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cGMP was measured on purified CD11b+, CD11c+, CD4+, or CD8+ cells using the Cyclic GMP EIA kit (Cayman Chemical). Data analysis was performed with the workbooks available at http://www.caymanchem.com/neptune/servlet/neptune/template/analysis%2CEIA.vm/a/z. Data are expressed as mean ± SE of quadruplicate wells.
Homeopathy for Erectile Dysfunction (ED)
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Most of the localization studies for PDE11 have been for PDE11A mRNA products. The data for protein are less certain as few highly specific antisera have been described. There also is likely to be substantial differences in expression between species. Nevertheless, it is clear that the PDE11A variants demonstrate differential tissue expression. In humans, PDE11A1 mRNA is most prominent in skeletal muscle and prostate (Fawcett et al., 2000; Yuasa et al., 2001a). PDE11A3 mRNA is found specifically in testis and PDE11A4 mRNA is highly expressed in prostate (Yuasa et al., 2000). PDE11A protein localization studies have been somewhat contradictory in their findings, probably because of differences in the specificity of the antibodies used. PDE11A1 protein was originally detected in prostate and skeletal muscle (Fawcett et al., 2000), although a later study did not detect PDE11A1 protein in any tissues (Loughney et al., 2005). In fact, only PDE11A4 protein has been verified and is found in prostate, pituitary, heart, and liver. Another study suggested that PDE11A is widely expressed, and immunohistochemistry using an antibody reported to recognize all PDE11A variants localized it to the epithelial, endothelial, and smooth muscle cells of many tissues, but at highest levels in the prostate, testis, kidney, adrenal gland, colon, and skin (D'Andrea et al., 2005). However, a separate study did not find any PDE11 protein expression in human testis (Loughney et al., 2005). As with many PDEs, it is still not clear if the same tissue, cellular, and subcellular localization is found among species. Future work will hopefully rectify the discrepancies regarding the tissue expression of PDE11A.
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Conclusions— Our study first shows a strong and independent association between ED and silent CAD in apparently uncomplicated type 2 diabetic patients. If our findings are confirmed, ED may become a potential marker to identify diabetic patients to screen for silent CAD. Moreover, the high prevalence of ED among diabetics with silent CAD suggests the need to perform an exercise ECG before starting a treatment for ED, especially in patients with additional cardiovascular risk factors.
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