The Quo-Lab HbA1c point-of-care analyser has successfully achieved International Federation of Clinical Chemistry and Laboratory Medicine (IFCC) certification. The IFCC maintains the JCTLM (Joint Committee for Traceability in Laboratory Medicine) endorsed reference measurement procedure for HbA1c, accepted worldwide as the analytical control for traceability of HbA1c measurement. To participate in the programme manufacturers are required to register and report the results of 24 samples (two per month) from across the measurement range. The samples are supplied by an IFCC Reference Laboratory. Together with the existing NGSP certification achieved from 2012, the IFCC award demonstrates that Quo-Lab meets all of the demanding standards set by independent certifying bodies.  

Doctors commonly use magnetic resonance imaging (MRI) to diagnose tumours, damage from stroke, and many other medical conditions. Neuroscientists also rely on it as a research tool for identifying parts of the brain that carry out different cognitive functions.

Now, a team of biological engineers at MIT is trying to adapt MRI to a much smaller scale, allowing researchers to visualise gene activity inside the brains of living animals. Tracking these genes with MRI would enable scientists to learn more about how the genes control processes such as forming memories and learning new skills, says Alan Jasanoff, an MIT associate professor of biological engineering and leader of the research team.

‘The dream of molecular imaging is to provide information about the biology of intact organisms, at the molecule level,’ says Jasanoff, who is also an associate member of MIT’s McGovern Institute for Brain Research. ‘The goal is to not have to chop up the brain, but instead to actually see things that are happening inside.’

To help reach that goal, Jasanoff and colleagues have developed a new way to image a ‘reporter gene’ — an artificial gene that turns on or off to signal events in the body, much like an indicator light on a car’s dashboard. In the new study, the reporter gene encodes an enzyme that interacts with a magnetic contrast agent injected into the brain, making the agent visible with MRI. This approach allows researchers to determine when and where that reporter gene is turned on.
MRI uses magnetic fields and radio waves that interact with protons in the body to produce detailed images of the body’s interior. In brain studies, neuroscientists commonly use functional MRI to measure blood flow, which reveals which parts of the brain are active during a particular task. When scanning other organs, doctors sometimes use magnetic ‘contrast agents’ to boost the visibility of certain tissues.

The new MIT approach includes a contrast agent called a manganese porphyrin and the new reporter gene, which codes for a genetically engineered enzyme that alters the electric charge on the contrast agent. Jasanoff and colleagues designed the contrast agent so that it is soluble in water and readily eliminated from the body, making it difficult to detect by MRI. However, when the engineered enzyme, known as SEAP, slices phosphate molecules from the manganese porphyrin, the contrast agent becomes insoluble and starts to accumulate in brain tissues, allowing it to be seen.

The natural version of SEAP is found in the placenta, but not in other tissues. By injecting a virus carrying the SEAP gene into the brain cells of mice, the researchers were able to incorporate the gene into the cells’ own genome. Brain cells then started producing the SEAP protein, which is secreted from the cells and can be anchored to their outer surfaces. That’s important, Jasanoff says, because it means that the contrast agent doesn’t have to penetrate the cells to interact with the enzyme.

Researchers can then find out where SEAP is active by injecting the MRI contrast agent, which spreads throughout the brain but accumulates only near cells producing the SEAP protein.
In this study, which was designed to test this general approach, the detection system revealed only whether the SEAP gene had been successfully incorporated into brain cells. However, in future studies, the researchers intend to engineer the SEAP gene so it is only active when a particular gene of interest is turned on.

Jasanoff first plans to link the SEAP gene with so-called ‘early immediate genes,’ which are necessary for brain plasticity — the weakening and strengthening of connections between neurons, which is essential to learning and memory.

‘As people who are interested in brain function, the top questions we want to address are about how brain function changes patterns of gene expression in the brain,’ Jasanoff says. ‘We also imagine a future where we might turn the reporter enzyme on and off when it binds to neurotransmitters, so we can detect changes in neurotransmitter levels as well.’ MIT

The apolipoprotein E gene ε4 allele is considered a negative factor for neural regeneration in late-onset Alzheimer’s disease cases. Apolipoprotein E genotyping is crucial to apolipoprotein E polymorphism analysis. Peripheral venous blood is the conventional tissue source for apolipoprotein E genotyping polymorphism analysis. Blood yields high-quality genomic DNA and can meet various research purposes. However, because of invasiveness, taking blood samples decreases compliance among the elderly, especially neuropsychiatric patients. Moreover, blood specimens often need cold storage, thereby increasing the cost. A research team from Department of Neurology, Peking University Shenzhen Hospital in China pointed out a non-invasive and fast method to genotype large samples to help to elucidate the role of apolipoprotein E gene ε4 allele in neural regeneration in the cases with late-onset Alzheimer’s disease. Genomic DNA from mouth swab specimens was extracted using magnetic nanoparticles, and genotyping was performed by real-time PCR using TaqMan-BHQ probes. Genotyping accuracy was validated by DNA sequencing. The method developed for apolipoprotein E genotyping is accurate and reliable, and also suitable for genotyping large samples, which may help determine the role of the apolipoprotein E ε4 allele in neural regeneration in late-onset Alzheimer’s disease cases.

UT Southwestern Medical Center researchers are developing a new predictive tool that could help patients with breast cancer and certain lung cancers decide whether follow-up treatments are likely to help.
Dr. Jerry Shay, Vice Chairman and Professor of Cell Biology at UT Southwestern, led a three-year study on the effects of irradiation in a lung cancer-susceptible mouse model. When his team looked at gene expression changes in the mice, then applied them to humans with early stage cancer, the results revealed a breakdown of which patients have a high or low chance of survival.

The findings offer insight into helping patients assess treatment risk. Radiation therapy and chemotherapy that can destroy tumours also can damage surrounding healthy tissue. So with an appropriate test, patients could avoid getting additional radiation or chemotherapy treatment they may not need, Dr. Shay said.

‘This finding could be relevant to the many thousands of individuals affected by these cancers and could prevent unnecessary therapy,’ said Dr. Shay, Associate Director for Education and Training for the Harold C. Simmons Comprehensive Cancer Center at UT Southwestern. ‘We’re trying to find better prognostic indicators of outcomes so that only patients who will benefit from additional therapy receive it.’

Dr. Shay’s study closely monitored lung cancer development in mice after irradiation. His group found some types of irradiation resulted in an increase in invasive, more malignant tumours. He examined the gene expression changes in mice well before some of them developed advanced cancers. The genes in the mouse that correlated with poor outcomes were then matched with human genes. When Dr. Shay’s team compared the predictive signatures from the mice with more than 700 human cancer patient signatures, the overall survivability of the patients correlated with his predictive signature in the mice. Thus, the classifier that predicted invasive cancer in mice also predicted poor outcomes in humans.

His study looked at adenocarcinoma, a type of lung cancer in the air sacks that afflicts both smokers and non-smokers. The findings also predicted overall survival in patients with early-stage breast cancer and thus offer the same helpful information to breast cancer patients; however the genes were not predictive of another type of lung cancer, called squamous cell carcinoma. Other types of cancers have yet to be tested.

UCSF scientists say new finding could lead to more accurate prognosis
The stiffening of breast tissue in breast-cancer development points to a new way to distinguish a type of breast cancer with a poor prognosis from a related, but often less deadly type, UC San Francisco researchers have found in a new study.
The findings may lead eventually to new treatment focused not only on molecular targets within cancerous cells, but also on mechanical properties of surrounding tissue, the researchers said.
In a mouse model of breast cancer, scientists led by Valerie Weaver, PhD, professor of surgery and anatomy and director of the Center for Bioengineering and Tissue Regeneration at UCSF, identified a biochemical chain of events leading to tumour progression. Significantly, this chain of events was triggered by stiffening of scaffolding tissue in the microscopic environment surrounding pre-cancerous cells. The stiffening led to the production of a molecule that can be measured in human breast cancer tissue, and which the researchers found was associated with worse clinical outcomes.
‘This discovery of the molecular chain of events between tissue stiffening and spreading cancer may lead to new and more effective treatment strategies that target structural changes in breast cancers and other tumours,’ Weaver said.
In the mouse experiments, Janna Mouw, PhD, a UCSF associate specialist who works in Weaver’s lab, found that tissue stiffening in microscopic scaffolding known as the extracellular matrix, or ECM, increases signalling by ECM-associated molecules, called integrins. The integrins in turn trigger a signalling cascade within cells that leads to the production of a tumour-promoting molecule called miR-18a.
Unlike most cellular signalling molecules thus far studied by scientists, miR-18a is not a protein or a hormone, but rather a microRNA, another type of molecule recognised in recent years to play an important role in the lives of cells. The miR-18a dials down the levels of a protective, tumour-suppressing protein called PTEN, which often is disabled in cancerous cells, leading to abnormal biochemical signalling that can promote cancer growth. University of California – San Francisco