Roche and Panasonic Healthcare partner for novel Point of Care system to improve diagnosis in metabolic syndrome.

Roche and Panasonic Healthcare have allied for a new medical testing solution to combine early diagnosis and control of blood lipid and average glucose concentration (HbA1c) levels. The new designed system will pioneer with a unique approach, as it enables healthcare professionals to early detect metabolic syndrome and to improve overall therapy guidance for patients with diabetes at point of care.

Manufactured by Panasonic Healthcare in Japan and marketed worldwide by Roche, the novel solution will respond to the growing needs of today’s cost conscious healthcare environment in primary care combining ease of use, reliability and cost effectiveness.

“I am convinced that the partnership with Panasonic Healthcare enables us to provide some pioneering improvements for healthcare professionals to early identify people with a metabolic syndrome, and to enhance overall therapy management for patients with chronic cardiovascular disease”, states Colin Brown, head of Roche Professional Diagnostics.

Starting at the end of 2012 [1], the novel blood glucose and lipid monitoring system will aid healthcare professionals with a rapid on-the-spot test for the two most important cardiovascular disease risk factors, as it also supports doctors with a user-friendly and failsafe handling for near patient testing.

“The new system will allow healthcare professionals to fully concentrate on their patients, as it will imply a convenient and safe handling of samples combined with a user friendly graphic interface for rapid and explicit result reporting. Seamless connectivity to the laboratory’s information system will allow consistent data management in established IT environments”, comments Kazuya Nakaya, Executive Managing Director of Panasonic Healthcare.

Metabolic syndrome affects 20 to 25% of the global adult population and it is a cluster of the most dangerous cardiovascular disease (CVD) risk factors: diabetes and elevated plasma glucose, abdominal obesity, high cholesterol and high blood pressure. [2]

In 2011, about 366 million people worldwide suffered from diabetes. According to the World Health Organization (WHO), this will increase to 552 million by 2030 and, the number of deaths will double to about 6 million annually. [3, 4] It is estimated that more than half of all people with diabetes type 2 remain undiagnosed. [4] As undiagnosed diabetes may affect serious cardiovascular problems it is important to be aware of its very early symptoms.

In the US, Japan and Europe there are more than 240 million people with abnormal lipoprotein levels and the prevalence is constantly increasing. [5] Dyslipidemia is a disorder of the lipoprotein metabolism, manifested by elevated low-density lipoprotein (LDL) cholesterol and triglyceride concentrations in the blood. The WHO estimates that this situation accounts for 18% of ischemic heart disease (IHD) and 56% of stroke and more than four million of deaths annually. [6]

Besides the chronic impact to the patients, dyslipidemia and diabetes have a financial impact for the healthcare systems worldwide as the global healthcare expenditures to treat and to prevent diabetes and its side effects were estimated at USD 376 billion in 2010 alone.

The alliance with Panasonic Healthcare will continue to expand Roche’s global leading position with innovative products and services to enable healthcare professionals for improved management of chronic cardiovascular disease at the point of care.

References
1. initially outside the US
2. www.idf.org/metabolic-syndrome, accessed 08/02/2012
3. IDF Diabetes Atlas 2011
4. Diabetes WHO Fact sheet N°312. Available at: http://www.who.int/mediacentre/factsheets/fs312/en/
5. Smith DG Am J Managed Care 2007; 13 (3): 69-71
6. Lozano et al. Miscoding and misclassification of ischaemic heart disease mortality. Global Programme on Evidence for Health Policy Working Paper No. 12. World Health Organization, September 2001.

A Yale University-led research team has developed a way to measure the loss of insulin-producing islet cells in the human pancreas. The death of those beta cells leads to diabetes. The finding is a crucial step in developing therapies to preserve insulin production and slow or halt the progress of diabetes.
Until now there has been no effective method for imaging pancreatic islet beta-cell mass in a non-invasive manner. Based on the work of Paul Harris and colleagues at Columbia University, the Yale team focused on the genetically expressed protein known as vesicular monoamine transporter type 2 (VMAT2). This protein facilitates the storage and release of some neurotransmitters, and is expressed simultaneously with insulin in pancreatic beta cells.
The Yale team infused both healthy patients and those with type-1 diabetes with a radioactive tracer that targets VMAT2. Patients were then scanned with a PET camera to calculate the radioactivity concentration in the pancreatic cells and measure the binding of the tracer.
Adjusting for dosage and body weight, the radiotracer binding among pancreatic cells was 40 percent less in type-1 diabetes patients than in healthy patients.
Senior author Gary W. Cline, associate professor of endocrinology at Yale School of Medicine, explained, ‘This tells us that we can now measure the loss of the pancreatic islet cells that produce insulin in diabetic patients. Being able to make these measurements will help in the development of a drug that can stop or slow the death of these cells, and thus prevent the damaging effects of type 1 diabetes.’ Yale University

Scientists have successfully sequenced the genome of a baby in the womb without tapping its protective fluid sac. Maternal blood sampled at about 18 weeks into the pregnancy and a paternal saliva specimen contained enough information for the scientists to map the foetus’ DNA. This method was later repeated for another expectant couple closer to the start of their pregnancy. The researchers checked the accuracy of their genetic predictions using umbilical cord blood collected at birth.
Jacob Kitzman and Matthew Snyder, working in the laboratory of Dr. Jay Shendure, associate professor of genome sciences at the University of Washington, led the study. Kitzman is a National Science Foundation Graduate Research Fellow.
Scientists have long known that a pregnant woman’s blood plasma contains cell-free DNA from her developing foetus. Foetal DNA appears in the mother’s plasma a few weeks after conception. It rises during gestation and normally vanishes after the baby arrives. While the concentration varies among individuals, about 10 percent of the cell-free DNA in a pregnant woman’s blood plasma comes from her foetus.
Based on this phenomenon, other research labs are designing maternal blood tests for major aberrations in the foetus’s genetic makeup. The tests are considered a safer substitute for the more invasive sampling of fluid from the uterus, a common procedure in obstetrical practice. These new tests search for just a few genetic disorders or specific congenital abnormalities. For example, a test targeted for Down syndrome would look for evidence of three copies of chromosome 21.
Kitzman explained what distinguishes his team’s latest methods is the ability to assess many and more subtle variations in the foetus’ genome, down to a minute, one-letter change in the DNA code.
‘The improved resolution is like going from being able to see that two books are stuck together to being able to notice one word misspelled on a page,’ said Kitzman.
With technical advances as well as statistical modelling, the research group overcame several obstacles that had stymied previous efforts to determine foetal genomes. With a preponderance of maternal rather than foetal DNA in plasma samples, a major problem was figuring out which genetic variants had passed from mother to child. The scientists applied a recently developed technique to resolve the mother’s haplotypes, which are groups of genetic variations residing on the same chromosome. From these groupings, the researchers could pick out the parts of the baby’s genetic material inherited from each parent with over 98 percent accuracy.
‘It was rewarding to apply biostatistics to help solve this problem,’ said Snyder, who came to genome sciences from the fields of statistics and economics.
Still, he added, there is more work to be done to improve this technique. The researchers pointed to the need for a more robust, scalable, overarching protocol, as well as ways to lower costs and automate and standardise parts of the process. Washington University

One of the largest studies to investigate birth complications and later mental health has found that premature birth constitutes a single, independent risk factor for a range of severe psychiatric disorders. Researchers at King’s College London in the UK and Karolinska Institutet suggest that neurodevelopmental differences in those born prematurely may be important in understanding the link.
Researchers identified all individuals registered in the Swedish birth register between 1973 and 1985 who were alive and living in Sweden at the age of 16, a total of nearly 1.5 million individuals. By analysing national hospital discharge registers, they identified all individuals admitted to hospital with their first episode of a psychiatric disorder.
The study found that individuals born extremely prematurely (less than 32 weeks gestation) were 2.5 times more likely to have psychosis as young adults, nearly 3 times more likely to have depression, and 7.4 times more likely to have bipolar disorder than those born at term (37-41 weeks gestation). The findings also revealed a smaller, yet still significant, increased risk of developing bipolar disorder, psychosis and depression for those born moderately prematurely (32-36 weeks).
The study also investigated the link between premature birth, eating disorders and alcohol and drug dependency, but association with these disorders was much weaker. Other adverse perinatal factors including newborn health, maternal socio-demographic characteristics and maternal psychiatric history were taken into account and were found to have no significant effect on the findings.
‘We believe that the increased risk of mental disorders in those born very prematurely can be explained by alterations of brain development’, says Professor Christina Hultman at Karolinska Institutet, who led the Swedish part of the study. ‘The immature nervous system in these children is particularly vulnerable to brain injury resulting from birth complications.’
Approximately 6 percent of babies in Sweden are born prematurely every year. Thanks to research and new technology, today many of prematurely born can be saved. Most of these babies go on to lead healthy lifestyles, although as a group they are more likely to require extra school support and be hospitalised with a variety of physical problems. Therefore the authors point to the importance of raising awareness of the increased risk of mental health disorders in people born prematurely, and suggest gestational age should be considered when investigating risk factors for psychiatric disorders in young adults. Karolinska Institute

Certain proteins, such as 14-3-3, conserve their basic functions of cell cycle control in diverse organisms, from worms to humans. In a study led by Julián Cerón and Simó Schwartz Jr, researchers from the Bellvitge Biomedical Research Institute (IDIBELL) and the Research Institute of Vall d’Hebron (VHIR) respectively, have described germ line functions of par-5, which is one of the two 14-3-3 proteins existing in Caenorhabditis elegans, worms used as experimental model in genetic studies. The overexpression of the 14-3-3 proteins is related to the resistance of tumours to chemotherapy, which could have implications for clinical practice.
Researchers found that par-5 gene, as its human homologues, is required for DNA damage response in C. Elegans validating the model to investigate chemotherapies and genetic modifications since 14-3-3 proteins are therapeutic targets in cancer
The powerful genetic tools of C. elegans have allowed a precise functional dissection of the single 14-3-3 protein present in their germline. The researchers have discovered that par-5 is not only necessary for proper cell cycle regulation, but also to prevent the accumulation of endogenous DNA damage and genomic instability.
Moreover, this study reveals that par-5 is required for DNA repair response when it is damaged by chemicals or ionizing radiation. In such response, the researchers propose a model where PAR-5 regulates CDK-1 phosphorylation to stop the cell cycle and repair the damage induced by chemotherapeutic agents.
The overexpression of the 14-3-3 protein has been related to chemotherapy resistance in cancer cell lines while its downregulation sensitises cells to therapy-induced cell death. Therefore, this study in C. elegans provides the basis for a model to study chemotherapy response in the context of a whole living organism.
Regulators proteins 14-3-3, evolutionarily conserved, bind to signalling proteins and affect their stability, activity or cellular localisation. So, they are involved in the regulation of various cellular processes, including apoptosis, the cell cycle and stress response.
In addition, the researchers found that par-5 is required for cell cycle arrest in response to replicative stress and ionizing radiation. IDIBELL-Bellvitge Biomedical Research Institute