The longest FlexLab automation system ever produced by Inpeco has been designed for a mega volume reference laboratory customer, Hermes Pardini group based in Minas Gerais, Brazil. Siemens Healthineers (Inpeco’s strategic automation partner who sold the solution) is implementing the FlexLab system for Hermes Pardini’s “Enterprise” project, which will result in the largest laboratory automation platform in the world, linking more than 100 analyzers and 7 clinical specialties.
The Hermes Pardini Group is highly innovative in diagnostics medicine, and will handle 110 million sample tubes every year to address diagnostic testing needs of patients and healthcare providers from all across Brazil. The Enterprise project is expected to be operating at its full capacity in 2019, and will automate the distribution of sample tubes to nearly 100 different analyzers with a total length of 330 meters, which will include more than 70 pre- and postanalytical modules to eliminate the need for error-prone and time-consuming manual interventions within the clinical laboratory. It is to be installed in the Vespasiano site (Belo Horizonte area) in the current laboratory testing area (3,500 square meters of floor space).
“Unlike conventional laboratory set-ups, where sample tubes must be moved manually between different analyzers, our enterprise lab will employ a ‘one-touch, one workflow’ concept to eliminate the need for manual interventions, ensure sample traceability, and reduce the turnaround time to results,” said Guilherme Collares, Chief Operations Officer of the Hermes Pardini Group.
Inpeco’s High Throughput FlexLab solution will contribute to make this concept a reality, and enable providers to receive results faster, thereby enabling better patient care. The project also includes refrigerated storage units, with capacity to hold more than 1.3 million samples, and a newly developed advanced vision system, which is able to detect sample deterioration such as hemolysis, icterus or lipemia. “We’ve been in touch with Hermes Pardini since they began 2 evaluating options to replace the automation system they were using – said Andrea Pedrazzini, President of Inpeco – and we are extremely proud and pleased that such a prestigious institution has decided to adopt the largest FlexLab system ever built to fully automate their samples process, from loading to storing and disposing.”

http://www.inpeco.com/en/

A multidisciplinary team at NUS BIGHEART has developed enVision – a portable, easy-to-use and inexpensive device for quick and accurate screening of diseases.
enVision takes between 30 minutes to one hour to detect the presence of diseases, which is two to four times faster than existing infection diagnostics methods. In addition, each test kit costs under S$1 – 100 times lower than the current cost of conducting similar tests.
“The enVision platform is extremely sensitive, accurate, fast, and low-cost. It works at room temperature and does not require heaters or special pumps, making it very portable. With this invention, tests can be done at the point-of-care, for instance in community clinics or hospital wards, so that disease monitoring or treatment can be administered in a timely manner to achieve better health outcomes,” said team leader Assistant Professor Shao Huilin from the Biomedical Institute for Global Health Research and Technology (BIGHEART) and Department of Biomedical Engineering at NUS. Asst Prof Shao is also an investigator with the Institute of Molecular and Cell Biology (IMCB) under the Agency for Science, Technology and Research (A*STAR).
The research team used the human papillomavirus (HPV), the key cause of cervical cancer, as a clinical model to validate the performance of enVision. In comparison to clinical gold standard, this novel technology has demonstrated superior sensitivity and specificity.
“enVision is not only able to accurately detect different subtypes of the same disease, it is also able to spot differences within a specific subtype of a given disease to identify previously undetectable infections," Asst Prof Shao added.
In addition, test results are easily visible – the assay turns from colourless to brown if a disease is present – and could also be further analysed using a smartphone for quantitative assessment of the amount of pathogen present. This makes enVision an ideal solution for personal healthcare and telemedicine.
“Conventional technologies – such as tests that rely on polymerase chain reaction to amplify and detect specific DNA molecules – require bulky and expensive equipment, as well as trained personnel to operate these machines. With enVision, we are essentially bringing the clinical laboratory to the patient. Minimal training is needed to administer the ,test and interpret the results, so more patients can have access to effective, lab-quality diagnostics that will substantially improve the quality of care and treatment,” said Dr Nicholas Ho, a researcher from NUS BIGHEART and A*STAR’s IMCB, and co-first author of the study.

National University of Singapore
news.nus.edu.sg/press-releases/envision-device-for-disease-screening

A new way to assess the impact of normal ageing on bones, joints and muscles has been proposed that could provide a benchmark for how well older people are able to keep moving.
The composition of the body changes as we get older, as muscle strength and bone density decline. But the challenge to date has been distinguishing between the normal effects of ageing and the first signs of disease.
As a result there has been limited consensus on appropriate biomarkers of normal ageing. This has led to an unreliable picture of musculoskeletal health in older people as bone, joints and muscle have been looked at in isolation, not as a complete system.
To address this, experts at the Medical Research Council-Arthritis UK Centre for Integrated Research into Musculoskeletal Ageing (CIMA) – a collaboration between Newcastle, Liverpool and Sheffield universities – have now proposed a set of measurements that can be used as a toolkit to assess bone, joint and muscle health.
The CIMA team say that the new toolkit will provide a consistent and holistic way to measure the gradual loss of function that everyone experiences as we get older.
In particular, they recommend the use of two biomarkers to assess bone condition – PINP and CTX, both well-established indicators of bone turnover. High levels of these biomarkers are often associated with greater fracture risk and faster rates of bone loss, particularly in older women.
The toolkit also proposes reliable indicators of cartilage damage, muscle mass, body composition and assessment of functional capability.
Professor John Mathers, from Newcastle University’s Institute for Ageing, said: “We know that when older people have limited mobility or stop being active altogether it can have a significant, negative impact on their cardio-vascular health, their neurological health and their quality of life overall, increasing the risk of disease.
“This new toolkit will help us better understand how well the whole musculoskeletal system functions as we age so that we can help people stay physically active and healthy for longer.”
The toolkit is a first step towards a comprehensive framework that could be used by researchers and clinicians – both with individuals as needed and, potentially, as part of a public health screening programme for older people.
Over time, this could identify parameters for normal musculoskeletal ageing according to gender and age. To aid this, the CIMA team say that the toolkit could be used earlier – when people are in their 50s and early 60s, before age-related disease or disability can occur – in order to get a better picture of how the musculoskeletal system ages.

Newcastle University
www.ncl.ac.uk/press/articles/latest/2018/09/toolkittoassessmusculoskeletalhealth/

G-protein-coupled receptors (GPCRs) are everywhere in our bodies. They are embedded in our cell membranes, where they act as signal transducers, allowing cells to respond to their external environments. GPCRs play a crucial role in most biological functions, including heart rate, blood pressure, vision, smell, taste and allergic responses. GPCR malfunction can lead to a number of diseases, and many therapeutic drugs work because they influence these proteins. Yet the basics of GPCR structure and functions are not well understood.
Researchers at University of California San Diego School of Medicine have unravelled new insights into the way cells leverage GPCRs and their cellular waste disposal systems to control inflammation. The findings suggest some existing cancer drugs that inhibit these cellular activities might be repurposed to treat vascular inflammation, which occurs when artery-blocking plaques form in atherosclerosis.
“We were surprised to discover that GPCRs and inflammation are influenced by ubiquitination — a process that was previously thought to only mark proteins for destruction,” said senior author JoAnn Trejo, PhD, professor in the Department of Pharmacology and associate dean of faculty affairs at UC San Diego School of Medicine. “Instead, we’ve unveiled new insights into both GPCR function and ubiquitination.”
When a molecule, such as a nutrient, binds to a GPCR on the outside of the cell, the GPCR changes shape. On the other side of the membrane, inside the cell, a G-protein docks on the newly re-positioned GPCR. Depending on the type of signal and cell, that G-protein then kicks off a cascade of molecular events.
Trejo and team focused on endothelial cells, the type that line blood vessels. In that context, they studied how GPCR functions are influenced by ubiquitination — a process in which enzymes tag proteins with small molecules called ubiquitin. Usually, an ubiquitin tag tells the cell’s garbage disposal machinery that a protein is ready for degradation. But in this case, ubiquitination has a different function.
The researchers found that the GPCR turns on an E3 ligase, the very enzyme that does the ubiquitinating, which triggers a cascade of molecular events that ultimately turn on another protein, p38, which in turn promotes inflammation.
According to Trejo, a handful of drugs that inhibit E3 ubiquitin ligases have been approved by the Food and Drug Administration (FDA) for the treatment of some cancers, including multiple myeloma and mantle cell lymphoma, and several others have entered clinical trials.
“But given the large number of E3 ligases in the human body — there are between 600 and 700 — and their diverse functions, the number of E3-targeting drugs approved or in clinical trials is remarkably small,” Trejo said. “And this is the first time E3 ligases have been shown to also play a role in vascular inflammation, which broadens the potential applications for drugs that inhibit these enzymes. The field is really in its infancy.”

University of California – San Diego
medschool.ucsd.edu/som/medicine/Pages/default.aspx

Glaucoma, a disease that afflicts nearly 70 million people worldwide, is something of a mystery despite its prevalence. Little is known about the origins of the disease, which damages the retina and optic nerve and can lead to blindness.
A new study from MIT and Massachusetts Eye and Ear has found that glaucoma may in fact be an autoimmune disorder. In a study of mice, the researchers showed that the body’s own T cells are responsible for the progressive retinal degeneration seen in glaucoma. Furthermore, these T cells appear to be primed to attack retinal neurons as the result of previous interactions with bacteria that normally live in our body.
The discovery suggests that it could be possible to develop new treatments for glaucoma by blocking this autoimmune activity, the researchers say.
“This opens a new approach to prevent and treat glaucoma,” says Jianzhu Chen, an MIT professor of biology, a member of MIT’s Koch Institute for Integrative Cancer Research, and one of the senior authors of the study.
Dong Feng Chen, an associate professor of ophthalmology at Harvard Medical School and the Schepens Eye Research Institute of Massachusetts Eye and Ear, is also a senior author of the study. The paper’s lead authors are Massachusetts Eye and Ear researchers Huihui Chen, Kin-Sang Cho, and T.H. Khanh Vu.
One of the biggest risk factors for glaucoma is elevated pressure in the eye, which often occurs as people age and the ducts that allow fluid to drain from the eye become blocked. The disease often goes undetected at first; patients may not realize they have the disease until half of their retinal ganglion cells have been lost.
Most treatments focus on lowering pressure in the eye (also known as intraocular pressure). However, in many patients, the disease worsens even after intraocular pressure returns to normal. In studies in mice, Dong Feng Chen found the same effect.
“That led us to the thought that this pressure change must be triggering something progressive, and the first thing that came to mind is that it has to be an immune response,” she says.
To test that hypothesis, the researchers looked for immune cells in the retinas of these mice and found that indeed, T cells were there. This is unusual because T cells are normally blocked from entering the retina, by a tight layer of cells called the blood-retina barrier, to suppress inflammation of the eye. The researchers found that when intraocular pressure goes up, T cells are somehow able to get through this barrier and into the retina.
The Mass Eye and Ear team then enlisted Jianzhu Chen, an immunologist, to further investigate what role these T cells might be playing in glaucoma. The researchers generated high intraocular pressure in mice that lack T cells and found that while this pressure induced only a small amount of damage to the retina, the disease did not progress any further after eye pressure returned to normal.
Further studies revealed that the glaucoma-linked T cells target proteins called heat shock proteins, which help cells respond to stress or injury. Normally, T cells should not target proteins produced by the host, but the researchers suspected that these T cells had been previously exposed to bacterial heat shock proteins. Because heat shock proteins from different species are very similar, the resulting T cells can cross-react with mouse and human heat shock proteins.
To test this hypothesis, the team brought in James Fox, a professor in MIT’s Department of Biological Engineering and Division of Comparative Medicine, whose team maintains mice with no bacteria. The researchers found that when they tried to induce glaucoma in these germ-free mice, the mice did not develop the disease.
The researchers then turned to human patients with glaucoma and found that these patients had five times the normal level of T cells specific to heat shock proteins, suggesting that the same phenomenon may also contribute to the disease in humans. The researchers’ studies thus far suggest that the effect is not specific to a particular strain of bacteria; rather, exposure to a combination of bacteria can generate T cells that target heat shock proteins.
One question the researchers plan to study further is whether other components of the immune system may be involved in the autoimmune process that gives rise to glaucoma. They are also investigating the possibility that this phenomenon may underlie other neurodegenerative disorders, and looking for ways to treat such disorders by blocking the autoimmune response.
“What we learn from the eye can be applied to the brain diseases, and may eventually help develop new methods of treatment and diagnosis,” Dong Feng Chen says.

MITnews.mit.edu/2018/glaucoma-autoimmune-disease-0810