Abstract. In aerosol chamber experiments optical properties of resuspended mineral dust samples of defined size distributions were measured. Extinction coefficients (b ext ) and mass specific extinction cross sections (σ ext ) were determined for Saharan dust samples from different locations. The results for σ ext were not very sensitive to the type of dust and varied at λ=550 nm between 3.3±0.4 m 2 g −1 and 3.7±0.4 m 2 g −1 .The absorption coefficients (b abs ) and mass specific absorption cross sections (σ abs ) were determined with a novel multiwavelength photo-acoustic absorption spectrometer (PAS). The single scattering albedo was close to 1 (0.98 to 0.99) at 532 nm and 1064 nm, but significantly lower (0.63 to 0.76) at 266 nm. Additionally the chemical and mineralogical composition of the dust samples were analysed with special regard to the iron oxide phases hematite and goethite. At λ=266 nm the mineral dust sample without any detectable iron oxides showed a significantly higher SSA compared to the sample with a hematite content of 0.6 wt-%.
Objective: The aim of the study was to evaluate the expression of tumor necrosis factor (TNF)-a protein in the subcutaneous and visceral adipose tissue in correlation with adipocyte cell volume, serum TNFa, soluble TNF-receptor-2 (sTNFR-2) and indirect parameters of insulin resistance in overweight/obese and lean healthy persons. Design: A cross-sectional case-control study was used. Patients: Twenty-eight overweight/obese probands with normal glucose tolerance (BMI . 27 kg/m 2 ) and 15 lean people (BMI , 25 kg/m 2 ), all of them undergoing planned surgical operation, participated in the study. Methods: Two to four grams of subcutaneous and visceral adipose tissue were removed and studied using semi-quantitative immunohistochemical staining of the TNF-a protein. Serum TNF-a, sTNFR-2 (ELISA) and fasting C-peptide (RIA) were measured. Results: TNF-a protein was expressed in adipocytes of both depots. The expression was evaluated visually and found to be greater in the obese patients. Significantly higher serum TNF-a (5.58^0.87 pg/ml vs 4.21^0.55, mean^S.D., P , 0.01, Mann -Whitney) and sTNFR-2 levels (7.84^3.56 ng/ml vs 4.59^1.35, P ¼ 0.005) were found in the obese subgroup in correlation with the fasting C-peptide level (r ¼ 0.49, P ¼ 0.003; and r ¼ 0.74, P ¼ 0.001) and the C-peptide/ blood glucose ratio (r ¼ 0.47, Spearman, P ¼ 0.005; and r ¼ 0.70, P ¼ 0.001). The cell volume of both adipocyte depots was found to have a significant positive correlation with serum TNF-a and sTNFR-2 levels in the total group of patients (subcutaneous: r ¼ 0.52, P ¼ 0.0003; r ¼ 0.69, P , 0.0001; visceral: r ¼ 0.65, P , 0.0001; r ¼ 0.63, P , 0.0001) and in both subgroups. Conclusions: Adipocyte cell volume of both the subcutaneous and visceral fat depots may be determinants of TNF-a, sTNFR-2 production and obesity-linked insulin resistance.
(1,25-D 3 ), is inhibition of cell growth and induction of cell differentiation and/or apoptosis. Synthesis and degradation of the secosteroid occurs not only in the kidney but also in normal tissue or malignant extrarenal tissues such as the colon. Because 25-hydroxyvitamin D 3 24-hydroxylase (CYP24A1) is considered to be the main enzyme determining the biological half-life of 1,25-D 3 , we have examined expression of the CYP24A1 mRNA (by real-time RT-PCR) and protein (by immunohistochemistry) in normal human colon mucosa, colorectal adenomas, and adenocarcinomas in 111 patients. Although 76% of the normal and benign colonic tissue was either completely devoid of or expressed very low levels of CYP24A1, in the majority of the adenocarcinomas (69%), the enzyme was present at high concentrations. A parallel increased expression of the proliferation marker Ki-67 in the same samples suggests that overexpression of CYP24A1 reduced local 1,25-D 3 availability, decreasing its antiproliferative effect. (J Histochem Cytochem 58:277-285, 2010) COLORECTAL CANCER (CRC) is the second leading cause of malignant mortality in Western industrialized countries (Boyle and Ferlay 2005). Geographical distribution of cancer mortality in the US correlates with exposure to solar (ultraviolet B) radiation; the highest mortality rates for CRC were observed in regions with less solar radiation (Freedman et al. 2002). Furthermore, epidemiological data have shown an inverse association of serum 25-hydroxyvitamin D 3 (25-D 3 ) levels with risk for prostate, breast, and colorectal malignancies (Garland et al. 1989;Ahonen et al. 2000;Bertone-Johnson et al. 2005). Estimating premature cancer mortality in the US, Grant and Garland (2006) implied that actually 20-30% of CRC cases could be avoided by sufficient exposure to sunlight.A recent meta-analysis of 18 cohort and case-control studies showed that an elevation of serum 25-D 3 concentration to levels $33 ng/ml led to a 50% lower incidence of CRC (Gorham et al. 2005). Cumulative epidemiological evidence suggests that there is a direct correlation between reduced CRC incidence and sunlight exposure, nutritional vitamin D intake, and high serum levels of 25-D 3 (Giovannucci et al. 2006).Vitamin D metabolism is a strictly regulated, multistep process, beginning with the formation of previtamin D 3 in the skin, mediated by ultraviolet radiation, or with absorption of vitamin D from dietary sources (Henry 1997;Sawada et al. 2000;Cheng et al. 2003). Vitamin D is hydroxylated by CYP27A1 to 25-hydroxyvitamin D 3 in the liver. The last step of the activation is accomplished by the 25-hydroxyvitamin D 3 1a hydroxylase (CYP27B1) in the kidney. The most active metabolite of vitamin D 3, 1a,25-dyhydroxyvitamin D 3 (1,25-D 3 , also known as calcitriol), has a crucial Correspondence to: Enikö Kállay,
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