, the higher the rates of MA. This result provides evidence that a gene or genes exist that cause both epilepsy and migraine.
Identification of genetic contributions to the comorbidity of epilepsy with other disorders, like migraine, has implications for epilepsy patients. Prior research has shown that coexisting conditions impact the quality of life, treatment success, and mortality of epilepsy patients, with some experts suggesting that these comorbidities may have a greater impact on patients than the seizures themselves. In fact, comorbid conditions are emphasised in the National Institutes of Health Epilepsy Research Benchmarks and in a recent report on epilepsy from the Institute of Medicine.
‘Our study demonstrates a strong genetic basis for migraine and epilepsy, because the rate of migraine is increased only in people who have close (rather than distant) relatives with epilepsy and only when three or more family members are affected,’ concludes Dr. Winawer. ‘Further investigation of the genetics of groups of comorbid disorders and epilepsy will help to improve the diagnosis and treatment of these comorbidities, and enhance the quality of life for those with epilepsy.’ Columbia University Medical Center