A team of researchers from UCLA’s Henry Samueli School of Engineering and Applied Science has developed a Google Glass application and a server platform that allow users of the wearable, glasses-like computer to perform instant, wireless diagnostic testing for a variety of diseases and health conditions.
With the new UCLA technology, Google Glass wearers can use the device’s hands-free camera to capture pictures of rapid diagnostic tests (RTDs), small strips on which blood or fluid samples are placed and which change colour to indicate the presence of HIV, malaria, prostate cancer or other conditions. Without relying on any additional devices, users can upload these images to a UCLA-designed server platform and receive accurate analyses — far more detailed than with the human eye — in as little as eight seconds.
The new technology could enhance the tracking of dangerous diseases and improve public health monitoring and rapid responses in disaster-relief areas or quarantine zones where conventional medical tools are not available or feasible, the researchers said.
‘This breakthrough technology takes advantage of gains in both immunochromatographic rapid diagnostic tests and wearable computers,’ said principal investigator Aydogan Ozcan, the Chancellor’s Professor of Electrical Engineering and Bioengineering at UCLA and associate director of UCLA’s California NanoSystems Institute. ‘This smart app allows for real-time tracking of health conditions and could be quite valuable in epidemiology, mobile health and telemedicine.’
In addition to designing the custom RDT–reader app for Google Glass, Ozcan’s team implemented server processes for fast and high-throughput evaluation of test results coming from multiple devices simultaneously. Finally, the researchers developed a web portal where users can view test results, maps charting the geographical spread of various diseases and conditions, and the cumulative data from all the tests they have submitted over time.
To submit images for test results, Google Glass users only need to take photos of RTD strips or other commonly available in-home tests, then upload the images wirelessly through the device to the UCLA-designed web portal. The technology permits quantified reading of the results to a few-parts-per-billion level of sensitivity — far greater than that of the naked eye — thus eliminating the potential for human error in interpreting results, which is a particular concern if the user is a health care worker who routinely deals with many different types of tests.
To gauge the accuracy and efficiency of the technology, the UCLA team used an in-home HIV test designed by OraSure Technologies and a prostate-specific antigen test made by JAJ International. The researchers took images of tests under normal, indoor, fluorescent-lit room conditions. They submitted more than 400 images of the two tests, and the RDT reader and server platform were able to read the images 99.6 percent of the time. In every case in which the technology successfully read the images, it returned accurate and quantified test results, according to the team.
The researchers also tested more than 300 blurry images or images of the testing device taken under various natural-usage scenarios and achieved a read rate of 96.6 percent. The UCLA Henry Samueli School of Engineering and Applied Science

Biomarkers for bone formation and resorption predict outcomes for men with castration-resistant prostate cancer, a team of researchers from UC Davis and their collaborators have found. Their study also found that the markers identified a small group of patients who responded to the investigational drug atrasentan. The markers’ predictive ability could help clinicians match treatments with individual patients, track their effectiveness and affect clinical trial design.
Castration-resistant prostate cancer does not respond to hormone treatments and often metastasises to bone. This led researchers to wonder if increased bone turnover markers might predict the course of the disease.
‘We found that patients with high levels of these markers in the blood had a much shorter lifespan compared to patients with low levels,’ said lead author Primo Lara, associate director for translational research at the UC Davis Comprehensive Cancer Center. ‘By measuring bone turnover in prostate cancer patients, we can determine how well they do.’
Healthy bone maintains a balance between formation and resorption, generating new bone while recycling old. Prostate cancer throws off this balance. Researchers hoped this mechanism would help them track the cancer. To investigate this potential link, the team tested blood serum in 778 patients for both resorption (N-telopeptide, pyridinoline) and formation markers (C-terminal collagen propeptide, bone alkaline phosphatase) and found elevated levels of each of the markers predicted poor prognosis.
Perhaps most interesting, elevated marker levels also predicted whether patients would respond to a specific drug. About 6 percent of patients with the highest marker levels responded to atrasentan, and investigational drug abandoned because it failed in clinical trials. Lara and colleagues believe this may be related to study design.
‘Atrasentan kept coming up short in randomised trials because the drug only works for a small group,’ Lara said. ‘Because certain drugs only succeed in a fraction of patients, drug makers need to factor in these bone metabolism markers in their trial design. They need to target the patients most likely to benefit.’
In addition to determining which patients might respond best to a specific treatment, these markers could be used to track their response during treatment. Marker status could also stratify patients equally within different study arms. Balancing these studies could potentially make them more accurate and identify the niche value of drugs like atrasentan whose effectiveness is not evident in large populations.
‘I think the days of doing empirical studies on all comers should end,’ Lara said. ‘You need to have an appropriate database of patients and perform a rigorous analysis to find the subset who will benefit from an investigational drug.’ UC Davis Comprehensive Cancer Center

The genetic disease ARVC leads to sudden cardiac death and is more common than it has been hitherto assumed. This is reported by an international team of researchers headed by Prof Dr Hendrik Milting from the Heart and Diabetes Center NRW. The molecular biologist working at the Ruhr-Universität’s clinic in Bad Oeynhausen revealed that all families who are known to be affected by the disease share the same genetic origin. There must be other families in Europe who also carry the genetic mutation but who are not yet known.
Scientists have thrown light on the genetic mutation that causes a particularly severe genetic disease (ARVC5) on the Canadian island Newfoundland in 2008. At first, they assumed that it was a genetic anomaly limited to this Canadian province. In 2010, Milting’s team – and at the same time a team of researchers from Copenhagen – proved that the ‘Newfoundland mutation’ did also occur in Europe. Today, the scientists know about affected families in Germany, Denmark, the USA and Canada. They all share common ancestors, as was demonstrated through genetic analysis. The scientists studied the environment of the TMEM43 gene in which the ARVC5-specific mutation is located. The genetic sequence in the neighbourhood of TMEM43 is typically highly variable; in all affected families, however, it was identical over long stretches. These findings verify a shared genetic origin.
The affected Danish and German families are not aware of the degree to which they are related; according to calculations, the mutation originated some 1300 to 1500 years ago. Thus, the ARVC5 mutation in the European families is not a novel mutation but an old European heritage. Therefore, there must be other families with that genetic mutation, who constitute the bridge between the patients in Europe and in North America. Two novel families with that mutation have recently been identified in Madrid. ‘In cases of sudden cardiac death in the family, people should sit up and take notice,’ says Prof Milting. ‘The families that are known to us have lost several male family members within a short space of time, even though they were under medical observation. Women frequently suffer from cardiac arrhythmias.’ Suspected cases must be looked into, warns the molecular biologist, because people carrying that mutation will definitely get the disease. Sudden cardiac death may be prevented if a defibrillator is implanted in good time.
Genetic analyses are increasingly gaining in importance in healthcare settings as prevention and diagnostic tools. ‘Nevertheless, healthcare professionals are called upon to exercise great discretion when deciding which analyses must necessarily be conducted for which patients,’ stresses Hendrik Milting. ‘After all, the objective is not to stigmatise the affected families, but to prevent severe heart diseases or even sudden cardiac death.’ A team of molecular biologists, cardiologists and human geneticists is in charge of this task at the Heart and Diabetes Center NRW.
The acronym ARVC stands for arrhythmogenic right ventricular cardiomyopathy. A considerable number of patients, most of them men, suffer sudden cardiac death without having ever shown any signs of a cardiovascular disease. The average life expectancy of men who have the ARVC5 genetic mutation is about 41 years. Ruhr University Bochum

Cornell researchers report they have discovered direct genetic evidence that a family of genes, called MicroRNA-34 (miR-34), are bona fide tumour suppressors.
Previous research at Cornell and elsewhere has shown that another gene, called p53, acts to positively regulate miR-34. Mutations of p53 have been implicated in half of all cancers. Interestingly, miR-34 is also frequently silenced by mechanisms other than p53 in many cancers, including those with p53 mutations.
The researchers showed in mice how interplay between genes p53 and miR-34 jointly inhibits another cancer-causing gene called MET. In absence of p53 and miR-34, MET overexpresses a receptor protein and promotes unregulated cell growth and metastasis.
This is the first time this mechanism has been proven in a mouse model, said Alexander Nikitin, a professor of pathology in Cornell’s Department of Biomedical Sciences and the paper’s senior author. Chieh-Yang Cheng, a graduate student in Nikitin’s lab, is the paper’s first author.
In a 2011 Proceedings of the National Academy of Sciences paper, Nikitin and colleagues showed that p53 and miR-34 jointly regulate MET in cell culture but it remained unknown if the same mechanism works in a mouse model of cancer (a special strain of mice used to study human disease).
The findings suggest that drug therapies that target and suppress MET could be especially successful in cancers where both p53 and miR-34 are deficient.
The researchers used mice bred to develop prostate cancer, then inactivated the p53 gene by itself, or miR-34 by itself, or both together, but only in epithelium tissue of the prostate, as global silencing of these genes may have produced misleading results.
When miR-34 genes alone were silenced in the mice, the mice developed cancer free. When p53 was silenced by itself, there were signs of precancerous lesions early in development, but no cancer by 15 months of age. When miR-34 and p53 genes were both silenced together, the researchers observed full prostate cancer in the mice.
The findings revealed that ‘miR-34 can be a tumour-suppressor gene, but it has to work together with p53,’ Nikitin said.
In mice that had both miR-34 and p53 silenced concurrently, cancerous lesions formed in a proximal part of the prostrate ducts, in a compartment known to contain prostate stem cells. The early lesions that developed when p53 was silenced alone occurred in a distal part of the ducts, away from the compartment where the stem cell pool is located. This suggested there was another mechanism involved when p53 and miR-34 were jointly silenced.
Also, the number of stem cells in mice with both p53 and miR-34 silenced increased substantially compared with control mice or mice with only miR-34 or p53 independently silenced.
‘These results indicated that together [miR-34 and p53] regulate the prostate stem cell compartments,’ said Nikitin.
This is significant, as cancer frequently develops when stem cells become unregulated and grow uncontrollably, he said.
Researchers further found that p53 and miR-34 affect stem cell growth by regulating MET expression. In absence of p53 and miR-34, MET is overexpressed, which leads to uncontrolled growth of prostate stem cells and high levels of cancer in these mice.
Future work will further examine the role of p53/miR-34/MET genes in stem cell growth and cancer. The findings have implications for many types of cancer. Cornell University

Cardiovascular calcification (deposits of minerals in heart valves and blood vessels) is a primary contributor to heart disease, the leading cause of death among both men and women in the United States according the Centers for Disease Control and Prevention (CDC).
‘Unfortunately, there currently is no medical treatment for cardiovascular calcification, which can lead to acute cardiovascular events, such as myocardial infarction and stroke, as well as heart failure,’ says Elena Aikawa, MD, PhD, Director of the Vascular Biology Program at the Center for Interdisciplinary Cardiovascular Sciences at Brigham and Women’s Hospital (BWH) and Associate Professor of Medicine at Harvard Medical School. ‘We have not found a way to reverse or slow this disease process, which is associated with ageing and common chronic conditions like atherosclerosis, diabetes, and kidney disease.’
Led by Dr. Aikawa, a team of researchers at BWH and Kowa Company, Ltd., a Japanese pharmaceutical company, has discovered certain proteins in osteoclasts, a precursor to bone, that may be used in helping to destroy cardiovascular calcification by dissolving mineral deposits. The research suggests a potential therapeutic avenue for patients with cardiovascular calcification.
Mature osteoclasts are not typically found in the vasculature. Using unbiased global proteomics (study of proteins), the researchers were able to examine osteoclast-like cells in the vasculature to determine which proteins induced osteoclast formation. They identified more than 100 proteins associated with osteoclast development. Follow-up study validated six candidate proteins, which serve as targets for possible medications that may help promote osteoclast development in the vasculature.
‘To advance this research, we need to further understand why osteoclasts are not prevalent in the vaculature, despite active calcification of the heart valves and blood vessels, and determine the difference between calcification in vasculature compared with calcification in bone,’ said Dr. Aikawa. ‘Then, we may examine ways to form osteoclasts in the vasculature.’ Brigham and Women’s Hospital