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BackgroundVitamin D deficiency and a high mean platelet volume (MPV) are related to cardiovascular disease. We investigated whether vitamin D deficiency is associated with high MPV.MethodsThis study included 434 patients without chronic disease who were not taking vitamin D or calcium supplements. Vitamin D was measured by chemiluminescent microparticle immunoassay on the Architect-I2000 system (Abbott Diagnostics, USA), and MPV was measured on the Cell-Dyn Ruby analyzer (Abbott Diagnostics). Patients were divided into Groups 1 (138 [men/women, 46/92]), 2 (148 [men/women, 54/94]), and 3 (148 [men/women, 50/98]) according to vitamin D levels of <10 ng/mL, 10-20 ng/mL, and >20 ng/mL, respectively.ResultsThe vitamin D level in Group 1 (7.7±1.9 ng/mL) was lower than that in Group 2 (15.1±1.6 ng/mL, P<0.001) and Group 3 (25.6±6.3 ng/mL, P<0.001). The MPV in Group 3 (7.5±1.0 fL) was lower than that in Group 1 (8.1±1.1 fL, P<0.001) and Group 2 (7.9±1.0 fL, P=0.009). Linear regression analysis showed that low levels of vitamin D (β=-0.109, P=0.019) was independently associated with increased MPV.ConclusionsThere was a strong association between a low vitamin D level and a high MPV; therefore, vitamin D deficiency may be associated with increased MPV.

IntroductionAlthough serum-providing blood tubes with a barrier are still widely used due to their significant advantages, the use of blood tubes with a barrier to provide plasma is becoming widespread. We compared 22 analytes in a BD Vacutainer® Barricor LH Plasma tube for local clinical validation of this new lithium heparin tube with a barrier.Materials and methodsSamples from 44 volunteers were collected in different tubes (Becton Dickinson and Company): Z tube without additive (reference), clot-activator tube with gel (SST), lithium heparin tube without gel (LiH), and lithium heparin tube with barrier (Barricor). Analyte concentrations in different tubes were compared with the reference tube. All tubes were also evaluated according to additional testing (different centrifugation durations, blood-sampling techniques and individual differences).ResultsAspartate aminotransferase (AST), glucose (Glc), potassium (K), lactate dehydrogenase (LD), sodium (Na), and total protein (TP) had a significant bias in Barricor (9.19%, - 3.24%, - 4.88%, 21.60%, - 0.40%, 5.03%, respectively) relative to the reference tube. There was no statistical difference between different centrifugation durations and individual differences for AST, K and LD in LiH and/or Barricor (P > 0.05). There was a significant bias for LD between LiH and Barricor in terms of blood-sampling techniques (21.2% and 12.4%, respectively).ConclusionsRecently, the use of plasma has become prominent due to some of its advantages. In this study, plasma AST, K, LD, Glc and TP levels in Barricor were clinically different in comparison to serum. The results of additional tests showed that higher levels of LD in Barricor did not result from haemolysis, and they might be related to other factors including number of platelets, cellular fragility, or functional environment.

This experiment was designed to investigate the lipid peroxidation and histological effects of chronic fluorosis on first and second generation rat lung tissues. Sixteen, virgin, female Wistar rats were mated with eight males (2:1) for approximately 12 h to obtain first-generation rats. Pregnant rats were divided into two experimental groups (control and fluoride supplemented). The pregnant rats in the fluoride-supplemented group were exposed to 30 mg/L sodium fluoride (NaF) in commercial drinking water containing 0.07 mg/L NaF throughout the gestation and lactation periods. After the lactation period, young animals (first generation; F1) were exposed to the same amount of NaF in drinking water for four months. At the end of the four-month experimental period, nine randomly-chosen male rats (F1) were sacrificed and lung tissues were removed for histopathological and enzymatic lipid peroxidation examination. The second generation rats were obtained from the remaining rats by the same method. They were also treated similarly. At the end of the four-month experimental period, nine randomly-chosen male rats (F2) were sacrificed, and the lungs were removed for histological and lipid peroxidation examination. The rats in the control groups underwent the same procedure without NaF supplementation. It was found that the plasma fluoride and the lung TBARS levels of fluoride supplemented F1 and F2 rats were higher than controls. There were marked histological changes in the lung tissues of fluoride supplemented F1 and F2 rats, as follows: in F1 rats; loss of alveolar architecture, emphysematous areas, descuamation of alveolar epithelium and alveolar congestion were observed. There were thickened interalveolar septae and congestion of alveolar septal vessels. Intraparenchymal thick-walled vessels were also observed. There were markedly perivascular and intraparenchymal focal mononuclear cell infiltrations. In F2 rats, in addition to these changes, there were lipid cell hyperplasia and increased connective tissue mass in the parenchymal areas. It is concluded that chronic fluorosis causes a marked destruction in lung tissues of F1 and F2 rats by causing lipid peroxidation.