ProtAffin AG Signs Manufacturing Contract for PA401 with CMC Biologics A/S

ProtAffin AG, a biotechnology company developing a novel class of
biopharmaceutical products that act by targeting cell-surface glycan structures,
today announced it has signed a manufacturing contract with CMC Biologics`
Danish operations, located in Copenhagen, Denmark for manufacture of its lead
product PA401 for the treatment of chronic obstructive pulmonary disease (COPD).
The contract will cover manufacture and supply of PA401 for preclinical
development and early clinical development in COPD and related respiratory
indications. PA401 is a glycan-binding decoy protein based on human chemokine
IL-8 (CXCL8), which has shown potent anti-inflammatory activity in both chronic
and acute preclinical models of lung inflammation. A composition of matter
patent covering PA401 has been granted in the USA and the EU.

ProtAffin`s novel class of biopharmaceutical products are first-in-class
engineered versions of human proteins which bind to cell surface glycans
(sugars) to affect their biological activity. Specific cell surface glycans
underlie inflammatory processes in several diseases including COPD, and
represent a rich and relatively under-investigated class of potential drug
targets for pharmaceutical and biotechnology companies. ProtAffin`s approach is
entirely innovative and opens up glycans as druggable targets through the use of
its CellJammer® discovery technology.

Dr. Andreas J Kungl, CSO of ProtAffin commented: “We are delighted to be working
with CMC Biologics A/S as our manufacturing partner for our first preclinical
product PA401. CMC have impressed us with their great expertise in process
development for early stage biopharmaceuticals, and their reputation for
customer service. Initiating manufacturing of PA401 to support preclinical and
early clinical development of PA401 is a major milestone for ProtAffin.”

David Kauffmann, Chairman of CMC Biologics, commented: “It is exciting to start
working with ProtAffin`s highly competent management and science team. We are
confident that this is the beginning of a long term relationship, and that
together our two companies will employ best and most timely manufacturing
solutions for development of ProtAffin`s lead product PA401″.

Notes to Editors:

About ProtAffin AG
ProtAffin is a European preclinical stage biotechnology company based in
Austria, developing protein-based products targeting inflammation and oncology.
Its novel class of biopharmaceuticals target heparin-like glycans (complex sugar
compounds) that drive inflammatory processes. ProtAffin has used its proprietary
CellJammer® discovery technology to develop a pipeline of preclinical
development candidates based on engineered human chemokine proteins. The
CellJammer® discovery technology has been successfully applied to a number of
chemokines, in addition to IL-8, central to inflammatory and autoimmune diseases
and is also applicable to many targets in the field of oncology.

Since 2007, the Company has raised over €18 million in venture capital from
Aescap Venture, Atlas Venture, SR One Ltd., Entrepreneurs Fund and Z-Cube Srl.
ProtAffin has also raised €2 million in non-dilutive financing in Austria. The
Company currently has 24 employees in Graz, Austria and Oxford, UK.

About PA401
ProtAffin`s lead anti-inflammatory product is PA401, a modified form of the
human chemokine IL-8. Human IL-8 (CXCL8) is a chemokine produced by macrophages
and other cells and its primary function is the induction of chemotaxis in
neutrophils. PA401 acts as a potent, targeted anti-inflammatory protein
preventing the infiltration of neutrophils which are a hallmark of many acute
and chronic respiratory diseases.

By binding to glycans that drive the infiltration of neutrophils in inflammation
with a higher affinity than wild-type IL-8, PA401 can prevent wild-type IL-8
from activating neutrophils and inhibit the events that would normally lead to
chronic lung inflammation. PA401 is in preclinical development for COPD and
related respiratory indications. A patent encompassing PA401 and other IL-8
variants was granted in the USA and EU in 2009. PA401 is a novel
biopharmaceutical product representing a very large commercial opportunity by
addressing the huge unmet medical need in respiratory diseases where chronic
neutrophilic infiltration is present, including COPD, cystic fibrosis, and
steroid-resistant asthma.

About Chronic Obstructive Pulmonary Disorder (COPD)
COPD is a chronic inflammatory disease characterised by airflow limitation that
is not fully reversible. The airflow limitation is usually both progressive and
associated with an abnormal inflammatory response of the lungs to noxious
particles or gases. It is typified by partially reversible obstruction of the
airways, with chronic bronchitis and/or emphysema, leading to a productive cough
and progressive difficulty in breathing. The disease affects about 60 million
people worldwide with more than 3 million people dying of the disease each year,
making it the 4th leading cause of death in the world. The number of affected
people is likely to increase in the next five years with the increased use of
tobacco, and increasing industrial pollution, especially in Asia-Pacific
countries.

Infiltration of neutrophils in the lung is one of the accepted hallmarks of
COPD, but this neutrophil infiltration is resistant to current therapies for
COPD, including inhaled corticosteroids. Interleukin-8 (IL-8) is accepted as one
of the most potent mediators of neutrophil infiltration in the lung and
targeting IL-8 or its receptors CXCR1 and CXCR2 is an approach under
investigation by a number of leading pharmaceutical companies for suppressing
the chronic lung inflammation seen in COPD. ProtAffin`s lead product PA401 is a
glycan-binding anti-inflammatory decoy version of human IL-8 and therefore
represents a promising new approach to reducing the IL-8 driven inflammation,
present in COPD.

About CMC Biologics A/S
CMC Biologics is a world leading company, in offering integrated services for
development and production of biopharmaceutical products. The Company
specializes in process development and large-scale manufacture of pharmaceutical
proteins, in compliance with the most stringent cGMP standards, for use in
preclinical studies, clinical trials and large-scale commercialization. CMC
Biologics offers a broad range of services, including the development of cell
lines, development of manufacturing processes, formulations, characterization
and analytical tests. CMC Biologics has manufacturing sites in Copenhagen,
Denmark and Seattle, Washington, USA.

For more information:
ProtAffin AG
Dr Jason Slingsby, Chief Executive Officer
T: +43 664 4187210
F: +43 316 382 541-4
E-mail: office@protaffin.com
www.protaffin.com
or
CMC Biologics
Mads Laustsen, Chief Executive Officer
Tel. +45 29488401
Email: ml@cmcbio.com
www.cmcbio.com
or
For media enquiries:
College Hill Life Sciences
Adam Michael, Dr Anastasios Koutsos
Tel: +44 20 7866 7861
Email: protaffin@collegehill.com
www.collegehill-lifesciences.com

Copyright Business Wire 2010

New effective strategy for treating tobacco addiction

Washington, May 12 (ANI): A group of researchers has developed a novel tea filter to treat cigarette addiction and have discovered the molecular mechanism behind the smoking cessation effect.

Professor Zhao Baolu and his group from the State Key Laboratory of Brain and Cognitive Science, Institute of Biophysics, Chinese Academy of Sciences identified theanine as the active ingredient in the tea filter that inhibits nicotine addiction.

Their work entitled “The cessation and detoxification effect of tea filters on cigarette smoke” was published in the X. edition Science of China in 2010.

Cigarette smoking has been linked to many life threatening diseases including heart disease, cancer and chronic obstructive pulmonary disease.

Many methods have been developed for smoking cessation by researchers and clinicians. Despite all efforts, currently available smoking cessation methods produce only modest success rates with frequent relapse. Due to the addictive nature of nicotine, quitting smoking remains an extremely difficult task. Therefore, the need for developing new smoking cessation strategies with better efficacy and fewer side effects is urgent.

Human tests using a newly developed tea filter were conducted at the Addiction Branch of Beijing Military Region General Hospital. A total of more than 100 male smokers participated in this study. The results from the first trial showed that the participants” average daily cigarette consumption decreased by about 43 percent and 56.5 percent after using the tea filters for 1 and 2 months, respectively. The results from the second trial showed that the participants” average daily cigarette consumption decreased by about 48 percent, 83 percent and 91 percent after using the tea filters for 1, 2 and 3 months, respectively.

The average daily cigarettes consumed by the participants decreased from about 24.5 per day to about 3 per day at the end of 3 months of treatment. In addition, most participants indicated that sputum and their smoking-related symptoms were reduced compared with the control group. Physical examinations of the participants did not reveal any apparent side effects.

The mechanism of action (MOA) studies indicated that theanine in the filter exerted an inhibitory effect similar to the nicotine acetylcholine receptor (nAChR) inhibitor. In addition, theanine could significantly inhibit the nicotine-induced increased expression of nAChR and the increase of the neurotransmitter dopamine (DA) released in mouse brains. The toxicological studies showed that the tea filters could significantly reduce the carcinogenic materials such as tar, free radicals, nitrosamine, benzo[a]pyrene, benzo[a]anthracene, chrysene and total polycyclic aromatic hydrocarbons (PAHs) generated in cigarette smoking. Animal studies also revealed that tea filters could significantly reduce the acute toxicity, mutagenicity, lung damage and carboxyhemoglobin (COHb) levels in the blood caused by cigarette smoking. (ANI)

Purple periwinkles may help fight inflammatory diseases

Washington, May 4 (ANI): Vinpocetine, a natural product derived from the periwinkle plant, can act as a novel anti-inflammatory agent that may one day be used for the treatment of chronic obstructive pulmonary disease, or COPD, as well as other inflammatory conditions, say scientists.

In the study published in the Proceedings of the National Academy of Sciences, researchers at the University of Rochester Medical Center were the first to find that vinpocetine acts as a potent anti-inflammatory agent when tested in a mouse model of lung inflammation, as well as several other types of human cells.

Results of the study show that vinpocetine greatly reduces inflammation, and, unlike steroids, does not cause severe side effects.

“What is extremely exciting and promising about these findings is vinpocetine”s excellent safety profile,” said Chen Yan, Ph.D., associate professor within the Aab Cardiovascular Research Institute at the Medical Center and a senior author of the study. “Previously, most drugs tested in this area have failed, not because of a lack of efficacy, but because of safety issues. We”re very encouraged by these results and believe vinpocetine has great potential for the treatment of COPD and other inflammatory diseases.”

Vinpocetine is a well-known natural product that was originally discovered nearly 30 years ago and is currently used as a dietary supplement for the prevention and treatment of cognitive disorders, such as stroke and memory loss, in Europe, Japan and China. (ANI)

Gene linked to lung cancer in non-smokers ‘identified’

Scientists have discovered what they claim is a common gene that raises the risk of developing lung cancer in non-smokers, a breakthrough which may pave the way for new targeted therapies for patients.

Despite several attempts to identify the specific genetic mechanisms responsible, the causes of lung cancer in “never-smokers” remain poorly understood.

Now, an international team, led by Mayo Clinic College of Medicine in New York, has identified the gene known as GPC5 which predisposes non-smokers to lung cancer, leading British newspaper ‘The Times’ reported.

In their research, the scientists, led by Ping Yang, examined DNA samples from 754 “never-smokers”, and analysed more than 300,000 DNA variants known as single nucleotide polymorphisms (SNP).

These were compared with samples from members of the public matched to patients by age, sex and ethnicity to show the genetic variations most likely to alter the risk of lung cancer in never-smokers.

The research also analysed possible links to lung cancer while controlling for history of chronic obstructive pulmonary disease, exposure to second-hand smoke, and family history of lung cancer.

Two specific genetic markers or SNPs emerged as significant. To validate their findings, the scientists took the 44 most frequently occurring genetic alterations from the research and assessed them in two additional independent groups of never smokers.

The two SNPs remained significant in both these replication sets, and further research backed the conclusion that they were associated with lung cancer in non-smokers through how they regulate the expression of the GPC5 gene.

Additional tests showed that GPC5 expression levels were 50 per cent lower in adenocarcinoma (the most common form of lung cancer) than in matched normal lung tissue, indicating that reduced GPC5 activity can be specific for adenocarcinoma in never smokers.

The findings have been published in the latest edition of ‘The Lancet Oncology’.

Blocking protein may prevent smoke-induced lung damage

London, March 19 (ANI): A new research has found that blocking a certain protein can reduce or prevent cigarette smoke-induced lung inflammation in mice.

Inflammation results in chronic obstructive pulmonary disease (COPD) and many other smoking-related ailments.

Cigarette smoke triggers the release of Granulocyte macrophage-colony stimulating factor (GM-CSF), which is linked to growth, activation and survival of leukocytes directly implicated in the pathogenesis of COPD.

It also causes activation and recruitment of more inflammatory cells into the lung, thereby perpetuating the inflammatory response and exacerbating ongoing inflammation.

These activated and recruited inflammatory cells also release proteases such as matrix metalloproteinase (MMP)-12, which destroy the lung tissue, resulting in emphysema.

The researchers from the University of Melbourne set out to determine whether blocking GM-CSF could reduce the inflammation and other deleterious effects of cigarette smoke exposure in mice.

They exposed a group of mice, half of which had been treated with a GM-CSF blocking agent, anti-GM-CSF, and half of which were controls, to the equivalent of nine cigarettes of smoke each day for four days. At the end of four days, the mice were killed and their lung tissue was examined for the presence of inflammatory cells.

Lead researcher on the study, Ross Vlahos, a senior research fellow with the lung disease research group at the University of Melbourne, said:

“We found that anti-GM-CSF strongly reduced the number of potentially harmful white blood cells that infiltrate the lung after smoke exposure, as well as inhibiting the pro-inflammatory cytokine tumor necrosis factor (TNF)-?, the chemokine macrophage inflammatory protein-2 (MIP-2), which coordinates the movement of white blood cells into the lung. It also inhibited the protease MMP-12, which is known as one of the main enzymes able to destroy lung tissue.

“Cigarette smoke-exposed mice that were treated with an anti-GM-CSF had significantly less lung inflammation in comparison to untreated mice. This indicates that GM-CSF is a key mediator in smoke-induced lung inflammation and its neutralization may have therapeutic implications in diseases such as COPD.”

He added: “Short-term models often translate into benefits in longer-term models. We still need to develop new methods and agents to test this idea long term and we also need to learn if it is effective in reversing longstanding disease.

Now, Dr. Vlahos plans to test whether GM-CSF could be a key target in other disease processes.

He concluded: “We want to understand exactly how blocking GM-CSF alters disease processes at the cellular and molecular levels so we can use this fine detail to make other treatments.

“Our treatment deals with cigarette smoke-induced lung inflammation involved in COPD, not cancer and other smoking-related ailments. Quitting remains the best and only cure for smoking-related lung disease.”

The study will soon be published in the American Thoracic Society”s American Journal of Respiratory and Critical Care Medicine. (ANI)

Action plan to phase out consumption of HCFC is on track: Ramesh

New Delhi, Sep 16 (ANI): Union Environment and Forest Minister Jairam Ramesh said on Wednesday that India has developed a comprehensive Road Map and Action Plan to phase-out of production and consumption of Hydrochlorofluorocarbons (HCFCs) in various sectors.

Addressing the gathering during the 15th International Ozone Day here Ramesh said: “The Government of India has taken a number of policy measures, fiscal and regulatory, to encourage the early adoption of alternative technologies in this area by existing and new enterprises.”

Ramesh hailed the Montreal Protocol as the most successful international treaty to ever achieve universal participation.

“At a time when the world is trying to solve the problem of climate change, the International Ozone Day provided a timely reminder of how international cooperation can help to solve major global environmental problems,” Ramesh added.

India is one of the first developing countries to join the Montreal Protocol and pledge its commitment to protect the Ozone Layer.

As a part of the accelerated phase-out of CFCs, India has completely phased out the production and consumption of CFCs as on 1 August 2008, 17 months prior to the agreed schedule.

Ramesh informed that over 97percent of controlled Ozone Depleting Substances (ODS) have been phased out by the Montreal Protocol.

“The end of 2009 will mark another significant milestone in the history of its implementation, with the use of potent ODSs -CFCs, Carbon Tetra Chloride (CTC) and Halons, except pharmaceutical-grade CFCs used in the manufacture of Metered Dose Inhalers (MDIs) – being ceased completely,” he said

The CFCs required for manufacturing for MDIs used by Asthma and Chronic Obstructive Pulmonary Disease (COPD) patients are still available in India, a national transition strategy to phase them out by 2013 is currently under implementation.

“The Ministry of Environment and Forests (MoEF), with support from the Global Environment Facility (GEF) and the World Bank recently also launched the India: Chiller Energy Efficiency Project to accelerate the conversion of CFC-based chillers using new, more energy efficient technologies,” Ramesh said.

This year’s theme for the ozone day was ‘Universal participation – Ozone protection unifies the World.’ (ANI)

New discovery may lead to improved therapies for lung disease

Washington, Sept 16 (ANI): Researchers at The University of Texas Health Science Centre at Houston have discovered a protein that appears to play a crucial role in development of chronic obstructive pulmonary disease (COPD).

The protein called osteopontin (OPN) could lead to a novel approach to the treatment of a devastating lung disease.

The research conducted on mice showed that genetically removing osteopontin could prevent COPD.

The mice without the protein had less inflammation and lung disease.

“The lack of osteopontin in the mice prevented the COPD features,” said Daniel Schneider, the study’s lead author and an M.D./Ph.D. candidate at the UT Health Science Center at Houston.

To understand the applicability of their findings to humans, the researchers analyzed the airways of people with COPD and found elevated levels of the protein.

“This is an important crossover study,” said Dr Michael Blackburn, the study’s senior author and professor in the Department of Biochemistry and Molecular Biology at The University of Texas Medical School at Houston.

“Because we can show osteopontin is elevated in people with COPD, this suggests that osteopontin could serve as both an indicator of disease progression and a therapeutic target,” he added.

The findings appear online in The FASEB Journal. (ANI)

New tool may help predict mortality risk in COPD patients

London, Aug 29 (ANI): Researchers have developed a new tool that would help predict a patient’s risk of dying from chronic obstructive pulmonary disease (COPD).

What’s more, it would also help determine the effective level of treatment.

Boffins have come up with an ADO index that can help physicians assess the severity of the illness.

Presently, the BODE index is used by chest physicians to estimate a patient’s risk of death from COPD. It assesses body-mass index, airflow obstruction, dyspnea and exercise capacity.

However, the BODE index is rarely used in primary care settings where most patient treatment options are managed, because exercise capacity cannot be easily measured in the typical doctor’s office.

“The burden from COPD is so enormous that we need to reach out to any doctors who care for COPD patients,” The Lancet quoted Dr Milo A. Puhan, associate professor in the Department of Epidemiology at the Johns Hopkins Bloomberg School of Public Health and lead author of the study.

“The ADO index can be used in any setting and we hope that it will serve as a basis for more individualized treatment selection in the near future,” Puhan added.

For the study, Puhan and colleagues developed a simplified BODE index and the ADO index, which included age, dyspnea and airflow obstruction.

The research team compared the predictions of the BODE index with the 3-year risk of all-cause mortality from 232 COPD patients from Switzerland.

The updated BODE index and the new ADO index were then validated with a cohort of 342 COPD patients from Spain.

The findings showed that updated BODE and ADO indices accurately predicted 3-year mortality compared to the original BODE index, which performed poorly at predicting 3-year risk of mortality. (ANI)

Superfood soy cuts smoker’s lung damage risk

Washington, June 26 (ANI): Smokers who eat large amounts of soy products are less likely to develop the smoking-associated lung disease COPD (Chronic Obstructive Pulmonary Disease), says a new study.

The research published in BioMed Central’s open access journal Respiratory Research has shown that consumption of a wide variety of soy products can be associated with a reduction in the risk of COPD and other respiratory symptoms.

To reach the conclusion, Dr. Fumi Hirayama and Professor Andy Lee from Curtin University of Technology, Australia, worked with a team of respiratory physicians to poll 300 patients with COPD from six Japanese hospitals and 340 age-matched control subjects from the same areas as the patients about their soy intake.

Hirayama said, “Soy consumption was found to be positively correlated with lung function and inversely associated with the risk of COPD. It has been suggested that flavonoids from soy foods act as an anti-inflammatory agent in the lung, and can protect against tobacco carcinogens for smokers. However, further research is needed to understand the underlying biological mechanism”.

Soy is a constituent of many foods, including tofu (soybean curd), natto (fermented soybeans), miso soup (fermented soybean paste), bean sprouts and soy milk.
t has been claimed that soy foods reduce cholesterol and can alleviate menopause symptoms.

COPD is characterized by progressive decline in lung function, and encompasses chronic bronchitis and emphysema. (ANI)

Women more prone to ill effects of smoking

Washington, May 19 (ANI): Women are more susceptible to smoking’s lung damaging effects than men, says a new study.

Inga-Cecilie Soerheim, M.D., and colleagues from Channing Laboratory, Brigham and Women’s Hospital and University of Bergen, Norway analyzed data from a Norwegian case-control study including 954 subjects with chronic obstructive pulmonary disease (COPD) and 955 controls.

All were current- or ex-smokers, and the COPD subjects had moderate or severe COPD.

“Overall our analysis indicated that women may be more vulnerable to the effects of smoking, which is something previously suspected but not proven,” said Dr. Soerheim.

The study results have been presented at the 105th International Conference of the American Thoracic Society in San Diego.

Examining the total study sample, there were no gender differences with respect to lung function (FEV1) and COPD severity, but the women were on average younger and had smoked significantly less than men.

To explore these differences further, they also analyzed two subgroups of the study sample: COPD subjects under the age of 60 (early onset group) and COPD subjects with less than 20 pack-years of smoking (low exposure group). In both subgroups, women had more severe disease and greater impairment of lung function than men.

“This means that female smokers in our study experienced reduced lung function at a lower level of smoking exposure and at an earlier age than men,” said Dr. Soerheim.

It has long been suspected that the effect of smoking on lung function may be modified by gender. Interaction analysis confirmed that being female represents a higher risk of reduced lung function and severe COPD, but this gender effect was most pronounced when the level of smoking exposure was low.

According to Dr. Soerheim, the reason why women may be more susceptible to the effects of cigarette smoke is still unknown, but there are several possible explanations: “Women have smaller airways; therefore each cigarette may do more harm. Also, there are gender differences in the metabolism of cigarette smoke. Genes and hormones could also be important.” (ANI)

Marijuana, ciggie smoke wreaks havoc on lungs

Washington, Apr 14 (ANI): People who smoke both tobacco and marijuana increase their risk of respiratory symptoms and chronic obstructive pulmonary disease (COPD), a new study has found.

Smoking only marijuana, however, was not associated with increased risks, the CMAJ study claimed.

The study, which surveyed 878 people aged 40 years or more in Vancouver, Canada, was part of the Burden of Obstructive Lung Disease (BOLD) Initiative that sought to determine the prevalence of COPD in adults over 40 years in the general population.
OPD is characterized by diseased lungs and narrowed airways and is associated with high mortality.

The researchers defined smokers as people who reported smoking at least 365 cigarettes in their lifetime, and a history of marijuana smoking as self-reporting of any previous smoking.

While tobacco smoking was associated with increased risk, smokers who reported using both tobacco and marijuana were 2.5 times more likely than nonsmokers to have respiratory symptoms and almost 3 times more likely to have COPD as defined by spirometric testing.

“We were able to detect a significant synergistic effect between marijuana smoking and tobacco smoking,” write Dr. Wan Tan of the University of British Columbia and St. Paul’s Hospital and coauthors.

“This effect suggests that smoking marijuana (at least in relatively low doses) may act as a primer, or sensitizer, in the airways to amplify the adverse effects of tobacco on respiratory health,” they added.

The researchers were limited by lack of data on the potential variations in marijuana potency, on differences in inhalation and the number of smokers who combine both substances in the same cigarette. (ANI)

More data regarding use of asthma drug Symbicort in younger children needed for approval: FDA

The Food and Drug Administration (FDA) has demanded more data from AstraZeneca Plc regarding its asthma drug Symbicort. The company is seeking approval for Symbicort for the long-term maintenance treatment of asthma in 6-11 year-olds.

Symbicort is already approved for patients aged 12 and over. Shares of the company slipped 1 percent after this decision of FDA. It is also approved for treating for chronic obstructive pulmonary disease, or COPD, in adults.

Food and Drug Administration (FDA) said AstraZeneca had not provided adequate data to establish the appropriate dose or doses of the drug’s two components — budesonide and formoterol — in this younger age group.

AstraZeneca said today that the FDA’s decision would have no impact on these existing patients or on children aged over 12 using it as a treatment for asthma.

Company officials said: “AstraZeneca is evaluating the CRL and will provide a response to the agency in due course.”

Supervised exercise therapy may help COPD patients

Washington, Apr 3 (ANI): Supervised exercise through pulmonary rehabilitation can help improve the condition of patients with chronic obstructive pulmonary disease (COPD), according to a study.

Richard Casaburi, at the Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center (LA BioMed), has found that supervised exercise can reduce the feelings of breathlessness, increase the tolerance for exercise, and improve quality of life in COPD patients.

Casaburi surveyed previous studies on pulmonary rehabilitation for COPD, and found that supervised exercise therapy improves aerobic function of the muscles, which helps reduce the breathlessness that is common in COPD.

“These findings are a clear indication that pulmonary rehabilitation can improve the quality of life for those living with COPD,” said Casaburi.

He added: “The studies also indicate that pulmonary rehabilitation results in decreased anxiety and depression for COPD patients because they find they can exercise more, and they enjoy the feeling that they have mastered something important in their lives.”

COPD is a group of lung diseases that includes chronic bronchitis and emphysema.

While the benefits of pulmonary rehabilitation programs for COPD are well documented, the study has reported that access to this type of therapy is limited, especially among lower-income, minority and rural populations.

Casaburi said: “A major stumbling block in providing pulmonary rehabilitation for COPD has been the lack of adequate funding for it. That should begin to change next January, when Medicare starts providing coverage for pulmonary rehabilitation for COPD.”

The study has been published in the New England Journal of Medicine. (ANI)

Genetic mutations may stunt kids’ lung development

Washington, Mar 27 (ANI): Scientists at the University of Pittsburgh Graduate School of Public Health and the German Research Center for Environmental Health have identified certain genetic mutations that may lead to poor lung development in children.

Poor lung development makes kids more vulnerable to diseases such as chronic obstructive pulmonary disease (COPD) later in life.

For the study, lead researchers Dr George Leikauf, and Dr Holger Schulz looked at a gene called superoxide dismutase 3 (SOD3), previously shown to protect the lungs from the effects of asbestos and oxidative stress.

They found that the presence of single nucleotide polymorphisms, or SNPs, variations in DNA sequences, in SOD3 that were linked to lung function in mice.

For further analysis, the researchers went on to assess SOD3 mutations in children ages 9 to 11 by testing for SNPs linked to lung function.

The researchers discovered two common SNPs associated with poorer lung function. One of these SNPs likely alters the expression levels of SOD3.

Lung function was tested with spirometry, which measures the amount and speed of exhaled air.

Previously, genetic variants in SOD3 have been associated with loss of lung function in COPD, which is mainly caused by cigarette smoking.

“We know SOD3 protects the lung against injury caused by chemicals in cigarette smoke, and it could be a link between childhood exposure to environmental tobacco smoke and poor lung development,” said Leikaf.

He said one day it might be possible to identify at-risk children and develop a medication that would foster optimal lung development.

The study appears online in Physiological Genomics. (ANI)

Genetics key to smokers’ lung disease risk

Washington, Mar 12 (ANI): It’s the genes that put some smokers at increased risk of developing chronic obstructive pulmonary disease (COPD) in later life, according to a study.

COPD is characterized by progressive decline in lung function, and encompasses chronic bronchitis and emphysema.

Around 90 percent of COPD is caused by long-term cigarette smoking, yet only 25 percent of chronic tobacco smokers go on to develop it.

For the study, US-based researchers Alireza Sadeghnejad, Jill Ohar, Eugene Bleecker and colleagues from the Wake Forest School of Medicine and Saint Louis University looked at a disintegrin and metalloprotease (ADAM) gene known as ADAM33 in 880 long-term heavy smokers.

ADAM33 is located on chromosome 20, and has been linked to asthma in previous studies.

The new study is unique in comparing long-term smokers with COPD versus a control group of long-term smokers without COPD.

And researchers found five single nucleotide polymorphisms (SNPs) – human DNA sequence variations – in ADAM33 that were more frequent in the COPD group than in the group of smokers without COPD. One SNP, known as S1, had a particularly strong link to lung abnormalities.

“Functional studies will be needed to evaluate the biologic significance of these polymorphisms in the pathogenesis of COPD,” said the authors.

The study has been published in BioMed Central’s open access journal Respiratory Research. (ANI)

Helium may be beneficial for lung patients

Washington, Mar 10 (ANI): Researchers from University of Calgary have suggested an innovative therapy to help patients with chronic obstructive pulmonary disease (COPD) breathe easier.

Lead researcher Neil Eves, PhD has found that patients who breathed a mix of 60pct helium and 40 pct oxygen during a rehabilitation program were able to exercise longer and harder than those who breathed normal air.

“COPD is not curable,” said Eves, a researcher with the Faculties of Kinesiology and Medicine.

“Our hope is that this research will help more individuals with COPD to realize the benefits of exercise,” he added.

Eves said he chose this specific gas mixture, because helium is a less dense gas that allows patients suffering with COPD to empty their damaged lungs better, while oxygen slows their breathing and further helps to reduce the shortness of breath these patients commonly suffer from.

During the study, individuals with COPD breathed either the helium/oxygen mix or air during cycling exercise.

While both groups improved their tolerance for exercise over a six-week rehabilitation program, the group that trained with helium could exercise significantly longer following rehabilitation than the control group.

“We are always interested in innovations that can help to improve the effectiveness of our health interventions,” said Dr. Sandra Delon, PhD, the director of Alberta Health Services’ Chronic Disease Management Program.

“We’ve already seen some promising results in this pilot program, so we’re very encouraged,” she added. (ANI)

Sunshine vitamin can protect against common cold

Washington, Feb 24 (ANI): Vitamin D a.k.a sunshine vitamin can protect people against common cold, a new study has found.

Investigators from the University of Colorado Denver (UC Denver) School of Medicine, Massachusetts General Hospital (MGH) and Children’s Hospital Boston found that people with the lowest blood vitamin D levels reported having significantly more recent colds or cases of the flu.

The risks were even higher for those with chronic respiratory disorders, such as asthma and emphysema. The report appears in the February 23 Archives of Internal Medicine.

“The findings of our study support an important role for vitamin D in prevention of common respiratory infections, such as colds and the flu,” says Adit Ginde, MD, MPH, UC Denver Division of Emergency Medicine and lead author of the study.

“Individuals with common lung diseases, such as asthma or emphysema, may be particularly susceptible to respiratory infections from vitamin D deficiency,” the expert added.

The study analyzed data from the Third National Health and Nutrition Examination Survey (NHANES III), conducted by the National Center for Health Statistics.
articipants were interviewed in their homes regarding their health and nutrition, and most participants also received a physical examination that included collection of blood and other samples for laboratory analysis.

The research team analyzed blood levels of 25-hydroxyvitamin D (25OHD) – the best measure of vitamin D status – from almost 19,000 adult and adolescent NHANES III participants, selected to be representative of the overall U.S. population.

Study participants with the lowest vitamin D blood levels – less than 10 ng per milliliter of blood – were about 40 percent more likely to report having a recent respiratory infection than were those with vitamin D levels of 30 or higher. The association was present in all seasons and even stronger among participants with a history of asthma or chronic obstructive pulmonary disease (COPD), including emphysema.

Asthma patients with the lowest vitamin D levels were five times more likely to have had a recent respiratory infection; while among COPD patients, respiratory infections were twice as common among those with vitamin D deficiency.

“A respiratory infection in someone with otherwise healthy lungs usually causes a few days of relatively mild symptoms,” explains Carlos Camargo, MD, DrPH, MGH Department of Emergency Medicine and senior author of the study.

“But respiratory infections in individuals with an underlying lung disease can cause serious attacks of asthma or COPD that may require urgent office visits, emergency department visits or hospitalizations. So the impact of preventing infections in these patients could be very large,” the expert added. (ANI)

Excessive weight loss should be seen as a wasting disease, says expert

Washington, January 22 (ANI): A Saint Louis University physician is concerned that doctors are not taking proper steps to pick up on problems with excessive weight loss, scientifically known as “cachexia”, pronounced kuh-kex-ee-uh.

“In sick people, weight loss is an important indicator of disease and potentially impending death,” said Dr. John Morley, an endocrinologist and director of the division of geriatric medicine at Saint Louis University School of Medicine.

“Cachexia is an extraordinary problem for people who are having other health problems, yet this is something that many physicians don’t pay attention to,” he added.

A group of physicians and scientists agreed on a definition of cachexia, published in the journal Clinical Nutrition recently.

“The definition is important because it gives physicians the guidelines to make a diagnosis and treat the condition. A definition of cachexia also makes it easier for scientists to conduct research and potentially develop new therapies for the problem,” Morley said.

He highlighted the fact that cochexia accompanies diseases like cancer, congestive heart failure, HIV, diabetes, kidney failure, and chronic obstructive pulmonary disease (COPD).

He suggests that people who traditionally have had difficulty taking off weight, and suddenly find the pounds melting off should, better beware because they may be ill, and could get even sicker as they become weaker and weaker.

“Cachexia should be seen as a wasting disease that requires specialized treatment from a physician who is familiar with the problem,” Morley said. (ANI)

Gene linked to reduced mortality from acute lung Injury identified

Washington, Jan 17 (ANI): Researchers at National Jewish Health and the University of Colorado Denver have identified a gene linked to improved survival among patients with acute lung injury.

Acute lung injury (ALI) is often caused by a respiratory infection and results in low oxygen levels in the blood, and fluid in the lungs.

“This discovery could benefit patients in two ways,” said James Crapo. MD, senior author and Professor of Medicine at National Jewish Health.

“By learning how this specific gene can alter the course of acute lung injury, we can gain insight into the biology of the disease, which could lead to better therapies.

“It also could become a tool in personalized medicine; by screening for this protective genotype and ones that make a person more susceptible to ALI, we can potentially tailor our treatment individual patients with respiratory infections and ALI to minimize the potential harm,” he added.

During the study, the researchers looked at the gene for extracellular superoxide dismutase (EC-SOD), a powerful antioxidant that has been associated with reduced lung injury in animal models, and better patient outcomes in chronic obstructive pulmonary disease.

The researchers then looked at the various forms of the EC-SOD gene in two groups of patients with infection-associated ALI.

They found that patients with a specific combination of four single nucleotide polymorphisms (SNPs), had an 75 percent reduced risk of being on a ventilator as all other ALI patients, and an 85 percent reduced risk of dying.

“This specific set of SNPs, which we call the GCCT haplotype, appears to reduce inflammation in the lung, thereby decreasing the severity of lung injury and ultimately protecting patients from mortality associated with ALI,” said John J. Arcaroli, PhD, first author and a post-doctoral fellow at the University of Colorado at Denver.

“Although We are not yet sure how these particular SNPs alter the action of the EC-SOD, these findings gives us a good starting point to learn more about possible protective mechanisms in ALI and other lung diseases,” he added.

The study appears in American Journal of Respiratory and Critical Care Medicine. (ANI)