Cross-border fertility treatment poses an increasing challenge to obstetricians. National data on its occurrence is urgently needed.”
“In previous experiments elevated but sub-symptomatic applications of Zn (0.1 mM

and 1 mM) caused impairments in growth parameters and photosynthetic performance of Populus x euramericana (Dode) Guinier clone I-214. The aim of this work was to evaluate leaf morphological and anatomical traits in this clone in response to the same Zn concentrations. The results showed that Zn treatments induced variations in leaf dry mass, area, mesophyll thickness, intercellular spaces, stomatal density and size. Stronger modifications, especially concerning stomata characteristics induced by 1 mM Zn, were consistent with physiological impairments while those induced by 0.1 mM Zn suggested a compensatory strategy for maintaining functional integrity.”
“To judiciously use Raoultella planticola Rs-2 JQ-EZ-05 inhibitor and develop its biodegradable and controlled-release formulations, Rs-2 was encapsulated with various combinations of sodium alginate (NaAlg) and starch. Sodium alginate, soluble starch, and CaCl2 showed good biocompatibility with Rs-2 for preparing microcapsules. These microcapsules were spherical in shape and their particle size, embedding

rate, swelling ratio of Rs-2 microcapsules and release numbers of viable Rs-2 cells increased with JPH203 the increasing of starch and NaAlg concentrations. Meanwhile, the biodegradability of the microcapsules constantly increases when the wt% of starch increased, but decreased when the amount of NaAlg increased. In addition, the release mechanism of microcapsules was consistent with that of the Ritger-Peppas model, which involves the Case II diffusion mechanism. In summary, the desired properties of the microcapsules can be modulated by varying the starch and alginate amounts of capsule materials. This click here process has broad application prospects to meet the needs of agricultural production. (C) 2014 Elsevier Ltd. All rights reserved.”
“The discovery of BMS-605339 (35), a tripeptidic inhibitor of the NS3/4A enzyme, is described. This compound incorporates a cyclopropylacylsulfonamide

moiety that was designed to improve the potency of carboxylic acid prototypes through the introduction of favorable nonbonding interactions within the S1′ site of the protease. The identification of 35 was enabled through the optimization and balance of critical properties including potency and pharmacokinetics (PK). This was achieved through modulation of the P2* subsite of the inhibitor which identified the isoquinoline ring system as a key template for improving PK properties with further optimization achieved through functionalization. A methoxy moiety at the C6 position of this isoquinoline ring system proved to be optimal with respect to potency and PK, thus providing the clinical compound 35 which demonstrated antiviral activity in HCV-infected patients.

The ghrelin-induced increase in the force of contractions was blocked when iberiotoxin (10(-7) mol L(-1)) was present in the bath solution.\n\nConclusions: Ghrelin reduces I(K(Ca)) in femoral selleckchem artery myocytes by a mechanism that requires activation of G alpha(i/o)-proteins, phosphatidylinositol phospholipase C, phosphatidylcholine phospholipase C, protein kinase C and IP(3)-induced Ca(2+) release.”
“Hepatocyte spheroids can maintain mature differentiated functions, but collide to form bulkier structures when in extended culture. When

the spheroid diameter exceeds 200 mu m, cells in the inner core experience hypoxia and limited access to nutrients and drugs. Here we report the development of a thin galactosylated cellulosic sponge to culture hepatocytes in multi-well plates as 3D spheroids, and constrain them within a macroporous scaffold network to maintain spheroid size and prevent detachment. The hydrogel-based soft sponge selleck screening library conjugated with galactose provided suitable mechanical and chemical cues to support rapid

formation of hepatocyte spheroids with a mature hepatocyte phenotype. The spheroids tethered in the sponge showed excellent maintenance of 3D cell morphology, cell cell interaction, polarity, metabolic and transporter function and/or expression. For example, cytochrome P450 (CYP1A2, CYP2B2 and CYP3A2) activities were significantly elevated in spheroids exposed to beta-naphthoflavone, phenobarbital, or pregnenolone-16 alpha-carbonitrile, respectively. The

sponge also exhibits minimal drug absorption compared to other commercially available scaffolds. As the cell seeding and culture protocols are similar to various high-throughput 2D cell-based assays, this platform is readily scalable and provides an alternative to current hepatocyte platforms used in drug safety testing applications. (C) 2011 Elsevier Ltd. All rights reserved.”
“Transient receptor potential (TRP) channels are a family of cation channels that play a key role Alvocidib datasheet in ion homeostasis and cell volume regulation. In addition, TRP channels are considered universal integrators of sensory information required for taste, vision, hearing, touch, temperature, and the detection of mechanical force. Seminal investigations exploring the molecular mechanisms of phototransduction in Drosophila have demonstrated that TRP channels operate within macromolecular complexes closely associated with the cytoskeleton. More recent evidence shows that mammalian TRP channels similarly connect to the cytoskeleton to affect cytoskeletal organization and cell adhesion via ion-transport-dependent and independent mechanisms.

5406; P = 0.0077) and ACR (r = 0.4772; P = 0.0284). The cellular accumulation of [C-14] tacrolimus in the peripheral blood mononuclear cells was 2-fold higher www.selleckchem.com/products/jnk-in-8.html in mdr1a/1b-knockout mice than in wild-type mice

(P = 0.0182). These results suggest that MDR1 in blood cells decreases the leukocytic concentration of tacrolimus, and it could be a useful marker to establish an individualized target concentration of tacrolimus to prevent ACR in pediatric patients after liver transplantation.”
“The process of nucleocytoplasmic shuttling is mediated by karyopherins. Dysregulated expression of karyopherins may trigger oncogenesis through aberrant distribution of cargo proteins. Karyopherin subunit alpha-2 (KPNA2) was previously identified as a potential biomarker for nonsmall cell lung cancer by integration of the cancer cell secretome and tissue transcriptome data sets. Knockdown of KPNA2 suppressed the proliferation and migration abilities of lung cancer cells. However, the precise molecular mechanisms underlying KPNA2 activity in cancer remain to be established. In the current study, we applied gene knockdown, subcellular fractionation, and stable isotope labeling by amino acids in cell culture-based quantitative proteomic

DZNeP order strategies to systematically analyze the KPNA2-regulating protein profiles in an adenocarcinoma cell line. Interaction network analysis revealed that several KPNA2-regulating proteins are involved in the cell cycle, DNA metabolic process, cellular component movements and cell migration. Importantly, E2F1 was identified as a potential novel cargo of KPNA2 in the nuclear proteome. The mRNA levels of potential effectors of E2F1 measured using quantitative PCR indicated that E2F1 is one of the “master molecule” responses to KPNA2 knockdown. Immunofluorescence staining and immunoprecipitation assays disclosed co-localization

and association between E2F1 and KPNA2. An in vitro protein binding assay further demonstrated that E2F1 interacts directly with KPNA2. Moreover, knockdown of KPNA2 led to subcellular redistribution of E2F1 in lung cancer see more cells. Our results collectively demonstrate the utility of quantitative proteomic approaches and provide a fundamental platform to further explore the biological roles of KPNA2 in nonsmall cell lung cancer. Molecular & Cellular Proteomics 11: 10.1074/mcp.M111.016592, 1105-1122, 2012.”
“Spinocerebellar ataxia type 7 (SCA7) is an autosomal-dominant neurodegenerative disorder characterized by progressive ataxia and retinal dystrophy. It is caused by a CAG trinucleotide expansion in the ataxin7 gene. Anatomical studies have shown severe cerebellar degeneration and region-specific neocortical atrophy in SCA7 patients. However, the impact of the neurodegeneration on the functional integration of the remaining tissue is still unknown.

Two discs of each material were AG-881 order mounted in individual oral splints and exposed to the oral cavity of 20 participants for 4 h. After this period the microbial adhesion to both materials’ surface was measured by two different approaches, the DAPI staining and the plate count. Statistical analysis was performed using non-parametric tests.\n\nResults. The surface roughness (R(a) parameter) was similar between the two materials and

lower than 0.2 mu m. Mean water and formamide contact angles were significantly higher for Filtek Silorane, which presented significantly lower surface free energy and greater degree of hydrophobicity in comparison to Synergy D6. The bioadhesion potential evaluated by either DAPI staining or plate count did not differ between the two

materials.\n\nSignificance. In contrast to previous in vitro studies, the present in situ study found no statistically significant differences with respect to bacterial adhesion between Filtek Silorane and Synergy D6, despite the differences found CA4P chemical structure for surface free energy and hydrophobicity. (C) 2011 Academy of Dental Materials. Published by Elsevier Ltd. All rights reserved.”
“How epithelial cells form a tubule with defined length and lumen diameter remains a fundamental question in cell and developmental biology. Loss of control of tubule lumen size in multiple organs including the kidney, liver and pancreas features selleck polycystic kidney disease (PKD). To gain insights into autosomal dominant polycystic kidney disease, we performed yeast two-hybrid screens using the

C-terminus of polycystin-1 (PC1) as bait. Here, we report that PC1 interacts with Pacsin 2, a cytoplasmic phosphoprotein that has been implicated in cytoskeletal organization, vesicle trafficking and more recently in cell intercalation during gastrulation. PC1 binds to a 107-residue fragment containing the 3 helix of the F-BAR domain of Pacsin 2 via a coiled-coil domain in its C-tail. PC1 and Pacsin 2 co-localize on the lamellipodia of migrating kidney epithelial cells. PC1 and Pacsin 2-deficient kidney epithelial cells migrate at a slower speed with reduced directional persistency. We further demonstrate that PC1, Pacsin 2 and N-Wasp are in the same protein complex, and both PC1 and Pacsin 2 are required for N-Wasp/Arp2/3-dependent actin remodeling. We propose that PC1 modulates actin cytoskeleton rearrangements and directional cell migration through the Pacsin 2/N-Wasp/Arp2/3 complex, which consequently contributes to the establishment and maintenance of the sophisticated tubular architecture. Disruption of this complex contributes to cyst formation in PKD.”
“The hepatitis E virus (HEV) was first identified in 1990, although hepatitis E-like diseases in humans have been recorded for a long time dating back to the 18th century.

\n\nRESULTS. Eighty-nine of 94 patients underwent one percutaneous drainage procedure and 5 of 94 patients underwent two drainages for a total of 99 drainages

in 94 patients (one drainage [n = 89] and two drainages [n = 5]). There were 62 men and 32 women with a mean age of 58.5 years (age range [+/- SD], 22.3-88.0 +/- 16 years). The abscess diameters ranged from 1.8 to 13 cm (mean, 5.3 +/- 2.5 cm), volume aspirated ranged from 0 to 200 mL (mean, 45 +/- 44 mL), and mean duration of drainage was 16.2 days (range, 2-110 +/- 18.7 days). The iliopsoas muscle was the most common site of drainage, accounting for 87.8% of the total. Catheter insertion was possible in all patients, with the muscular component successfully drained in 82% (81/99) overall: 85% (46/54) of those with muscle involvement alone and 77% https://www.selleckchem.com/products/mi-503.html (35/45) of those with musculoskeletal collections. Catheter drainage and antibiotic administration resulted in 65.6% (65/99) not requiring any surgical intervention and resolution of abnormal white cell count or fevers in 98.8% (79/80) of those with abnormal parameters before treatment. Skeletal infection was associated with increased risk of drainage failure (p = 0.0001).\n\nCONCLUSION. Percutaneous imaging-guided musculoskeletal drainage is clinically useful, safe, and effective for draining complex musculoskeletal

collections. It is highly effective for draining collections LXH254 ic50 https://www.selleckchem.com/products/gm6001.html involving muscle alone; however, skeletal infection is associated with a higher risk of drain failure.”
“Objectives This review discusses the limitations and applications of the everted gut sac model in studying drug absorption, metabolism, and interaction.\n\nKey findings The mechanism of drug absorption,

interaction and the effect of factors such as age, sex, species, chronic therapy, and disease state on drug absorption have been summarized. The experimental conditions and their effects on the outcomes of trials have been discussed also.\n\nSummary The everted sac model is an efficient tool for studying in-vitro drug absorption mechanisms, intestinal metabolism of drugs, role of transporter in drug absorption, and for investigating the role of intestinal enzymes during drug transport through the intestine.”
“The rapid growth of infant brains places an exceptionally high demand on the supply of nutrients from the diet, particularly for preterm infants. Sialic acid (Sia) is an essential component of brain gangliosides and the polysialic acid (polySia) chains that modify neural cell adhesion molecules (INCAM). Sia levels are high in human breast milk, predominately as N-acetylneuraminic acid (Neu5Ac). In contrast, infant formulas contain a low level of Sia consisting of both Neu5Ac and N-glycolylneuraminic acid (Neu5Gc). Neu5Gc is implicated in some human inflammatory diseases.

“
“Local calcium (Ca2+) changes regulate central nervous system metabolism and CCI-779 chemical structure communication integrated by subcellular processes including mitochondrial Ca2+ uptake. Mitochondria take up Ca2+ through the calcium uniporter (mCU) aided by cytoplasmic microdomains of high Ca2+. Known only in vitro,

the in vivo impact of mCU activity may reveal Ca2+-mediated roles of mitochondria in brain signaling and metabolism. From in vitro studies of mitochondrial Ca2+ sequestration and cycling in various cell types of the central nervous system, we evaluated ranges of spontaneous and activity-induced Ca2+ distributions in multiple subcellular compartments in vivo. We hypothesized that inhibiting (or enhancing) mCU activity would attenuate (or augment) cortical neuronal activity as well as activity-induced hemodynamic responses in an overall cytoplasmic and mitochondrial Ca2+-dependent manner. Spontaneous and sensory-evoked

P505-15 solubility dmso cortical activities were measured by extracellular electrophysiology complemented with dynamic mapping of blood oxygen level dependence and cerebral blood flow. Calcium uniporter activity was inhibited and enhanced pharmacologically, and its impact on the multimodal measures were analyzed in an integrated manner. Ru360, an mCU inhibitor, reduced all stimulus-evoked responses, whereas Kaempferol, an mCU enhancer, augmented all evoked responses. Collectively, the results confirm aforementioned hypotheses and support the Ca2+ uptake-mediated integrative role of in vivo mitochondria on neocortical activity.”
“Background: The mechanisms of endothelial dysfunction induced by hemodialysis are unclear. To gain a mechanistic view we have evaluated some of the biochemical markers which directly or indirectly lead to SHP099 endothelial dysfunction during a single dialysis session.\n\nMethods: Time course changes in plasma nitrate levels, arginine (ARG), citrulline, asymmetric dimethylarginine (ADMA), homocysteine (Hcy), malondialdehyde (MDA) and lipoprotein-associated phospholipase

A2 (LpPLA2) were evaluated in 27 patients with end-stage renal disease on maintenance hemodialysis. Statistical evaluation of changes was done using analysis of variance for repeated measures and linear regression using generalized estimating equations for repeated measures.\n\nResults: Nitrate levels significantly increased as a result of dialysis (p<0.001). Hcy (p<0.05) and ADMA (p<0.001) levels were found to be significantly decreased. ARG/ADMA ratio showed an increase (p<0.001). Presence of oxidative stress (OS) was observed in the form of increased plasma MDA levels. Nitrate levels were negatively associated with Hcy, ADMA and LpPLA2 activity.\n\nConclusion: Our results show an increased production of nitric oxide (NO) during dialysis, which however is affected by increased OS ultimately favoring endothelial dysfunction.

Once more, it is shown that drug challenges should be performed at home and prolonged in children reporting non-immediate reactions, at the risk of underdiagnosing drug hypersensitivity. Finally, hymenoptera venom immunotherapy is efficient in children, and its efficacity persists during 7-8 years at least. (C) 2014 Elsevier Masson

SAS. All rights reserved.”
“The roles of hypoxia-induced and stem cell-associated genes in the development of malignancy and tumour progression are well known. However, PF-03084014 purchase there are a limited number of studies analysing the impact of mRNA expression levels of hypoxia-induced and stem cell-associated genes in the tissues of brain tumours and glioblastoma patients. In this study, tumour tissues from patients with glioblastoma multiforme and tumour adjacent tissues were

analysed. We investigated mRNA expression levels of hypoxia-inducible factor-la (HIF-1 alpha), hypoxia-inducible factor-2 alpha (HIF-2 alpha), carbonic anhydrase 9 (CA9), Bafilomycin A1 supplier vascular endothelial growth factor (VEGF), glucose transporter-1 (GLUT-1) and osteopontin (OPN), and stem cell-associated genes survivin, epidermal growth factor receptor (EGFR), human telomerase reverse transcriptase (hTERT), Nanog and octamer binding transcription factor 4 (OCT4) using quantitative real-time polymerase chain reaction (qRT-PCR). Our data revealed higher mRNA expression levels of hypoxia-induced and stem cell-associated genes in tumour tissue than levels in the tumour adjacent tissues in patients with glioblastoma multiforme. A strong

positive correlation between the mRNA expression levels of HIF-2 alpha, CA9, VEGF, GLUT-1 and OPN suggests a specific hypoxia-associated profile of mRNA expression in glioblastoma multiforme. Additionally, the results indicate the role of stem-cell-related genes in tumour hypoxia. Kaplan-Maier analysis revealed that high mRNA expression levels of hypoxia-induced markers showed a trend towards shorter overall survival in glioblastoma patients (P=0.061). Our data suggest that selleck kinase inhibitor mRNA expression levels of hypoxia-induced genes are important tumour markers in patients with glioblastoma multiforme.”
“All three classes of serine beta-lactamases are inhibited at micromolar levels by 1: 1 complexes of catechols with vanadate. Vanadate reacts with catechols at submillimolar concentrations in aqueous buffer at neutral pH in several steps, initially forming 1:1, 1:2, and, possibly, 1:3 complexes. Formation of these complexes is followed by the slower reduction of vanadate (V-v) to vanadyl (V-IV) and oxidation of the catechol. Vanadyl-catechol complexes, however, do not inhibit the beta-lactamases. Rate and equilibrium constants of formation of the 1:1 and 1:2 complexes of vanadate with catechol itself and with 2,3-dihydroxynaphthalene were measured by stopped-flow spectrophotometry.

As the type of anchorage of adhesion ligands to materials surfaces is known to determine the mechanical balance of adherent cells, we investigated herein the behaviour of endothelial cells under physiological shear stress conditions. The adhesion ligand fibronectin was anchored to polymer surfaces of four physicochemical characteristics exhibiting covalent and non-covalent attachment as well as high and low hydrophobicity. The in situ analysis combined with cell tracking of shear stress-induced effects on cultured isolated cells and monolayers under venous (0.5 dyn/cm(2)) and arterial LY2606368 mw (12 dyn/cm(2)) shear stress over a time period of 24 h revealed distinct differences in their morphological and migratory

features. Most pronounced, unidirectional and bimodal migration

patterns of endothelial cells in or against flow direction were found in dependence on the type of substrate-matrix anchorage. Combined by an immunofluorescent analysis of the actin cytoskeleton, cell-cell junctions, cell-matrix adhesions, and matrix reorganization these results revealed a distinct balance of laminar shear stress, cell-cell contacts and substrate-matrix anchorage in affecting endothelial cell fate under flow conditions. This analysis underlines the importance of materials surface parameters as well as primary and secondary adhesion ligand anchorage in the GW4869 context of artificial blood Caspase pathway vessels for future therapeutic devices. (C) 2011 Elsevier Ltd. All rights reserved.”
“Although axonal regeneration after CNS injury is limited, partial injury is frequently accompanied by extensive functional recovery. To investigate mechanisms

underlying spontaneous recovery after incomplete spinal cord injury, we administered C7 spinal cord hemisections to adult rhesus monkeys and analyzed behavioral, electrophysiological and anatomical adaptations. We found marked spontaneous plasticity of corticospinal projections, with reconstitution of fully 60% of pre-lesion axon density arising from sprouting of spinal cord midline-crossing axons. This extensive anatomical recovery was associated with improvement in coordinated muscle recruitment, hand function and locomotion. These findings identify what may be the most extensive natural recovery of mammalian axonal projections after nervous system injury observed to date, highlighting an important role for primate models in translational disease research.”
“B23 (NPM/nucleophosmin) is a multifunctional nucleolar protein and a member of the nucleoplasmin superfamily of acidic histone chaperones. B23 is essential for normal embryonic development and plays an important role in genomic stability, ribosome biogenesis, and anti-apoptotic signaling. Altered protein expression or genomic mutation of B23 is encountered in many different forms of cancer. Although described as multifunctional, a genuine molecular function of B23 is not fully understood.

Patients with NSCLC had a significantly higher frequency of IL-22 rs2227484 CT genotype (odds ratio [OR] = 1.917, 95% confidence interval [CI] 1.001-3.670, EVP4593 in vitro p = 0.038) and T allele (OR = 1.878, 95% CI 1.010-3.491, p = 0.049) as compared with controls. The rs2227484 genotype was associated with a 2.263-fold increased risk for advanced NSCLC (p = 0.041). Among different subtypes of NSCLC, these associations were more obvious in the adenocarcinoma. Moreover, patients with high

frequencies of genotypic polymorphisms had high plasma levels of IL-22. IL-22 polymorphisms and corresponding high levels of IL-22 in plasma may contribute to the development of NSCLC, especially adenocarcinoma.”
“The bioactivities of two novel compounds (TAE-1 and TAE-2) that contain a sym-triazine scaffold with acetylcholine-like substitutions are examined as promising

candidate agents against Alzheimer’s disease. Inhibition of amyloid-beta fibril formation in the presence of A beta(1-42), evaluated by Thioflavin T fluorescence, demonstrated comparable or improved activity to a previously reported pentapeptide-based fibrillogenesis inhibitor, iA beta 5p. Destabilization of A beta(1-42) assemblies by TAE-1 and TAE-2 was confirmed by scanning electron microscopy imaging. sym-Triazine inhibition of acetylcholinesterase (AChE) activity was observed in cytosol extracted from differentiated human SH-SY5Y neuronal cells and also using human erythrocyte AChE. The sym-triazine derivatives were well tolerated by these PR-171 Proteases inhibitor cells and promoted beneficial effects on human neurons, upregulating expression of synaptophysin, a synaptic marker protein, and MAP2, a neuronal differentiation marker.”
“For many subjectively experienced outcomes, such as pain and depression, rather large placebo effects have been reported. However, there is increasing evidence that placebo interventions also affect end-organ functions regulated by the autonomic nervous system (ANS). After discussing three psychological find more models for autonomic

placebo effects, this article provides an anatomical framework of the autonomic system and then critically reviews the relevant placebo studies in the field, thereby focusing on gastrointestinal, cardiovascular and pulmonary functions. The findings indicate that several autonomic organ functions can indeed be altered by verbal suggestions delivered during placebo and nocebo interventions. In addition, three experimental studies provide evidence for organ-specific effects, in agreement with the current knowledge on the central control of the ANS. It is suggested that the placebo effects on autonomic organ functions are best explained by the model of ‘implicit affordance’, which assumes that placebo effects are dependent on ‘lived experience’ rather than on the conscious representation of expected outcomes.

Mild to moderate asymptomatic hyperglycemia is observed with figitumumab therapy, but it is generally manageable and well tolerated. Because of its extended half-life and absence of dose-limiting toxicity and hypersensitivity, figitumumab compares well to other compounds in its class. Furthermore,

recent data suggest that figitumumab might be active in combination with platinum doublets for the treatment of chemotherapy-naive non-small-cell lung cancer (NSCLC). This article discusses the results to date of the figitumumab development program and the rationale for further testing of this agent as a therapeutic Rapamycin molecular weight option for the treatment of patients with NSCLC.”
“Recent studies have implicated glial cells in modulation of synaptic transmission, so it is plausible that glial cells may have a functional role in the hyperexcitability characteristic of epilepsy. Indeed, alterations in distinct

astrocyte membrane channels, receptors, and transporters have all been associated with the epileptic state. This review focuses on the potential roles of the glial water channel aquaporin-4 (AQP4) in modulation of brain excitability and in epilepsy. We will review studies of mice lacking AQP4 (Aqp4-/- mice) or a-syntrophin (an AQP4 anchoring protein) and discuss the available human studies demonstrating alterations of AQP4 in human epilepsy tissue specimens. We will conclude with new studies of AQP4 regulation and discuss the potential role of AQP4 in the development of epilepsy (epileptogenesis). While many questions remain unanswered, click here the available data indicate that AQP4 and its molecular partners may represent important new therapeutic targets. (c) 2012 Wiley Periodicals, Inc.”
“Objective. Altered calcium homeostasis has been linked to increased intima-media thickness (IMT) and plaques. We aimed to investigate whether serum 25-hydroxyvitamin

D (25(OH) D) and serum calcium are associated with IMT and plaques in nonsmoking population. Methods. Ultrasound of the right carotid artery with the measurements of IMT and plaques was performed Linsitinib in 4194 nonsmoking subjects with available measurements of serum 25(OH) D and total calcium. Linear regression was applied to study the linear relationships between variables. Multinomial logistic regression was used to evaluate predictors of increased IMT and total plaque area (TPA), adjusted for age, body mass index, systolic blood pressure, and total cholesterol. Results. There was no significant linear relationship between mean IMT, TPA, and either serum 25(OH) D or total serum calcium. One SD increase in serum 25(OH) D was independently associated with increased odds of being in the highest quartile of IMT in men (OR 1.30, 95% CI 1.12, 1.51). In women, 1 SD increase in serum 25(OH) D was independently associated with increased risk of being in the upper tertile of TPA (OR 1.