Introduction
The presence of erectile dysfunction (ED) could be a warning of vascular disease in different arterial territories.
Aim
The aim of this study was to investigate the association between ED and the presence of atherosclerosis in 2 different vascular beds: carotid and lower limbs.
Methods
A total of 614 volunteers between 45 and 74 years of age (mean age 61.0 years) were randomly selected from the general population. ED was assessed using the International Index of Erectile Function (IIEF-5). Ankle-brachial index (ABI) measurement and carotid atherosclerosis were evaluated by echo-Doppler.
Main Outcome Measures
Mean carotid intima-media thickness (IMT), prevalence of carotid plaques, mean ABI, and prevalence of ABI < 0.9 were the main outcome measures.
Results
ED was present in 373 subjects (59.7%). Mean carotid IMT was significantly higher in men with ED (0.762 ± 0.151 mm vs 0.718 ± 0.114 mm, P < .001). Also the global prevalence of carotid plaques was more frequent in men with ED (63.8% vs 44.8%, P < .001), even after adjusting by age, cardiovascular risk factors, and ongoing treatment (P = .039). Both the IMT and the prevalence of carotid plaques increased significantly with ED severity (P trend .004 and <.001, respectively). There were no significant differences between groups neither in mean ABI nor in the prevalence of subjects with ABI < 0.9. However, there was a trend to a lower ABI and a higher prevalence of ABI < 0.9 with increasing ED severity.
Conclusion
In the general population, the presence of ED identifies subjects with higher atherosclerosis burden in carotid arteries but not in the lower extremities.
Morphine and other opioids have been reported to modulate phagocytosis in the ciliate Tetrahymena. However, the endogenous signaling molecule responsible for these effects remains uncharacterized. In this work we present evidence for the presence of beta-endorphin-like protein(s) in Tetrahymena thermophila. Subcellular extracts and cell-free culture supernatants were fractionated by hydrophobic chromatography on Sep Pack C18 columns and by affinity chromatography on polyclonal anti-beta-endorphin columns. Both preparations exhibited opioid-like effects in two different systems: 1) they inhibited phagocytosis in murine peritoneal macrophages, and 2) they blocked the response to mechanical stimuli in the ciliate Stentor. Both of these effects were reversed by naloxone, consistent with an opioid receptor-mediated mechanism. Chromatographic (HPLC) fractionation of the subcellular extracts resolved a component with beta-endorphin-like immunoreactivity, whose retention time was similar to that of the human beta-endorphin standard. Fractions were also analyzed by immunoblots using a monoclonal antibody that recognizes the N-terminus of human beta-endorphin. This antibody detected two antigenic components (corresponding to Mr 9,000 and Mr 12,000 polypeptides) in subcellular extracts, but only a single antigen (corresponding to a Mr 7,000 polypeptide) in culture supernatants. These results indicate that Tetrahymena produces one or more proteins that share some properties with beta-endorphin and that these may form part of an opioid mechanism that originated early in evolution.
Background: Mounting data suggest that exposure to chronic stress is associated with worse breast cancer outcomes. This study aimed to explore the impact of social environmental adversity (SEA, e.g., child abuse, crime, sexual, and physical violence), depressive symptomatology, and anxiety on immune cell infiltration into the breast tumor microenvironment. Methods: Participants (n = 33) completed a series of surveys assessing depression and anxiety symptoms, adverse childhood events (ACE), and trauma history. Tumor-associated macrophages (CD68+), B cells (CD19+), and T cells (CD3+) were identified by immunohistochemical analyses of formalin-fixed paraffin-embedded tumor samples and quantified. Spearman rank tests were used to explore the relationships between the variables studied. Results: Exposure to SEA was high (ACE = 72%, exposure to crime = 47%, and exposure to physical/sexual assault = 73%) among participants. Moreover, 30% reported a comorbid history of depression and ACE; 39% reported one or more traumatic events, and clinically significant depression symptomatology, while 21% reported trauma history and significant anxiety symptomatology. Increased tumor-infiltrating B cells were significantly correlated with exposure to crime, anxiety symptoms, and exposure to an ACE. The ACE plus anxiety group presented the highest infiltration of B cells, T cells, and macrophages. Conclusion: These findings support a role for SEA, anxiety symptoms, and depression as potential modulators of the immune tumor microenvironment in breast cancer.
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