New sensor for early detection of heart attack in humans, providing results in just 1 minute.
Heart disease is the leading cause of death for both men and women. Therefore, a fast and reliable diagnosis of heart attack is urgently needed.
A new study, led by Prof. Jaesung Jang (School of Mechanical and Nuclear Engineering) has developed an electrical immunosensor to detect the acute myocardial infarction, also known as a heart attack within a minute. The system works by measuring the level of cardiac troponin I (cTnI), a protein that is excreted by the heart muscle into the blood following a heart attack.
Prof. Jang states, “This new immunosensor is constructed in a different way than any other sensor.” He adds, “Owing to the new design of this immunosensor, this device is able to rapidly diagnose the level of heart attacks at the point of care.”
Using just a single droplet of blood, this immunosensor detects the target protein present in the blood serum following a heart attack and provides a result in 1 minute.
In the study, dielectrophoretic (DEP) forces have been applied to attract the target protein. The incubation time required for the detection is decreased through DEP-mediated biomarker concentration, in which the target protein is attracted onto the sensing areas via electrical forces. Therefore, the dielectrophoretic concentration of cTnI reduced the incubation time required from 60 min to 1 min.
Chang-Ho Han (School of Mechanical and Nuclear Engineering), a combined master’s-doctoral student in Prof. Jang’s group notes, “The level of cTnI within a single droplet of blood serum is not great.” He continues, “However, we were able to attract the target protein onto the sensing areas via electrical forces, thereby greatly improvingdetection time and detection limit.”
According to the research team, this novel immunosensor holds considerable potential for use as a platform for sensing distinct types of proteins, along with the feasibility of miniaturization and integration for biomedical diagnosis.
The findings of the research have been published in the August issue of the prestigious biotechnology journal Biosensors & Bioelectronics.
A multidisciplinary research team discovers how cells know to rush to a wound and heal it — opening the door to new treatments for diabetes, heart disease and cancer
Researchers at the University of Arizona have discovered what causes and regulates collective cell migration, one of the most universal but least understood biological processes in all living organisms.
The findings, published in the March 13, 2015, edition of Nature Communications, shed light on the mechanisms of cell migration, particularly in the wound-healing process. The results represent a major advancement for regenerative medicine, in which biomedical engineers and other researchers manipulate cells’ form and function to create new tissues, and even organs, to repair, restore or replace those damaged by injury or disease.
“The results significantly increase our understanding of how tissue regeneration is regulated and advance our ability to guide these processes,” said Pak Kin Wong, UA associate professor of mechanical and aerospace engineering and lead investigator of the research.
“In recent years, researchers have gained a better understanding of the molecular machinery of cell migration, but not what directs it to happen in the first place,” he said. “What, exactly, is orchestrating this system common to all living organisms?”
Leaders of the Pack
The answer, it turns out, involves delicate interactions between biomechanical stress, or force, which living cells exert on one another, and biochemical signaling.
The UA researchers discovered that when mechanical force disappears — for example at a wound site where cells have been destroyed, leaving empty, cell-free space — a protein molecule, known as DII4, coordinates nearby cells to migrate to a wound site and collectively cover it with new tissue. What’s more, they found, this process causes identical cells to specialize into leader and follower cells. Researchers had previously assumed leader cells formed randomly.
Wong’s team observed that when cells collectively migrate toward a wound, leader cells expressing a form of messenger RNA, or mRNA, genetic code specific to the DII4 protein emerge at the front of the pack, or migrating tip. The leader cells, in turn, send signals to follower cells, which do not express the genetic messenger. This elaborate autoregulatory system remains activated until new tissue has covered a wound.
The same migration processes for wound healing and tissue development also apply to cancer spreading, the researchers noted. The combination of mechanical force and genetic signaling stimulates cancer cells to collectively migrate and invade healthy tissue.
Biologists have known of the existence of leader cells and the DII4 protein for some years and have suspected they might be important in collective cell migration. But precisely how leader cells formed, what controlled their behavior, and their genetic makeup were all mysteries — until now.
Broad Medical Applications
“Knowing the genetic makeup of leader cells and understanding their formation and behavior gives us the ability to alter cell migration,” Wong said.
With this new knowledge, researchers can re-create, at the cellular and molecular levels, the chain of events that brings about the formation of human tissue. Bioengineers now have the information they need to direct normal cells to heal damaged tissue, or prevent cancer cells from invading healthy tissue.