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Causes of Erectile Dysfunction (ED)
Often abbreviated as ED, erectile dysfunction is a consistent or reoccurring inability to obtain or maintain an erection satisfactory for sexual performance. It affects an estimated 30 million men in the United States. Erectile dysfunction is occurs frequently in men with diabetes, high blood pressure, high cholesterol, heart disease, vascular disease, neurological diseases and other major illnesses and disorders.
Psychological factors include stress, anxiety, depression and relationship problems. Lifestyle risk factors include obesity, lack of physical activity, smoking and excessive alcohol consumption. Other contributing factors include various prescribed medications. Studies have shown that men who suffer from erectile dysfunction were twice as likely to have diabetes as compared to healthy, unaffected men.
Erectile Dysfunction (ED) and Other Health Risks
Research has shown recently that erectile dysfunction can be an early warning symptom of important diabetes and cardiovascular problems. Erectile dysfunction predicts and precedes the metabolic syndrome several years in advances. Similarly erectile dysfunction predicts and precedes a heart attack 3 years in advance. Such new information affords a great warning for middle aged men to go to the doctor and get the appropriate evaluation. Furthermore, sexual health becomes the portal to men’s health motivating men to pursue healthy lifestyle such as weight control, physical exercise, quitting smoking and controlling alcohol.
Read more information on site: http://www.drridwan.com/urology-health-issues/erectile-dysfunction.php.
In Vivo Studies
Cigarette Smoke Up-regulates CLCA1 and EGFR mRNA and Protein Expressions and MUC5AC mRNA Expression in Rats: In the nonsmoking group, CLCA1, EGFR, and MUC5AC mRNA expressions were constitutively expressed in rat lung and trachea. The smoke-exposed group showed significant up-regulation of all the three mRNA expressions from day 21 onwards (p < 0.001) [Fig 1]. This effect was stronger in the trachea than in the lung. Similarly, the protein expressions of CLCA1 and both resting EGFR and activated pEGFR were significantly increased on day 28 (p < 0.001) [Fig 2].
Niflumic Acid, AG-1478, or Both Inhibit the Cigarette Smoke-Induced MUC5AC Gene Expression: Niflumic acid is a blocker of the CLCAs, and AG-1478 is an inhibitor of EGFR tyrosine kinase. In the smoke-exposed treatment group, niflumic acid, AG-1478, or both significantly inhibited the upreglation of MUC5AC mRNA expression (p < 0.001) without affecting the upregulation of CLCA1 and EGFR mRNAs. Combining both drugs did not show a significant synergistic effect on MUC5AC mRNA expression (Fig 3). On the protein level, neither niflumic acid, AG-1478, nor both could inhibit the upregulation of CLCA1 protein by cigarette smoke. However, EGFR upregulation was partially inhibited by AG-1478, while pEGFR expression was abolished by it (p < 0.001). Niflumic acid had no effect on the protein expressions of EGFR and pEGFR (Fig 2). Continue reading “Canadian Health&Care Mall: Outcomes of Niflumic Acid and AG-1478 Reduce Cigarette Smoke-Induced Mucin Synthesis”
Although the idea of reducing tobacco toxin exposure among continuing smokers is not a new concept, recent efforts by the tobacco industry to develop and market potential reduced-exposure products have resulted in an increased interest in examining this approach. The escalating introduction of potential reduced-exposure products has prompted the US Food and Drug Administration to sponsor a report from the Institute of Medicine and for the National Cancer Institute to convene an expert panel to consider the feasibility of this approach, the necessary science and systems that need to be in place in order to ensure public health, and the specific research areas that will need to be pursued. The identification of reliable and valid biomarkers for tobacco toxin exposure was determined to be a particularly important area of research.
Biomarkers can be considered as measures of the following: (1) toxins specifically related to exposure of tobacco constituents, such as nicotine or tobacco-specific nitrosamines; (2) risk contributors to disease, such as lipoproteins, C-reactive protein, WBC count; (3) disease markers such as pulmonary function; or (4) clinical outcome measures, such as hospitalizations, occurrence of disease, or death. Smokers compared to nonsmokers have significantly elevated risk factors for cardiovascular disease (CVD), and these risk factors improve among smokers after cessation of cigarettes. To date, few studies have examined the effects of changes in cigarette dose on cardiovascular risk factors. Of the studies that currently exist, the results show significant improvement on these measures; however, the sample sizes have tended to be small, and no control groups have been used.