Nanoparticles: A High-Tech Solution for Lung Cancer Treatment

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Lung cancer is the leading cause of cancer-related death for both men and women in the U.S., according to the American Cancer Society (ACS). Responsible for 1 in 4 cancer deaths, there were approximately 224,390 new cases and 158,000 lung cancer deaths in 2016 alone.

Despite the seemingly grim outlook for lung cancer patients, many people diagnosed with the disease are cured. The key for these positive outcomes is early cancer detection and treatment. A number of new and innovative therapies have been developed that have contributed greatly to the prolonged survival of patients. However, as the statistics show, there is still a vital need for better treatment options to further improve survival rates.

A main focus in cancer research has been to target the cell communication that causes normal cells to change into cancerous cells. Our understanding of these processes has grown significantly during the past decade, and scientists have been able to point to a number of proteins that are involved in this transformation. Recently, a group of scientists combined its knowledge of these cellular processes with a high-tech anti-cancer drug delivery method to wipe out lung cancer cells. They used nanoparticles with a drug that specifically targeted a protein known to be involved in this cell-changing process. Nanoparticles are very tiny particles between 1 and 100 nanometers—about 1,000 times smaller than a cell—that are made of special material depending on their use. Here, they used a special type of nanoparticle that allowed the drug to get into the lung cancer cells.

In addition to new therapies to fight cancer, there are low-tech ways you can reduce your cancer risk. One of the main causes of lung cancer is smoking tobacco products. The No. 1 way to stay healthy is to avoid tobacco, including smokeless tobacco products, which can also cause cancer. Tomorrow, November 17, is the Great American Smokeout—a good day to make a commitment to quit. ACS has a number of stop-smoking resources available on its website. Additionally, eating healthy and staying active will reduce your risk for cancer-related illness.

audrey-vasauskasAudrey A. Vasauskas, PhD, is an assistant professor of physiology at the Alabama College of Osteopathic Medicine.

The Antioxidant-Activity Connection

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Antioxidants: It’s one of the biggest health buzzwords today. The fabled powers of these mysterious compounds have been featured on daytime TV, plastered on age-defying beauty products and foods in the grocery store, and sold to us as a major reason to frequent juice bars and smoothie shops. Antioxidants are not just an overblown fad, though. They play an important role in keeping our bodies healthy, and they are critical for some people, such as patients with chronic obstructive pulmonary disease (COPD), who can’t get enough oxygen and are inactive as a result.

Antioxidants neutralize molecules called reactive oxygen species (ROS). ROS compounds are byproducts of our body’s metabolism, and too much of them can damage DNA, change cell structure and even kill cells. We can acquire antioxidants to combat ROS by eating foods such as berries, nuts and sweet potatoes. In addition, the body has its own array of natural antioxidants to destroy ROS. Inactivity and low oxygen in the blood (hypoxia) that occur in COPD alter the body’s levels of ROS and antioxidants and can worsen the disease. Maintaining healthy levels of ROS and antioxidants in patients with COPD is a concern for health care providers.

A new study published in the Journal of Applied Physiology found that a low level of activity may be enough to raise antioxidant levels. In a 10-day study, healthy women were confined to strict bed rest, confined to bed rest while breathing air with 32 percent less oxygen, or breathed the low-oxygen air but could stand, walk and conduct normal daily activity. Blood samples were taken before, during and after the experiment to compare the balance between ROS and antioxidant levels. ROS levels increased in all three groups, but the most noticeable difference was in the active group, which had higher antioxidant levels than those on bed rest. Although low oxygen in the blood increased the ROS levels of the participants in the active group, maintaining a somewhat active lifestyle allowed their bodies to produce more antioxidants to buffer the damaging ROS compounds.

There’s a growing population of patients with lung disease who experience both inactivity and hypoxia, so research that helps identify additional consequences of hypoxia and inactivity is paramount for improving care. This study suggests that if these patients can maintain some degree of their physical routine, they may be protected from some of the damaging effects of ROS. This research also provides evidence health care workers can use to educate and encourage healthy behaviors in their patients to reduce complications caused by too much ROS.

Thomas J. Otskey, Hannah Grace Deery, Sandra Bigirwa, Sarah Small and Erin Feldott are students in the Department of Health and Human Physiology at the University of Iowa studying respiratory physiology with Melissa Bates, PhD.

Why Do You Gasp for Air on a Cold Winter’s Day?

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I live in South Dakota where the winter days can be frigid and very dry. Many people, including me, have difficulty breathing while exercising in the winter because our airways temporarily narrow during exercise. This condition is called exercise-induced bronchoconstriction (EIB), formerly known as exercise-induced asthma, and it’s often triggered by working out in cold, dry air.

Scientists believe it’s the dryness of the air breathed in and the quality of the air, not the coldness, that cause the airways to narrow. The lungs have a number of defense mechanisms and reflexes to protect the small airspaces from dry air and particles in the air. The extensive network of airways moistens and warms inhaled air so that by the time the air arrives at the gas-exchange areas—where oxygen enters the blood and carbon dioxide leaves—it is humidified and the same temperature as the body. The airways are lined with mucus that helps catch inhaled particles through its stickiness. The airways also can constrict to prevent particles and dry air from getting farther into the lungs. Narrowing causes problems, however, because less air reaches the gas-exchange areas, preventing the body from getting enough oxygen.

How can you tell if you have EIB? You will experience one or more of the following symptoms, which last 10 to 15 minutes after you’ve finished exercising:

  • shortness of breath or wheezing,
  • decreased endurance,
  • tightness in the chest,
  • cough,
  • upset stomach and
  • sore throat

While 90 percent of people with asthma have EIB, not everyone with EIB has asthma. You’ll need to see an allergist to determine whether your symptoms are solely exercise-induced, are a reaction to irritants in the air or are indications you have asthma.

EIB doesn’t have to keep you from exercising in the winter. In fact, many elite cross-country skiers, world-class figure skaters and ice hockey players have EIB. Here are some suggestions from the American College of Allergy, Asthma and Immunology to relieve your symptoms:

  • Warm up with gentle exercises for 15 minutes before starting intense exercise.
  • Cover your mouth and nose with a scarf or face mask.
  • Try to breathe through your nose.

Medicine that widens the airways can also be prescribed to help prevent your symptoms and attacks. I try not to take a deep breath when I go outside on a cold South Dakota winter day. Then, I head out on a four-mile walk with my golden retriever.

Barb Goodman, PhD

Barb Goodman, PhD, is a  a professor of physiology at the University of South Dakota.

Bee-ware the Cause of Childhood Asthma

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Childhood asthma has reached epidemic proportions across the globe for unknown reasons. Maternal smoking is associated with childhood asthma, but a study published in 2005 suggested that if your grandmother smoked, you were at greater risk of developing asthma than if your mother smoked. How could this happen?

 
Your genes determine the traits you have, and changing a gene’s DNA sequence can affect the trait. However, a trait can also be altered by changing how the cell reads the DNA sequence. This is called “epigenetic changes.” We hypothesized that nicotine—the primary chemical in cigarette smoke that affects fetal lung development—altered genes in this way and conducted several studies to test our hypothesis.

 
In our research, we saw that rats given nicotine while in the womb developed asthma. What was interesting, however, was that their offspring also developed asthma, even though those offspring weren’t directly exposed to nicotine. This effect lasted at least three generations. We think the reason is because nicotine caused epigenetic changes in the egg and sperm cells, cells that are inherited by the next generation. These changes made the next generation’s developing lung hyper-reactive, which is characteristic of asthma.

 
We also saw that repeated environmental exposure to nicotine amplified the asthma symptoms. Nicotine dissolves in fat and can be stored in fat tissue in the body. When it crosses the placenta, we think it can accumulate in the fetus because the fetus is rich in fat.

 
The news coverage on neonicotinoid pesticides harming the honey bee population has been catching our attention. Neonicotinoids are chemically similar to nicotine and have similar biological effects. Although neonicotinoid pesticides are supposed to be far less toxic to mammals, such as humans, than they are to bees, our studies show that nicotine has serious transgenerational effects on lung health and that repeated exposure worsens the impact. In light of the increasing incidence of childhood asthma, we wonder if stopping cigarette smoking and the use of neonicotinoid pesticides could reduce the occurrence of asthma.

 

John S. Torday, PhD

 

John S. Torday, PhD, is a professor of pediatrics at Harbor-UCLA Medical Center, Torrance, Calif. 

 

 

 

Virender K. Rehan, MD

 

Virender K. Rehan, MD, is a professor of pediatrics at Harbor-UCLA Medical Center, Torrance, Calif.

Life After A Life-Saving Treatment: Lung Health in Young Adults Who Were Born Prematurely

Credit: Melissa Bates

Credit: Melissa Bates

In 1963, President John Kennedy’s wife, Jackie, gave birth to a little boy three weeks early. The baby survived only 39 hours before dying of hyaline membrane disease, more commonly known as respiratory distress syndrome. The first successful treatments began in 1991, and now nearly 99 percent of babies like the Kennedy baby survive prematurity. Physicians are even able to treat babies born as much as 16 weeks early. This also means that the first large-scale group of people with hyaline membrane disease to survive being born prematurely is only 24 years old. What does the future hold for this population?

Hyaline membrane disease is caused by a deficiency in the molecule surfactant. Surfactant is produced in the lung starting shortly before birth and is critical for the lungs to inflate and the lungs’ surface to stay dry. To treat the disease, premature babies are given surfactant derived from animals. In addition to surfactant, supplemental oxygen is given and babies are placed on mechanical ventilators.

We recently found that adults who had been born prematurely had important, but unexpected, changes in their physiology.  For example, unlike their peers who were born at full term, prematurely born adults couldn’t increase their breathing in a low-oxygen environment. We also discovered that their exercise capacity and the ability of their lungs to take up oxygen were reduced. We were really struck by this because these prematurely born adults looked just as healthy as adults born at term, until they were stressed with exercise or a low-oxygen environment.

Although we studied minor stresses in a healthy population, we think that our experiments offer a clue that a bigger problem exists on the horizon. Soon, this young population will begin to age. We’ve already found that their physiology is different. Given the current success in treating premature infants now, it is absolutely vital that we shift some of our scientific focus to figuring out whether their different physiology puts them at higher risk of age-related diseases, such as high blood pressure, pulmonary hypertension and diabetes, in the future.

Melissa Bates, PhD, is an assistant professor of human physiology at the University of Iowa.

Correction (10/22/15): An earlier version had said that the baby was born in 1967. The correct year was 1963, and the post has been revised.