Chemotherapy Plus Synthetic Compound Provides Potent Anti-Tumor Effect in Pancreatic Cancers

Human pancreatic cancer cells dramatically regress when treated with chemotherapy in combination with a synthetic compound that mimics the action of a naturally occurring "death-promoting" protein found in cells, researchers at UT Southwestern Medical Center have found.

Researchers led by Dr. Rolf Brekken have shown in mice that pancreatic cancer cells dramatically regress when treated with chemotherapy in combination with a synthetic "death-promoting" compound. 

The research, conducted in mice, appears in the March 23 issue of Cancer Research and could lead to more effective therapies for pancreatic and possibly other cancers, the researchers said.
"This compound enhanced the efficacy of chemotherapy and improved survival in multiple animal models of pancreatic cancer," said Dr. Rolf Brekken, associate professor of surgery and pharmacology and the study's senior author. "We now have multiple lines of evidence in animals showing that this combination is having a potent effect on pancreatic cancer, which is a devastating disease."
In this study, Dr. Brekken and his team transplanted human pancreatic tumors into mice, then allowed the tumors to grow to a significant size. They then administered a synthetic compound called JP1201 in combination with gemcitabine, a chemotherapeutic drug that is considered the standard of care for patients with pancreatic cancer. They found that the drug combination caused regression of the tumors.
"There was a 50 percent regression in tumor size during a two-week treatment of the mice," Dr. Brekken said. "We also looked at survival groups of the animals, which is often depressing in human therapeutic studies for pancreatic cancer because virtually nothing works. We found not only significant decrease in tumor size, but meaningful prolongation of life with the drug combination."
The drug combination was also effective in an aggressive model of spontaneous pancreatic cancer in mice.
The compound JP1201 was created in 2004 by UT Southwestern researchers to mimic the action of a protein called Smac. The researchers discovered Smac in 2000 and found that this protein plays a key role in the normal self-destruction process present in every cell.
Cell death, or apoptosis, is activated when a cell needs to be terminated, such as when a cell is defective or is no longer needed for normal growth and development. In cancer cells, this self-destruct mechanism is faulty and lead to breaks in the cell-death cascade of events. The synthetic Smac, or Smac mimetic, developed at UT Southwestern inhibits these breaks, allowing the cell to die.
"In essence, we're inhibiting an inhibitor," Dr. Brekken said. "And we're allowing the apoptotic cascade to kick off, resulting in the death of cancer cells."
UT Southwestern researchers are using Smac mimetics in breast and lung cancer research, as well. Dr. Brekken said the next step is to develop a compound based on JP1201 that can be tested in humans in clinical trials.
Other UT Southwestern researchers involved in the study included lead author Dr. Sean Dineen, surgery resident; Dr. Christina Roland, surgery resident; Rachel Greer, student research assistant in the Nancy B. and Jake L. Hamon Center for Therapeutic Oncology Research; Juliet Carbon, senior research associate in surgery and in the Hamon Center; Jason Toombs, research assistant in surgery and in the Hamon Center; Dr. Puja Gupta, a pediatric hematology/oncology fellow; Dr. Noelle Williams, associate professor of biochemistry; and Dr. John Minna, director of the W.A. "Tex" and Deborah Moncrief Jr. Center for Cancer Genetics and of the Hamon Center.
The research was supported by Susan G. Komen for the Cure and Joyant Pharmaceuticals, a Dallas-based company and UT Southwestern spinoff that is developing medical applications of Smac-mimetic compounds.

Just One Cigarette Has Harmful Effect On Arteries Of Young Healthy Adults

Even one cigarette has serious adverse effects on young adults, according to research presented by Dr. Stella Daskalopoulou at the Canadian Cardiovascular Congress 2009, co-hosted by the Heart and Stroke Foundation and the Canadian Cardiovascular Society.Her study found that smoking one cigarette increases the stiffness of the arteries in 18 to 30 year olds by a whopping 25 per cent.

Arteries that are stiff or rigid increase resistance in the blood vessels, making the heart work harder. The stiffer the artery, the greater the risk for heart disease or stroke.

"Young adults aged 20-24 years have the highest smoking rate of all age groups in Canada," says Dr. Daskalopoulou, an internal medicine and vascular medicine specialist at McGill University Health Centre. "Our results are significant because they suggest that smoking just a few cigarettes a day impacts the health of the arteries. This was revealed very clearly when these young people were placed under physical stress, such as exercise."

The study compared the arterial stiffness of young smokers (five to six cigarettes a day) to non-smokers. The median age was 21 years. Arterial measurements were taken in the radial artery (in the wrist), the carotid artery (in the neck), and in the femoral artery (in the groin), at rest and after exercise.

Arterial stiffness in both smokers and non-smokers was measured using a new but well established method called applanation tonometry. Dr. Daskalopoulou introduced the 'arterial stress test' which measures the arteries' response to the stress of exercise. The test is comparable to a cardiac stress test, which measures the heart's response to the stress of exercise.

"In effect we were measuring the elasticity of arteries under challenge from tobacco," explains Dr. Daskalopoulou.

An initial arterial stress test was carried out to establish a baseline measurement for both the non-smokers and the smokers, who were asked not to smoke for 12 hours prior to the test. After the first meeting, smokers returned and smoked one cigarette each and then repeated the stress test. During the final meeting, smokers were asked to chew a piece of nicotine gum prior to the stress test.

Dr. Daskalopoulou found that after exercise the arterial stiffness levels in non-smokers dropped by 3.6 per cent. Smokers, however, showed the reverse: after exercise their arterial stiffness increased by 2.2 per cent. After nicotine gum, it increased by 12.6 per cent. After one cigarette, it increased by 24.5 per cent.

Interestingly, there was no difference in the arterial stiffness measurements between smokers and non-smokers at rest.

"In effect, this means that even light smoking in otherwise young healthy people can damage the arteries, compromising the ability of their bodies to cope with physical stress, such as climbing a set of stairs or running to catch a bus," says Dr. Daskalopoulou. "It seems that this compromise to respond to physical stress occurs first, before the damage of the arteries becomes evident at rest."

"More than 47,000 Canadians will die prematurely each year due to tobacco use, which often starts in the teen years," warns Heart and Stroke Foundation spokesperson Dr. Beth Abramson. "We know that over 90 per cent of teenagers who smoke as few as three to four cigarettes a day may be trapped into a lifelong habit of regular smoking, which typically lasts 35 to 40 years."

Smoking contributes to the build up of plaque in the arteries, increases the risk of blood clots, reduces the oxygen in the blood, increases blood pressure, and makes the heart work harder. Smoking also nearly doubles the risk of ischemic stroke.

Dr. Abramson says this study reinforces the importance of education, prevention programs, and legislation such as the recently passed Bill C-32, Cracking Down on Tobacco Marketing Aimed at Youth Act.

Protein May Be Strongest Indicator Of Rare Lung Disease

Researchers at the University of Cincinnati (UC) have discovered a protein in the lungs that can help in determining progression of the rare lung disease Idiopathic Pulmonary Fibrosis (IPF).Researchers say the protein—Serum surfactant protein A—is superior to other IPF predictors and could lead to better decisions about treatment and timing of lung transplantation.

The study, led by Brent Kinder, MD, is published in the June 4 edition of the journal Chest.

Surfactant proteins are lipoproteins that allow the lungs to stretch and function. These have previously been investigated by UC pulmonary researchers Frank McCormack, MD, and Jeffrey Whitsett, MD.

Kinder and colleagues report that Serum surfactant protein A is the strongest predictor of a patient's survival in the first year after diagnosis with IPF.

"A simple blood test may give us the information we need to help determine the short term risk of death in a patient with IPF," says Kinder, an assistant professor of medicine at the UC College of Medicine and pulmonologist with UC Physicians. "This protein is a stronger predictor of the severity of illness than age, symptoms or prognostic data, like breathing tests."

IPF is scarring of the lung. As the disease progresses, air sacs in the lungs become replaced by fibrotic scar tissue. Lung tissue becomes thicker where the scarring forms, causing an irreversible loss of the tissue's ability to carry oxygen into the bloodstream.

IPF is one of about 200 disorders called interstitial lung diseases, which affect the thick tissue of the lung as opposed to more common lung ailments—such as asthma or emphysema—that affect the airways.

IPF is the most common form of interstitial lung diseases and affects about 128,000 people in the United States, with an estimated 48,000 new cases diagnosed each year. There currently are no proven therapies or cures for IPF.

Kinder, director of UC's Interstitial Lung Disease Center, says this new indicator will allow doctors to determine the severity of the disease in a fast, effective manner and will help them decide the best way to go about treating it.

"It will allow us to come to a decision about how or if to treat the IPF patient and get them enrolled in clinical trials immediately," he says. "In severe cases, it can help in scheduling a lung transplant at the most optimal time for the patient.

"Overall, this discovery could help us define the window of opportunity to appropriately try more aggressive therapies and could greatly help improve the lives of those living with IPF."

This study was funded in part by a Support of Continuous Research Excellence (SCORE) grant from the National Institutes of Health and a UC Dean's Scholars award for clinical research.

Environmental Exposure To Particulates May Damage DNA In As Few As Three Days

Exposure to particulate matter has been recognized as a contributing factor to lung cancer development for some time, but a new study indicates inhalation of certain particulates can actually cause some genes to become reprogrammed, affecting both the development and the outcome of cancers and other diseases.The research will be presented on May 17, at the 105th International Conference of the American Thoracic Society in San Diego.

"Recently, changes in gene programming due to a chemical transformation called methylation have been found in the blood and tissues of lung cancer patients," said investigator Andrea Baccarelli, M.D., Ph.D., assistant professor of applied biotechnology at the University of Milan. "We aimed at investigating whether exposure to particulate matter induced changes in DNA methylation in blood from healthy subjects who were exposed to high levels of particulate matter in a foundry facility."

Researchers enrolled 63 healthy subjects who worked in a foundry near Milan, Italy. Blood DNA samples were collected on the morning of the first day of the work week, and again after three days of work. Comparing these samples revealed that significant changes had occurred in four genes associated with tumor suppression.

"The changes were detectable after only three days of exposure to particulate matter, indicating that environmental factors need little time to cause gene reprogramming which is potentially associated with disease outcomes," Dr. Baccarelli said.

"As several of the effects of particulate matter in foundries are similar to those found after exposure to ambient air pollution, our results open new hypotheses about how air pollutants modify human health," he added. "The changes in DNA methylation we observed are reversible and some of them are currently being used as targets of cancer drugs."

Dr. Baccarelli said the study results indicate that early interventions might be designed which would reverse gene programming to normal levels, reducing the health risks of exposure.

"We need to evaluate how the changes in gene reprogramming we observed are related to cancer risk," he said. "Down the road, it will be particularly important not only to show that these changes are associated with increased risk of cancer or other environmentally-induced diseases, but that, if we were able to prevent or revert them, these risks could be eliminated."

Session # A45: "Genetic Basis for Environmental and Occupational Respiratory Diseases." Abstract # 2589: "Effects of Particulate Matter Exposure on p16, p53, APC and RASSF1A Promoter Methylation" Poster Board # C51

Specific Lung Cancer Susceptibility Gene Identified

University of Cincinnati (UC) cancer cell biologists have identified a distinct gene linked to increased lung cancer susceptibility and development. They say this gene—known as RGS17—could result in a genetic predisposition to develop lung cancer for people with a strong family history of the disease.With further investigation, they believe the gene could be used to identify high-risk patients who may benefit from earlier, more aggressive lung cancer screening.

Marshall Anderson, PhD, and his colleagues report their findings in the April 15, 2009, issue of the journal Clinical Cancer Research.

“Understanding how the RGS17 gene impacts cancer development could change clinical diagnosis and treatment as radically as discovery of the breast cancer genes (BRCA1 and BRCA2) did,” explains Anderson, who has led the multi-institutional Genetic Epidemiology of Lung Cancer Consortium (GELCC) studying the genetic basis of lung cancer since 1997. “A proven genetic test could help us identify people at risk before the disease progresses.”

According to the American Cancer Society, lung cancer is the leading cause of cancer related disease and death. Although tobacco smoke is the primary environmental cause of the disease, science has shown there is also a strong genetic component to the disease.

“This study represents a significant contribution to our understanding of lung cancer susceptibility and is another step toward to the goal of preventive medicine,” says David Christiani, MD, MPH, a professor of occupational medicine and environmental health at the Harvard School of Public Health, whose two-page commentary on the study is published in conjunction with the GELCC team’s scientific findings. “The authors undertook a daunting challenge of performing a family-based study of lung cancer in an effort to identify specific causal genes.”

Genes, which are located in fixed positions on the cell's chromosomes, carry the DNA code that determines inherited characteristics, including a risk of certain diseases.

For this study, Anderson and his multi-institutional team collected biological samples from numerous multigenerational families with five or more members who were affected by lung cancer. Through a combination of what is known as “fine mapping”—where genetic information is dissected and analyzed—and genetic association studies, researchers identified RGS17 as a major candidate susceptibility gene for familial lung cancers.

Research has shown that lung cancer can occur sporadically—where people have no known risk factors or family history—or hereditarily, occurring in multiple members of the same family. In 2004, Anderson’s team reported the first genetic evidence of a major lung cancer “susceptibility locus” on chromosome 6, and evidence of a susceptibility region on three other chromosomes.

The region of the original chromosome where the lung cancer markers were found contained about 100 genes, including several genes suspected to be involved in tumor suppression and cell growth.

Using a genetically altered mouse model, researchers determined that when RGS17 was suppressed, lung tumors shrank, proving the gene was involved in cancer development and must be present for cancer growth.

“What was most interesting is that this same gene was over-expressed in 60 percent of the samples from non-hereditary lung tumors,” explains Anderson. “This suggests that perhaps epigenetic factors may be contributing to abnormal genetic development.”

The UC-led team will conduct additional research to investigate how environmental factors may influence familial cancer development.

Funding for this research comes from the National Institutes of Health through the Genetic Epidemiology of Lung Cancer Consortium, a collaborative research effort established in 1997 to research the genetic origins of familial lung cancers. Anderson serves as principal investigator. Collaborating institutions include Washington University-St. Louis, Mayo Clinic-Rochester, University of Colorado, University of Texas Southwestern Medical Center, Louisiana State University, Saccomanno Research Institute, National Cancer Institute, National Human Genome Research Institute, Karmanos Cancer Institute, University of Toledo and M.D. Anderson Cancer Center-Houston.

Catching The Common Cold Virus Genome

A new study by Brigham Young University researchers on the virus behind nearly half of all cold infections explains how and where evolution occurs in the rhinovirus genome and what this means for possible vaccines."There are a lot of different approaches to treating the cold, none of which seem to be effective," said Keith Crandall, professor of biology and co-author of the study. "This is partly because we haven't spent a lot of time studying the virus and its history to see how it's responding to the human immune system and drugs."

The BYU team studied genomic sequences available online and used computer algorithms to estimate how the rhinovirus is related to other viruses.

According to Nicole Lewis-Rogers, a postdoctoral fellow in the Biology Department and lead author on the study, the rhinovirus is similar to the polio virus, whose vaccine was announced in 1955. But while the polio virus has just three subspecies, the rhinovirus has more than 100 subspecies, which continually evolve.

"These viruses could be under the same constraints and yet change differently," Lewis-Rogers said. "That's why it is so hard to create a vaccine."

Through a computer program developed at BYU, Lewis-Rogers' team was able to identify the parts of the virus genome that enable resistance to drugs and the human immune system.

The immune system does a good job of recognizing viral contaminants and getting rid of them, as do new drugs, but the rhinovirus has responded to these defenses by changing its genome so that it is not so easily recognized.

"The virus is evolving solutions against the immune system and drugs," Crandall said. "The more we can learn about how the virus evolves solutions, the better we can rid the body of these infections."

Understanding where change occurs in the virus genome will help virologists who work to design drugs that target the rhinovirus.

"If you've got 10,000 bits of information, this narrows it down to a handful," Lewis-Rogers said. "Here is where you can start looking."

Lewis-Rogers and Crandall hope scientists will use these insights to build better drugs to combat the virus in the most effective way.

The study is reported in the April issue of the journal Molecular Biology and Evolution. BYU undergraduate Matthew Bendall is also a co-author on the study, which was funded by the USDA. Bendall will next pursue a master's in bioinformatics at BYU.

Broccoli May Help Protect Against Respiratory Conditions Like Asthma

Here's another reason to eat your broccoli: UCLA researchers report that a naturally occurring compound found in broccoli and other cruciferous vegetables may help protect against respiratory inflammation that causes conditions like asthma, allergic rhinitis and chronic obstructive pulmonary disease.Published in the March edition of the journal Clinical Immunology, the research shows that sulforaphane, a chemical in broccoli, triggers an increase of antioxidant enzymes in the human airway that offers protection against the onslaught of free radicals that we breathe in every day in polluted air, pollen, diesel exhaust and tobacco smoke. A supercharged form of oxygen, free radicals can cause oxidative tissue damage, which leads to inflammation and respiratory conditions like asthma.

"This is one of the first studies showing that broccoli sprouts — a readily available food source — offered potent biologic effects in stimulating an antioxidant response in humans," said Dr. Marc Riedl, the study's principal investigator and an assistant professor of clinical immunology and allergy at the David Geffen School of Medicine at UCLA.

"We found a two- to three-fold increase in antioxidant enzymes in the nasal airway cells of study participants who had eaten a preparation of broccoli sprouts," Riedl said. "This strategy may offer protection against inflammatory processes and could lead to potential treatments for a variety of respiratory conditions."

The UCLA team worked with 65 volunteers who were given varying oral doses of either broccoli or alfalfa sprout preparations for three days. Broccoli sprouts are the richest natural source of sulforaphane; the alfalfa sprouts, which do not contain the compound, served as a placebo.

Rinses of nasal passages were collected at the beginning and end of the study to assess the gene expression of antioxidant enzymes in cells of the upper airways. Researchers found significant increases of antioxidant enzymes at broccoli sprout doses of 100 grams and higher, compared with the placebo group.

The maximum broccoli sprout dosage of 200 grams generated a 101-percent increase of an antioxidant enzyme called GSTP1 and a 199-percent increase of another key enzyme called NQO1.

"A major advantage of sulforaphane is that it appears to increase a broad array of antioxidant enzymes, which may help the compound's effectiveness in blocking the harmful effects of air pollution," Riedl said.

According to the authors, no serious side effects occurred in study participants receiving broccoli sprouts, demonstrating that this may be an effective, safe antioxidant strategy to help reduce the inflammatory impact of free radicals.

Riedl notes that more research needs to be done to examine the benefits of sulforaphane for specific respiratory conditions. It is too early to recommend a particular dosage.

Riedl recommends including broccoli and other cruciferous vegetables as part of a healthy diet.

The study was supported by the National Institutes of Health, the National Institute of Environmental Health Sciences and the U.S. Environmental Protection Agency.

Other study authors include Dr. Andrew Saxon of the Hart and Louis Lyon Laboratory, division of clinical immunology and allergy in the department of medicine at the David Geffen School of Medicine at UCLA, and Dr. David Diaz-Sanchez of the human studies division of the U.S. Environmental Protection Agency.

Pollution-related Asthma May Start In The Womb

Children born in areas with increased traffic-related pollution may be at greater risk of developing asthma due to genetic changes acquired in the womb, according to new research from the University of Cincinnati (UC) and Columbia University Mailman School of Public Health.
In a study of umbilical cord blood from New York City children, researchers have discovered evidence of a possible new biomarker—an epigenetic alteration in the gene ACSL3—associated with prenatal exposure to polycyclic aromatic hydrocarbons (PAHs). These chemical compounds are created as byproducts of incomplete combustion from carbon-containing fuels, resulting in high levels in heavy-traffic areas. Exposure to PAHs has been linked to diseases such as cancer and childhood asthma.

Researchers say this finding provides a potential clue for predicting environmentally related asthma in children—particularly those born to mothers who live in high-traffic areas like Northern Manhattan and South Bronx when pregnant.

This is the first study to examine the effects of prenatal ambient air pollutant exposure on epigenetic changes linked to asthma. Epigenetic changes may disrupt the normal functioning of genes by affecting their expression but do not cause structural changes or mutations in the genes.

The team reports its findings in the Feb. 16, 2009, issue of PLoS One.

For this study, UC researchers teamed with Columbia's Mailman School of Public Health to study the relationship between prenatal PAH exposure and childhood asthma, hypothesizing that transplacental exposure to PAHs could "reprogram" fetal genes and lead to airway inflammation or asthma during childhood. Epigenetic reprogramming is the result of an organism's genes interacting with the environment.

"Our data support the concept that environmental exposures can interact with genes during key developmental periods to trigger disease onset later in life, and that tissues are being reprogrammed to become abnormal later," says Shuk-mei Ho, PhD, senior author of the paper, chair of UC's Department of Environmental Health and the director of the Center for Environmental Genetics.

"This research is aimed at detecting early signs of asthma risk so that we can better prevent this chronic disease that affects as many as 25 percent of children in Northern Manhattan and elsewhere," adds Frederica Perera, DrPH, professor of environmental health sciences and director of the Columbia Center for Children's Environmental Health (CCCEH) at the Mailman School of Public Health and co- first author on the paper.

Using biological specimens from the CCCEH birth cohort of mothers and children living in Northern Manhattan and the South Bronx, UC scientists analyzed umbilical cord white blood cell samples from 56 children for epigenetic alterations related to prenatal PAH exposure. (The mothers' exposure to PAHs was monitored during pregnancy using backpack air monitors).

The researchers found a significant association between changes in ACSL3 methylation—a gene expressed in the lung—and maternal PAH exposure. ACSL3 also was associated with a parental report of asthma symptoms in the children prior to age 5.

With confirmation in further studies, researchers say changes in the ACSL3 gene could serve as a novel biomarker for early diagnosis of pollution-related asthma.

"This study provides a blueprint for the discovery of epigenetic biomarkers relevant to other investigations of exposure-disease relationships in birth cohorts," says Wan-yee Tang, PhD, a UC research scientist and a co-first author on the paper.

"Understanding early predictors of asthma is an important area of investigation," adds Rachel Miller, MD, director of the CCCEH asthma project and study co-author, "because they represent potential clinical targets for intervention."

The CCCEH birth cohort was launched in 1998 to study the effects of prenatal exposure to common urban pollutants on the health of mothers and their children. Children in the cohort were born to non-smoking Dominican and African-American women in Northern Manhattan or the South Bronx and follow-up is ongoing.

Funding for the multi-institutional study comes from the National Institute of Environmental Health Sciences (NIEHS), the U.S. Environmental Protection Agency (EPA) and private foundations. UC's Linda Levin, PhD and Columbia University Mailman School's Julie Herbstman, PhD, and Deliang Tang, MD, DrPH, were also co-authors of the study.

Toothbrushing Can Prevent Hospital-borne Pneumonia

Hospital-borne infections are a serious risk of a long-term hospital stay, and ventilator-associated pneumonia (VAP), a lung infection that develops in about 15% of all people who are ventilated, is among the most dangerous. With weakened immune systems and a higher resistance to antibiotics, patients who rely on a mechanical ventilator can easily develop serious infections — as 26,000 Americans do every year.

Thanks to a proven new clinical approach developed by Tel Aviv University nurses, though, there is a new tool for stopping the onset of VAP in hospitals.

This new high-tech tool? An ordinary toothbrush.

Three Times a Day Keeps Pneumonia Away

“Pneumonia is a big problem in hospitals everywhere, even in the developed world,” says Nurse Ofra Raanan, the chief researcher in the new study and a lecturer at Tel Aviv University’s Department of Nursing. “Patients who are intubated can be contaminated with pneumonia only 2 or 3 days after the tube is put in place. But pneumonia can be effectively prevented if the right measures are taken.”

Raanan, who works at the Sheba Academic School of Nursing at The Chaim Sheba Medical Center, collaborated with a team of nurses at major medical centers around Israel. The nurses found that if patients — even unconscious ones — have their teeth brushed three times a day, the onset of pneumonia can be reduced by as much as 50%.

A Pioneering Study with Measurable Effects

It’s difficult to quantify the effects precisely, the researchers say. “While the research shows a definite improvement in reducing the incidence of hospital-borne pneumonia, it’s hard to say by exactly how much toothbrushing prevents VAP,” says Raanan, but the published evidence shows a direct correlation for intubated patients.

“Sometimes, however, doctors and nurses do everything right and the patient still gets pneumonia. But this approach will certainly improve the odds for survival.”

Normally, the teeth and oral cavity in a healthy mouth maintain a colony of otherwise harmless bacteria. Infection takes root when a breathing tube allows free passage of the “good” bacteria into the lower parts of the lung. The bacteria travel in small water droplets through the tube and colonize the lung. Once there, the bacteria take advantage of a patient’s weakened immune system and multiply. A regular toothbrushing kills the growth and subsequent spread of the bacterium that leads to VAP.

Augmenting the Preventative Routine

There are additional steps for preventing the onset of VAP. Today, nurses typically use a mechanical suction device to remove secretions from the mouth and throat. They also put patients in a seated position and change the position every few hours. Toothbrushing, say Tel Aviv University nurses, should be added to the routine.

Although nurses in some American hospitals already practice toothbrushing on ventilated patients, these new results may convince medical centers around the world to invest more resources in this routine practice, thereby saving lives.

The research and recommendations are scheduled for publication in a leading nursing journal.