Antibacterial resistance a cause for major concern, cystic fibrosis experts say

 

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World-leading cystic fibrosis experts, from Queen's University Belfast, have called for greater research to address the major concern of antibacterial resistance.

Professor Stuart Elborn, an international authority on respiratory medicine, said that more funding and further research are required into antibiotic resistance in order to improve patient outcomes for people with Cystic Fibrosis.

In his paper, Infections in chronic lung diseases 2, which was recently published in The Lancet, Professor Elborn reviews current research into infections in chronic lung diseases. Professor Elborn and his colleagues state that while not all resistance found in bacteria is caused by antibiotics, the increasing resistance to antibiotics is proving a major problem in treating people with Cystic Fibrosis.

Speaking about his research Professor Elborn, Dean of the School of Medicine, Dentistry and Biomedical Sciences at Queen's, said: "Our review of current research has found a need for further investigation into antibacterial resistance. While antibiotic treatment has undeniably resulted in increased life expectancy for patients with Cystic Fibrosis during the past 50 years, the emergence of antimicrobial resistance is a cause for major concern.

"We need more research into how to improve cystic fibrosis patient outcomes while reducing antibiotic resistance. We need to look at the use of compounds that may work against bacteria in a way that helps our current antibiotics to be more effective. Such compounds are readily available for treatment of other conditions. At Queen's we are leading the way and are working on developing some of these compounds.

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Story Source:

The above story is based on materials provided by Queen's University, Belfast. Note: Materials may be edited for content and length.

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Journal Reference:

1. Laura J Sherrard, Michael M Tunney, J Stuart Elborn. Antimicrobial resistance in the respiratory microbiota of people with cystic fibrosis. The Lancet, 2014; 384 (9944): 703 DOI: 10.1016/S0140-6736(14)61137-5

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Secret to raising well behaved teens? Maximize their zzzzz's

 

September 26, 2014

Taylor & Francis

While American pediatricians warn sleep deprivation can stack the deck against teenagers, a new study reveals youth’s irritability and laziness aren’t down to attitude problems but lack of sleep. This paper exposes the negative consequences of sleep deprivation caused by early school bells, and shows that altering education times not only perks up teens’ mood, but also enhances learning and health.

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In puberty, shifts in our body clocks push optimal sleep later into the evening, making it extremely difficult for most teenagers to fall asleep before 11.00pm. This, coupled with early school starts in the morning, results in chronically sleep-deprived and cranky teens as well as plummeting grades and health problems.

While American pediatricians warn sleep deprivation can stack the deck against teenagers, a new study from Taylor & Francis reveals youth's irritability and laziness aren't down to attitude problems but lack of sleep.

Recently published in the journal of Learning, Media and Technology, this interesting paper exposes the negative consequences of sleep deprivation caused by early school bells, and shows that altering education times not only perks up teens' mood, but also enhances learning and health.

It is no secret that human biology and education measure time in different ways; however, 'our ability to function optimally [and learn], varies with biological time rather than conventional social times', explain the team leading the research. When the two are more closely aligned, like in the early years of education, this is not so critical.

But things drastically change during adolescence, when 'the conflict between social and biological time is greater than at any point in our lives', continue the academics. Our sleep-wake cycle, or circadian rhythm, is the result of a complex balance between states of alertness and sleepiness regulated by a part of the brain called Suprachiasmatic Nucleus (SNC); in puberty, shifts in our body clocks push optimal sleep later into the evening, making it extremely difficult for most teenagers to fall asleep before 11.00pm. This, coupled with early school starts in the morning, results in chronically sleep-deprived and cranky teens as well as plummeting grades and health problems.

There is a body of evidence showing the benefits of synchronizing education times with teens' body clocks; interestingly, while 'studies of later start times have consistently reported benefits to adolescent sleep health and learning, there [is no evidence] showing early starts have a positive impact on such things', add the researchers. In spite of examples corroborating this theory -- crucial is the case of the United States Air Force Academy where a later start policy has been instrumental in trumpeting the marks of a group of 18-19 year olds -- educators still fail to grasp it's not laziness that keeps teens in bed in the morning but their biological clocks.

However, regardless of reluctance to alter the way things have always been done, a number of initiatives -- including the Start School Later campaign and the establishment of the National Sleep Foundation -- indicate a change may be in the air for education policies and practices in the US.

'Good policies should be based on good evidence and the data show that children are currently placed at an enormous disadvantage by being forced to keep inappropriate education times', argue the team. Will priorities be reshuffled to allow teenagers to cop some more z's then? This still remains to be seen.

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Story Source:

The above story is based on materials provided by Taylor & Francis. Note: Materials may be edited for content and length.

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Journal Reference:

1. Paul Kelley, Steven W. Lockley, Russell G. Foster, Jonathan Kelley. Synchronizing education to adolescent biology: ‘let teens sleep, start school later’. Learning, Media and Technology, 2014; 1 DOI: 10.1080/17439884.2014.942666

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Graphene looks promising as a flexible, low-cost touchscreen solution

 

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New research published today in the journal Advanced Functional Materials suggests that graphene-treated nanowires could soon replace current touchscreen technology, significantly reducing production costs and allowing for more affordable, flexible displays.

The majority of today's touchscreen devices, such as tablets and smartphones are made using indium tin oxide (ITO) which is both expensive and inflexible. Researchers from the University of Surrey and AMBER, the materials science centre based at Trinity College Dublin have now demonstrated how graphene-treated nanowires can be used to produce flexible touchscreens at a fraction of the current cost.

Using a simple, scalable and inexpensive method the researchers produced hybrid electrodes, the building blocks of touchscreen technology, from silver nanowires and graphene.

Dr Alan Dalton from the University of Surrey said, "The growing market in devices such as wearable technology and bendable smart displays poses a challenge to manufacturers. They want to offer consumers flexible, touchscreen technology but at an affordable and realistic price. At the moment, this market is severely limited in the materials to hand, which are both very expensive to make and designed for rigid, flat devices."

Lead author, Dr Izabela Jurewicz from the University of Surrey commented, "Our work has cut the amount of expensive nanowires required to build such touchscreens by more than fifty times as well as simplifying the production process. We achieved this using graphene, a material that can conduct electricity and interpret touch commands whilst still being transparent."

Co-author, Professor Jonathan Coleman, AMBER, added, "This is a real alternative to ITO displays and could replace existing touchscreen technologies in electronic devices. Even though this material is cheaper and easier to produce, it does not compromise on performance."

"We are currently working with industrial partners to implement this research into future devices and it is clear that the benefits will soon be felt by manufacturers and consumers alike."

The research benefitted from funding and collaboration with M-SOLV, a touchscreen manufacturer.

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Story Source:

The above story is based on materials provided by University of Surrey. Note: Materials may be edited for content and length.

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Journal Reference:

1. Izabela Jurewicz, Azin Fahimi, Phillip E. Lyons, Ronan J. Smith, Maria Cann, Matthew L. Large, Mingwen Tian, Jonathan N. Coleman, Alan B. Dalton. Insulator-Conductor Type Transitions in Graphene-Modified Silver Nanowire Networks: A Route to Inexpensive Transparent Conductors. Advanced Functional Materials, 2014; DOI: 10.1002/adfm.201402547

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Biochemists solve 'address problem' in cells that leads to lethal kidney disease

 

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Carla Koehler, UCLA professor of chemistry and biochemistry, is shown in her laboratory.

Research by UCLA biochemists may lead to a new treatment -- or even a cure -- for PH1, a rare and potentially deadly genetic kidney disease that afflicts children. Their findings also may provide important insights into treatments for Parkinson's disease, Alzheimer's disease and other degenerative diseases.

Led by Carla Koehler, a professor of chemistry and biochemistry in the UCLA College, the researchers identified a compound called dequalinium chloride, or DECA, that can prevent a metabolic enzyme from going to the wrong location within a cell. Ensuring that the enzyme -- called alanine: glyoxylate aminotransferase, or AGT -- goes to the proper "address" in the cell prevents PH1.

The findings were published online in the Proceedings of the National Academy of Sciences and will appear later in the journal's print edition.

In humans, AGT is supposed to go to an organelle inside the cell called the peroxisome, but for people with a particular genetic mutation, the enzyme mistakenly goes instead to the mitochondria -- tiny power generators in cells that burn food and produce most of the cells' energy -- which causes PH1.

Koehler's team demonstrated that adding small amounts of DECA, which is FDA-approved, to cells in a Petri dish prevents AGT from going to the mitochondria and sends it to its proper destination, the peroxisome.

"In many mutations that cause diseases, the enzyme doesn't work," Koehler said. "In PH1 the enzyme does work, but it goes to the wrong part of the cell. We wanted to use DECA in a cell model to block AGT from going to the wrong address and send it back to the right address. DECA blocks the mitochondria 'mailbox' and takes it to the peroxisome address instead."

How often did it work?

"All the time," said Koehler, a member of UCLA's Jonsson Comprehensive Cancer Center, Molecular Biology Institute and Brain Research Institute.

For people with the mutation, the correct peroxisome address is present in AGT, but it is ignored because it is accompanied by the address of the mitochondria, which the cell reads first, Koehler said.

Koehler, who also is a member of the scientific and medical advisory board of the United Mitochondrial Disease Foundation, hopes to find out whether a similar "correct address" strategy can slow cancer down. Her laboratory has identified approximately 100 other small molecules, which she calls MitoBloCKs, that she and her colleagues are testing for their ability to combat Parkinson's, Alzheimer's and other diseases.

PH1 -- short for primary hyperoxaluria 1 -- starts at birth and is usually fatal for patients who do not receive both kidney and liver transplants. Approximately half of those with the disease have kidney failure by age 15. Koehler has presented her findings to the Oxalosis and Hyperoxaluria Foundation, which provides support for PH1 patients and their families.

Scientists' ability to diagnose rare diseases has improved in recent years because technological advances in genomics have made it easier to identify more genetic mutations, Koehler said.

According to Koehler, to treat diseases, scientists must first understand how proteins like AGT move inside the cell. Her research, which encompasses biochemistry, genetics and cell biology, studies how mitochondria are assembled and function, how proteins enter the mitochondria and reach the right location inside cells, and how mitochondria communicate with the rest of the cell.

Her laboratory uses model systems that enable them to study the biochemistry in a way that is not possible with humans. Much of the work is conducted in yeast.

"It's exciting that our studies in baker's yeast, a typical laboratory model, might be able to help kids with a complicated disease," Koehler said.

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Story Source:

The above story is based on materials provided by University of California - Los Angeles. The original article was written by Stuart Wolpert. Note: Materials may be edited for content and length.

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Journal Reference:

1. N. Miyata, J. Steffen, M. E. Johnson, S. Fargue, C. J. Danpure, C. M. Koehler. Pharmacologic rescue of an enzyme-trafficking defect in primary hyperoxaluria 1. Proceedings of the National Academy of Sciences, 2014; DOI: 10.1073/pnas.1408401111

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Celiac disease: A wriggly solution to a first-world problem

 

September 25, 2014

James Cook University

Groundbreaking results were achieved in a clinical trial using hookworms to reduce the symptoms of celiac disease. The results are good news for sufferers of other inflammatory conditions such as asthma and Crohn's disease. In the small trial run over a year, 12 participants were each experimentally infected with 20 Necator americanus (hookworm) larvae. They were then given gradually increasing doses of gluten, with their daily dose in the final stage being equivalent to a medium-sized bowl of spaghetti.

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Australian researchers have achieved groundbreaking results in a clinical trial using hookworms to reduce the symptoms of celiac disease.

The results are also good news for sufferers of other inflammatory conditions such as asthma and Crohn's disease.

In the small trial run over a year, 12 participants were each experimentally infected with 20 Necator americanus (hookworm) larvae.

They were then given gradually increasing doses of gluten -- beginning with just one-tenth of a gram per day (the equivalent of less than a one-inch segment of spaghetti) and increasing in two further stages to a final daily dose of three grams (75 spaghetti straws).

"By the end of the trial, with worms onboard, the trial subjects were eating the equivalent of a medium-sized bowl of spaghetti, with no ill effects," James Cook University (JCU) immunologist Paul Giacomin said.

"That's a meal that would usually trigger a debilitating inflammatory response, leaving a celiac patient suffering symptoms like diarrhea, cramps and vomiting."

Four participants withdrew in the earlier stages of the trial (for various reasons mostly unrelated to gluten) but the remaining eight experienced significant and ongoing benefits. "The eight who stuck with the trial were able to increase their gluten tolerance by a factor of 60, a massive change," said Alex Loukas, head of the Centre for Biodiscovery and Molecular Development of Therapeutics at JCU, and joint principal investigator of the study. "We and others have had promising results in earlier trials but this is clear proof-of-principle of the benefits of hookworm in treating inflammatory disease," Professor Loukas said.

Significantly, all the trial subjects rejected the researchers' offer of drugs that would eliminate the hookworms. "They all chose to keep their worms, and they continue to report good health. However they were instructed to return to a gluten-free diet after the trial," Professor Loukas said.

The potential of helminths (parasitic worms) in treating inflammatory diseases lies in their ability to dial back the human immune response -- a skill that enables them to survive, and thrive, in the human gut, without compromising their host's ability to fight off other infectious diseases.

A collaboration between JCU scientists in Cairns and gastroenterologist Dr John Croese at The Prince Charles Hospital in Brisbane, this study investigated the mechanism by which hookworms reduce the inflammatory response. "In gut biopsies collected before, during and at the end of the trial, we identified specific cells of the immune system, known as T cells, that we suspected were targeted by hookworm proteins," Dr Giacomin said. "We found that over the duration of the trial the T cells within the intestine changed from being pro-inflammatory to anti-inflammatory."

Hookworm infestation can be devastating in poorer tropical countries, where Professor Loukas and Dr Giacomin are working on a vaccine to help the 740 million who are infected. "With poor sanitation, repeated infections result in blood loss that can cause severe anemia. For newborns, children, pregnant women and the malnourished, the result can be debilitating illness or death," Professor Loukas said.

"People can get treated, but then they get reinfected -- a vaccine could break that cycle."

Conversely, inflammatory conditions such as celiac disease, inflammatory bowel disease, Crohn's disease and asthma are less common in developing countries, but are rife in affluent nations where helminths have been largely eradicated. 'In the one out of every 70 Australians who suffer from celiac disease, the immune system reacts abnormally to gluten, resulting in small bowel damage," Dr Croese said. "Symptoms vary, with the most common being gastrointestinal upsets. Others symptoms, some more severe, may include fatigue, anemia, unexplained weight loss or gain, bone or joint pains and swelling of the mouth or tongue."

Professor Loukas said his research team was aiming for a win-win. "We're working on both a vaccine to break that cycle of reinfection in developing countries, and a treatment for the inflammatory conditions that are a growing first-world problem."

The researchers believe that the key to the hookworm's anti-inflammatory prowess lies within the proteins that the worms secrete. They are actively seeking these molecules for further research, with the ultimate goal of developing an entirely new class of anti-inflammatory drug.

"This trial has confirmed hookworms as our choice of parasite for clinical applications," Professor Loukas said.

"But despite our growing fondness for them, we do acknowledge that a protein pill will have broader market appeal than a dose of worms."

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Story Source:

The above story is based on materials provided by James Cook University. Note: Materials may be edited for content and length.

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Journal Reference:

1. John Croese, Paul Giacomin, Severine Navarro, Andrew Clouston, Leisa McCann, Annette Dougall, Ivana Ferreira, Atik Susianto, Peter O'Rourke, Mariko Howlett, James McCarthy, Christian Engwerda, Dianne Jones, Alex Loukas. Experimental hookworm infection and gluten microchallenge promote tolerance in celiac disease. Journal of Allergy and Clinical Immunology, 2014; DOI: 10.1016/j.jaci.2014.07.022

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Minority background, low education, and low income negatively influence HPV vaccine series completion

 

According to a recent study in the journal Human Vaccines & Immunotherapeutics (HV&I), only 60% of young US women who received the first dose of the human papilloma virus (HPV) vaccine went on to complete the three-dose vaccine series. The study found that minority backgrounds, low income, and low education were associated with non-completion.

To better understand why women who initiate HPV vaccination do not complete the series, a team of researchers led by Dr. Abbey Berenson from the University of Texas Medical Branch examined the correlates of vaccine series completion among young women using data from the Behavioral Risk Factor Surveillance System (BRFSS), a cross-sectional telephone health survey conducted by the Centers for Disease Control and Prevention.

Based on data from 2008-2010, about 25% of the 2,700 respondents who ranged in age from 18-26 initiated HPV vaccination. The overall weighted vaccine series completion rate was 60.7%. Ethnic differences were noted, illuminating higher completion rates among white compared with black and Hispanic women.

A higher income and a college degree also were associated with higher completion rates of the vaccine series. The authors also observed higher vaccine series completion among those who had undergone a routine medical check-up during the past year.

Dr. Ronald Ellis, Editor-in-Chief of HV&I, comments HPV vaccine is one of the most highly effective vaccines, and one of only two vaccines (along with hepatitis B) that has been shown to prevent an infection that can result in cancer, as well as morbidity and mortality.

"The primary issue with reducing the incidence of cervical carcinoma is the problem of increasing the rate of vaccine utilization," Ellis said.

Four HPV strains are responsible for roughly 70% of cervical cancer and about 90% of genital warts in women. These strains are included in the licensed HPV vaccines Cervarix (types 16 and 18) and Gardasil (types 6, 11, 16 and 18), which are recommended for girls 11-12 years of age and may be given from age 9-26. HPV vaccines are highly effective in protecting against precancerous lesions and genital warts; nevertheless, vaccine uptake and series completion are still low.

"The authors' identification of factors that influence the likelihood of a woman being vaccinated should lead to actions for increasing vaccination rates, thus serving women's health in a significant way," Ellis said.

Story Source:

The above story is based on materials provided by Taylor & Francis. Note: Materials may be edited for content and length.

Journal Reference:

 

1. Mahbubur Rahman, Tabassum H Laz, Christine McGrath, Abbey B Berenson. Correlates of human papillomavirus vaccine series completion among young adult female initiators. Human vaccines & immunotherapeutics, 2014; 10 (8) DOI: 10.4161/hv.29633

    

    

Protecting the body from itself: How defense cells fight disease, but not themselves

 

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Autoimmune B cells cause the over-activation and death of NKT cells via presentation of altered lipids.

Scientists from A*STAR's Bioprocessing Technology Institute (BTI) have established a clearer relationship between two cells which serve our body's natural defence mechanisms against diseases and infections. Their findings, published in the journal CELL REPORTS, will help the medical community better understand autoimmunity and could pave the way for treatment of autoimmune diseases.

Natural killer T (NKT) cells and B cells are two of many immune cell types that work in tandem to help the body fight against foreign infectious agents. NKT cells have very potent functions and are crucial to the immune system despite making up only a small percentage of white blood cells. While scientists have established that NKT cells can promote the production of antibodies by B cells to combat infection, little is known about the effect of B cells on NKT cells until now.

Patients with autoimmune disorders have been observed to have drastically reduced numbers of NKT cells. The study conducted by BTI scientists revealed that autoimmune B cells had altered lipid compositions, causing NKT cells to be over-activated and resulting in their eventual death and depletion in numbers. The scientists further found that removal of a lipid-presenting molecule from B cells resulted in recovery in the numbers of NKT cells.

Dr Andy Tan, a research scientist at BTI who led the study, said, "Our findings provide an alternative theory to current understanding of how autoimmune B cells affect NKT cells. This will allow new therapeutic strategies to be devised, rectifying NKT cell deficiency in autoimmune patients and improving their health."

Autoimmune diseases, including lupus and some forms of arthritis and diabetes, develop when the immune system fails to distinguish between its own cells and foreign pathogens such as bacteria and viruses, resulting in attacks on the patient's own healthy tissue. Autoimmunity affects between three to 10 percent of the general population, depending on gender, disease type and geographical location. Future studies to identify particular lipids responsible for NKT cell over-activation might thus present therapeutic opportunities for those with autoimmune diseases and disorders.

Prof Lam Kong Peng, senior author for the study and Executive Director of BTI, added, "One of the central questions in the field of immunology is how the immune system is able to maintain a delicate balance in effectively fighting foreign pathogens and avoiding attack of the body itself. Our findings have brought us one step closer to unravelling the mechanisms that govern the balance between immunity and autoimmunity."

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Story Source:

The above story is based on materials provided by A*Star Agency for Science, Technology and Research. Note: Materials may be edited for content and length.

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Journal Reference:

1. Andy Hee-Meng Tan, William Pooi-Kat Chong, Sze-Wai Ng, Nurhidayah Basri, Shengli Xu, Kong-Peng Lam. Aberrant Presentation of Self-Lipids by Autoimmune B Cells Depletes Peripheral iNKT Cells. Cell Reports, 2014; DOI: 10.1016/j.celrep.2014.08.043

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Strategy to reduce side effects in modern cancer therapy

 

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The new strategy activates the EGFR inhibitor specifically under hypoxic conditions (indicated by blue fluorescence).

The occurrence of severe side effects and the development of resistance are two of the biggest problems facing modern cancer therapy. Even the latest, highly targeted cancer drugs such as the tyrosine kinase inhibitors Tarceva(R) or Sutent(R) are affected by these problems, which can ultimately lead to treatment having to be stopped. The effect of this class of inhibitors is based on the specific inhibition of proteins that are over-activated in cancer cells and which drive abnormal cell growth. However, clinical practice has shown that, as a result of the physiological functions of these proteins in healthy tissue, their inhibition can cause severe side effects. As a result, there is an acute need for strategies to restrict the effect of these highly promising new drugs more selectively to the malignant tumour.

The aim of the research was to develop an improved tyrosine kinase inhibitor that is actually inactive and which is only activated selectively in the malignant tissue. This is intended to prevent damage to healthy tissue and therefore minimise side effects for patients. As part of the paper published in the journal Angewandte Chemie [Applied Chemistry], International Edition, a new inhibitor has been successfully synthesised and coordinated to cobalt(III). This leads to initial drug inactivation and, thus, no activity under normal physiological conditions. Only in tumour tissue where, due to the rapid growth, unusually low-oxygen conditions prevail, the inactive cobalt(III) compound is reduced to cobalt(II) and as a result releases the active drug. The tumour-selective effectiveness of this approach has been demonstrated both in living cells and in tumor-bearing organisms.

The development of this complex idea and strategy was made possible by the outstanding interdisciplinary collaboration organised in the context of the "Translational Cancer Therapy Research" platform led by Bernhard Keppler, Dean of the Faculty of Chemistry at the University of Vienna, and Walter Berger, Professor at the Medical University of Vienna. This research platform promotes constant scientific exchange between synthetic chemists at the University of Vienna and cancer researchers at the Medical University of Vienna. It is only through these opportunities that the team of university assistants Christian Kowol (University of Vienna) and Petra Heffeter (Medical University of Vienna) has been able, based on two diploma theses (by Claudia Karnthaler-Benbakka, MSc., and Diana Groza, MSc.), to produce these results. The study was funded by the City of Vienna fund for "innovative interdisciplinary cancer research," the Austrian Science Fund (FWF) and COST CM1105. In view of the highly promising results, the new combination class has been patented by the two universities and currently a partner for further (clinical) development is searched.

So far there has been no comparable strategy for reducing the (severe) side effects of tyrosine kinase inhibitors. As a result, there is hope that, in future, the approach presented here will improve the tolerance of the therapy and allow this treatment to benefit patients who have previously had to discontinue it.

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Story Source:

The above story is based on materials provided by University of Vienna. Note: Materials may be edited for content and length.

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Journal Reference:

1. Claudia Karnthaler-Benbakka, Diana Groza, Kushtrim Kryeziu, Verena Pichler, Alexander Roller, Walter Berger, Petra Heffeter, Christian R. Kowol. Tumor-Targeting of EGFR Inhibitors by Hypoxia-Mediated Activation. Angewandte Chemie International Edition, 2014; DOI: 10.1002/anie.201403936

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Child maltreatment underreported in medicaid claims, study finds

 

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Medicaid claims are a poor way to identify child abuse and neglect at a population level, according to a study from the Brown School at Washington University in St. Louis.

Lead author Ramesh Raghavan, PhD, associate professor at the Brown School and of psychiatry at the School of Medicine, examined Medicaid records from 36 states for 1,921 children in the National Survey of Child and Adolescent Well-Being, whom caseworkers had identified as having been maltreated, and who had received Medicaid-funded services.

Only 15 percent had relevant codes for abuse or neglect in any of their Medicaid files over four years of observation.

Maltreated children are frequent users of health and mental health services; almost all are entitled to Medicaid.

Medicaid records of maltreated boys, older children, and African Americans were less likely to reflect abuse than those of other children, the study found.

Previous research has documented the reasons clinicians may not enter maltreatment codes while billing Medicaid, but the magnitude at a national level has not been known.

"This study has important implications for Medicaid scholarship conducted on abused and neglected children," said Raghavan, who also is a faculty scholar in the Institute for Public Health. "It seems clear that relying upon Medicaid claims yields unacceptably low rates of ascertained maltreatment."

Instead, he said, researchers should include data from child welfare or other administrative data sets to better capture the prevalence of abuse or neglect at a population level.

The study was published online in the August issue of Child Maltreatment.

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Story Source:

The above story is based on materials provided by Washington University in St. Louis. Note: Materials may be edited for content and length.

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Journal Reference:

1. R. Raghavan, D. S. Brown, B. T. Allaire, L. D. Garfield, R. E. Ross, D. Hedeker. Challenges in Using Medicaid Claims to Ascertain Child Maltreatment. Child Maltreatment, 2014; DOI: 10.1177/1077559514548316

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