Log In to The Paramus Post - Greater Paramus News and Lifestyle Webzine

Please enter your user name and password below.

No Account Yet? Sign Up!

The Paramus Post - Greater Paramus News and Lifestyle Webzine
Saturday, December 05 2020 @ 08:26 PM EST
Advertisement
The Paramus Post - Greater Paramus News and Lifestyle Webzine
Saturday, December 05 2020 @ 08:26 PM EST
Advertisement
The Paramus Post - Greater Paramus News and Lifestyle Webzine

April 27: Local Internist and Pulmonologist to Present COPD Seminar at Heritage Pointe of Teaneck


Informative Lecture Made Possible by Recent Medical Alliance with Rental Retirement Community

Dr. Glenn Brauntuch, an Englewood-based internist and pulmonologist, will present an educational seminar on chronic obstructive pulmonary disease (COPD) at Heritage Pointe of Teaneck on Tuesday, April 27, at 2 p.m. The event is free and open to the public.

Breathing problems such as asthma and COPD often arise in older adults, especially those with a history of smoking. COPD is one of the most common lung diseases, which often makes for difficultly breathing.
Symptoms of COPD include cough with mucus, shortness of breath that gets worse with mild activity, fatigue, frequent respiratory infections and wheezing. As the symptoms of COPD develop slowly, some people may be unaware that they are sick.

Brauntuch, who is a specialist in COPD, asthma and lung cancer, will present this information and more, including testing and prevention, during the program. The event is made possible by a recent alliance between the full-service rental retirement community and area physicians. As a result of the relationship, Brauntuch and other area physicians provide medical services to Heritage Pointe residents.

Heritage Pointe of Teaneck is located at 600 Frank W. Burr Blvd. in Teaneck, N.J. For more information or to RSVP for this event, contact Heritage Pointe at (201) 836-9260, or visit www.RetireAtHeritage.com.
Advertisement
Advertisement

Share It!

Comments are closed

harleyrider1978

Thursday, April 15 2010 @ 07:50 PM EDT
http://www.6minutes.com.au/articles/z1/view.asp?id=515462

Childhood asthma rather than a history of smoking appears to be the main risk factor for developing COPD in later life, New Zealand researchers have found.



A diagnosis of asthma in childhood conferred the same risk as 60 pack years of smoking, a study by Dr Philippa Shirtcliffe and Professor Richard Beasley of the Medical Research Institute of New Zealand in Wellington suggests.



In a study of almost 750 people they found that the risk of COPD as defined using GOLD guidelines, (post-bronchodilator FEV1/FVC ratio <0.7), was increased in smokers by 30% for every 10 pack years of smoking.



However, they also found that childhood asthma showed with the strongest association for COPD, equivalent to adding about 20 years to lung age.



The researchers say their findings support the so-called ‘Dutch hypothesis’ that asthma and COPD share common origins and should be considered as points on a common disease continuum, at least in some patients.



“The findings of this analysis … challenge the dogma that the vast majority of cases of GOLD-defined COPD are due to smoking,” they write in the Internal Medicine Journal (April 12).



They note that there have been several other studies showing that childhood asthma is a risk factor for COPD, and they suggest that “these findings highlight the inadequacy of current definitions and the need to review the taxonomy for the disorders of airways obstruction.”

harleyrider1978

Thursday, April 15 2010 @ 07:54 PM EDT
Adenoviruses Cause COPD
It has always been obvious merely from looking at the scatter plots in old studies of lung function that, among both smokers and nonsmokers, certain individuals were distinctly abnormal. They had much higher rates of loss than the others. There was a higher proportion of abnormal individuals among the smokers, and, by ignoring these individual differences and lumping together all smokers versus all nonsmokers, the anti-smoking ideologues falsely implicated tobacco as the cause of chronic obstructive pulmonary disease (COPD).

COPD IS A SYSTEMIC, NOT LOCAL, DISEASE
Mitochondrial Abnormalities in COPD include tissues with no exposure to cigarette smoke

Systemic effects of COPD. M Decramer, F De Benedetto, A Del Ponte, S Marinari. Respir Med 2005 Dec;99 Suppl B:S3-10. "Chronic obstructive pulmonary disease (COPD) is characterised by a range of pathological changes of the respiratory system, including airflow limitation secondary to structural changes of the small airways and loss of alveolar attachments, inflammation, ciliary dysfunction, and increased mucous production. COPD also has significant systemic consequences.... Although improving lung function and disease symptoms have been the main focus of COPD management, these parameters alone do not reflect the full burden of disease. More recent endeavours have highlighted the potential role of addressing physical limitations imposed by systemic alterations. It is evident that systemic manifestations are common in COPD. Indeed, many patients demonstrate a gradual and significant weight loss that exacerbates the course and prognosis of disease. This weight loss is often accompanied by peripheral muscle dysfunction and weakness, which markedly contribute to exercise limitation and impaired quality of life."


Decramer - Respir Med 2005 abstract / PubMed

Reduced mitochondrial density in the vastus lateralis muscle of patients with COPD. HR Gosker, MK Hesselink, H Duimel, KA Ward, AM Schols. Eur Respir J 2007 Jul;30(1):73-79. "Mitochondrial number (0.34 versus 0.63 n.microm(-2)) and fractional area (1.95 versus 4.25%) were reduced in the vastus of COPD patients compared with controls."


Gosker / Eur Respir J 2007 full article

E1A oncogene enhancement of caspase-2-mediated mitochondrial injury sensitizes cells to macrophage nitric oxide-induced apoptosis. JR Radke, ZK Siddiqui, TA Miura, JM Routes, JL Cook. J Immunol 2008 Jun 15;180(12):8272-8279. "E1A expression did block cellular recovery from NO-induced mitochondrial injury and converted the reversible, NO-induced cytostasis response of cells to an apoptotic response. This viral oncogene-induced phenotypic conversion of the cellular injury response of mouse and human cells was mediated by an E1A-related increase in NO-induced activation of caspase-2, an apical initiator of intrinsic apoptosis. Blocking caspase-2 activation or expression eliminated the NO-induced apoptotic response of E1A-positive cells."


Radke - J Immunol 2008 abstract / PubMed

Abnormal mitochondrial function in locomotor and respiratory muscles of COPD patients. L Puente-Maestu, J Pérez-Parra, R Godoy, N Moreno, A Tejedor, F González-Aragoneses, JL Bravo, FV Alvarez, S Camaño, A Agustí. Eur Respir J 2009 May;33(5):1045-1052. "Skeletal muscle mitochondria of patients with chronic obstructive pulmonary disease show electron transport chain blockade and excessive production of reactive oxygen species. The concurrent involvement of both vastus lateralis and external intercostalis suggests a systemic (rather than a local) mechanism(s) already occurring in relatively early stages (Global Initiative for Chronic Obstructive Lung Disease stage II) of the disease."


Puente-Maestu - Eur Respir J 2009 abstract / PubMed

Adenovirus Infection in COPD

Latent adenoviral infection in the pathogenesis of chronic airways obstruction. T Matsuse, S Hayashi, K Kuwano, H Keunecke, WA Jefferies, JC Hogg. Am Rev Respir Dis 1992 Jul;146(1):177-184. The American Review of Respiratory Disease and its successor, the American Review of Critical Care Medicine, is the organ of the American Thoracic Society, which was formed as a division of the American Lung Association.

Matsuse - Am Rev Respir Dis 1992 abstract / PubMed
Endotoxin-specific NF-kappa-B activation in pulmonary epithelial cells harboring adenovirus E1A. N Keicho, Y Higashimoto, GP Bondy, WM Elliot, JC Hogg, S Hayashi. Am J Physiol 1999;277(Lung Cell Mol Physiol 21):L523-L532. "Studies from our laboratory showed that greater copy numbers of the E1A DNA from Group C adenovirus are found in the lungs of smokers with chronic obstructive pulmonary disease than in smokers without airways obstruction and that E1A proteins are detected in lung epithelial cells of these patients."

Keicho / Am J Physiol 1999 full article
Effect of adenovirus E1A on ICAM-1 promoter activity in human alveolar and bronchial epithelial cells. Y Higashimoto, N Keicho, WM Elliot, JC Hogg, S Hayashi. Gene Expr 1999;8(5-6):287-297. "Because adenovirus E1A gene products are known to regulate the expression of many genes by interacting with cellular transcription factors, we postulated that E1A enhances the production of inflammatory mediators and exacerbates the inflammatory process in smokers' lungs." This is pure Political Correctness, because contrary to the lies we've been brainwashed with, most smokers don't have any such "inflammatory process" and some nonsmokers do.

Higashimoto - Gene Expr 1999 abstract / PubMed
New treatments proposed for chronic obstructive pulmonary disease. Lisa Melton, The Lancet Interactive 2000 Feb 5. "James Hogg (St. Paul's Hospital, Vancouver, Canada) believes that, in patients with COPD, latent adenoviral infection might amplify the inflammation that cigarettes trigger in all smokers. His team has detected large amounts of an adenoviral protein in lung samples from patients with COPD, localised to areas of inflammation and emphysema."

The Lancet Interactive 2000 Feb 5 / findarticles.com
Amplification of inflammation in emphysema and its association with latent adenoviral infection. I Retamales, WM Elliott, B Meshi, HO Coxson, PD Pare, FC Sciurba, RM Rogers, S Hayashi, JC Hogg. Am J Respir Crit Care Med 2001 Aug 1;164(3):469-473. These charlatans compare "patients with similar smoking histories and either no (n=7), mild (n=7), or severe emphysema (n=7), and illogically conclude that "cigarette smoke-induced lung inflammation [which most smokers don't have -cast] is amplified in severe emphysema and that latent expression of the adenoviral E1A protein expressed by alveolar epithelial cells influenced this amplification process."

Retamales - Am J Respir Crit Care Med 2001 abstract / PubMed
Retamales - Am J Respir Crit Care Med 2001 Full Article
(Comment on Retamales et al.) End-stage chronic obstructive pulmonary disease: the cigarette is burned out but inflammation rages on. SD Shapiro. Am J Respir Crit Care Med 2001 Aug 1;164(3):339-340.

Shapiro - Am J Respir Crit Care Med 2001 abstract / PubMed
Shapiro - Am J Respir Crit Care Med 2001 Full Article
[Latent adenovirus infection in chronic obstructive pulmonary disease.] B He, M Zhao, X Li. Zhonghua Jie He He Hu Xi Za Zhi 2001 Sep;24(9):520-523. "The E1A region of adenovirus was found in the epithelial cells of COPD and chronic bronchitis patients (27%), not found in the patients with asthma and normal volunteers. Furthermore, E1A DNA was much more commonly in the COPD patients (50%) than in the patients with chronic bronchitis (8%) (P<0.05). CONCLUSIONS: Latent adenoviral infection was present in the stable stage of COPD and may be related to the pathogenesis of the disease."

He - Zhonghua Jie He He Hu Xi Za Zhi 2001 abstract / PubMed
Role of latent viral infections in chronic obstructive pulmonary disease and asthma. JC Hogg. Am J Respir Crit Care Med 2001 Nov 15;164(10 Pt 2):S71-S75. A propaganda study with guinea pigs. Quoth Hogg: "Acute viral respiratory tract infections are well known to precipitate asthma attacks and acute exacerbations of chronic obstructive pulmonary disease, but their role in the pathogenesis of chronic disease is poorly designed." And why is this this case, Dr. Hogg? Haven't you and your ATS cronies known about the disintegrating effects of adenoviruses since the 1950s? And purposely stifled the research so you could blame smoking?

Hogg - Am J Respir Crit Care Med 2001 abstract / PubMed
Hogg - Am J Respir Crit Care Med 2001 Full Article
Emphysematous lung destruction by cigarette smoke. The effects of latent adenoviral infection on the lung inflammatory response. B Meshi, TZ Vitalis, D Ionescu, WM Elliot, C Liu, XD Wang, S Hyashi, JC Hogg. Am J Respir Cell Mol Biol 2002 Jan;26(1):52-57. Another rehash of Hogg's guinea pig study. Another question: Why does it seem as if James C. Hogg and his friends are the only ones allowed to investigate and/or publish on this subject, at least in the western literature?

Meshi - Am J Respir Cell Mol Biol 2002 abstract / PubMed
Meshi - Am J Respir Cell Mol Biol 2002 Full Article
COPD Prevalence in Lifetime Nonsmokers
While admitting that COPD occurs in only "15-20% of heavy, long-term cigarette smokers," they fail to acknowledge that 4 to 6% of lifelong nonsmokers have physician-diagnosed COPD as well (Chronic obstructive pulmonary disease in lifelong nonsmokers: results from NHANES. AS Whittemore, SA Perlin, Y DiCiccio. Am J Public Health 1995 May;85(5):702-706), with COPD defined as chronic bronchitis or emphysema. The lie the health establishment has been pounding into us for decades that COPD is "vanishingly rare" in lifelong nonsmokers is explicitly rejected by Whittemore et al. While spin-doctoring their work with the specious reservation that it failed to measure exposure to environmental tobacco smoke, they nevertheless admit that "Despite these reservations, some conclusions seem warranted. In particular, the disease is not vanishingly rare in nonsmokers. The overall prevalence in [never-smoking] adults aged 18 to 74 is about 4% to 6%."

Whittemore - Am J Public Health 1995 full article / PubMed Central

Airway obstruction in never smokers: results from the Third National Health and Nutrition Examination Survey. BR Celli, RJ Halbert, RJ Nordyke, B Schau. Am J Med 2005 Dec;118(12):1364-1372. "Never smokers represented 42% of the Third National Health and Nutrition Examination Survey population aged 30 to 80 years, with obstruction prevalence of 91 per 1000. Never smokers accounted for 4.56 million cases of obstruction, or 23% of the total burden."


Celli - Am J Med 2005 abstract / PubMed

COPD and Social Class
It has long been known that adenovirus infection is more common in the lower socioeconomic classes, just as Whittemore et al. found in their study of lifelong nonsmokers, where the percentages of physician-diagnosed COPD by income ranged from 2.7% to 5.6% in men, and 3.8% to 6.9% among women. Since smokers are more likely to be from the lower socioeconomic classes, smokers are more likely to be exposed to this infection. Exposure to infection, not ETS, is the most important confounder, and socioeconomic class is only an inadequate proxy for this true confounder. Furthermore, it has been known since 1962 that certain strains of adenovirus, notably Ad12, are known to be carcinogenic in animals, and the main difference between the carcinogenic and noncarcinogenic strains is in their ability to escape immune detection to cause a chronic infection. It has also long been known that adenoviruses interact with other oncogenic viruses, inlcuding polyoma, papilloma, and hepatitis viruses. The health establishment has purposely eschewed research of the appropriate level of sophistication in order to falsely blame smoking and passive smoking.

Advertisement
Advertisement
Advertisement
Advertisement
Trinity Presbyterian Church
Join the purpose driven church exercising faith, hope, and love because nothing else matters...
www.TrinityFamily.org
StoneMicro Web Technologies
Dynamic Website Development, Content Management System, Blogs, Web design, Web hosting services
www.StoneMicro.com
Sponsor ParamusPost