Ethnicity and social deprivation contribute to vitamin D deficiency in an urban UK population.

We receive a large number of 25 hydroxyvitamin D (25OHD) assay requests from General Medical Practitioners (GPs) in primary care. We have investigated whether this rate of requesting is related to the ethnicity of the local urban population based in Central Manchester or Trafford areas with very different ethnic populations. Data on assay requesting was collected from January-December 2013. Samples were assayed using an ABSciex 5500 tandem mass spectrophotometer and the Chromsystems 25OHD kit for LC-MS/MS. 11,291 requests for 25OHD measurement received from Central Manchester GPs and 5176 requests from Trafford GPs. Overall 29% of patients were profoundly deficient (<25nmol/L) and a further 32% were insufficient (25-50nmol/L). Using the 2011 Census data we have analysed our data by ethnicity (categorized here as white, Asian, black, Chinese, other) based on patient's home postcode and related this to the Index of Multiple Deprivation (IMD). In areas where >70% of the population were non-white (NW), 69% had 25OHD <50nmol/L. Areas where <5% of patients were NW, 42% of patients were still insufficient. There was a significant correlation between the Index of Social Deprivation (IMD) and the percentage of patients with 25OHD <50nmol/L (p<0.0001). Areas with the highest Index of Social Deprivation (IMD ranking <16,000) showed no association between ethnicity and IMD (p=0.69). We have shown that over 61% of all patients in these urban areas of Manchester and Trafford showed increased risk of bone, and potentially other diseases, based on their 25OHD assay results alone and that social deprivation, as well as ethnicity, contribute to the poor 25OHD levels seen in these patients.

Angiogenic characteristics of circulating and tumoural thrombospondin-1 in breast cancer.

In cancer models, thrombospondin-1 (TSP-1) has been shown to inhibit angiogenesis or promote metastasis by increasing adhesion of malignant cells to endothelium. To determine the role of TSP-1 in breast cancer and breast cancer angiogenesis, we have measured TSP-1 in plasma and tumour cytosols and compared levels to established clinicopathological prognostic parameters and intratumoural microvessel density. TSP-1 was measured, by radioimmunoassay, in plasma (pTSP-1) and tumour cytosols (cTSP-1) of women with early breast cancer (EBC) (n=71). pTSP-1 in EBC was compared to pTSP-1 levels in women with advanced breast cancer (ABC) (n=66), normal controls (n=77) and was correlated with prognostic features and microvessel density (MVD) (measured by CD31 immunostaining). cTSP-1 levels were compared to prognostic features and microvessel density. pTSP-1 in women with EBC (median 484, IQR 344-877 ng/ml) and ABC (median 588, IQR 430-952 ng/ml) were elevated when compared to normal controls (median 21, IQR 175-247) (p<0.001). Women with lymph node metastases (n=35) had higher levels of TSP-1 (median 799 ng/ml, IQR 455-943) than women who were node negative (median 343 ng/ml, IQR 267-514) (n=36) (p<0.05). Levels of pTSP-1 in EBC correlated with MVD (R=0.39, p<0.05). Levels of TSP-1 in tumour cytosols of women with EBC (median 1714, IQR 893-5283 ng/ml) correlated with microvessel density (R=0.46, p<0.01). Circulating levels of TSP-1 appear to be a marker of breast cancer aggressiveness and in breast cancer may have a pro-angiogenic rather than anti-angiogenic role.

Power frequency magnetic field exposure and gap junctional communication in Clone 9 cells.

Exposure to a power-frequency magnetic field has been reported to produce a statistically significant inhibition of gap junctional communication (GJC) in Clone 9 cells that have been pre-stressed by treatment with low concentrations of chloral hydrate (CH) [C.F. Blackman, J.P. Blanchard, S.G. Benane, D.E. House, J.A. Elder, Double blind test of magnetic field effects on neurite outgrowth, Bioelectromagnetics, 19 (1998) 204-209]. This observation might provide mechanistic insight into the possible role of electromagnetic fields (EMFs) in the carcinogenic process, since cancer cells frequently show decreased or absent GJC, and tumor promoting chemicals have been observed to inhibit GJC. Magnetic field exposure conditions were 45 Hz, 23.8 microT rms + parallel DC 36.6 microT, for 30 min of exposure. The responses of Clone 9 cells to the GJC-inhibiting effects of the tumor promoter 12-O-tetradecanoylphorbol 13-acetate and the chemical CH were evaluated and compared to reported results [S.G. Benane, C.F. Blackman, D.E. House, Effects of perchloroethylene and its metabolites on intercellular communication in Clone 9 rat liver cells, J. Toxicol. Environ. Health, 48 (1996) 427-437]. Before magnetic field exposure, cells were exposed for 24 h to either 3 (nine experiments) or 5 mM (11 experiments) CH to produce GJC of 67% or 50%, respectively, relative to unexposed controls. GJC was assessed microscopically using the scrape-loading technique and a blinded protocol. No statistically significant effect was observed due to magnetic field exposure with either CH concentration.