As well as announcing the launch of a new global diagnostics business unit at Medica last month, Avantor Performance Materials also announced the creation of a new diagnostics product brand: BeneSpheradiagnostics solutions, which will include a broad and expanding range of reliable, affordable diagnostic technologies and easy-to-use products, focused on three segments: in vitro reagents and instruments for clinical chemistry, immunology, haematology, microbiology, histology and cytology and genetic testing; instruments for in vivo diagnostics, currently sold under the Diagnova name in India; and consumables and instruments for life sciences research in academia, government and pharmaceutical labs, also currently sold under the Diagnova name in India.
At the moment Avantor’s performance diagnostics solutions include J.T.Baker clinical reagents, which have provided world-class solutions for haematology and histology applications for over 30 years, and BeneSphera diagnostics solutions built on Diagnova, the company’s Indian-based diagnostics business with a 25-year legacy offering products, engineering and application support for immunology, clinical chemistry, haematology, microbiology, endoscopy and life science needs.
Avantor’s plans are to grow the new global diagnostics business through organic development and the strategic acquisition of R&D-backed manufacturing and distribution companies in targeted locations to support a strong global brand and supply chain.

The discovery of a gene that causes a form of hereditary spastic paraplegia may provide scientists with an important insight into what causes axons, the stems of our nerve cells, to degenerate in conditions such as multiple sclerosis.An international team of scientists led by Dr Evan Reid at the University of Cambridge and Dr Stephan Zuchner from the University of Miami reports that mutations in the gene known as reticulon 2 on chromosome 19 cause a form of hereditary spastic paraplegia (HSP). HSP is characterised by progressive stiffness and contraction (spasticity) of the legs, caused by selective and specific degeneration of axons.
The team identified three mutations in the reticulon 2 gene as causing a type of HSP – in one case, this mutation included an entire deletion of the gene. In addition, the researchers showed that reticulon 2 interacts with another gene, spastin. Mutations in this gene cause the most common form of hereditary spastic paraplegia.
Reticulon 2 provides the genetic code for a reticulon protein that is a member of a family of proteins recently shown to have a key role in shaping the endoplasmic reticulum. The endoplasmic reticulum is a network of interconnected sheets and tubules that extends throughout the cytoplasm in nearly all cells.
The endoplasmic reticulum has several functions, including protein synthesis, calcium signalling and the regulation of other components of the cell. Recent data suggest the sheets are involved in protein synthesis, whereas the tubules are specialised to carry out the other functions.
This new study provides the most direct evidence to date that defects in how the endoplasmic reticulum is shaped and formed could underlie axon degeneration. When axons degenerate, signals are unable to pass through the nerve cells, leading to a breakdown of communication within the central nervous system. This is common in degenerative diseases of the nervous system, such as multiple sclerosis.
‘Our work highlights important new disease mechanisms, which may provide a platform for us to study how axons are damaged in devastating illnesses such as HSP, and perhaps even in multiple sclerosis, which in some cases is very similar to HSP,’ explains Dr Reid, a Wellcome Trust Senior Research Fellow in Clinical Science. ‘But we must not forget how this work may immediately directly benefit families affected by HSP, for whom the discovery now opens up the possibility of genetic counselling and testing.’ Wellcome Trust

Roche Accu-Chek^® Inform II test strips chosen by CEGA Air Ambulance requirements for accuracy and ease-of-use

CEGA Air Ambulance has recently upgraded its blood glucose monitoring system to use the advanced Accu-Chek Inform II test strips from Roche.  Ensuring accurate and reliable results across a wide range of glucose levels, these easy to use blood glucose test strips provide the performance criteria necessary for monitoring critically ill patients prior to, during and after emergency flight transfers.

“We require a reliable, easy to use, professional tool for blood glucose measurement,” comments CEGA Senior Flight Nurse, Stuart Cox.  “After reviewing all the kits that are available on the market, we felt that the Roche Accu-Chek Inform II test strips best met our requirements for high quality patient care in the air ambulance environment.  The user interface is very simple and straightforward to use anywhere and by any of our trained staff.  In addition, the strips have a very good range compared to other systems, giving accurate results at both high and low glucose levels, which is essential for patient safety.”

Stress-induced insulin resistance and hyperglycaemia is common in critically ill patients [1,2,3] and so close monitoring of blood glucose levels is an important part of their care.  Studies have shown that maintenance of appropriate glycaemic control in such patients improves morbidity and mortality [1,4,5].

“Providing international medical assistance, including the transportation of critical care patients around Europe, we use the Accu-Chek Inform II glucose strips to assess patients prior to the flight to make sure they are stable; during the transfer to monitor them and guide any necessary treatment; and then after the flight to assess their status before handing them over to the next medical team.  The accuracy of the Accu-Chek Inform II strips ensures that patients get the right care at the right time, and we can have confidence in the results.”

The Accu-Chek Inform II test strips have undergone extensive evaluation, including studies at over 30 external sites as well as thorough internal testing [6]. The results of these evaluations demonstrate that the Accu‑Chek Inform II strips provide accurate and reliable blood glucose measurements under a variety conditions, including wide haematocrit and environmental ranges and in presence of maltose. Furthermore, the strips require a minimal sample volume of just 0.6µl and deliver accurate results from alternative sampling sites, such as the palm and forearm.

“The Accu-Chek Inform II strips mirror our needs for air ambulance work,” concludes Stuart.  “They are well researched, with evidence-based performance.  We also value the after sales and technical support we have received from Roche, which has been invaluable in the training of our staff.” www.roche.co.ukwww.cega-air-ambulance.com.

<sup>1.  Van den Berghe, G., Wouters, P., Weekers, F. et al (2001) N Engl. J. Med. 345: 1359-67
2. Van den Berghe, G. (2004) J. Clin. Invest. 114: 1187-1195
3. Mizock, B.A. Best Pract. Res. Clin. Endocrinol. Metab. 2001,15(4): 533 – 551.
4. Krinsley, J.S. (2004) Mayo Clin. Proc. 79:992-1000 
5.  Insulin in Intensive Care – The Leuven Protocol.  Intensive Care Society website: http://www.ics.ac.uk/icmprof/pubsother.asp?menuid=86. Information available on request, Roche Diagnostics, Burgess Hill, UK.</sup>

Binding Site, the Birmingham-based healthcare manufacturer, develops and produces laboratory-based tests for the diagnosis and monitoring of blood cancers and immunodeficiency diseases. The company recently won the EEF Midlands Outstanding Export Award, sponsored by UK Trade and Investment (UKTI), and will go on to compete in the National Awards final in January. The annual awards are hosted by EEF, the manufacturers’ organisation, and recognise excellence in enterprise, innovation, environmental performance and skills development among UK manufacturers.
Binding Site’s export strategy has been developed and refined for more than ten years to become integral to all aspects of the business. Initially, the export initiative was led by the sales and marketing team, but as overseas expansion gathered pace, the company drew on the support of technical, R&D, HR and finance departments.As a result of this highly successful multi-disciplinary approach, Binding Site currently exports around 90% of its products, with the United States accounting for 47% of total sales. The judging panel, led by Cranfield University, praised Binding Site’s achievements, stating that it was extremely impressed by the challenging target market featured in the story, the United States. Despite tough regulations, Binding Site had broken through and was now experiencing progressive growth.

Tilting the scales in an ongoing debate, University of Wisconsin-Madison researchers have found new evidence that human cytomegalovirus (HCMV) is associated with glioblastoma multiforme (GBM), the brain cancer that killed Sen. Edward Kennedy.
The findings confirm what only a handful of scientists have found, but in a manner that University of Wisconsin School of Medicine and Public Health researchers believe enhances the scientific rigor of earlier studies.
The study hints for the first time that HCMV may work differently than other cancer-related viruses – possibly by affecting only tumour stem cells, self-renewing cells that keep the tumour growing. The new research may place HCMV in an expanding group of viruses associated with cancer.
‘As many as 15 to 20 percent of all human cancers are caused by viruses, and the number is growing,’ says HCMV expert Dr. Robert Kalejta, associate professor of oncology at the UW School of Medicine and Public Health (SMPH). ‘The viruses may not cause cancer on their own, but they play a critical role in the process.’
Among others, human papilloma virus (HPV) causes cervical cancer, Epstein-Barr virus (EBV) causes lymphoma and hepatitis C virus (HCV) causes liver cancer.
HCMV’s role in GBM has been debated, with many scientists and clinicians remaining skeptical. Oncologist Dr. Charles Cobbs of California Pacific Medical Center has been the main proponent of the theory that HCMV contributes to GBM.
Dr. John Kuo, assistant professor of neurological surgery and human oncology and a cancer stem cell scientist at the School of Medicine and Public Health, was one of the skeptical ones, but he says he’s now convinced that HCMV is associated with human GBM specimens.
Still, the association does not prove a causal relationship between HCMV and the development of GBM, he says.
‘This study may open up a new unexplored area of research for this incurable disease,’ says Kuo, who is director of the Comprehensive Brain Tumor Program at UW Hospital and Clinics. He also co-ordinates clinical trials as chair of the brain tumour group at the Carbone Cancer Center.
Two years ago, Kalejta’s team added support to Cobb’s position when it showed that two HCMV proteins shut down a key protein that restricts tumour growth in general.
‘HCMV can also do every one of the things that are generally considered the 10 hallmarks of cancer,’ says Kalejta, a member of the McArdle Laboratory for Cancer Research, Carbone Cancer Center, Stem Cell and Regenerative Medicine Center and Institute for Molecular Virology at UW-Madison.
The problem with studying HCMV is that the virus is present in a harmless way in almost everyone, so scientists can’t ask if HCMV-positive people are more likely to get cancer than people without HCMV.
Kalejta’s postdoctoral fellow Dr. Padhma Ranganatan used a standard laboratory test, rather than the ultra-sensitive test Cobb has used, to see if HCMV was present in 75 GBM samples. The UW-Madison researchers also looked to see if the entire virus genome – all of its DNA – rather than just a portion of it was present in the tissues. Finally, they wanted to learn if all cells within the tumour or just some of them were infected.
The analysis showed that HCMV is statistically more likely to be present in GBM sample tissues than in other brain tumour and epileptic brain tissues. The whole virus genome, not a portion of it, was present in GBM samples. And the data suggested that a minority of GBM cells were infected with HCMV.
‘We hypothesize that HCMV may be infecting only tumour stem cells, unlike other viruses, which infect every single tumour cell,’ says Kalejta. ‘This leads us to predict that HCMV functions by a unique mechanism that no other virus uses.’ University of Wisconsin-Madison