There's nothing subtle about a migraine. Yet the cause of one type has baffled medical experts for years – perhaps until now.

Dr. Barbara Lee Peterlin, D.O., and her team of researchers from John Hopkins University School of Medicine in Baltimore, may have discovered a biomarker for episodic migraines.

America's headache
Chronic Migraines plague more than 3.2 million Americans, according to MyChronicMigraine.com. Only about 20 percent of cases are diagnosed, which means most people experience these painful episodes and either can't or aren't getting health care experts' input.

Different from the occasional migraine, episodic migraines occur more frequently. MyChronicMigraine.com explained that people who get them experience 15 headaches per month on average. They can strike at anytime and a number of environmental factors can trigger them, including an abrupt change in climate, an alteration in meal times, a difference in sleep patterns and excess stress. 

A treatment has yet to be found, which is why the findings from the John Hopkins' study are exciting, explained Peterlin.

"While more research is needed to confirm these initial findings, the possibility of discovering a new biomarker for migraine is exciting," said Peterlin.

Blood tests might help
Researchers arrived at this conclusion, which was published in the journal Neurology, by conducting neurological exams on 52 women who were diagnosed with episodic migraines. Additionally, researchers examined 36 women who were not diagnosed with the condition.

Study authors checked each participants body mass index and took blood samples to measure the level of ceramades in the bloodstream, which controls inflammation in the brain. As it turns out, women whose ceramide levels decreased were more at risk of developing a migraine than those who had higher levels.

Researchers used blood tests to learn more about migraines.

More specifically, participants with episodic migraines had about 6,000 nanograms of ceramides in their blood. Those who experienced the painful headaches had about 10,500 nanograms.

While scientists believe that this experiment should be duplicated to strengthen its results, potentially finding a biomarker for episodic migraines is certainly a beacon of hope for many Americans.

"This study is a very important contribution to our understanding of the underpinnings of migraine and may have wide-ranging effects in diagnosing and treating migraine if the results are replicated in further studies," explained Dr. Karl Ekbom, of the Karolinska Institutet in Stockholm, Sweden.

Unrestrained growth is one of the signatures of cancer cells. Consequently, to slow or halt the progression of the disease, it is important to first determine what causes this kind of tumor growth.

Researchers at the University of Pennsylvania hoped to make progress in understanding the growth of cancerous tumors by studying mitochondria. The team found that when key components of the mitochondria were disrupted by silencing specific proteins in the organelle, normal cells began to show characteristics of the cells found in cancerous tumors.

"That result alone couldn't tell us whether that was the cause or effect of tumors, but our cell system clearly says that mitochondrial dysfunction is a driving force in tumorigenesis," Narayan Avadhani, Ph.D., a professor of biochemistry in UPenn's School of Veterinary Medicine, said in a statement. The study was led by members of Avadhani's lab.  

Exploring the powerhouse 
The mitochondria is often referred to as the "powerhouse" of the cell because it produces most of the cell's adenosine triphosphate, more commonly known as ATP, which is used as energy. The researchers were interested in examining the organelle to determine if defects would contribute to the growth of cancerous tumors.

Researchers found that cells where the powerhouse was disrupted exhibited characteristics of cancer cells.

"The first part of the Warburg hypothesis has held up solidly in that most proliferating tumors show high dependence on glucose as an energy source and they release large amounts of lactic acid," Avadhani said in a press release. "But the second part, about the defective mitochondrial function causing cells to be tumorigenic, has been highly contentious."The study was built on observations made by German biologist Otto Heinrich Warburg. According to the official website of the Nobel Prize, Warburg's studies included the respiration of cells and tumor metabolism, and he was particularly interested in cancer cells. In 1924, Warburg observed that glucose was consumed at a higher rate in cancerous cells than in normal cells and that those malignant cells additionally had defects in the mitochondria.  

Testing the theory
The team tested the second part of Warburg's postulation by taking cells and silencing the expression of particular parts of the mitochondria's cytochrome oxidase C or CcO using RNA molecules. 

According to the report, the scientists observed major changes in the mitochondria and cells after disrupting only a single protein subunit of CcO. Avadhani reported that the resulting cells showed all the signs of a cancer cell.  

The researchers similarly silenced the subunits in lines that were already cancerous and found that it made the cells more invasive, increasing their malignant potency. They further found that when human tumors were examined, the most oxygen-starved areas contained versions of CcO that were defective.

The findings suggest that these defects in cytochrome oxidase C could be potential biomarkers during cancer screening.  

The research was published in the journal "Oncogene." 

Fixing a broken heart may boil down to a science. Researchers have just designed a patch proven to work in reversing damage in pig and mouse hearts. If effective in humans, the patch can potentially help millions of people who've had heart attacks. 

The leading cause of death
According to the American Heart Association, cardiovascular disease is the leading cause of death, accounting for 17.3 million deaths per year. By 2030, this number is predicted to inflate to more than 23.6 million deaths. Moreover, roughly 85 million Americans are living with a form of cardiovascular disease or the side effects of stroke. 

Despite the staggering number of lives cardiovascular disease has affected, many people can take action to reduce their risk of developing it. The AHA pointed out that maintaining physical activity, a healthy diet, body weight – and a person's levels of cholesterol, blood pressure and blood sugar are pivotal in avoiding a heart attack.

While the AHA and a swath of other organizations have their sights set on shrinking the number of people with heart disease, there has yet to be a successful solution to improve heart muscles once someone has had a heart attack. 

Why scar tissue develops
As explained by Medical News Today, when a person has a heart attack, he or she is unable to repair those heart muscles and subsequently develops scar tissue. The heart muscle cells, called cardiomyocytes​, die following a heart attack because there's a lack of oxygen due to reduced blood flow.

The human body compensates by forming scar tissue around the heart. However, new research published in the journal Nature might indicate that scientists are a step closer to keeping those cells alive. 

In fact, it's this shortcoming of cardiomyocytes that inspired Pilar Ruiz-Lozano, Ph.D., study author and professor at Stanford University, California, to conduct the study. 

The heart patch 
Dr. Ruiz-Lozano's jumping off point for the experiment was based on the fact that zebrafish have heart cells that can regenerate. The epicardium plays a significant role in regeneration. It's located on the inner layer of the pericardium, which lines the heart walls. 

With these vital facts in mind, the researchers analyzed mammal hearts with the goal of finding a single compound that can regenerate cariomyocytes. After examining more than 300 proteins produced in the inner layer of the pericardium, researchers determined that a natural protein known as Faollistatin-like 1 (FSTL1) prompts cell regeneration. 

The patch helped cells regenerate.

Does it work on humans? 
The study authors learned that this protein vanishes after a heart attack, which is why they decided to create a patch embedded with it, intended to stimulate epicardial tissue. The patches were tested on pigs and mice that have experienced heart attacks. They were soon found to be effective in regenerating heart cells in as early as 2-4 weeks. 

This finding is considered an exciting one, as it might pave the way for producing a similar product that can help humans who've had heart attacks. Human trials are slated to begin within the next two years.

Sometimes when you don't have the material you need for an experiment, you just have to create it yourself. 

According to a press release from the University of Illinois at Chicago, researchers at the university were able to create a prostate "organoid," the first of its kind, using human embryonic stem cells. The team found that when exposed to bisphenol A, a common chemical, the organoid produced an excess of prostate stem cells. This overproduction suggests that BPA exposure could increase the risk of prostate cancer in men. 

A controversial additive
According to the U.S. National Institute of Environmental Science, BPA is a chemical created primarily in the production of epoxy resins and polycarbonate plastics. It is typically found in food and drink packaging, such as cans and plastic water bottles, as well as in compact disks, medical devices and other commonly used items. Even some dental sealants and composites can lead to BPA exposure. 

Disposable plastic water bottles are a common way that people are exposed to BPA.

This is not the first research that has linked BPA with prostate cancer. Many studies have looked at the correlation, including one published in April 2014, in which researchers at the University of Cincinnati found that urine BPA levels could potentially be used as a marker for prostate cancer. 

Lab-created test materials
The organoid grown by the UIC researchers was about a millimeter in length and resembled a miniature prostate, a statement reported. 

When the research team exposed the growing organoid to low amounts of BPA, it produced an overabundance of prostate stem cells in bunches throughout the tissue. A normal gland only has a few stem cells spread throughout that serve to develop new prostate tissue during a man's life. An abnormally high amount of stem cells in any body tissue could increase the risk for cancer. 

"The higher number of stem cells we saw in developing organoids given very low doses of BPA may be the underlying mechanism by which BPA increases the risk for prostate cancer," study leader Gail Prins, Ph.D., director of UIC's andrology laboratory and a professor of physiology in the UIC College of Medicine, said in a statement.  

Prins reported that the abnormally high number of stem cells after BPA exposure is a strong candidate to explain why exposure to the chemical has previously been associated with prostate cancer development later in life.

One of the reasons that cancer is such a difficult disease to treat is because it comes in so many different varieties. There is, at least for now, no cure-all that will address every form of the sickness with a simple solution. This is one of the reasons why it's so important to understand different forms of the disease and the way that they develop.

Researchers at Florida State University who were specifically looking at how viruses can cause cancer may have made significant progress by identifying a protein that inhibits the body's response to viral infection. With this information, the team hopes that it might be possible to manipulate the cellular pathway, helping a person to fight the cancer caused by the virus. 

The role of viruses
Viruses are small organisms that require living hosts – such as humans – in order to multiply, the Mayo Clinic reported. When it enters the body of its host, the virus takes over some of the cells, forcing them to produce more of the virus. Common diseases caused by viruses included chicken pox, AIDS and the common cold.  

Researchers have found that common viruses are involved in the development of particular kinds of cancer. While knowledge regarding the process is far from complete, research has already led to the development of vaccines to help prevent certain forms of the disease, the American Cancer Society reported. A common vaccine, for example, protects against human papilloma viruses, a group of more than 150 viruses of which at least a dozen are known to be associated with cancer.

While vaccinations can help protect against some viruses associated with cancer, they are only effective prior to exposure.

However, the problem with these vaccines is that they're only effective if the person receives the vaccination before being exposed to the virus. Researchers are investing time into learning more about the relationship between cancer and viruses in the hopes that the information will help to find ways to fight the disease once exposure has already occurred. 

Understanding the mechanisms
The research team at Florida State University, led by Fanxiu Zhu, the FSU Margaret and Mary Pfeiffer Endowed Professor for Cancer Research, specifically studied Kaposi's sarcoma-associated herpesvirus. According to a statement from the school, the virus is associated with forms of lymphoma and Kaposi's sarcoma. The team screened all 90 proteins is the KSHV cell and found one that directly inhibited cGAS, a DNA sensor. 

After identifying the protein that inhibited the sensor, which they named KicGas, the researchers mimicked natural infection by infecting cell lines from humans with the Kaposi's sarcoma virus. When they eliminated KicGas in the cells, a much stronger immune response was produced. 

To better understand how the inhibitor functions, Hong Li, an FSU professor of chemistry and biochemistry who collaborated with Zhu, is building three-dimensional model of the interactions in the next stage of the research. Li, whose specific focuses are molecular biophysics and molecular biology, has already examined the protein's role in inhibiting the activity of cGAS in test tubes, the statement reported. 

"These are hard problems to solve, and there is still much to learn here," Li said.

There is certainly more to learn in the area, but figuring out how KicGas functions would be a big next step. 

Working toward increased defense
The researchers hope that understanding how the inhibitor functions will eventually lead to discovering ways that the cellular pathway can be manipulated so that a person can more effectively fight cancer.

"Once we figure that out, we can hopefully design something to fight the disease," Zhu said.

While fighting cancer is a clear application of the research, the benefits are not limited to patients with that particular disease alone.

"We can manipulate the protein and/or the sensor to boost or tune down the immune response in order to fight infectious and autoimmune diseases, as well as cancers," Zhu said.

By increasing understanding of how viruses cause cancer in this way, scientists will be able to use it to come up with more effective therapy options, potentially increasing patient outcomes.