Incipient sex chromosomes have been found in New Zealand’s eponymous export, the kiwifruit. Researchers writing in the open access journal BMC Genomics have mapped the kiwifruit genome and pin-pointed the sex-determining locus.

It has previously been suggested that, among the kiwifruit plant’s small (<1um) chromosomes, lie a pair of X/Y-like chromosomes that result in its dioecism. Now a team led by Lena Fraser and colleagues at the New Zealand Institute for Plant and Food Research has confirmed this suggestion by mapping the genome of the golden kiwifruit.

The genome has been mapped with 644 microsatellite markers from three genetic libraries (two from the New Zealand Institute for Plant and Food Research and one from the University of Udine, Italy). These showed 29 linkage groups, represented expression of 587 genes, and revealed that sex-linked sequence characterised amplified region (SCAR) markers and the flower sex phenotype were mapping to a subtelomeric region that bears the hallmarks of an early sex-determining locus.

The mapping of this sex-determining locus to a subtelomeric region fits with previous published work on chromosome pairing and also the authors own observations. Whilst studying kiwifruit karyotypes, the research team observed that in the pollen mother cells undergoing meiosis one of the 29 pairs of chromosomes did not pair tightly in a region close to one end. An absence of pairing means that the male-specific region on the Y is inherited as a unit, maintaining sexual dimorphism.

Based on the genetic structure they have now defined for this non-recombining sex-determining region, the authors suggest that at least two linked genes on the putative Y chromosome are responsible for dioecy: one suppressing pistil formation and one for pollen development.

Of more than 60 species of Actinidia (kiwifruit), only two have been widely cultivated so far, and there is potential for breeding new varieties. All Actinida species are dioecious, and the authors say they are likely to have similar sex-determining regions. The authors work in producing female, male and consensus genetic linkage maps for the golden kiwifruit, A. chinensis and identifying the sex-determining region may provide the key to fully exploiting this relatively recent cultivar.

According to Fraser, ‘The gene-rich map we have constructed will be a valuable resource for quantitative trait loci analysis to identify markers related to traits of importance in breeding new and novel kiwifruit for the markets of the world.’

Source: BioMed Central.

Interest in personal health records as an electronic tool to manage health information is increasing dramatically. A group led by a UCSF researcher has identified cost, privacy concerns, design shortcomings and difficulties sharing information across different organizations as critical barriers hindering broad implementation of electronic personal health records.

The barriers are discussed in a paper appearing in the March-April 2009 issue of the journal “Health Affairs.”

“It is imperative that these barriers hampering adoption of personal health records be addressed. We do not have the ‘best of breed’ yet, but I do believe that if we encourage nimble innovative solutions, we can achieve the ideal personal health record,” said James S. Kahn, MD, professor of clinical medicine at UCSF’s Positive Health Program at San Francisco General Hospital.

The paper notes that costs may be offset by improvement in health activities and reduced administrative costs. The difficulty of making personal health record data portable for patients as they change health organizations is a key factor limiting wider and more rapid adoption.

“Personal health records controlled by patients that are interoperable with other systems so that they can take their records with them are also essential for empowering patients and ensuring their control over their own health care. Exploring other technologies such as mobile phones as an easier entry point for consumers to access their records could play an important role as well,” said Kahn.

The authors posit a dynamic relationship as patients’ behavior influences personal health record acceptance and personal health record adoption influences consumers’ behavior.

“For instance, a personal health record could interact with patients through automated mechanisms such as alerts or reminders and improve medication adherence. Consumer-to-consumer interactions through social networking sites could provide group support for healthy behavior changes such as tobacco abatement,” said Kahn.

Kahn has directed the development of the Health Care Evaluation Record Organizer (HERO) at Ward 86, UCSF’s outpatient HIV/AIDS clinic at San Francisco General Hospital, a public hospital where many patients are in a safety net situation.

“In addition, we need to recognize that some established personal health record vendors may not respond to all patient needs. We are actively trying to understand how personal health records can be used in a safety net setting in a public hospital,” added Kahn.

Source: University of California – San Francisco

A large group of California physicians given financial incentives to improve the quality of medical care have begun to embrace an array of changes important to advancing quality, according to a RAND Corporation study issued today.

Measures adopted by medical groups include speeding up adoption of information technology such as electronic medical records, more closely tracking the improvement of physician performance and sharpening institutional focus on quality, according to findings published in the March/April edition of the journal Health Affairs. The project was supported by a grant from the California HealthCare Foundation.

“Physician groups are responding to pay-for-performance programs by making practice changes and altering how they compensate physicians to reward quality, but health plans and purchasers say that those investments are not yet translating into substantial gains in quality,” said Cheryl Damberg, the study’s lead author and a senior policy researcher at RAND, a nonprofit research organization.

“The true benefits of these programs may take more time to be realized and it is likely that investments in other quality efforts will be needed in addition to performance-based pay,” Damberg said.

The RAND Health study found that medical groups are providing some payments to individual physicians based on quality measures and physicians in the program are receiving more feedback about whether they are attaining quality goals.

Pay-for-performance programs in health care have grown rapidly in recent years as a way to improve the quality of care delivered by doctors, hospitals and other health care providers. Despite the rapid adoption of these programs, there is little research about how well they work and what types of strategies work best.

RAND researchers are evaluating a statewide pay-for-performance program launched by the California Integrated Healthcare Association in 2003. The initiative includes seven major California health plans and 225 physician groups. The groups employ 35,000 physicians who care for 6.2 million people enrolled in commercial health maintenance organizations and point-of-service plans.

Under the program, physician groups receive financial bonuses if they meet certain performance guidelines such as increasing the number of patients with diabetes who receive recommended blood tests. Other performance measures include improving patient experience with getting care and adopting health information technology capabilities. Between 2003 and 2007, the participating health plans paid $203 million in incentives to participating physician groups.

The RAND study reports findings gathered from surveys of 35 medical groups, the seven health plans and representatives from two employers that are involved in the pay-for-performance experiment.

Most of the medical groups surveyed suggested that the program’s financial incentives — generally about $1,500 to $2,000 annually per physician — were too small to stimulate significant change among most doctors. They suggested the incentives needed to be two to five times higher in order to achieve quality improvements.

Health plans thought increasing the incentives was a low priority because of the relatively small quality improvements attained thus far and questions about whether other types of investments might produce greater quality gains, according to the study.

Although there is some concern that pay-for-performance might cause physicians to drop patients who decline to follow recommendations, few reports of such events were received. More than two-thirds of the medical groups reported that the pay-for-performance program resulted in more positives than negatives.

Most physician organizations said they collected more bonus payments than they had spent to comply with the program, although six said it was barely enough to cover their costs. Twenty of the medical groups surveyed said the program had affected the behavior of their individual physicians, prompting them to embrace quality efforts such as performing more-intensive outreach to patients.

Source: RAND Corporation

PORTLAND, Ore. – Oregon patients who request physician aid in dying under Oregon’s Death With Dignity Act often rate concerns about future illness symptoms as a leading motivator. The findings are the result of an Oregon Health & Science University study published in the March 9 edition of the Archives of Internal Medicine.

“Our data suggests that patients who request physician-assisted death do so not because of physical symptoms or their current quality of life. They often make their requests based on an anticipation of future suffering,” explained Linda Ganzini, M.D., a professor of psychiatry in the OHSU School of Medicine.

Previous studies of the factors for requests of physician aid in dying were based on interviews and surveys conducted with health care providers and family members following a loved one’s death. The goal of this study was to directly survey patients about their reasons for requesting assistance, before death via physician aid or other circumstances.

A total of 56 Oregonians took part in the study. All of the patients had requested physician aid in dying or had contacted an advocacy organization for information. The vast majority of patients were diagnosed with terminal cancer.

Each of these patients was asked to rate on a 5-point scale the importance of 29 factors in influencing their request for aid in dying. The highest ranked reasons for aid in dying were: wanting to control the circumstances of their death, concerns about future poor quality of life, concerns about future pain, concerns about the future ability to care for oneself, a loss of independence and the desire to die at home. Among the lowest rated reasons for requesting assistance were: depression, lack of support, financial concerns, current pain and quality of life.

The findings are being published as a second U.S. state enacts a law allowing physician-assisted suicides to take place. On Thursday, March 5, Washington became the second state in the country to allow physicians to prescribe lethal medications. Oregon’s assisted suicide law was enacted in 1998.

“We hope that the results of this study will help guide providers in counseling patients who inquire about physician aid in dying,” added Ganzini. “Based on this data, health care providers should first focus on providing information about future symptom control and improving the patient’s sense of control.”

Source: Oregon Health & Science University

DALLAS – March 9, 2009 – A newly discovered receptor in a strain of Escherichia coli might help explain why people often get sicker when they’re stressed.

Researchers at UT Southwestern Medical Center are the first to identify the receptor, known as QseE, which resides in a diarrhea-causing strain of E coli. The receptor senses stress cues from the bacterium’s host and helps the pathogen make the host ill. A receptor is a molecule on the surface of a cell that docks with other molecules, often signaling the cell to carry out a specific function.

The study is available online and in a future issue of the Proceedings of the National Academy of Sciences. Dr. Vanessa Sperandio, associate professor of microbiology at UT Southwestern and the study’s senior author, said QseE is an important player in disease development because the stress cues it senses from a host, chiefly epinephrine and phosphate, are generally associated with blood poisoning, or sepsis.

“Patients with high levels of phosphate in the intestine have a much higher probability of developing sepsis due to systemic infection by intestinal bacteria,” Dr. Sperandio said. “If we can find out how bacteria sense these cues, then we can try to interfere in the process and prevent infection.”

Millions of potentially harmful bacteria exist in the human body, awaiting a signal from their host that it’s time to release their toxins. Without those signals, the bacteria pass through the digestive tract without infecting cells. What hasn’t been identified is how to prevent the release of those toxins.

“There’s obviously a lot of chemical signaling between host and bacteria going on, and we have very little information about which bacteria receptors recognize the host and vice versa,” Dr. Sperandio said. “We’re scratching at the tip of the iceberg on our knowledge of this.”

In 2006, Dr. Sperandio’s lab was the first to identify the receptor QseC sensor kinase, a molecule found in the membrane of a diarrhea-causing strain of E coli known as enterohemorrhagic Escherichia coli, or EHEC. Prior research by Dr. Sperandio found that when a person ingests EHEC – which is usually transmitted through contaminated food such as raw meat – it travels peacefully through the digestive tract until reaching the intestine. There, chemicals produced by the friendly gastrointestinal microbial flora and the human hormones epinephrine and norepinephrine alert the bacteria to its location.

Once QseC recognizes the stress hormones, it initiates a cascade of genetic activations in which EHEC colonizes the intestine and moves toxins into human cells, altering the makeup of the cells and robbing the body of nutrients.

“The bacteria get what they want – nourishment – and the person ends up getting diarrhea,” Dr. Sperandio said.

The new study identifies QseE, a receptor only found in intestinal bacteria, as the receptor that ends this QseC-initiated cascade. It also provides the timing for the bacterium’s actions, including the regulation of the genes necessary for EHEC to cause diarrhea.

“EHEC needs both receptors to be fully virulent and express its toxins,” Dr. Sperandio said. “When people are stressed they have more epinephrine and norepinephrine being released. Both of these human hormones activate the receptors QseC and QseE, which in turn trigger virulence. Hence, if you are stressed, you activate bacterial virulence.”

Dr. Sperandio said the findings also suggest that there may be more going on at the genetic level in stress-induced illness than previously thought.

“The problem may not only be that the stress signals are weakening your immune system, but that you’re also priming some pathogens at the same time,” she said. “Then it’s a double-edged sword. You have a weakened immune system and pathogens exploiting it.”

Previous research by Dr. Sperandio found that phentolamine, an alpha blocker drug used to treat hypertension, and a new drug called LED209 prevent QseC from expressing its virulence genes in cells.

The next step is to test whether phentolamine has the same effect on QseE.

Source: UT Southwestern Medical Center

Credit: University of Iowa

A new study led by University of Iowa researchers has found an unexpected new link between this inflammation in heart muscle following a heart attack and a previously known enzyme called calcium/calmodulin-dependent protein kinase II or CaM kinase II. The findings also reveal the involvement of an immune system gene — complement factor B — that has been implicated in other inflammatory diseases.

The study, published online March 9 in the Journal of Clinical Investigation, suggests that CaM kinase II inhibition could be a therapeutic target in heart disease, but by previously unknown pathways.

CaM kinase II is a pivotal enzyme that registers changes in calcium levels and oxidative stress and translates these signals into cellular effects, including changes in heart rate, cell proliferation and cell death. CaM kinase II also regulates gene expression — which genes are turned on or off at any given time. Inhibition of CaM kinase II in mice protects the animals’ hearts against some of the damaging effects of a heart attack.

To better understand how CaM kinase II pathways are involved in damage caused by heart attack, the UI researchers investigated the effect of CaM kinase II activity on gene expression during a heart attack. The study’s lead author was Madhu Singh, Ph.D., UI research scientist, and the senior author was Mark Anderson, M.D., Ph.D., professor of internal medicine and molecular physiology and biophysics at the UI Roy J. and Lucille A. Carver College of Medicine and director of the Division of Cardiovascular Medicine.

“We used a mouse model in which CaM kinase II is inhibited in heart muscle cells. These mice are protected from many of the ill effects of heart attack,” Singh said. “We compared a large number of genes that were expressed in the protected mice compared to the non-protected control mice. A particularly interesting finding was that a cluster of inflammatory genes was differently expressed depending on whether CaM kinase II was active or inhibited.”

Specifically, the research showed that heart attack triggered increased expression of a set of pro-inflammatory genes, and inhibition of CaM kinase II substantially reduced this effect.

The team focused on the most highly regulated of these inflammatory genes — complement factor B. The protein produced by this gene is involved in the innate immune system called the alternative complement pathway.

The team found that complement factor B protein is synthesized in heart muscle cells as part of an autoimmune response to heart attack and that complement factor B protein participates in the formation of the so-called membrane attack complex, which punctures holes in heart cell membranes.

“It was very surprising that heart muscle cells express complement factor B, an immune system protein, because traditionally these cells are known for their contraction function, which supports heart pumping, not as part of the immune response to injury,” Singh said.

Complement factors are part of the first line of defense against pathogens. When complement pathways are triggered, a biological cascade is set in motion that results in the formation of a membrane attack complex – a group of proteins that can literally punch holes in the cell membrane of an invading microbe or an injured cell.

The UI team showed that the complement factor B produced in heart muscle cells helped form membrane attack complexes that were able to puncture the cell membranes of heart muscle cells in a petri dish. In addition, the researchers found that genetically engineered mice that did not express functional complement factor B were partly protected from heart attack — showing reduced mortality and heart damage.

“Clearly, if this immune system response is induced during heart attack injury, it might amplify heart damage by poking holes in the cell membrane,” Singh said. “Not only is the heart trying to recover from the injury induced by the heart attack, but it also has to deal with the consequences of the induced activity of the complement pathway, which is attacking the cell membranes.

“If we can reduce the extra burden on the heart by some means of inhibiting this activity, then clinically that might be useful, he added.

“These findings show a previously unanticipated connection between CaM kinase II activity and inflammation in heart muscle and show that this connection drives maladaptive responses to heart attack,” said Anderson, who also holds the Potter-Lambert Chair in Cardiology. “By understanding these CaM kinase II signaling mechanisms that occur inside the cell we might arrive at new and better drug targets that act more specifically to treat a variety of heart problems.”

Source: University of Iowa

Credit: University of Iowa

Even for those without a heart condition, it’s a peculiar feeling when your heart “races” in response to stress. That pacing change happens in part because of how the enzyme calcium/calmodulin-dependent protein kinase II (CaM kinase II) is called into action by the body’s ‘fight or flight’ stress response, University of Iowa researchers have found.

The finding challenges traditional concepts of the heart’s peacemaking function and adds support to the idea that finding ways to inhibit CaM kinase II could help control heart rate problems in people with arrhythmias and other heart conditions. The study results appear March 9 in the online Early Edition of the Proceedings of the National Academy of Sciences.

Previous understanding of the heart’s pacemaking functions was focused on beta-adrenergic receptors, said Yuejin Wu, Ph.D., the study’s lead investigator and a research scientist in internal medicine at the UI Roy J. and Lucille A. Carver College of Medicine.

“Beta-adrenergic receptor stimulation during stress ultimately increases activity of a particular ion channel, previously known as the ‘pacemaker channel’, and our current treatments for fast heart rates involve drugs that directly inhibit these beta-adrenergic receptors,” Wu said. “In fact, we found that a significant part of the ‘fight or flight’ heart rate response depends on activation of the enzyme CaM kinase II during beta-adrenergic stimulation.”

In a recent study from Germany, a mouse model that was missing the gene for the pacemaker ion channel surprisingly responded normally to the drug isoproterenol. Similar to adrenaline, isoproterenol can increase heart rate. This response meant that the ion channel, by itself, does not explain the physiological “fight or flight” heart rate response.

Based on this observation, Wu and other colleagues in the lab of the paper’s senior author, Mark Anderson, M.D., Ph.D., head of the UI Division of Cardiovascular Medicine, developed mice in which the CaM kinase II function was inhibited in heart cells. When these mice were exposed to the adrenaline-like agent isoproterenol, the stimulant’s effect did not occur. As a result, the mice without CaM kinase II function had much slower heart rates than mice that had normal CaM kinase II function. The finding underscored that CaM kinase II activation can increase heart rates.

“In a person whose heart beats at a normal rate, you would not want to inhibit CaM kinase II function,” Wu said. “But our findings suggest that in people with rapid heart rates it could be beneficial to inhibit the enzyme’s function. When the heart beats too fast, it does not pump well, and if a fast heart rate, persists it can damage the heart’s muscle.”

This research focused specifically on specialized heart cells called sinoatrial nodal cells, which help maintain the heart’s normal rhythm. Compared to other heart cells, which affect contraction, there are very few sinoatrial cells — perhaps only a few hundred. This scarcity means each cell is critical for normal heart function. The same scarcity also has made it challenging to find enough cells for research purposes.

Based on research done in France, Wu and colleagues were able to develop a method to extract single sinoatrial nodal cells from mouse models for examination. Unlike ventricular cells, sinoatrial nodal cells can beat on their own without electrical stimulation, allowing scientist to see their activity when extracted.

“By examining single cells, we were able to see very basic mechanisms”, Wu said. “The sinoatrial cells taken from mice with inhibited CaM kinase II were not able to facilitate calcium function, and thus, each cell’s ability to beat slowed down. Since people with arrhythmias have a heart beat that is too fast, the opposite problem may be true — there is too much CaM kinase II function, resulting in calcium overload.”

The team will continue to study pathways by which CaM kinase II functions and affects the heart.

Source: University of Iowa

Fifteen-year-old males who ate fish at least once a week displayed higher cognitive skills at the age of 18 than those who it ate it less frequently, according to a study of nearly 4,000 teenagers published in the March issue of Acta Paediatrica.

Eating fish once a week was enough to increase combined, verbal and visuospatial intelligence scores by an average of six per cent, while eating fish more than once a week increased them by just under 11 per cent.

Swedish researchers compared the responses of 3,972 males who took part in the survey with the cognitive scores recorded in their Swedish Military Conscription records three years later.

“We found a clear link between frequent fish consumption and higher scores when the teenagers ate fish at least once a week” says Professor Kjell Torén from the Sahlgrenska Academy at the University of Gothenburg, one of the senior scientists involved in the study. “When they ate fish more than once a week the improvement almost doubled.

“These findings are significant because the study was carried out between the ages of 15 and 18 when educational achievements can help to shape the rest of a young man’s life.”

The research team found that:

• 58 per cent of the boys who took part in the study ate fish at least once a week and a further 20 per cent ate fish more than once a week.
• When male teenagers ate fish more than once a week their combined intelligence scores were on average 12 per cent higher than those who ate fish less than once a week. Teenagers who ate fish once a week scored seven per cent higher.
• The verbal intelligence scores for teenagers who ate fish more than once a week were on average nine per cent higher than those who ate fish less than once a week. Those who ate fish once a week scored four per cent higher.
• The same pattern was seen in the visuospatial intelligence scores, with teenagers who ate fish more than once a week scoring on average 11 per cent higher than those who ate fish less than once a week. Those who ate fish once a week scored seven per cent higher.

“A number of studies have already shown that fish can help neurodevelopment in infants, reduce the risk of impaired cognitive function from middle age onwards and benefit babies born to women who ate fish during pregnancy” says Professor Torén.

“However we believe that this is the first large-scale study to explore the effect on adolescents.”

The exact mechanism that links fish consumption to improved cognitive performance is still not clear.

“The most widely held theory is that it is the long-chain polyunsaturated fatty acids found in fish that have positive effects on cognitive performance” explains Professor Torén.

“Fish contains both omega-3 and omega-6 fatty acids which are known to accumulate in the brain when the foetus is developing. Other theories have been put forward that highlight their vascular and anti-inflammatory properties and their role in suppressing cytokines, chemicals that can affect the immune system.”

In order to isolate the effect of fish consumption on the study subjects, the research team looked at a wide range of variables, including ethnicity, where they lived, their parents’ educational level, the teenagers’ well-being, how frequently they exercised and their weight.

“Having looked very carefully at the wide range of variables explored by this study it was very clear that there was a significant association between regular fish consumption at 15 and improved cognitive performance at 18″ concludes lead author Dr Maria Aberg from the Centre for Brain Repair and Rehabilitation at the University of Gothenburg.

“We also found the same association between fish and intelligence in the teenagers regardless of their parents’ level of education.”

The researchers are now keen to carry out further research to see if the kind of fish consumed – for example lean fish in fish fingers or fatty fish such as salmon – makes any difference to the results.

“But for the time being it appears that including fish in a diet can make a valuable contribution to cognitive performance in male teenagers” says Dr Aberg.

Source: Wiley-Blackwell

The Department of Applied Physics, Northwestern Polytechnical University (NPU) in Xi’an, China-Research, has shown that the substantial undercooling of liquid state brings about novel microstructural transition for Al-Cu-Si ternary eutectic alloy. The study is reported in Issue 54 (January, 2009) of Chinese Science Bulletin because of its significant research value.

Al–Cu–Si alloy is widely applied in industry mainly as a light construction material. It is also a promising material for applications such as engine block and cylinder heads. It is important for designers to have an intimate knowledge of how Al–Cu-Si alloy solidifies because its mechanical performance is usually controlled by solidification mechanism and microstructural characteristics. However, so far there has been little research on its rapid solidification mechanism under the extremely nonequilibrium condition.

In this work, Al80.4Cu13.6Si6 eutectic alloy was undercooled up to 147 K (0.18TE). Generally speaking, under the conventional solidification condition, a liquid aluminium alloy can be hardly undercooled because of oxidation. Dr. Ruan and Prof. Wei made it realized by choosing dehydrated B2O3 agent as a denucleating agent and providing a high-vacuum environment and special melting processing. In addition, the experimental parameters, such as cooling rate, superheating, and holding time, were controlled in order to get a wider undercooling range for comparison.

The undercooling level of alloy melt has a strong effect on its crystallization kinetics, structure morphology, and final physical and chemical properties. This study presents the microstructural characteristics of highly undercooled Al80.4Cu13.6Si6 ternary eutectic alloys. So far, most investigations on eutectic growth focus on binary alloy systems. The rapid solidification of undercooled ternary alloys involves the competitive nucleation and coupled growth of three eutectic phases from one liquid phase, which makes it more complicated than the case of binary alloys. The authors showed that the phase selection of Al80.4Cu13.6Si6 ternary eutectic alloy is influenced by undercooling, which makes the competitive nucleation and cooperative growth among (Al), (Si) and (CuAl2) phases become more drastic. Once undercooling exceeds 73 K, the primary phase will transform from (Al) dendrite to faceted (Si) block.

“This paper emphasizes the phase selection and microstructure formation of substantially undercooled ternary eutectic alloys. The result is of academic and practical significance.” said one journal reviewer. A series of papers about rapid solidification of ternary eutectic alloys written by Dr. Ruan and Prof. Wei have been published in Chin. Sci. Bull., Sci. Chin. G, etc. “It enriched and expanded the research results on nonequilibrium solidification. It offered us new references to develop solidification and nonequilibrium phase transition theory,” said another reviewer.

Source: Science in China Press

The possibility of remote monitoring for chronically ill patients will soon become a reality. Now, researchers in South Africa and Australia have devised a decentralized system to avoid medical data overload. They describe the peer-to-peer system in a forthcoming issue of the International Journal of Computer Applications in Technology.

People with a range of chronic illnesses, including diabetes, high blood pressure, and heart problems can benefit from advances in monitoring technology. Such devices could send data on a person’s symptoms directly to a centralized computer server at their health center. This would allow healthcare workers to take appropriate action, whether in an emergency or simply to boost or reduce medication in response to changes in the patient’s symptoms.

However, as tele-monitoring is set to become widespread, there will inevitably be an issue of data overload with which a centralized computer will not be able to cope. Computer scientists Hanh Le, Nina Schiff, and Johan du Plessis at the University of Cape Town, working with Doan Hoang at the University of Technology, Sydney, suggest a decentralized approach.

Computer users are familiar with the concept of peer-to-peer (P2P) networks in which individual users share the workload across equivalent personal computers on a network. This avoids overloading any single server or swamping bandwidth on individual connections. The P2P approach is commonly employed by software companies and others to distribute large digital files, such as operating system updates, and high-definition movies.

A P2P network overlays a network on the individual peers, known as nodes, without a central control point and uses their idle processing cycles, storage, and bandwidth via the internet.

Le and colleagues have developed an application to demonstrate proof of principle of how a P2P network could incorporate patient sensors including thermometers, blood-pressure units and electrocardiograms (ECG). It is the latter on which the team has focused to build a P2P heart-monitoring network.

The system builds on the team’s concept of a physically-aware reference model (a PARM). Their PARM acts as a small-scale, but scalable model of the kind of network overlay that could be built on the internet. Tests have already demonstrated that a continual and unintrusive heart monitoring application could be developed into a working e-health system quickly and simply at low cost using P2P.

Source: Inderscience Publishers