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Clinical Trials in Emphysema
Alabama
Birmingham : Research Site: New! TESRA: (Treatment of Emphysema with a gamma-Selective Retinoid Agonist)
Birmingham : Cardiothoracic Surgery ,University of Alabama, Birmingham The IBV Trial . An Investigational treatment for people suffering from Emphysema
Mobile : Pulmonary Associates of Mobile, PC The IBV Trial . An Investigational treatment for people suffering from Emphysema
Arizona
Phoenix : Pulmonary Associates Phoenix The EASE Trial: An investigation of the Exhale� Drug-Eluting Stent in homogeneous emphysema patients with severe hyperinflation . . .
Bulgaria
Pleven : Research Site: New! TESRA: (Treatment of Emphysema with a gamma-Selective Retinoid Agonist)
Ruse : Research Site: New! TESRA: (Treatment of Emphysema with a gamma-Selective Retinoid Agonist)
Sofia : Research Site: New! TESRA: (Treatment of Emphysema with a gamma-Selective Retinoid Agonist)
Canada
Toronto, ON : Research Site: New! REPAIR Tier 2 - (Retinoids in Emphysema Patients on the Alpha-1-Antitrypsin International Registry)
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Emphysema
If you are aged 40 to 74, have severe emphysema, are able to participate in standard exercise testing, are willing to abstain from smoking for four months prior and during the trial, and can complete at least one overnight clinic stay, you may qualify for this study.
The research site is in Chicago, Ill.
More information
Please see http://www.centerwatch.com/patient/studies/cat59.html.
Mice that inhaled cigarette smoke five hours daily avoided lung damage in a study by eating a chemical compound.
The mice were exposed to smoke in a laboratory to study emphysema, a progressive lung disease that causes shortness of breath and often is fatal. The compound, CDDO-imidazole, boosted the animals’ production of antioxidants that keep lung cells from dying and decrease inflammation, according to a report today in the Proceedings of the National Academy of Sciences.
Cigarette smoke is the most common cause of emphysema. The research, from the Bloomberg School of Public Health at Johns Hopkins University in Baltimore, may show drugmakers where to focus efforts to treat the malady, said James Kiley, the director of the division of lung diseases at the National Heart, Lung, and Blood Institute.
“Is it going to bring a new therapy tomorrow?” said Kiley, who wasn’t involved in the study. “Absolutely not. We don’t have any therapies that will cure the disease or halt the progression once it’s started, so it’s a step toward that.
An experimental drug protected mice exposed to tobacco smoke from developing chronic lung disease, raising hope for a treatment in humans, U.S. researchers said on Monday.
They said the chemical CDDO-Im helped activate a master gene called Nrf2 that bolsters the lung's ability to fight off chronic obstructive pulmonary disease, or COPD, a condition that includes emphysema, chronic bronchitis and some types of serious chronic asthma.
"COPD is the 4th-largest killer in the world with no effective drugs," Shyam Biswal of Johns Hopkins School of Medicine in Maryland, who worked on the study, said in an e-mail.
In prior research, Biswal and colleagues found that Nrf2 works as a "master gene," turning on genes involved in protecting the lungs from pollution and cigarette smoke.
"The Nrf2 pathway is the major antioxidant and detoxifying response in the lungs. Therapies targeting this pathway need to be developed and tested in patients," said Biswal, whose study was published in the Proceedings of the National Academy of Sciences.
a new drug may protect the animals from the respiratory damage caused by cigarettes.
The finding holds out hope for patients with chronic obstructive pulmonary disease (COPD) -- a chronic progressive lung disease involving both emphysema and chronic obstructive bronchitis.
COPD, most commonly linked to smoking, is the fourth leading cause of death in the United States and there are no effective treatments.
"Our previous studies have shown that there is a defect in Nrf2 -- a master regulator of antioxidant and detoxifying pathways -- in the lungs of COPD patients that may be involved in the severity of this disease," explained lead researcher Shyam Biswal, an associate professor at the Johns Hopkins Bloomberg School of Public Health in Baltimore.
In this study, the researchers used a novel drug molecule called CDDO-imidazole (CDDO-Im) to curb the progression of the disease by targeting the Nrf2 pathway.
Scientists have shown in experiments with mice, that a new drug may protect the animals from respiratory damage caused by cigarettes. The chemical CDDO-Im helped activate a master gene called Nrf2 that bolsters the lung's ability to fight off chronic obstructive pulmonary disease, or COPD, a condition that includes emphysema, chronic bronchitis and some types of serious chronic asthma.
COPD the 4th-largest killer in the world, most commonly linked to smoking, is the fourth leading cause of death in the United States and there are no effective treatments.
The report is published in this week's online edition of the Proceedings of the National Academy of Sciences.
Using a molecule similar to one found in an experimental cancer drug, researchers at the Johns Hopkins Bloomberg School of Public Health demonstrated that activation of a key component of the lung’s antioxidant defense system, Nrf2, can prevent emphysema in mice. The researchers believe that activation of Nrf2 could be a novel target for therapies to prevent chronic obstructive pulmonary disease (COPD), which comprises emphysema and chronic bronchitis. COPD is a major public health problem and it is the fourth leading cause of death in the U.S.
Newswise -- Using a molecule similar to one found in an experimental cancer drug, researchers at the Johns Hopkins Bloomberg School of Public Health demonstrated that activation of a key component of the lung’s antioxidant defense system, Nrf2, can prevent emphysema in mice. The researchers believe that activation of Nrf2 could be a novel target for therapies to prevent chronic obstructive pulmonary disease (COPD), which comprises emphysema and chronic bronchitis. COPD is a major public health problem and it is the fourth leading cause of death in the U.S. The study is published in the online Early Edition of PNAS: Proceeding of the National Academy of Sciences.
The nation's first scientific study on the relationship between smoking and respiratory disease among Hispanic versus non-Hispanic white (NHW) women revealed that NHW women smokers were at greater risk of developing airflow obstruction and diminished lung function than Hispanic women who smoke - a surprising finding given that many diseases more adversely affect ethnic minorities. Smoking-related respiratory diseases are a major cause of death among all women.
The objective was to evaluate the risk of airflow obstruction and to assess lung function among Hispanic and NHW female smokers in a New Mexican group of participants.
Lead investigators at Lovelace Respiratory Research Institute (LRRI) - in collaboration with the University of New Mexico School of Medicine, Harvard Medical School and the University of Southern California, Los Angeles - conducted the study, which was financed by the Tobacco Settlement Commission of New Mexico. Of the 1,433 women who participated, 248 (17.3 percent) were Hispanic, 830 (57.9 percent) were current smokers, 517 (36.1 percent) smoked 40 pack-years and 422 (29.4 percent) were obese.
The party never stops for mice in Todd Wyatt's laboratory at the University of Nebraska Medical Center, where researchers hope to learn how chronic heavy drinking and smoking often inflicts a double whammy on lungs.
The drinking water for some mice there is 40 proof, raising blood alcohol to the point they can't legally be at the wheel. The mice also smoke the equivalent of a pack a day, based on blood cotinine levels.
They lack only some Texas hold 'em tables and a country western jukebox, but sacrifices must be made to serious science.
Wyatt, a Ph.D researcher, hopes the five-year, $1.5 million study will explain everybody's apocryphal uncle Joe -- the relative who smokes and drinks daily, even on his 87th birthday.
Wyatt said whenever he talks about his research, someone always brings up uncle Joe.
Understanding what makes Joe immune to lung disease could lead to better treatments for COPD -- chronic obstructive pulmonary disease, an incurable syndrome afflicting 40 million people and for which there are no good treatments.
Boston University School of Medicine (BUSM) is one of seven centers to receive a four-year grant from the National Institutes of Health (NIH) to use cutting edge genomic technologies to better understand lung disease. The $2.9 million awarded to BUSM will fund a study to probe the causes of chronic obstructive pulmonary disease (COPD), a disease associated with smoking that is characterized by airflow limitation.
COPD is the fourth leading cause of death in the United States and a significant public health burden. There is currently no cure for COPD, and the limited available therapies are mainly used to treat symptoms of the disease. While the role cigarette smoke plays in COPD is undisputed, the mechanism by which inhaled smoke contributes to disease pathogenesis remains unclear. The purpose of this study is to develop an understanding of the processes that contribute to COPD pathogenesis, ultimately yielding tools for stratifying and treating COPD patients based on the molecular processes that are responsible for their disease.
During the two-week stay in hospital that followed, his lungs were found to be operating at 25-per-cent capacity and he was diagnosed with chronic obstructive pulmonary disease, or COPD.
An estimated 1.5 million Canadians suffer from the lung-damaging disease, which includes emphysema and chronic bronchitis. Another 1.6 million are believed to have it, but haven't been diagnosed.
More people are hospitalized and readmitted because of COPD than with heart failure, angina and other serious chronic diseases. It is the fourth leading cause of death of adult Canadians.
In 85 to 90 per cent of cases, COPD is the result of smoking tobacco, says Dr. Ron Damant, an associate professor of respirology at the University of Alberta. But any kind of chronic inhalation -- second-hand smoke, occupational pollutants, outdoor air pollution -- can cause it as well.
Early symptoms are coughing and bringing up a little sputum (saliva and mucus). Smokers often think that's normal, so they don't worry about it, but it's the first sign of irreversible damage to the lungs and other parts of the body, Damant says.
"A chronic cough is always a sign of trouble because it's not a normal thing to have."
Most of the full-blown cases of COPD doctors see today are in patients who were smoking 20 to 50 years ago.
Scientific Knowledge on the Subject
Patients with chronic obstructive pulmonary disease (COPD) are at an increased risk of cardiovascular disease. The mechanism for this relationship, however, remains unknown.
What This Study Adds to the Field
Impaired flow-mediated dilation was strongly related to systemic inflammation and airway obstruction, which may help explain the increased cardiovascular morbidity in patients with COPD.
Patients with idiopathic pulmonary fibrosis (IPF) are three times as likely to experience severe coronary events--including heart attacks--than people without the disease, according to a recent study that analyzed the risk of cardiovascular disease in nearly 1,000 patients with IPF and more than 3,500 matched controls.
"If you look at them over time, people with IPF have roughly a three-fold increased risk of acute coronary syndrome, which is a greater increase than you get from smoking," said Richard B. Hubbard, M.D., British Lung Foundation professor of epidemiology at the University of Nottingham and lead author of the study.
The study was published in the second issue for December of the American Thoracic Society's American Journal of Respiratory and Critical Care Medicine. . . .
Unfortunately, medical knowledge about IPF is limited. "We know that genetic factors play some role in IPF because it clusters in families in about 10 percent of cases-- and in a similar number of people there is evidence that environmental factors, such as exposure to metal dust at work and cigarette smoking may have a role," said Dr. Hubbard. "[But] studies from the U.S.A. and the U.K. suggest that IPF is becoming more common, and the reasons for this are unclear."
People with the deadly lung disease idiopathic pulmonary fibrosis (IPF) are three times more likely than people without the disease to suffer severe cardiac events such as a heart attack, according to a British study.
"If you look at them over time, people with IPF have roughly a threefold increased risk of acute coronary syndrome, which is a greater increase than you get from smoking," lead author Dr. Richard B. Hubbard, a professor of epidemiology at the University of Nottingham, said in an American Thoracic Society news release. . . .
The study was published in the second issue for December of the American Journal of Respiratory and Critical Care Medicine. . . .
"We know that genetic factors play some role in IPF, because it clusters in families in about 10 percent of cases, and in a similar number of people, there is evidence that environmental factors, such as exposure to metal dust at work and cigarette smoking may have a role,"
Chronic Obstructive Pulmonary Disease (COPD), a lung disease related to smoking, is one of the leading causes of chronic morbidity and mortality around the world. One goal in COPD research is the identification of biomarkers for early diagnosis of the disease. Here, we sought COPD-specific changes in the proteome from human lung tissue. This revealed increased levels of surfactant protein A (SP-A) in COPD but not in the normal or fibrotic lung. The results were confirmed by immunohistochemistry, morphometry and Western blotting. Furthermore, elevated SP-A protein levels were detected from the induced sputum supernatants of COPD patients. The levels of other surfactant proteins (SP-B, SP-C, SP-D) were not altered. Our results suggest that SP-A is linked to the pathogenesis of COPD and could be considered as a potential COPD biomarker.