Advances in molecular biology greatly contributed, in the past decades, to a deeper understanding of the role of gene function in disease development. Environmental as well as nutritional factors are now well acknowledged to interact with the individual genetic background for the development of several diseases, including cancer, cardiovascular disease, and neurodegenerative diseases. The precise mechanisms of such gene-nutrient interactions, however, are not fully elucidated yet. Many micronutrients and vitamins are crucial in regulating mechanisms of DNA metabolism. Indeed, folate has been most extensively investigated for its unique function as mediator for the transfer of one-carbon moieties for nucleotide synthesis/repair and biological methylation. Cell culture, animal, and human studies, clearly demonstrated that folate deficiency induces disruption of DNA synthesis/repair pathways as well as DNA methylation anomalies. Remarkably, a gene-nutrient interaction between folate status and a polymorphism in methylenetetrahydrofolate reductase gene has been reported to modulate genomic DNA methylation. This observation suggests that the interaction between a nutritional status and a mutant genotype may modulate gene expression through DNA methylation, especially when such polymorphism affects a key enzyme in one-carbon metabolism and limits the methyl supply. DNA methylation, both genome-wide and gene-specific, is of particular interest for the study of aging, cancer, and other pathologic conditions, because it affects gene expression without permanent alterations in the DNA sequence such as mutations or allele deletions. Understanding the patterns of DNA methylation through the interaction with nutrients is a critical issue, not only to provide pathophysiological explanations of a disease state, but also to identify individuals at-risk to conduct targeted diet-based interventions.

The objective of the present review is to highlight the relationship between low vitamin B 6 status and CVD through its link with inflammation. While overt vitamin B 6 deficiency is uncommon in clinical practice, increasing evidence suggests that marginal vitamin B 6 deficiency is rather frequent in a consistent proportion of the population and is related to an increased risk of inflammation-related diseases. Ample evidence substantiates the theory of atherosclerosis as an inflammatory disease, and low plasma vitamin B 6 concentrations have been related to increased CVD risk. Several studies have also shown that low vitamin B 6 status is associated with rheumatoid arthritis and chronic inflammatory bowel diseases, both of which hold an underlying chronic inflammatory condition. Furthermore, the inverse association observed between inflammation markers and vitamin B 6 supports the notion that inflammation may represent the common link between low vitamin B 6 status and CVD risk. In addition to the epidemiological evidence, there are a number of cell culture and animal studies that have suggested several possible mechanisms relating impaired vitamin B 6 status with chronic inflammation. A mild vitamin B 6 deficiency characterises, in most cases, a subclinical at-risk condition in inflammatory-linked diseases which should be addressed by an appropriate individually tailored nutritional preventive or therapeutic strategy.

While overt vitamin B6 deficiency is not a frequent finding nowadays in medical practice, evidence suggests that insufficiency of this vitamin is rather widespread in a quite large portion of the population such as the elderly or in not unusual conditions such as that of alcohol addiction. Moreover, a mild deficiency in B6 vitamin is a state that may be associated with an increased risk of cardiovascular disease. Epidemiologic evidence from case control and prospective studies have suggested that low dietary intake or reduced blood concentrations of vitamin B6 is associated with an increased risk of cardiovascular disease, although most recent trials demonstrated the ineffectiveness of vitamin B6 supplementation on the prevention of cardiovascular events recurrence. Due to limited and somewhat inconsistent data together with the ample variety of critical functions in which vitamin B6 is involved in the human body, it is very challenging to attempt at establishing a cause and effect relationship between vitamin B6 and risk of cardiovascular disease as it is to delineate the exact mechanism(s) by which vitamin B6 may modulate such risk. In the present chapter we review the currently available knowledge deriving from both epidemiological and mechanistic studies designed to define potential candidate mechanisms for the association of vitamin B6 impairment and risk of cardiovascular disease development.

PurposeThe aim of this study was to investigate the effect of transurethral resection of the prostate (TURP) on erectile function.Materials and MethodsA total of 108 patients treated with TURP were retrospectively evaluated. All patients were evaluated 1, 3, and 6 months after TURP by use of the International Prostate Symptom Score (IPSS), International Index of Erectile Function (IIEF), peak urinary flow rate (Qmax), and post-void residual urine (PVR).ResultsOne and 3 months after TURP, the erectile function domain score of the IIEF was significantly decreased. However, after 6 months, there was no longer a significant decrease in the erectile function domain score. The change in erectile function was compared with the IPSS score. There was no statistically significant correlation, but patients who had better voiding symptoms after TURP had improved erectile function.ConclusionsOur study showed that there was a significant decrease in erectile function for 3 months after TURP. However, no significant change in erectile function was observed 6 months after TURP.

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Purpose Hybrid imaging techniques can provide functional and anatomical information about sentinel lymph nodes in breast cancer. Our aim in this study was to evaluate which imaging parameters on hybrid sentinel lymphoscintigraphy predicted metastatic involvement of sentinel lymph nodes (SLNs) in patients with breast cancer. Methods Among 56 patients who underwent conventional sentinel lymphoscintigraphy, 45 patients (age, 53.1±9.5 years) underwent hybrid sentinel lymphoscintigraphy using a singlephoton emission computed tomography (SPECT)/computed tomography (CT) gamma camera. On hybrid SPECT/CT images, we compared the shape and size (long-to-short axis [L/S] ratio) of the SLN, and SLN/periareolar injection site (S/P) count ratio between metastatic and non-metastatic SLNs. Metastatic involvement of sentinel lymph nodes was confirmed by pathological biopsy. Results Pathological biopsy revealed that 21 patients (46.7 %) had metastatic SLNs, while 24 (53.3 %) had non-metastatic SLNs. In the 21 patients with metastatic SLNs, the SLN was mostly round (57.1 %) or had an eccentric cortical rim (38.1 %). Of 24 patients with non-metastatic SLNs, 13 patients (54.1 %) had an SLN with a C-shape rim or eccentric cortex. L/S ratio was 2.04 for metastatic SLNs and 2.38 for non-metastatic SLNs. Seven (33 %) patients had T1 primary tumors and 14 (66 %) had T2 primary tumors in the metastatic SLN group. In contrast, 18 (75 %) patients had T1 primary tumors and six (25 %) had T2 tumors in the non-metastatic SLN group. S/P count ratio was significantly lower in the metastatic SLN group than the non-metastatic SLN group for those patients with a T1 primary tumor (p=0.007). Conclusions Hybrid SPECT/CT offers the physiologic data of SPECT together with the anatomic data of CT in a single image. This hybrid imaging improved the anatomic localization of SLNs in breast cancer patients and predicted the metastatic involvement of SLNs in the subgroup of breast cancer patients with T1 primary tumors.

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The functional parameter, especially summed systolic thickening score on QG-SPECT had prognostic values, despite normal perfusion, in predicting cardiac events in diabetic patients, and QG-SPECT provides clinically useful risk stratification in diabetic patients with normal perfusion.