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Smokers fuel prediction of steep rise in lung disease 

DUBAI // The prevalence of a progressive and irreversible lung disease is increasing rapidly.

Chronic obstructive pulmonary disease (COPD) affects 4 per cent of the Abu Dhabi population, according to a study by UAE University, Zayed Military Hospital and the Emirates Allergy and Respiratory Society (Ears).

Worldwide, the disease, caused mainly by smoking and characterised by severely restricted breathing as a result of lung damage and inflammation, affects between 2 and 9 per cent of the population, placing Abu Dhabi slightly below the average.

However, with smokers making up nearly a quarter of the adult population in the emirate, experts project that the prevalence of COPD could increase to 7 per cent in the next five years.

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Smokers prone to lung deterioration  

If you smoke and remain in the basement most of the time, or near an area with compost materials, there are more chances of lung deterioration following Chronic Obstructive Pulmonary Disorder (COPD). There exists a fungus that can worsen the condition of patients suffering from COPD.

The relation of smoking with fungus has been established for the first time in medical literature by a PGI doctor.

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• Rapidly spreading COPD threatens to snuff out smokers’ lives 

DUBAI: While there are ways, experts aver, to control the spread of most chronic diseases, the incidence of Chronic Obstructive Pulmonary Disease (COPD) is threatening to rapidly increase in the UAE, with four per cent of the Abu Dhabi population already afflicted by the disease, a recent study reveals.

The research has been carried out by Dr Ashraf H Alzaabi, Chair and Clinical Assistant Professor at the UAE University, and Head of Respiratory Division at Zayed Military Hospital.

Another study on COPD is being conducted by Emirates Allergy and Respiratory Society (EARS) to cover the whole of the GCC region, details of which are soon expected to be out.

Dr Mirza Ali Al Sayegh, president of EARS, said that COPD is an under-diagnosed, life-threatening lung disease.

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Soda Linked to Lung Disease  

Action Points

People who consumed at least a half a liter of soft drinks a day were more than twice as likely to develop either asthma or chronic obstructive pulmonary disease (COPD), compared with those who didn't partake at all.

Point out that the study design was cross-sectional study and therefore could not prove causality.

More bad news for soda lovers: in addition to obesity and heart disease, the sugary drinks may be tied to asthma and chronic obstructive pulmonary disease (COPD), Australian researchers found.

People who consumed at least a half a liter of soft drinks a day were more than twice as likely to develop either lung condition compared with those who didn't partake at all (OR 2.33, 95% CI 1.51 to 3.60), Zumin Shi, MD, of the University of Adelaide in Australia, and colleagues reported in Respirology.

The cross-sectional study, however, couldn't prove causality, and researchers not involved in the study suspect an overall unhealthy diet effect might be at play.

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Soft Drinks May Raise Odds for Respiratory Ills: Study 

Drinking a lot of soft drinks may increase the risk for asthma and/or chronic obstructive pulmonary disease (COPD), a new study suggests.

Nearly 17,000 people aged 16 and older in South Australia were asked about their consumption of soft drinks such as Coke, flavored mineral water, lemonade, Powerade and Gatorade. . . .

Smoking increased the risk even further, especially for COPD. People who smoked and consumed more than half a liter of soft drinks a day had a 6.6 times greater risk of COPD than those who didn't smoke and didn't consume soft drinks.

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Coughing and other respiratory symptoms improve within weeks of smoking cessation 

If the proven long-term benefits of smoking cessation are not enough to motivate young adults to stop smoking, a new study shows that 18- to 24-year olds who stop smoking for at least two weeks report substantially fewer respiratory symptoms, especially coughing. The study findings are detailed in Pediatric Allergy, Immunology, and Pulmonology.

Karen Calabro, DrPH and Alexander Prokhorov, MD, PhD, The University of Texas MD Anderson Cancer Center, Houston, compared self-reported respiratory symptoms among two groups of college students who participated in programs designed to motivate them to stop smoking. One group achieved smoking cessation for two weeks or longer and the other group failed to stop smoking. More than half of the students smoked 5-10 cigarettes a day and had smoked for 1-5 years.

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LETTER: Encourage butting out 

Re: Stop forcing no smoking, Feb. 1.

I think the majority of the Ottawa public are fed up with second-hand smoke and want the city to update and expand its smoke-free indoor bylaw, to include outdoor spaces.

This is indeed a big issue. . . .

I'm 61 years old, living with chronic obstructive pulmonary disease, with only 12-per-cent lung capacity left, and am waiting on a lung transplant waiting list for donor lungs, to be able to breathe.

I'm on supplemental oxygen therapy at a two-and-a-half flow rate with additional corticosteroid and bronchodilator medication.

Most smokers want to quit. Smoke-free spaces encourage them to quit. I'm looking forward to a smoke-free Ottawa.

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Respiratory Symptoms After Smoking Cessation among College Students  

Data on respiratory symptoms after smoking cessation are available for mature adults, but for young adults these data are limited to observational studies. This retrospective analysis of smoking cessation trials addresses the gap. A cohort of 18- to 24-year-olds without chronic respiratory illness was developed from 2 randomized trials of behavioral interventions versus standard care to promote smoking cessation. This secondary analysis was performed to determine whether short-term respiratory health improvements occurred among those who achieved smoking cessation for 2 weeks or more. Self-reported respiratory symptoms were assessed at baseline and last follow-up. The sample numbered 327, 60% smoked 5–10 cigarettes a day and 56% smoked for 1–5 years. Abstinence periods among those achieving cessation ranged from 2 to 78 weeks. The mean overall baseline respiratory symptom score was 14.3, standard deviation (SD)=11.5. Respiratory symptoms for those achieving cessation were mean=13.3, SD=11.2, decreasing to mean=3.8, SD=5.9 symptom days at the last follow-up. Baseline symptoms for those who continued smoking were mean=14.6, SD=11.6, decreasing to mean=10.3, SD=10.3 at follow-up. Five fewer respiratory symptom days per week were noted for those who stopped smoking (mean=5.2, SD=1.5, P<0.0001). Smoking cessation is associated with reduced respiratory symptoms. Feedback of short-term health consequences may be relevant to younger populations who may perceive smoking hazards as in the distant future.

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• Coughing and other respiratory symptoms improve within weeks of smoking cessation 

a new study shows that 18- to 24-year olds who stop smoking for at least two weeks report substantially fewer respiratory symptoms, especially coughing. The study findings are detailed in Pediatric Allergy, Immunology, and Pulmonology, a peer-reviewed journal published by Mary Ann Liebert, Inc.

Karen Calabro, DrPH and Alexander Prokhorov, MD, PhD, The University of Texas MD Anderson Cancer Center, Houston, compared self-reported respiratory symptoms among two groups of college students who participated in programs designed to motivate them to stop smoking. One group achieved smoking cessation for two weeks or longer and the other group failed to stop smoking. More than half of the students smoked 5-10 cigarettes a day and had smoked for 1-5 years.

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COPD Clinical Trials 

Your search returned 115 studies:

Emphysema/COPD (Chronic Obstructive Pulmonary Disease) - Multiple Locations in the US

COPD (Chronic Obstructive Pulmonary Disorder) - Multiple Locations in the US

COPD (Chronic Obstructive Pulmonary Disease) - Birmingham AL

COPD (Chronic Obstructive Pulmonary Disease) - DeLand FL

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Smoke-Activated Cells Ravage Lungs in Emphysema  

Action Points

* Explain that the destruction of lung tissue in emphysema was mediated by antigen-presenting cells (APCs) that were activated by the smoke.

* Point out that transfer of lung APCs from mice with emphysema showed that this population was capable of transferring disease even in the absence of tobacco smoke exposure, a process dependent on IL-17A expression.

The destruction of lung tissue in emphysema was mediated by antigen-presenting cells (APCs) that were activated by the smoke, according to an experimental study.

Four months of active smoke exposure in a chamber that mimicked smoking habits in humans significantly increased dendritic cells and neutrophils compared with controls. The exposed mice also showed significant increases in lung volume (417 ± 8 mm3 air-exposed mice versus 500 ± 9 mm3 smoke-exposed) and decreases in density (-428 ± 9 HU versus -478 ± 7 HU, P<0.05) reported Farrah Kheradmand, MD, from the Baylor College of Medicine in Houston, and colleagues, in Science Translational Medicine.

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Smoke-Activated Cells Ravage Lungs in Emphysema 

Action Points

* Explain that the destruction of lung tissue in emphysema was mediated by antigen-presenting cells (APCs) that were activated by the smoke.

* Point out that transfer of lung APCs from mice with emphysema showed that this population was capable of transferring disease even in the absence of tobacco smoke exposure, a process dependent on IL-17A expression.

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The pathogenesis of COPD and IPF: distinct horns of the same devil? 

New paradigms have been recently proposed in the pathogenesis of both chronic obstructive pulmonary disease (COPD) and idiopathic pulmonary fibrosis (IPF), evidencing surprising similarities between these deadly diseases, despite their obvious clinical, radiological and pathologic differences. There is growing evidence supporting a "double hit" pathogenic model where in both COPD and IPF the cumulative action of an accelerated senescence of pulmonary parenchyma (determined by either telomere dysfunction and/or a variety of genetic predisposing factors), and the noxious activity of cigarette smoke-induced oxidative damage are able to severely compromise the regenerative potential of two pulmonary precursor cell compartments (alveolar epithelial precursors in IPF, mesenchymal precursor cells in COPD/emphysema). The consequent divergent derangement of signalling pathways involved in lung tissue renewal (mainly Wnt and Notch), can eventually lead to the distinct abnormal tissue remodelling and functional impairment that characterise the alveolar parenchyma in these diseases (irreversible fibrosis and bronchiolar honeycombing in IPF, emphysema and airway chronic inflammation in COPD).

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Cigarette Smoke Induction of Osteopontin (SPP1) Mediates TH17 Inflammation in Human and Experimental Emphysema 

We have shown that CD1a+ antigen-presenting cells (APCs) from lungs of patients with emphysema can induce autoreactive T helper 1 (TH1) and TH17 cells. Similarly, the canonical cytokines interferon-γ (IFN-γ) and interleukin-17A (IL-17A) are specifically linked to lung destruction in smokers, but how smoke activates APCs to mediate emphysema remains unknown. Here, we show that, in addition to increasing IFN-γ expression, cigarette smoke increased the expression of IL-17A in both CD4+ and γδ T cells from mouse lung. IL-17A deficiency resulted in attenuation of, whereas lack of γδ T cells exacerbated, smoke-induced emphysema in mice. Adoptive transfer of lung APCs isolated from mice with emphysema revealed that this cell population was capable of transferring disease even in the absence of active smoke exposure, a process that was dependent on IL-17A expression. Spp1 (the gene for osteopontin) was highly expressed in the pathogenic lung APCs of smoke-exposed mice and was required for the TH17 responses and emphysema in vivo, in part through its inhibition of the expression of the transcription factor Irf7. Thus, the Spp1-Irf7 axis is critical for induction of pathological TH17 responses, revealing a major mechanism by which smoke activates lung APCs to induce emphysema and identifying a pathway that could be targeted for therapeutic purposes.

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Study Maps Path From Smoking to Emphysema in Mice 

Smoking activates certain genes and portions of the immune system, which in turn causes inflammation that leads to emphysema.

So say researchers who mapped the destructive path from smoking to the debilitating lung disease in mice.

"Previously, emphysema was thought to be a nonspecific injurious response to long-term smoke exposure," study author Dr. Farrah Kheradmand, a professor of medicine and immunology at Baylor College of Medicine, said in a college news release. "These studies show for the first time that emphysema is caused by a specific immune response induced by smoke."

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