Key words: prostate cancer; 25(OH)-vitamin D 3 ; serum bankVitamin D deficiency has been implicated as risk factor for prostate cancer. 1 In cell culture studies, vitamin D metabolites have had protective action against cancer development (for review see Ylikomi et al. 2 ). Normal and malignant prostate cells contain vitamin D receptor (VDR), 3-5 which mediates the antiproliferative action of 1,25(OH) 2 -vitamin D 3 . 6 In addition to the antiproliferative action of 1,25(OH) 2 -vitamin D 3 , it can cause apoptosis, 7 induce differentiation, 8 inhibit telomerase expression, 9 inhibit tumor cell invasiveness 10 and suppress tumor-induced angiogenesis. 11 Several epidemiologic studies have reported that high serum vitamin D levels or sunlight may protect against prostate cancer. 3,4,[12][13][14][15] Factors that affect prostate cancer include age, dark skin and environment, e.g., latitude and diet. 16 These factors might be linked to vitamin D availability. 17,18 Furthermore, high fish (rich in vitamin D) consumption appears to correlate with lower prostate cancer risk. 19 In addition, VDR gene polymorphism may contribute to the risk of prostate cancer. 20 -24 There is also a study showing no correlation between serum vitamin D metabolites and prostate cancer in Maryland (USA), 25 but the authors concluded that the power of their study was limited. In another study on U.S. male physicians, only a weak protection against prostate cancer was found with the highest quartile of serum 1␣,25(OH) 2 -vitamin D 3 . 26 Similarly, no correlation was found in Hawaii. 27 There are 2 physiologically interesting metabolites of vitamin D, 1␣,25(OH) 2 -vitamin D 3 , regulating calcium homeostasis for bones and muscles in extremely narrow limits, and 25(OH)-vitamin D 3 , regulating target (prostate) cell proliferation and differentiation through activation to 1␣,25(OH) 2 -vitamin D 3 in the target (prostate) cell. Serum 25(OH)-vitamin D 3 is produced by liver 25-hydroxylase, the rate of the synthesis being directly proportional to vitamin D 3 serum concentration. 28 Therefore, serum 25(OH)-vitamin D 3 reflects vitamin D availability in the organism. Serum concentration of 25(OH)-vitamin D 3 is so high that it might possess a significant biologic activity in target cells, but it is also a precursor for the biologically more active 1␣,25(OH) 2 -vitamin D 3 . Prostate as well as many other target organs can activate 25(OH)-vitamin D 3 through 1␣-hydroxylation 29,30 and inactivate it through 24-hydroxylation. 31 In an epidemiologic study, we found that low concentrations (Ͻ40 nmol/l) of 25(OH)-vitamin D in serum were associated with a 1.7-fold increased risk of prostate cancer. 3,4 Since the power of our study was limited, preventing extensive analysis of the data, and we are partners in the Nordic Specimen Banks for Cancer Causes and Control, we had an opportunity to extend our study to other Scandinavian countries located geographically at the same latitude. Our aim was to determine whether our finding could be replicated in a la...

Vitamin D emerges as an important neurosteroid hormone in the brain, with a strong potential for age-specific applications in clinical nutrition.

Clinical trials of vitamin D supplementation are needed to investigate whether it enhances immunity to microbial infections.

Grooming is a commonplace, robust behavior in rodent species. It has been shown to be highly sensitive to a number of experimental factors, making it an ideal target for manipulation. The complex patterning of grooming in rodents, which usually proceeds in a cephalo-caudal direction and involves several distinct stages, can be dissected into its constituent parts and microstructures. Several grooming patterning analysis methods are described in the protocol that allow for an assessment of this behavior based on measurements of grooming activity and its sequencing. Additionally, grooming can be evaluated in reference to the regional distribution and syntax in which it occurs. Owing to the ever-increasing number of rodent models that have strong grooming phenotypes, this high-throughput in-depth analysis is becoming crucial for biomedical research.

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A correlation has also been found between low femoral BMD and stress fractures. We measured serum 25(OH)D concentration in a population sample of military recruits to determine if vitamin D is a predisposing factor for fatigue bone stress fracture. Materials and Methods: We prospectively followed 800 randomly selected, healthy Finnish military recruits with a mean age of 19 years for developing stress fractures in homogenous circumstances. Blood for serum 25(OH)D concentration was drawn at entry into military service, and the weight, height, body mass index (BMI), muscle strength, and 12-minute running were measured for all subjects. Serum 25(OH)D concentrations were measured with enzyme immunoassay. At end of the 90-day follow-up, 756 subjects completed the study. Subjects without fracture constituted controls. Results: Twenty-two recruits with stress fracture were identified (2.9%), the incidence being 11.6 (95% CI: 6.8-16.5) per 100 person-years. In the final multivariate analysis, the significant risk factor for stress fracture in conscripts was a below median serum 25(OH)D level (75.8 nM), OR being 3.6 (95% CI: 1.2-11.1). No significant associations between BMI (p ‫ס‬ 0.255), age (p ‫ס‬ 0.216), or smoking (p ‫ס‬ 0.851) and bone stress fracture were found in this study population. Conclusions: A lower level of serum 25(OH)D concentration may be a generally predisposing element for bone stress fractures. Considering the obvious need of additional vitamin D in prevention of stress fractures, the effects of vitamin D fortification of foods and supplementation will be subjects of interest for future research.

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According to the present paradigm, 1alpha,25-dihydroxyvitamin D3 [1alpha,25-(OH)2D3] is a biologically active hormone; whereas 25-hydroxyvitamin D3 (25OHD3) is regarded as a prohormone activated through the action of 25-hydroxyvitamin D3 1alpha-hydroxylase (1alpha-hydroxylase). Although the role of vitamin D3 in the regulation of growth and differentiation of prostatic epithelial cells has been well studied, its action and metabolism in prostatic stroma are still largely unknown. We investigated the effects of 25OHD3 and 1alpha,25-(OH)2D3 on two human stromal primary cultures termed P29SN and P32S. In a cell proliferation assay, 25OHD3 was found at physiological concentrations of 100-250 nM to inhibit the growth of both primary cultures, whereas 1alpha,25-(OH)2D3 at a pharmacological concentration of 10 nM exhibited the growth-inhibitory effects on P29SN cells but not on P32S cells. Quantitative real-time RT-PCR analysis revealed that both 25OHD3 and 1alpha,25-(OH)2D3 induced 25-hydroxyvitamin D3 24-hydroxylase (24-hydroxylase) mRNA in a dose- and time-dependent manner. By inhibiting 1alpha-hydroxylase and/or 24-hydroxylase enzyme activities, the induction of 24-hydroxylase mRNA by 250 nM 25OHD3 was clearly enhanced, suggesting that 1alpha-hydroxylation is not a prerequisite for the hormonal activity of 25OHD3. Altogether our results suggest that 25OHD3 at a high but physiological concentration acts as an active hormone with respect to vitamin D3 responsive gene regulation and suppression of cell proliferation.