Nova Biomedical has been awarded a multi-year group purchasing agreement for critical care blood gas analysers from Premier. This agreement provides Premier members access to Nova’s new Stat Profile Prime Plus® critical care blood gas analyser. Prime Plus features maintenance-free sensor technology to provide 20 essential critical care tests including BUN, creatinine, ionized magnesium, blood gases, electrolytes, metabolites, hematology, and co-oximetry. Prime Plus also provides new and patented, non-lysing whole blood co-oximetry technology, along with automated quality control (QC), powerful data management, bidirectional connectivity, and extensive cybersecurity protection. The current agreement allows Premier members, at their discretion, to take advantage of special, pre-negotiated pricing and terms for Prime Plus analysers and consumables in addition to Nova’s 10-test Prime analysers.
“We are pleased that Premier has awarded a group purchasing agreement to our innovative, maintenance-free Prime Plus,” said John Britt, Director of Corporate Accounts for Nova. “This agreement allows Premier members access to the entire Stat Profile Prime platform including its new flagship analyser, Prime Plus. Prime Plus introduces innovative technology that expands critical care testing with unique assays and eliminates sensor and co-oximeter maintenance, all of which improves uptime and reliability while reducing costs. Prime Plus represents the latest in critical care testing technology and further demonstrates Nova’s leadership and history of innovation.”
Prime Plus incorporates Nova’s innovative, maintenance-free sensor technology with individual MicroSensor cards, calibrator cartridges, and quality control cartridges. This design eliminates sensor and co-oximeter maintenance, improves analyser uptime, and reduces testing costs for the compact and easy-to-use Prime Plus.
Premier is a leading healthcare improvement company, uniting an alliance of approximately 4,000 U.S. hospitals and 165,000 other providers.
www.novabiomedical.com

Levels of a gene that helps the immune system differentiate the good cells from the bad could be a good indicator of prognosis in people with colorectal cancers, Medical College of Georgia researchers report.
Looking at 15 genes known to be associated with colorectal cancers — eight associated with lower survival rates and seven with higher — the researchers found that one gene, CCR4, was present in higher levels in patients with a good prognosis, even in those diagnosed with late stage disease.
The gene is part of the chemokine family, which is involved in trafficking the body’s white blood cells, which then fight off invaders. Through genetic analysis, MCG researchers found that patients with higher levels had responded better to treatment, had more incidences of remission and lived longer, says second-year MCG student Chance Bloomer.
“If the cancer is expressing this gene, it makes it easier for the immune system to attack those cells,” he says. “There is no good type of colorectal cancer, but if you’re going to have it, you want higher levels of this gene.” Bloomer is presenting his findings at the American Association for Cancer Research Annual Meeting this week in Atlanta.
Bloomer worked with Dr. Ravindra Kolhe, molecular pathologist and director of MCG’s Georgia Esoteric & Molecular Laboratory, to design the two genetic panels — one that he hoped could be used to predict good outcomes and one for poorer outcomes. They started by combing through cBioPortal for Cancer Genomics, which houses large-scale cancer genomics data sets.
“Essentially this was raw data,” Bloomer says. “There are thousands of gene expression levels for thousands of patients with all types of cancers. I was looking for genes that had been shown to be associated with better survival rates.”
Bloomer started with nearly 800 genes — all with known and strong associations to cancer progression — and narrowed those down to 38 with significant associations to increased or decreased survival rates for colon cancer. He narrowed the group further by grouping those with similar mechanisms — whether they were involved in immune system response, rates of tumour growth or treatment response, for example. “I wanted a holistic approach that looked at tumour genetics and how these genes worked,” he says.
After settling on an eight gene panel he hoped would help determine decreased survival rates, and a seven gene panel to determine better survival rates, they analysed tissue samples of 750 colorectal cancer patients from the Georgia Cancer Center. Patients were grouped by tumour stage, determined by using its size and/or whether it has spread; whether they survived less than or more than three years; tumour grade, a measure of how quickly it is likely to grow and spread; and age — over or under age 76.
While the entire panel did not work as well as Bloomer had hoped, increased levels of CCR4 did show multiple significant associations with better prognosis, even in patients with stage 4 cancer. Patients with stage 3 cancer and better survival rates also had higher levels of CCR4 than those with stage 1 tumours and poorer survival rates. Young patients with better survival rates also had higher levels than those with worse survival rates.
“We’re not entirely sure what the association is, but those are next steps,” Bloomer says. “If we are able to design a panel that can predict prognosis, and we are able to tell people they may have a worse prognosis, maybe that helps justify the more aggressive treatments, which can be uncomfortable and come with worse side effects. It’s important, though, that we tell patients that their results are not a certainty. They indicate, not ensure.”
Medical College of Georgia https://jagwire.augusta.edu/archives/63148

In late July, Svar Life Science signed a strategic agreement to transfer the portfolio of radioimmunoassays (RIA) and the Chromogranin A Neolisa™ (ELISA) product to DIAsource ImmunoAssays, a BioVendor group company.
Svar Life Science AB (formerly Euro Diagnostica AB), a Swedish life science company that has been working across the clinical diagnostic value chain for over 30 years, and DIAsource ImmunoAssays, a leading diagnostics company delivering manual RIA and ELISA kits and open automation solutions to international markets, today announced a strategic agreement, under which Svar Life Science will transfer its portfolio of RIA products and the Neolisa™ CgA ELISA product to DIAsource, securing the continued production and sales of these products.
Svar Life Science will continue to invent, develop and apply the best analytical technologies, with a focus on helping deliver the answers needed in drug discovery and clinical diagnostics, and the impact this has on human lives.
This transaction strengthens DIAsource and BioVendor’s position as one of the top RIA and larger ELISA manufacturers, committed to servicing customers worldwide that use manual assays and open automation to complement their portfolio on closed automated systems.
The portfolio to be transferred includes the complete line of radioimmunoassays for the quantification of a number of peptide hormones involved in critical physiological processes. These endocrinological parameters are mainly used as tumour markers and for diabetology and salt balance analysis. The portfolio transfer also includes the ELISA Chromogranin A Neolisa™ product which complements the RIA Chromogranin A product.
In order to support a smooth transition with minimal disruption for customers, the companies have agreed to a transition period. Starting 1st of September 2018 DIAsource ImmunoAssays assumes sales of the RIA product portfolio. During the remainder of 2018 the RIA production will be transferred. Sales of the Neolisa™ CgA ELISA product will be assumed by DIAsource as of January 2019, with production transfer to follow during 2019.
Ron Long, CEO, Svar Life Science, said: “The agreement with DIAsource ImmunoAssays forms part of our strategy of focusing our product portfolio and core technologies to help deliver the answers needed in drug discovery and clinical diagnostics today. It also enables us to strengthen our support for life science customers providing high quality solutions, the best analytical technologies for drug development and clinical research.
DIAsource ImmunoAssays are committed to being a complete diagnostic provider and we’re confident that this agreement enables them to increase their support for customers in the field of radioimmunoassays.”  
Jef Vangenechten, CEO of DIAsource ImmunoAssays, said: “This acquisition is another step in our strategy to position DIAsource as a consolidator of manual specialty assays, after previous acquisitions of the Intertech RIA product line in 2012, Viro-Immun ELISA and IFA product lines in 2017, and more recently the RIA product line from ZenTech.”www.diasource-diagnostics.com

In the brain, as in business, connections are everything. To maintain cellular associates, the outer surface of a neuron, its membrane, must express particular proteins—proverbial hands that reach out and greet nearby cells. And, like a creepily long handshake, surface molecules can overstay their welcome: A protein that lingers too long on the membrane may compromise the connections, or synapses, between cells.
In a new study, Rockefeller scientist Mary E. Hatten and research associate Hourinaz Behesti demonstrate that the protein ASTN2 helps move proteins away from the membrane in a timely fashion. The researchers also propose a mechanism by which ASTN2 defects lead to neurodevelopmental disorders such as autism and intellectual disabilities.
Neurons send messages to one another in the form of chemicals, or neurotransmitters, which activate receptor proteins on the surface of neighboring cells. Chemical communication is highly dynamic, which means that receptors must be dynamic too: they perpetually rotate on and off the membrane, ensuring rapid response to incoming signals. This process requires assistance from additional proteins, so-called traffickers that nudge receptors to move along.
Hatten, the Frederick P. Rose Professor, has demonstrated that the protein ASTN2 acts as such a trafficker during cell migration in early development. When Behesti joined Hatten’s lab, she proposed that the protein might also play a role later in life, an idea supported by the fact that ASTN2 had been shown to be present in the adult brain. Specifically, the protein appears to be disproportionally expressed in the cerebellum—a brain region that some researchers suspect may govern complex aspects of cognition, in addition to its more-established role in regulating movement.
Hatten and Behesti wanted to better understand the function of ASTN2 in the adult cerebellum. An initial clue came by way of collaborators at Johns Hopkins University, who identified a family that had multiple members with ASTN2 mutations and neurodevelopmental disorders, including autism and language delays.
Concurrently, an independent study of a large population showed that ASTN2 mutations are associated with a wide variety of brain disorders. Hatten and Behesti therefore set out to determine how defects in this protein might disrupt cerebellar circuitry, and brain activity at large.
The researchers used a special microscopy technique to determine where ASTN2 is expressed in the mouse cerebellum. They found that it appears primarily in components of neurons responsible for moving proteins around, and they identified a collection of molecules that attach to ASTN2. These “binding partners” included proteins involved in synapse formation and protein trafficking.
When the researchers increased the expression of ASTN2 in mouse neurons, levels of its binding partners decreased, suggesting that ASTN2 attaches to these proteins and then ushers them away from the membrane for degradation within the cell. Working with researchers at Duke University, the scientists also observed that cells with heightened ASTN2 formed stronger synapses; and they suspect that decreased ASTN2 yields the opposite effect.
“Our data suggest that people who have mutations in ASTN2 make less of the protein, which leads to slower or weaker synapses,” says Behesti.
The researchers propose that without sufficient ASTN2, proteins accumulate on the cell surface, which hinders neuronal connections and communication.
“Synapses aren’t static. They need to respond in real time to dynamic stimuli; and one of the ways they do this is by changing their surface protein expression,” says Behesti.
This research supports a broader view that the disruption of surface protein composition may underlie a number of neurodevelopmental disorders. It also points to the cerebellum as a potentially fruitful research subject for understanding these conditions.
“People are just beginning to realize that the cerebellum isn’t just there to control movement and motor learning,” says Hatten. “It has much more complex roles in cognition and language.

Rockefeller University
www.rockefeller.edu/news/23712-study-protein-trafficker-provides-insight-autism-brain-disorders/

Opitz C syndrome (OCS), an ultra-rare disease that causes serious physical and intellectual disabilities, has an heterogeneous genetic base that makes its medical diagnostic and therapeutic intervention difficult, according to a new study by professors Daniel Grinberg, Susanna Balcells and Roser Urreizti, from the Group on Human Molecular Genetics of the of the Faculty of Biology of the University of Barcelona and the Rare Diseases Networking Biomedical Research Centre (CIBERER).
The new study concludes this severe and extremely rare disease could be considered a “private syndrome” for each patient.
Described in 1969 by geneticist John M. Opitz, this ultra-rare pathology –with only a few diagnosed cases worldwide- shows a great clinical variability in different levels of severity (trigonocephaly, intellectual disability, psychomotor retardation, among others). Therefore, clinical symptomatology of Opitz C syndrome can overlap other similar minority pathologies (Kleefstra, Kabuki, Bohring-Opitz syndromes, etc.).
However, despite sharing several clinical manifestations, “this disease does not show a genetic base shared by the affected people, and its hereditary transmission model is still unknown”, note the authors, also members of the Institute of Biomedicine of the University of Barcelona (IBUB) and the Research Institute Sant Joan de Déu (IRSJD).
Since 2007, several genes have been related to this pathology, which is hard to diagnose due its wide clinical pattern (for instance, ASXL1, CD96, ASXL3 and MAGEL2). In this context, research lines of the Group on Human Molecular Genetics (UB-CIBERER-HSJD) –in which Raquel Rabionet and Laura Castilla take part too- are broadening the knowledge of the genetic basis of this pathology which so far does not have any chance of receiving treatment, prenatal diagnosis nor genetic counselling.
“In these ultra-rare diseases, the application of new massive sequencing technologies is a determining factor regarding the molecular diagnosis for patients and therefore, to progress in the exploration of therapeutic applications”, comment the authors. 
In some cases, affected patients can receive an early diagnose –incomplete and too general- that makes any therapeutic intervention difficult. This is the case of a recent research study in which the Group on Human Molecular Genetics participated, and found two mutations in the PIGT gen in a patient who had initially been diagnosed Opitz C syndrome.
This study could profile a precise molecular diagnose of the causes of the real pathology –with a few cases gathered in the scientific bibliography- affecting the patient, considered as Opitz C at the beginning.
The international scientific collaboration has been determining in the genetic diagnosis of other cases with severe affectations in the neuro-development that had been considered to be Opitz C syndrome. In particular, the UB team has participated in the identification of new genetic mutations associated with DPH1 syndrome –a minority disease with a low prevalence among population- in patients of two different families from Malta and Yemen.
University of Barcelona https://tinyurl.com/yxdrze2f