Biomedical Engineering News

Qualcomm Life, a subdivision of the major telecom product company that aspires to be a market leader in the developing wireless health network, recently unveiled their new 2net™ Platform and Hub.  Qualcomm Life was formed last week as a wholly owned subsidiary to operate the formerly known Qualcomm Wireless Health. 2net™ includes a wireless hub hardware that integrates signals from many health monitoring devices around the home, collects and encrypts the data,  then sends it to the cloud for physicians or other permitted parties to view.

Roughly 133 million Americans suffer from chronic diseases and their homes are littered with health monitoring devices such as blood pressure monitors or glucose meters. These devices collect data that would greatly benefit health providers in making more efficient treatment decisions if only they had access to that data.

While it is possible to use apps on smartphones to collect and transmit health data, not all signals from the array of health monitoring devices can communicate with smartphone technology. Qualcomm Life Vice President Rick Valencia purports that the new 2net™ Platform not only meets all medical standards, but is “technology agnostic, and can pair with virtually anything”. Qualcomm life is in the process of establishing partnerships with several device manufacturers and their case studies show positive results for the growing wireless healthcare user market.

“There are plenty of apps that will monitor your heart rate or glucose, but if it’s involved in any clinical decision making, that will need to be sent over secure channels and have backup capabilities,” says Andy Castonguay, principal analyst for handsets and devices at Informa.

2net™ is likely the first product on the market with its level of connectivity, security and ease-of-use. 2net™ Platform will probably include a service fee, but Qualcomm Life supports that the convenience and widely informative technology will be worth the price.

Cancer can be caused by a complex cascade of events, one of which is believed to be chronic inflammation.

Inflammation is the body’s immune response to the presence of foreign particles such as pathogens or irritants, and is designed to remove such particles. Immune cells are called to the site of inflammation to envelop foreign particles or secrete oxidative chemicals like hydrogen peroxide to kill invaders. Unfortunately this process can persist, in the case of prolonged irritation, resulting in a pathology known as chronic inflammation.

Chronic inflammation has been suggested to be one of the main causes of many degenerative diseases and cancers. Things like irritating implants, undetected allergies, and poor diet can all illicit an extended inflammatory response. As the concentration of immune cells and harmful chemical secretions increase, the surrounding tissue begins to suffer, resulting in prompt cellular death. The inflammatory process also enhances healing and cellular propagation, causing cells in the affected area to multiply quickly and compensate for the dying cells. This leads to a highly proliferative state in which a mutation is more likely to occur, increasing the chance of tumor formation.

With this knowledge, it follows that reducing inflammation should reduce risk of cancer, which is exactly what a recent study has demonstrated. A 2011 article published in The Lancet has shown a decreased risk of death from cancer in patients consuming Aspirin daily over a long period of time (five years or longer). Aspirin inhibits certain inflammatory precursor enzymes, and plays a role in reducing chronic inflammation. The areas of decreased cancer risk include lung, brain, pancreas, and esophagus. Aspirin seems to have the greatest effect on cancers of the digestive track, showing decreased risk of gastrointestinal tumors. This could be in relation to Aspirin being most effective at the site of absorption (the gastrointestinal tract). The study concluded that long term treatment with Aspirin decreases the risk of death in multiple cancer types, and further research on anti-inflammatory agents for the treatment of cancer should be conducted.

As published earlier this month in the peer-reviewed journal Public Library of Science (PLoS) Pathogens, researchers have discovered that fatal prion diseases such as Bovine spongiform encephalopathy (a.k.a. Mad Cow Disease) show signs of destroying a particular protein up to seven months prior to infection. This protein called shadoo is found in lower concentrations as the early stage of prion disease unfolds in an infected brain.

“This is telling us there is a process within the disease that we were previously unaware of, a process that is happening before the infected animals are getting sick. It’s telling us that the brain cells are more active in defending themselves than we thought. The brain cells are in fact trying to get rid of the prion protein, and as a consequence, this bystander shadoo protein is being destroyed unintentionally,” says lead author and co-principal investigator, David Westaway.

Westaway, who works for both the Centre for Prions and Protein Folding Diseases and the Division of Neurology at the University of Alberta, collaborated with several other researchers from scientific departments in Canada, the US and Germany to make this discovery. A thorough study of how the brain cells attempt to fend off the prion protein may lead to scientific advancements in aiding this process to better protect the animal hosts and reduce the fatalities in such prion diseases.

Co-principal investigator George Carlson of the McLaughlin Research Institute in Montana noted that increasing the amount of shadoo protein in laboratory models did nothing to deter the course of prion disease, meaning the role of shadoo protein itself is not yet fully understood. Nonetheless, the only reproducible sign of prion disease thus far is reduction in the levels of shadoo protein.

Parkinson’s is caused primarily by the degeneration of dopamine producing neurons in the brain, which results in loss of motor and speech control, imbalance, and cognitive disfunction. Recently it has been found that these symptoms are only indirectly caused by low dopamine levels. In reality, the degeneration of dopamine neurons prevents transmittance of the inhibitory neurotransmitter GABA (Gamma-Aminobutryic Acid) to the subthalamic region of the basal ganglia. The subthalamic nucleus (within the subthalamic region of the basal ganglia) is believed to control action selection and impulsivity and research has shown that disinhibition of this region contributes to the severity of Parkinson’s symptoms.

In short, lowered GABA transmittance into the subthalamic nucleus results in overexcitement of the region (since GABA is inhibitory), leading to a worsening of the effects of Parkinson’s. A recent article published in The Lancet: Neurology demonstrates a potential gene therapy treatment based on this knowledge which significantly increases motor control in patients with Parkinson’s.

Genetic engineers used an adenovirus to deliver the GAD gene (Glutamic Acid Decarboxylase) to the subthalamic region of the brain, where it initiates the production of GAD in native neurons. GAD is an enzyme which breaks down the excitatory neurotransmitter glutamate into the inhibitory neurotransmitter GABA. Thus, an increase in the level of GAD leads to an increase in the level of GABA and a decrease in the level of glutamate, all of which acts to remediate the overexcitement of the subthalamic nucleus (as GABA is inhibitory and glutamate is excitatory).

In the study of this gene therapy, 22 advanced stage Parkinson’s patients were given this genetic treatment, while 23 other patients received fake therapies as an experimental blind. Patient condition was assessed using the UPDRS (Unified Parkinson’s Disease Rating Scale) motor control scale before therapy and six months post therapy. From an average UPDRS of 25 (before therapy), the genetic therapy group improved their average score by 8 points, while the experimental blind group improved their average score by 4 points, a statistically significant improvement. Gene therapy recipients also saw improvements in other symptomatic areas affected by Parkinson’s besides basic motor control.

With further research, gene therapy could become a key treatment in the battle against neurological disorders such as Parkinson’s and Alzheimer’s disease.

Researchers at the University of California San Diego School of Medicine, in collaboration with Australian colleagues, have genetically modified zebrafish to serve as a model for atherosclerosis, a disorder where arterial walls are hardened from the buildup of LDL (or bad cholesterol) and other substances that form rigid structures called plaques. Atherosclerosis is a dangerous condition that can lead to blood clots, heart attacks or strokes. In a recent press release summarizing their methods and findings, the team outlines the advantages of the zebrafish model.

Young zebrafish are transparent, allowing researchers to literally see and capture the effects of dietary changes and the efficacy of different drugs on plaque formation. To clarify the results, an antibody that recognizes oxidized LDL conjugated with green fluorescent protein was introduced into the zebrafish genome, inducing them to create fluorescent antibodies that would bind to the bad cholesterol and make them visible as in the image above (top right).

Using appropriate imaging techniques, the team observed that treating a fish with an antioxidant drug proved therapeutically equivalent to switching the fish to a low cholesterol diet. Results showed up in just ten days, compared to the nearly six months required to complete similar experiments in mice, marking an order of magnitude improvement in the time required to conduct such studies.

“I see this cholesterol-fed, transgenic zebrafish model as a novel way to study early vascular lipid accumulation and lipoprotein oxidation, the processes that lead to heart disease in humans,” said team leader Yuri Miller, MD, PhD. “Since it is relatively easy and cost-effective to establish and maintain new transgenic zebrafish lines, this offers an in-vivo test for new antioxidants and other drug candidates that could affect development of human atherosclerosis.”

For more information, check out the full research article in the December 1st issue of The Journal of Clinical Investigation.

The vascularization of fabricated tissues presents a considerable challenge to tissue engineers. Tissues thicker than three cell layers cannot maintain physiological function (gas transfer) without vesicular perfusion. Even when tissues are implanted into the body, blood vessels can fail to form, resulting in implant tissue death.

When native tissues suffer from lack of oxygen they release Hypoxia Induced Factors (HIFs) which spark the production of Vascular Endothelial Growth Factor (VEGF). VEGF in turn begins a biochemical cascade which results in vessel formation from the walls of existing vessels, satisfying the starved tissue’s need for nutrients and waste disposal.

To facilitate this process for implanted tissues, researchers at Wake Forest University have recently developed an injectable collagen-based gel which contains the chemical messenger VEGF in minute concentrations. The gel releases 100 ng of VEGF to an isolated area of injection over the course of 12 days, promoting vessel development at a designated implant site. Vessel development increases the chance of implant survival, and researchers hope to extend the period of VEGF release to ensure vascularization.

The molecular structure of gelatin makes this extended release possible. Gels, composed of a molecular matrix (in this case collagen), trap water within its structure. In addition to water, the matrix can be loaded with a solution containing chemicals such as VEGF, and depending on matrix porosity, the rate of release (of the chemicals/solution contained within) can be controlled.

The gel has shown promising results in small animal trials, with findings published in the Journal of the American College of Surgeons. To learn about other scientist’s attempts at tissue vascularization, read more here.